Endocrinologist - Thyroid - Thyrax - TSH - Candesartan

Endocrinologist Terapi Pengganti (Thyrax) TSH Level Candesartan
Terapi Pengganti (Replacement Therapy) Sesudah Pengangkatan

Kelenjar Tiroid
1. Sumber: http://mediasehat.com/tanyajawab3482
Thyrax adalah obat yang berisi levothyroxin, yaitu hormon sintetik untuk tiroksin
(salah satu hormon tiroid). Levothyroxin diberikan untuk kondisi-kondisi dimana
seseorang tidak mampu memproduksi hormon tiroid pada jumlah yang cukup,
misalnya pada penderita hipotiroid, atau dalam kasus Bapak, karena mengalami
pengangkatan kelenjar tiroid. Levothyroxin juga diberikan untuk mereka yang
mengalami penyakit gondok (pembesaran kelenjar tiroid) akibat kekurangan iodium.
Dosis obat sebaiknya tidak Anda stop atau dikurangi, atau dilebihkan, di luar anjuran
dokter. Hal ini karena bisa menyebabkan Anda menderita hipotiroid (kekurangan
hormon tiroid) atau malah hipertiroid (kelebihan hormon tiroid). Kedua kondisi
tersebut akan berakibat buruk pada kesehatan Bapak (untuk kondisi tersebut bisa
di-search di mediasehat tentang hipotiroid dan hipertiroid). Namun jika Anda
mengalami gejala-gejala hipertiroid, sebaiknya diskusikan kembali dengan dokter
Anda untuk kemungkinan meninjau kembali dosisnya. Jangan pernah mengambil
kesimpulan sendiri untuk menambah ataupun mengurangi karena yang Anda
konsumsi adalah hormon, dan dampak lebih/kurang akan berakibat langsung pada
fungsi tubuh Anda.
Selama Anda berada dalam jalur yang benar, artinya mengkonsumsi obat dalam
jumlah yang tepat, justru Anda akan baik-baik saja. Karena Thyrax fungsinya bukan
mengobati, tapi melengkapi apa yg kurang. Secara medis disebut sebagai terapi
pengganti (replacement therapy). Pengangkatan kelenjar tiroid menyebabkan tubuh
Anda kehilangan 'pabrik' hormon tiroid, dan fungsi Thyrax adalah untuk melengkapi
apa yang hilang dari tubuh Anda. Jadi fungsinya lebih untuk menjaga agar semua
aktivitas yang terjadi pada tubuh Anda berjalan normal, atau setidaknya diusahakan
agar tetap berjalan normal. Efek samping akan muncul justru jika Anda tidak
mengkonsumsi secara benar.
2. Sumber: http://www.kerjanya.net/faq/8035-thyrax.html
Thyrax tersedia dalam bentuk tablet dengan isi sebesar 100 mcg. Dosis dewasa dan
anak di atas 12 tahun adalah sebesar 150 200 mcg per hari. Sedangkan anakanak usia 6-12 tahun 100-150 mcg, 1-5 tahun 75-100 mcg, 6-12 bulan 50-75 mcg,
<6 bulan 25-50 mcg. Biasanya obat harus diberikan secara terus menerus seumur
hidup.
Dosis obat tidak boleh dikurangi atau ditambahkan sendiri di luar anjuran dokter.
Kekurangan atau kelebihan dosis dapat menyebabkan gangguan pada tubuh
penderita. Selain itu, untuk mencegah terjadinya ketidakcocokan dosis, maka

penderita harus memeriksakan diri ke dokter untuk menyesuaikan dosisnya. Agar
efektif, thyrax harus diberikan dalam keadaan perut kosong atau sekitar setengah
jam sebelum makan. Perlu diketahui juga, beberapa jenis obat juga dapat
mengganggu penyerapan thyrax antara lain kalsium, zat besi, atau obat maag.
3. Sumber: http://www.medicinenet.com/thyroid_replacement-oral/page2.htm
Pharmacy Author: Eni Williams, PharmD, PhD

Medical and Pharmacy Editor: Jay W. Marks, MD
What are the side effects of thyroid replacement hormones?
Thyroid replacement hormones usually are well tolerated. Symptoms that occur
during treatment are often due to toxic, elevated levels of thyroid hormones and
resulting symptoms from hyperthyroidism. Symptoms may include chest pain,
increased heart rate or pulse rate, excessive sweating, heat intolerance,
nervousness, headache, insomnia, diarrhea, vomiting, weight loss, and fever. Some
women may experience irregular menstrual cycles.
What are some examples of thyroid replacement hormones?

The following is a list of the thyroid replacement hormones that are available in the
United States:
levothyroxine sodium (Levothroid, Levoxyl, Synthroid, Tirosint, Unithroid)
liothyronine sodium (Cytomel, Triostat)
liotrix (Thyrolar)
For what conditions are thyroid replacement hormones used?

Thyroid replacement hormones are used to treat hypothyroidism (low production of
thyroid hormone) and myxedema, a condition that is caused by prolonged
hypothyroidism. Thyroid replacement hormones prevent thyroid hormone release
from cancerous thyroid nodules and are used therefore to treat thyroid cancers.
They also are used to manage thyrotoxicosis, a condition in which there are high
levels of thyroid hormones resulting from over-active thyroid glands and too much
thyroid hormone. Thyrotoxicosis may progress to hypothyroidism or cause the
growth of goiters necessitating the use of thyroid replacement hormones.
Are there any differences among the different types of thyroid replacement
hormones?
There is conflicting evidence regarding which hormone replacement therapy should

be preferred. The American Association of Clinical Endocrinologists recommends
that clinical hypothyroidism is best treated with synthetic T4 levothyroxine (for
example levothyroxine and sodium [Synthroid, Levoxyl and Levothroid]). There is
variability between the absorption and distribution of generic T4 compared to brand
name preparations. Hence it is recommended that patients remain with specific
brand names during treatment. There is also variability between generic formulations
and brand names of pure T3 (liothyronine [Cytomel, Triostat]), combined T4/T3
formulations (liotrix [Thyrolar]) and thyroid extracts from animal sources (Armour
Thyroid, Nature-Throid etc.). Thyroid extracts from animal sources are no longer
available in the United States. Emerging information shows that combination of
T4/T3 therapy may have some advantages over T4 in cognitive performance and
mood but studies are not conclusive.
With which drugs do thyroid replacement hormones interact?

Thyroid replacement hormones should be used cautiously in people with diabetes
since starting or discontinuing therapy may lead to a loss of control of the blood
sugar requiring adjustments in doses of insulin or oral antidiabetic drugs (for
example, glyburide [Micronase]). The effects of blood thinners such as warfarin
(Coumadin) may be increased by thyroid replacement hormones warranting a
decrease in the dose of warfarin in addition to monitoring of blood clotting.
Intravenous epinephrine administration in patients with coronary artery disease who
are taking thyroid replacement hormones may increase the risk of complications
such as difficulty in breathing and possibly heart attacks. The effectiveness of some
beta blockers [for example, metoprolol (Lopressor) orpropranolol (Inderal)] may be
reduced when a patient is converted from a state of hypothyroidism (under activity)
to a normal state (euthyroid state). It also may be necessary to modify the dose of
digoxin (Lanoxin) and theophylline (Slo-Bid) when a patient is converted from
hypothyroidism (under activity) to a normal state (euthyroid state). There is
increased elimination of theophylline in a euthyroid state compared to a state of
hypothyroidism.
The effectiveness of thyroid replacement hormones may be decreased when given
with drugs such as calcium carbonate, ferrous sulphate, cholestyramine (Questran)
and colestipol (Colestid) that binds thyroid replacement hormones and prevent their
absorption. This interaction may be reduced by separating the administration of
these drugs from thyroid replacement hormones by four hours.
4. Sumber: http://www.thyroid.org/thyroid-hormone-treatment/
THYROID HORMONE REPLACEMENT THERAPY
Many people have a thyroid gland that cannot make enough thyroid hormone for the
bodys needs. This is called Hypothyroidism and may be caused by a nonfunctioning thyroid gland (for example Hashimotos disease), by destruction of
thyroid gland by surgery or radiation treatment or by a non-functioning pituitary gland
(see Hypothyroidism Brochure). Hypothyroidism, is the most common reason for
needing thyroid hormone replacement.
The goal of thyroid hormone treatment is to closely replicate normal thyroid
functioning. Pure, synthetic thyroxine (T4) works in the same way as a patients own
thyroid hormone would. Thyroid hormone is necessary for the health of all the cells
in the body. Therefore, taking thyroid hormone is different from taking other
medications, because its job is to replace a hormone that is missing. The only safety
concerns about taking thyroid hormone are taking too much or too little. Your thyroid
function will be monitored by your physician to make sure this does not happen.
When thyroid hormone is used to treat hypothyroidism, the goal of treatment is to
keep thyroid function within the same range as people without thyroid problems.
Keeping the TSH level in the normal range does this. The best time to take thyroid
hormone is probably first thing in the morning on an empty stomach. This is because
food in the stomach can affect the absorption of thyroid hormone. However, the most
important thing is to be consistent, and take your thyroid hormone at the same time,
and in the same way, every day. If you are taking several other medications, you
should discuss the timing of your thyroid hormone dose with your physician.
Do not stop your thyroid hormone without discussing this with your physician. Most
thyroid problems are permanent, and therefore most patients require thyroid
hormone for life. If you miss a dose of thyroid hormone, it is usually best to take the
missed dose as soon as you remember. It is also safe to take two pills the next day;
one in the morning and one in the evening. It is very important that your thyroid
hormone and TSH levels are checked periodically, even if you are feeling fine, so
that your dose of thyroid hormone can be adjusted if needed.
Warning Too Much Thyroid Hormone

Increases Bone Fractures In The Elderly
References:
Singer PA, Cooper DS, Levy EG, Ladenson PW, Braverman LE, Daniels G,
Greenspan FS, McDougall IR, Nikolai TF 1995 Treatment guidelines for patients
with hyperthyroidism and hypothyroidism. Standards of Care Committee, American
Thyroid Association. J A M A 273:808-812
Canaris GJ, Manowitz NR, Mayor G, Ridgway EC 2000 The Colorado thyroid
disease prevalence study. Arch Int Med 160:526-534
Sheppard MC, Holder R, Franklyn JA 2002 Levothyroxine treatment and occurrence

of fracture of the hip. Arch Int Med 162:338-343
Bauer DC, Ettinger B, Nevitt MC, Stone KL 2001 Risk for fracture in women with
low serum levels of thyroid-stimulating hormone. Ann Int Med 134:561-568
Murphy E, Williams GR 2004 The thyroid and the skeleton. Clinical Endocrinology
61:285-298
Imam A, Iqbal J, Blair HC, Davies TF, Huang CL, Zallone A, Zaidi M, Sun L 2009
Role of the pituitary-bone axis in skeletal pathophysiology. Curr Op Endocrinol Diab
16:423-429
Flynn RW, Bonellie SR, Jung RT, MacDonald TM, Morris AD, Leese GP 2010
Serum thyroid-stimulating hormone concentration and morbidity from cardiovascular
disease and fractures in patients on long-term thyroxine therapy. J Clin Endocrinol
Metab 95:186-193
Turner MR, Camacho X, Fischer HD, Austin PC, Anderson GM, Rochon PA,
Lipscombe LL 2011 Levothyroxine dose and risk of fractures in older adults: nested
case-control study. BMJ 342:d2238
Syed FA, Ng AC 2010 The pathophysiology of the aging skeleton. Curr Osteoporos
Rep
Kabadi UM 1997 Influence of age on optimal daily levothyroxine dosage in patients
with primary hypothyroidism grouped according to etiology. Southern Medical
Journal 90:920-924
Sawin CT, Herman T, Molitch ME, London MH, Kramer SM 1983 Aging and the
thyroid. Decreased requirement for thyroid hormone in older hypothyroid patients.
Am J Med 75:206-209
Boucai L, Hollowell JG, Surks MI 2011 An approach for development of age-,
gender-, and ethnicity-specific thyrotropin reference limits. Thyroid 21:5-11
Cooper DS, Doherty GM, Haugen BR, Kloos RT, Lee SL, Mandel SJ, Mazzaferri EL,
McIver B, Pacini F, Schlumberger M, Sherman SI, Steward DL, Tuttle RM 2009
Revised American Thyroid Association management guidelines for patients with
thyroid nodules and differentiated thyroid cancer. Thyroid 19:1167-1214
For many years the American Thyroid Association has recommended close
monitoring of all patients treated with thyroid hormone (1). The reason for this
recommendation is that many patients are either overtreated or undertreated based
on their blood TSH (thyroid stimulating hormone) levels (2), which may lead to
adverse effects .
This problem has been found to be especially important in post menopausal women
and older men (3) who are at increased risk for fractures from worsening
osteoporosis when overtreated with thyroid hormones (4). Thyroid hormones have a
direct action on bone cells leading to bone loss (5) . TSH, which may play a role in
protecting bone (6), is also low in overtreated patients. On the other hand, patients
with hypothyroidism treated with doses of thyroxine that keep TSH within the normal
range, do not appear to be at increased risk of fracture (4,7). For this reason, regular
monitoring of thyroid replacement therapy every 6-12 months once stabilized, using
serum TSH as a gauge, is the current standard of care (1).
This issue is again emphasized by a new study from Toronto, Canada published in
the British Medical Journal examining the health records of 213,511 patients over
the age of 70 years who were taking thyroxine over a 3.8 year period (8). 10.4% had
a fracture during this time and 88% of the fractures were in women. The risk of
fracture was almost double for those currently taking thyroid hormone as compared
to those who only used it years ago. Those patients taking higher doses of thyroxine
were more likely to have had a fracture than those taking lower doses. Unfortunately
serum TSH data were not available so it is not certain which patients were properly
treated, but it is plausible that many patients were overtreated, especially those who
received higher doses. This supports the importance of avoiding overtreatment with
thyroxine by adjusting the dose carefully through TSH monitoring.
Age itself is a risk factor for osteoporosis and fracture (9). Additionally, older patients
need less thyroxine to maintain a euthyroid state (10,11). Failure to recognize the
relationship of age and thyroxine requirements will lead to over dosage if the dose of
thyroxine is not titrated down as patients age. Unnecessary treatment of elderly
patients adds to this danger. The diagnosis of thyroid failure in the elderly needs to
be carefully evaluated with the knowledge that the upper normal value for TSH in
people over 80 yrs is ~7.5 uU/ml, compared to 4.0 uU/ml in young adults (12).
Therefore careful selection of which elderly patients should be treated with thyroxine
is critical. Thyroid hormone overtreatment of elderly patients is an avoidable
problem.
Individuals vary in their absorption of thyroxine, sometimes because of use of
interfering medications, higher thyroxine doses may be required for some patients to
achieve normal TSH levels. This should not contribute to bone loss as long as
overtreatment is avoided. Further, some patients with thyroid cancer need to have a
lower TSH levels to prevent cancer recurrence (13). In these selected patients the
risk of bone loss is outweighed by beneficial effects on control of the cancer. Hence,
it is important is to adjust the dose of thyroxine to achieve TSH levels that are
appropriate for each individual patient.
5. Sumber: http://www.cancer.org/cancer/thyroidcancer/detailedguide/thyroid-cancertreating-thyroid-hormone-therapy
Thyroid hormone therapy

Taking daily pills of thyroid hormone (thyroid hormone therapy) can serve 2
purposes:
It can help maintain the bodys normal metabolism (by replacing missing
thyroid hormone after surgery).
It can help stop any remaining cancer cells from growing (by lowering TSH
levels).
After a thyroidectomy, the body can no longer make the thyroid hormone it needs, so
patients must take thyroid hormone (levothyroxine) pills to replace the loss of the
natural hormone.
Taking thyroid hormone may also help prevent some thyroid cancers from returning.
Normal thyroid function is regulated by the pituitary gland. The pituitary makes a
hormone called TSH that causes the thyroid gland to make thyroid hormone for the
body. TSH also promotes growth of the thyroid gland and probably of thyroid cancer
cells. The level of TSH, in turn, is regulated by how much thyroid hormone is in the
blood. If the level of thyroid hormone is low, the pituitary makes more TSH. If the
level of thyroid hormone is high, not as much TSH is needed, so the pituitary makes
less of it.
Doctors have learned that by giving higher than normal doses of thyroid hormone,
TSH levels can be kept very low. This may slow the growth of any remaining cancer
cells and lower the chance of some thyroid cancers (especially high-risk cancers)
coming back.
Possible side effects
Taking higher than normal levels of thyroid hormone seems to have few short-term
side effects, but some doctors have expressed concerns about taking them for long
periods of time. High levels of thyroid hormone can lead to problems with a rapid or
irregular heartbeat. Over the long run, high doses of thyroid hormone can lead to
weak bones (osteoporosis). Because of this, high doses of thyroid hormone may be
reserved for people with differentiated thyroid cancers who are at high risk of
recurrence.
TSH (thyroid-stimulating hormone) Level

1. Sumber: http://www.everydayhealth.com/hs/healthy-living-withhypothyroidism/understanding-test-results/
Understanding Your Hypothyroidism Test Results

By Beth W. Orenstein Reviewed by Farrokh Sohrabi, MD
A simple regular blood test is used to guide treatment for hypothyroidism and
monitor the condition. Here's what the numbers mean.
If theres a bright side to hypothyroidism, or an underactive thyroid, its that treatment
usually just involves taking daily medication, and testing is limited to a simple blood
test. Your hypothyroidism test results are your doctors blueprint for prescribing the
right dose of synthetic thyroid hormone medication and tracking how well its
working.
Thyroid Hormones: Names and Numbers
The main job of the thyroid gland is to make the hormone thyroxine, also known as
T4 because it has four iodine molecules. The thyroid also makes the hormone
triiodothyronine, known as T3 because it has three iodine molecules, but in smaller
amounts, explains Cathy Doria-Medina, MD, an endocrinologist with HealthCare
Partners Medical Group in Torrance, Calif. The thyroid gland makes mostly T4,
[and] the T4 has to be converted to T3 because T3 is the part of thyroxine that

actually does the work," she says.
The pituitary gland at the base of the brain controls hormone production in your
body. It makes thyroid-stimulating hormone, or TSH, which tells the thyroid gland
how much T4 and T3 to produce. The TSH level in your blood reveals how much T4
your pituitary gland is asking your thyroid gland to make. If your TSH levels are
abnormally high, it could mean you have an underactive thyroid, or hypothyroidism.
TSH levels go in the opposite direction of your thyroid hormone, Dr. Doria-Medina
explains. If youre making too little thyroid hormone, your TSH will go up. If youre
making too much thyroid hormone, your TSH will go down.
Whats normal can vary, depending on a number of factors, including the laboratory
where your blood test is done, she adds. A normal range for TSH in most
laboratories is 0.4 milliunits per liter (mU/L) to 4.0 mU/L.
If your TSH is higher than 4.0 mU/L on repeat tests, you probably have
hypothyroidism.
Your doctor may also order a T4 test. Most of the T4 in your blood attaches to a
protein, and when it does, it cant get into your cells. Only T4 that is unattached or
free can get into your cells to go to work. A blood test can measure how much free
T4 is available.
Hypothyroidism Tests: A Measure of Treatment Success
Hypothyroidism is treated with daily medication. Taking synthetic thyroid hormone
medication can bring your T4 and TSH levels back to their normal ranges. Once
youre on the right dose, you should have no symptoms.
When you first start taking medication, your doctor will need to monitor your blood to
fine- tune the dosage. Initially you will need to be tested more frequently, DoriaMedina says. A person who is newly diagnosed and taking medication for
hypothyroidism should be tested every six weeks until the dosage is just right.
The dose you start with is your doctors educated guess about whats best for you,
most likely the lowest dose possible to avoid side effects, which can include a rapid
heartbeat and restlessness.
Medication for hypothyroidism is slow-acting, and it can take several weeks for your
body to adjust. If your TSH is still high and your symptoms havent subsided after six
to 10 weeks, your doctor will likely increase the dose, and youll need your blood
tested again after another six to 10 weeks.
Keeping Hypothyroidism Under Control
Because youll need to take thyroid medication every day for the rest of your life,
even after the right dose is found, your hormone levels will be monitored regularly to
be sure that your treatment is working properly. Eventually, most people with
hypothyroidism can just be seen yearly by their doctor, Doria-Medina says.
The American Thyroid Association recommends that you keep your TSH within a
narrow range of 0.5 to 2.0 mU/L, but dont be alarmed if your test results vary a little.
Some variation is normal because your pituitary gland sends out TSH in pulses, not
a steady stream. Also, the time of day you're tested can make a difference. TSH
levels are likely to be higher at night and lower during the day.
If you have new or worsening symptoms or your health-status changes such as if
you become pregnant, go through menopause, or are given another medicine that
can interfere with your thyroid hormones you should see your doctor and have
your blood tested again, even if its ahead of schedule.
Making the Most of Your Hypothyroidism Treatment

By Dennis Thompson, Jr. Reviewed by Niya Jones, MD, MPH
Determining the right dose for levothyroxine can be tricky. Find out how to get
your medication right and discover the pitfalls of getting it wrong.
For people with hypothyroidism, the most common medication is levothyroxine, a
synthetic form of thyroid hormone. It's an effective hypothyroidism treatment, but
it's also a very tricky one it can take weeks or even months to figure out the
daily dosage that works best for you. Even then, if you don't follow your doctors
instructions closely and take your medication properly, you could throw your
hormone levels out of whack.
Finding the Right Dose of Thyroid Medication
To determine your levothyroxine dosage, your doctor will draw your blood to test
for thyroid-stimulating hormone (TSH). This test measures how much thyroid
hormone your body is asking your thyroid gland to make. The higher your TSH
level, the more starved your body is for thyroid hormone a sign that your
doctor needs to increase your dose of the synthetic replacement hormone.
Unless your TSH levels are unusually high, your doctor typically will start you out
at a low dose of about 50 micrograms a day. Then you'll probably have a TSH
test every three to four weeks, and the readings from those tests will be used to
determine your precise hypothyroidism treatment. Based on the test results, your
doctor may increase or decrease the dose until your thyroid hormone levels
stabilize.
"Youll likely get to a steady level in around a month, and then four to six weeks is
the rule of thumb to re-check your levels again," says Stephanie Lee, MD, PhD
associate chief of endocrinology, nutrition, and diabetes at Boston Medical
Center and an associate professor at the Boston University School of Medicine.
If you find that your levels are not stabilizing, you and your doctor will need to
discuss alternatives. Your doctor might prescribe another type of levothyroxine or
see if you respond better to natural thyroid hormone or a combination of different

thyroid hormones.
Following Thyroid Treatment Instructions
It's very important to follow your doctor's instructions when taking medication as
part of your hypothyroidism treatment. If you don't, your body may not be able to
fully absorb the levothyroxine and your hormone levels could fluctuate.
"This hormone is potent in very small amounts, so any little change in your
routine can change your hormone levels," says Laura Pizzi, PharmD, a professor
at the Jefferson School of Pharmacy at Thomas Jefferson University in
Philadelphia.
Small changes that can influence the effect of thyroid medication on your body
include:
Changing the time of day you take your dose

Taking the medication on an empty stomach, then switching to taking it
with food
Switching brands of levothyroxine
For the best levothyroxine absorption, Hossein Gharib, MD, a professor of

endocrinology at the Mayo Clinic in Rochester, Minn., recommends that it be
taken in a fasting state, just after you wake up. "If you can't take it in a fasting
state, they you should take it in the evening, two to three hours after your
evening meal, Dr. Gharib says.
Watching for Interactions With Levothyroxine
Other drugs and some dietary supplements can interact with levothyroxine. For
example, iron and calcium supplements can interfere with the absorption of
levothyroxine. The iron or calcium can bind with the synthetic hormone,
preventing your body from using it. "You're basically snatching away some of the
levothyroxine that otherwise wouldve been absorbed into the body," Dr. Pizzi
says.
The hormone estrogen also can interfere with the body's ability to use
levothyroxine. That means women taking birth control pills may need an
increased dose of thyroid medication, Pizzi says.
Other medications that can interfere with the absorption of levothyroxine include:
Aspirin
Amphetamines
Anticoagulants
Some antidepressants
Anti-anxiety drugs
Arthritis medications
Beta blockers
Insulin
10
Monitoring Potential Side Effects of Thyroid Medication

Not taking levothyroxine the right way or experiencing drug interactions can
make your thyroid hormone levels swing high or low and cause side effects.
Elevated hormone levels can make you feel shaky, jittery, and jumpy, Pizzi says.
You might notice your heart racing or have trouble sleeping at night. You might
even lose some weight.
Hormone levels that are too low can cause fatigue and sluggishness. You might
experience a slow heart rate, lose some of your hair, feel depressed, or gain
weight.
If you experience any of these problems, call your doctor. "Your doctor will likely
ask you to come in and get your blood checked," Pizzi says. Based on the
results, he or she will probably change your thyroid medication dosage to
address the side effect.
Overall, if you establish and maintain a regular routine with your hypothyroidism
treatment, the condition should have little effect on your long-term health and
well-being, Pizzi says.
2. Sumber: http://www.md-health.com/High-Tsh.html
What Does a High TSH Mean?

What does a high TSH mean? High levels of TSH in the blood stream typically
signal that the thyroid is underperforming. High TSH levels are a common signal
of hypothyroidism that will require medical treatment to avoid potential health
risks.
TSH or thyroid stimulating hormone is a hormone produced in the anterior
pituitary gland. This is used to help stimulate the thyroid to produce
triiodothyronine (T3) or thyroxine (T4), hormones that help stimulate the
metabolism. If your pituitary gland is producing TSH trying to stimulate the thyroid
but the thyroid does not respond, it can result in an excessive amount of TSH in
the bloodstream. This can be caused by stress, illness, an obstruction or surgery
causing the thyroid to malfunction or be sluggish.
What is a TSH Test?
A TSH test is a lab test that analyzes your blood to determine the body's overall
TSH levels. If you begin to show signs of a malfunctioning thyroid your doctor my
order a test to check for the TSH levels in your system. If these show a high level
of TSH you may have a sluggish thyroid, but low levels of TSH signal that your
thyroid may be overactive.
During a TSH test, your doctor will take a blood sample to check the hormone
levels. A needle will be placed in a sterilized are of your arm, then attached to a
11
tube to collect the blood. After this is finished the needle removed and you will be
asked to put pressure and a bandage on the site to stop the bleeding. In some
cases an elastic band may be placed around the arm to make it easier to collect
the blood. You should not feel a great deal of pain from the elastic band or the
needle, though you may develop a bruise at the injection site.
Your doctor will be focusing on the two hormones that control the metabolism,
triiodothyronine (T3) and thyroxine (T4). Results of the TSH test are typically
available 2-3 days after the test is given. If your hormones do not fall within a
healthy range your doctor will explain what may be going wrong and what you
can do treat this condition.
What is the Normal Range of TSH?
There are a range of levels that your TSH levels can be. Learning what these
levels mean will help you work with your doctor to address your condition
adequately.
Normal TSH - Adults should have TSH hormone levels that range from
0.4-4.2 mU/L. This indicates that the signals from your pituitary gland
match the activity of your thyroid gland. Your doctor will use this hormone
level alongside the other signals and side affects you may be showing to
determine if there is an underlying health issue at hand.
Low TSH - Low TSH levels can be a sign that you are dealing with an
overactive thyroid gland from conditions such as goiter, noncancerous
tumors or Graves's disease. The thyroid may also become overactive
during the first trimester of pregnancy. If you are already being treated for
thyroid issues, you may develop low TSH levels if you are taking too much
thyroid medication. If you are not showing signs of overactive thyroid you
may have damaged the pituitary gland, causing it to produce less TSH.
High TSH - High levels of TSH are typically caused by an underactive
thyroid or hypothyroidism. This is typically caused by Hashimoto's
thyroiditis. If you are already being treated for a thyroid disorder this can
be a sign that you need to increase your medication. In rare cases, you
may be showing high TSH levels because you have developed a tumor
that is causing the pituitary gland to over-produce TSH.
Conditions that Cause High TSH

Once it is determined that you have excessive levels of TSH in your system, your
doctor will start narrowing down what is causing the trouble.
Hypothyroidism - Hypothyroidism is a condition that is defined by your

body failing to produce enough hormones to adequately manage your
metabolism. Patients suffering from this condition will typically experience
dry skin, increased sensitivity to cold, thinning hear, impaired memory,
muscle aches, puffy face, unexplained weight gain, constipation, fatigue,
hoarseness, elevated cholesterol, irregular menstrual periods or
depression. A number of circumstances such as surgery, taking
psychiatric medications, radiation therapy or an autoimmune disease can
12
lead to this condition. Hypothyroidism is typically managed with

medication that will artificially replace these hormones.
Pituitary Tumors - In rare cases, excessive TSH levels are a sign that your
pituitary gland is not functioning properly. In some cases this is because a
group of cells has begun to grow on top of the gland. In most cases these
tumors are not cancerous, but they can cause interference in your bodily
functions that can lead to other negative side effects which could be
dangerous to the body. The overproduction of TSH can lead to an
overactive thyroid.
Thyroid Disorder - Thyroid disorders such as enlarged thyroid gland,
cancer or abnormal hormone production can cause the thyroid to function
poorly. Some of these conditions are harmless, but many will require
medical intervention to avoid unpleasant side effects such as a sluggish
metabolism that will lead to damage throughout the body.
3. Sumber: http://www.endocrineweb.com/conditions/thyroid/hypothyroidism-toolittle-thyroid-hormone-
Hypothyroidism: Too Little Thyroid Hormone

Part 1: Introduction, Causes, and Symptoms of Hypothyroidism
Written by James Norman MD, FACS, FACE
Hypothyroidism is a condition in which the body lacks sufficient thyroid hormone.
Since the main purpose of thyroid hormone is to "run the body's metabolism," it is
understandable that people with this condition will have symptoms associated
with a slow metabolism. The estimates vary, but approximately 10 million
Americans have this common medical condition. In fact, as many as 10% of
women may have some degree of thyroid hormone deficiency. Hypothyroidism
is more common than you would believe, and millions of people are currently
hypothyroid and don't know it. For an overview of how thyroid hormone is
produced and how its production is regulated, check out our thyroid hormone
production page.
Hypothyroidism Slideshow: Causes, Symptoms, and Treatments
Causes of Hypothyroidism
There are two fairly common causes of hypothyroidism. The first is a result of
previous (or currently ongoing) inflammation of the thyroid gland, which leaves a
large percentage of the cells of the thyroid damaged (or dead) and incapable of
producing sufficient hormone. The most common cause of thyroid gland failure is
called autoimmune thyroiditis (also called Hashimoto's thyroiditis), a form of
thyroid inflammation caused by the patient's own immune system.
The second major cause is the broad category of "medical treatments." The
treatment of many thyroid conditions warrants surgical removal of a portion or all
of the thyroid gland. If the total mass of thyroid producing cells left within the
13
body are not enough to meet the needs of the body, the patient will develop
hypothyroidism. Remember, this is often the goal of the surgery for thyroid
cancer.
But at other times, the surgery will be to remove a worrisome nodule, leaving half
of the thyroid in the neck undisturbed. Sometimes, this remaining thyroid lobe
and isthmus will produce enough hormone to meet the demands of the body. For
other patients, however, it may become apparent years later that the remaining
thyroid just can't quite keep up with demand.
Similarly, goiters and some other thyroid conditions can be treated with
radioactive iodine therapy. The aim of the radioactive iodine therapy (for benign
conditions) is to kill a portion of the thyroid to prevent goiters from growing larger
or producing too much hormone (hyperthyroidism).
Occasionally, the result of radioactive iodine treatment will be that too many cells
are damaged so the patient often becomes hypothyroid within a year or two.
However, this is usually greatly preferred over the original problem.
There are several other rare causes of hypothyroidism, one of them being a
completely "normal" thyroid gland that is not making enough hormone because of
a problem in the pituitary gland. If the pituitary does not produce enough thyroid
stimulating hormone (TSH) then the thyroid simply does not have the "signal" to
make hormone. So it doesn't.
Symptoms of Hypothyroidism
Fatigue
Weakness
Weight gain or increased difficulty losing weight
Coarse, dry hair
Dry, rough pale skin
Hair loss
Cold intolerance (you can't tolerate cold temperatures like those around
you)
Muscle cramps and frequent muscle aches
Constipation
Depression
Irritability
Memory loss
Abnormal menstrual cycles
Decreased libido
Each individual patient may have any number of these symptoms, and they will
vary with the severity of the thyroid hormone deficiency and the length of time the
body has been deprived of the proper amount of hormone.
You may have one of these symptoms as your main complaint, while another will
not have that problem at all and will be suffering from an entirely different
symptom. Most people will have a combination of these symptoms. Occasionally,
14
some patients with hypothyroidism have no symptoms at all, or they are just so
subtle that they go unnoticed.
If you have these symptoms, you need to discuss them with your doctor.
Additionally, you may need to seek the skills of an endocrinologist. If you have
already been diagnosed and treated for hypothyroidism and continue to have any
or all of these symptoms, you need to discuss it with your physician.
Potential Dangers of Hypothyroidism
Because the body is expecting a certain amount of thyroid hormone the pituitary
will make additional thyroid stimulating hormone (TSH) in an attempt to entice the
thyroid to produce more hormone. This constant bombardment with high levels of
TSH may cause the thyroid gland to become enlarged and form a goiter (termed
a "compensatory goiter").
Left untreated, the symptoms of hypothyroidism will usually progress. Rarely,
complications can result in severe life-threatening depression, heart failure, or
coma.
Hypothyroidism can often be diagnosed with a simple blood test. In some
persons, however, it's not so simple and more detailed tests are needed. Most
importantly, a good relationship with a good endocrinologist will almost surely be
needed.
Hypothyroidism is completely treatable in many patients simply by taking a small
pill once a day. However, this is a simplified statement, and it's not always so
easy. There are several types of thyroid hormone preparations and one type of
medicine will not be the best therapy for all patients. Many factors will go into the
treatment of hypothyroidism and it is different for everybody.
Hypothyroidism: Too little thyroid hormone

Part 2: Diagnosis and Treatments of Hypothyroidism.
Too little thyroid hormone produced.Since hypothyroidism is caused by too little
thyroid hormone secreted by the thyroid, the diagnosis of hypothyroidism is
based almost exclusively upon measuring the amount of thyroid hormone in the
blood. There are normal ranges for all thyroid hormones which have been
calculated by computers which measured these hormones in tens of thousands
of people. If your thyroid hormone levels fall below the normal range, that is
consistent with hypothyroidism These tests are very accurate and reliable and
are so routine that they are available to everybody. More about these tests on
another page. However, its not always so simple...keep reading.
REMEMBER
hypo = too little
thyroidism = disease of the thyroid
Thus, hypo-thyroidism = a disease of too little thyroid activity.
15
The idea is to measure blood levels of T4 and TSH. In the typical person with an
under-active thyroid gland, the blood level of T4 (the main thyroid hormone) will
be low, while the TSH level will be high. This means that the thyroid is not
making enough hormone and the pituitary recognizes it and is responding
appropriately by making more Thyroid Stimulating Hormone (TSH) in an attempt
to force more hormone production out of the thyroid. In the more rare case of
hypothyroidism due to pituitary failure, the thyroid hormone T4 will be low, but the
TSH level will also be low. The thyroid is behaving "appropriately" under these
conditions because it can only make hormone in response to TSH signals from
the pituitary. Since the pituitary is not making enough TSH, then the thyroid will
never make enough T4. The real question in this situation is what is wrong with
the pituitary? But in the typical and most common form of hypothyroidism, the
main thyroid hormone T4 is low, and the TSH level is high.
The next question is: When is low too low, and when is high too high? Blood
levels have "normal" ranges, but other factors need to be taken into account as
well, such as the presence or absence of symptoms. You should discuss your
levels with your doctor so you can interpret how they are helping (or not?) fix
your problems.
Oh, if only it were this simple all the time! Although the majority of individuals
with hypothyroidism will be easy to diagnose with these simple blood tests, many
millions will have this disease in mild to moderate forms which are more difficult
to diagnose. The solution for these people is more complex and this is due to
several factors. First we must realize that not all patients with hypothyroidism are
the same. There are many degrees of this disease from very severe to very mild.
Additionally, and very importantly, we cannot always predict just how bad (or
good) an individual patient will feel just by examining his/her thyroid hormone
levels. In other words, some patients with very "mild" deviations in their thyroid
laboratory test results will feel just fine while others will be quite symptomatic.
The degree of thyroid hormone abnormalities often, but NOT ALWAYS will
correlate with the degree of symptoms. It is important for both you and your
physician to keep this in mind since the goal is not necessarily to make the lab
tests go into the normal range, but to make you feel better as well! We must also
keep in mind that even the "normal" thyroid hormone levels in the blood have a
fairly large range, so even if a patient is in the "normal" range, it may not be the
normal level for them.
For the majority of patients with hypothyroidism, taking some form of thyroid
hormone replacement (synthetic or natural, pill or liquid, etc) will make the
"thyroid function tests" return to the normal range, AND, this is accompanied by a
general improvement in symptoms making the patient feel better. This does not
happen to all individuals, however, and for these patients it is very important to
find an endocrinologist who will listen and be sympathetic. (We aim to help you
find this type of doctor.) Because most patients will be improved (or made
completely better) when sufficient thyroid hormone is provided on a daily basis to
make the hormone levels in the blood come into the normal range, physicians will
often will rely on test results to determine when a patient is on the appropriate
dose and therefore doing well. Remember, these tests have a wide normal
16
range. Find a doctor who helps make you FEEL better, not just make your labs
better because once given this diagnosis, you are likely to carry it for a long, long
time. There is more than one drug, there is more than one lab test, and there is
a "just right" doctor for everybody.
Treatment of Hypothyroidism
Hypothyroidism is usually quite easy to treat (for most people)! The easiest and
most effective treatment is simply taking a thyroid hormone pill (Levothyroxine)
once a day, preferably in the morning. This medication is a pure synthetic form of
T4 which is made in a laboratory to be an exact replacement for the T4 that the
human thyroid gland normally secretes. It comes in multiple strengths, which
means that an appropriate dosage can almost always be found for each patient.
The dosage should be re-evaluated and possibly adjusted monthly until the
proper level is established. The dose should then be re-evaluated at least
annually. If you are on this medication, make sure your physician knows it so
he/she can check the levels at least yearly. Note: Just like we discussed above,
however, this simple approach does not hold true for everybody. Occasionally
the correct dosage is a bit difficult to pin-point and therefore you may need an
exam and blood tests more frequently. Also, some patients just don't do well on
some thyroid medications and will be quite happy on another. For these reasons
you should not be shy in discussing with your doctor your blood hormone tests,
symptoms, how you feel, and the type of medicine you are taking. The goal is to
make you feel better, make your body last longer, slow the risk of heart disease
and osteoporosis...in addition to making your blood levels normal! Sometimes
that's easy, when its not, you need a physician who is willing to spend the time
with you that you deserve while you explore different dosages other types of
medications (or alternative diagnoses).
Some patients will notice a slight reduction in symptoms within 1 to 2 weeks, but
the full metabolic response to thyroid hormone therapy is often delayed for a
month or two before the patient feels completely normal. It is important that the
correct amount of thyroid hormone is used. Not enough and the patient may have
continued fatigue or some of the other symptoms of hypothyroidism. Too high a
dose could cause symptoms of nervousness, palpitations or insomnia typical of
hyperthyroidism. Some recent studies have suggested that too much thyroid
hormone may cause increased calcium loss from bone increasing the patient's
risk for osteoporosis. For patients with heart conditions or diseases, an optimal
thyroid dose is particularly important. Even a slight excess may increase the
patient's risk for heart attack or worsen angina. Some physicians feel that more
frequent dose checks and blood hormone levels are appropriate in these
patients.
After about one month of treatment, hormone levels are measured in the blood to
establish whether the dose of thyroid hormone which the patient is taking is
appropriate. We don't want too much given or subtle symptoms of
hyperthyroidism could ensue, and too little would not alleviate the symptoms
completely. Often blood samples are also checked to see if there are antibodies
against the thyroid, a sign of autoimmune thyroiditis. Remember, this is the most
common cause of hypothyroidism. Once treatment for hypothyroidism has been
17
started, it typically will continue for the patient's life. Therefore, it is of great
importance that the diagnosis be firmly established and you have a good
relationship with a physician you like and trust.
Synthetic T4 can be safely taken with most other medications. Patients taking
cholestyramine (a compound used to lower blood cholesterol) or certain
medications for seizures should check with their physician about potential
interactions. Women taking T4 who become pregnant should feel confident that
the medication is exactly what their own thyroid gland would otherwise make.
However, they should check with their physician since the T4 dose may have to
be adjusted during pregnancy (usually more hormone is needed to meet the
increased demands of the mother's new increased metabolism). There are other
potential problems with other drugs including iron-containing vitamins. Once
again, pregnant women (and all women and men for that matter) taking iron
supplements should discuss this with your physician. There are three brand
name Levothyroxine tablets now available. You may want to consult with your
physician or pharmacist on the most cost effective brand since recent studies
suggest that none is better than the other.
4. Sumber: http://www.endocrineweb.com/conditions/thyroid/thyroid-gland-function
Thyroid Gland Function Tests

Common Tests to Examine
Written by James Norman MD, FACS, FACE
Some information on this page is a little more advanced. If you have trouble
understanding the process of normal thyroid function, please go to our page describing
this process first.
As we have seen from our overview of normal thyroid
physiology, the thyroid gland produces T4 and T3. But this
production is not possible without stimulation from the
pituitary gland (TSH) which in turn is also regulated by the
hypothalamus's TSH Releasing Hormone. Now, with
radioimmunoassay techniques it is possible to measure
circulating hormones in the blood very accurately.
Knowledge of this thyroid physiology is important in
knowing what thyroid test or tests are needed to diagnose
different diseases. No one single laboratory test is 100%
accurate in diagnosing all types of thyroid disease; however,
a combination of two or more tests can usually detect even the slightest abnormality
of thyroid function.
For example, a low T4 level could mean a diseased thyroid gland ~ OR ~ a nonfunctioning pituitary gland which is not stimulating the thyroid to produce T4. Since the
pituitary gland would normally release TSH if the T4 is low, a high TSH level would
confirm that the thyroid gland (not the pituitary gland) is responsible for the
18
hypothyroidism.
If the T4 level is low and TSH is not elevated, the pituitary gland is more likely to be
the cause for the hypothyroidism. Of course, this would drastically effect the treatment
since the pituitary gland also regulates the body's other glands (adrenals, ovaries, and
testicles) as well as controlling growth in children and normal kidney function. Pituitary
gland failure means that the other glands may also be failing and other treatment than just
thyroid may be necessary. The most common cause for the pituitary gland failure is a
tumor of the pituitary and this might also require surgery to remove.
Modern measurement of thyroid hormones is done by a new technique, radioimmunoassay

(RIA), discovered by Dr. Solomon Berson and Dr. Rosalyn Yallow. They were awarded the 1977
Nobel Prize in Medicine for this discovery which revolutionized the study of thyroid disease as
well as the entire field of endocrinology.
The following are commonly used thyroid tests
Measurement of Serum Thyroid Hormones: T4 by

RIA
T4 by RIA (radioimmunoassay) is the most used thyroid
test of all. It is frequently referred to as a T7 which
means that a resin T3 uptake (RT3u) has been done to correct for certain medications
such as birth control pills, other hormones, seizure medication, cardiac drugs, or even
aspirin that may alter the routine T4 test. The T4 reflects the amount of thyroxine in
the blood. If the patient does not take any type of thyroid medication, this test is usually
a good measure of thyroid function.
Measurement of Serum Thyroid Hormones: T3 by RIA
As stated on our thyroid hormone production page, thyroxine (T4) represents 80% of the
thyroid hormone produced by the normal gland and generally represents the overall
function of the gland. The other 20% is triiodothyronine measured as T3 by RIA.
Sometimes the diseased thyroid gland will start producing very high levels of T3 but still
produce normal levels of T4. Therefore measurement of both hormones provides an even
more accurate evaluation of thyroid function.
Thyroid Binding Globulin
Most of the thyroid hormones in the blood are attached to a protein called thyroid binding
globulin (TBG). If there is an excess or deficiency of this protein it alters the T4 or T3
measurement but does not affect the action of the hormone. If a patient appears to have
normal thyroid function, but an unexplained high or low T4, or T3, it may be due to an
increase or decrease of TBG. Direct measurement of TBG can be done and will explain
the abnormal value. Excess TBG or low levels of TBG are found in some families as an
hereditary trait. It causes no problem except falsely elevating or lowering the T4 level.
These people are frequently misdiagnosed as being hyperthyroid or hypothyroid, but they
have no thyroid problem and need no treatment.
Measurement of Pituitary Production of TSH
Pituitary production of TSH is measured by a method referred to as IRMA
(immunoradiometric assay). Normally, low levels (less than 5 units) of TSH are sufficient
to keep the normal thyroid gland functioning properly. When the thyroid gland becomes
inefficient such as in early hypothyroidism, the TSH becomes elevated even though the
T4 and T3 may still be within the "normal" range. This rise in TSH represents the
pituitary gland's response to a drop in circulating thyroid hormone; it is usually the
first indication of thyroid gland failure. Since TSH is normally low when the thyroid
gland is functioning properly, the failure of TSH to rise when circulating thyroid
19
hormones are low is an indication of impaired pituitary function. The new "sensitive"
TSH test will show very low levels of TSH when the thyroid is overactive (as a normal
response of the pituitary to try to decrease thyroid stimulation). Interpretations of the
TSH level depends upon the level of thyroid hormone; therefore, the TSH is usually
used in combination with other thyroid tests such as the T4 RIA and T3 RIA.
TRH Test
In normal people TSH secretion from the pituitary can be increased by giving a shot
containing TSH Releasing Hormone (TRH...the hormone released by the hypothalamus
which tells the pituitary to produce TSH). A baseline TSH of 5 or less usually goes up to
10-20 after giving an injection of TRH. Patients with too much thyroid hormone
(thyroxine or triiodothyronine) will not show a rise in TSH when given TRH. This "TRH
test" is presently the most sensitive test in detecting early hyperthyroidism. Patients who
show too much response to TRH (TSH rises greater than 40) may be hypothyroid. This
test is also used in cancer patients who are taking thyroid replacement to see if they are
on sufficient medication. It is sometimes used to measure if the pituitary gland is
functioning. The new "sensitive" TSH test (above) has eliminated the necessity of
performing a TRH test in most clinical situations.
Iodine Uptake Scan
A means of measuring thyroid function is to measure how much iodine is taken up by the
thyroid gland (RAI uptake). Remember, cells of the thyroid normally absorb iodine from
our blood stream (obtained from foods we eat) and use it to make thyroid hormone
(described on our thyroid function page). Hypothyroid patients usually take up too little
iodine and hyperthyroid patients take up too much iodine. The test is performed by giving
a dose of radioactive iodine on an empty stomach. The iodine is concentrated in the
thyroid gland or excreted in the urine over the next few hours. The amount of iodine that
goes into the thyroid gland can be measured by a "Thyroid Uptake". Of course, patients
who are taking thyroid medication will not take up as much iodine in their thyroid gland
because their own thyroid gland is turned off and is not functioning. At other times the
gland will concentrate iodine normally but will be unable to convert the iodine into
thyroid hormone; therefore, interpretation of the iodine uptake is usually done in
conjunction with blood tests.
Thyroid Scan
Taking a "picture" of how well the thyroid gland is
functioning requires giving a radioisotope to the patient
and letting the thyroid gland concentrate the isotope (just
like the iodine uptake scan above). Therefore, it is
usually done at the same time that the iodine uptake
test is
performed. Although other isotopes, such as technetium, will be concentrated by the
thyroid gland; these isotopes will not measure iodine uptake which is what we really want
to know because the production of thyroid hormone is dependent upon absorbing iodine.
It has also been found that thyroid nodules that concentrate iodine are rarely cancerous;
this is not true if the scan is done with technetium. Therefore, all scans are now done with
radioactive iodine. Both of the scans above show normal sized
thyroid glands, but the one on the left has a "HOT" nodule in the
lower aspect of the right lobe, while the scan on the right has a
"COLD" nodule in the lower aspect of the left lobe (outlined in red
and yellow). Pregnant women should not have thyroid scans
performed because the iodine can cause development troubles within
the baby's thyroid gland.
Two types of thyroid scans are available. A camera scan is performed
most commonly which uses a gamma camera operating in a fixed
position viewing the entire thyroid gland at once. This type of scan takes only five to ten
minutes. In the 1990's, a new scanner called a Computerized Rectilinear Thyroid (CRT)
20
scanner was introduced. The CRT scanner utilizes computer technology to improve the
clarity of thyroid scans and enhance thyroid nodules. It measures both thyroid function
and thyroid size. A life-sized 1:1 color scan of the thyroid is obtained giving the size in
square centimeters and the weight in grams. The precise size and activity of nodules in
relation to the rest of the gland is also measured. CTS of the normal thyroid gland In
addition to making thyroid diagnosis more accurate, the CRT scanner improves the
results of thyroid biopsy. The accurate sizing of the thyroid gland aids in the follow-up of
nodules to see if they are growing or getting smaller in size. Knowing the weight of the
thyroid gland allows more accurate radioactive treatment in patients who have Graves'
disease.
Thyroid Scans are used for the following reasons:
Identifying nodules and determining if they are "hot" or "cold".

Measuring the size of the goiter prior to treatment.
Follow-up of thyroid cancer patients after surgery.
Locating thyroid tissue outside the neck, i.e. base of the tongue or in the chest.
Thyroid Ultrasound
Thyroid ultrasound refers to the use of high frequency sound waves to obtain an image of
the thyroid gland and identify nodules. It tells if a nodule is "solid" or a fluid-filled cyst,
but it will not tell if a nodule is benign or malignant. Ultrasound allows accurate
measurement of a nodule's size and can determine if a nodule is getting smaller or is
growing larger during treatment. Ultrasound aids in performing thyroid needle biopsy by
improving accuracy if the nodule cannot be felt easily on examination. Several more
pages are dedicated to the use of ultrasound in evaluating thyroid nodules.
Thyroid Antibodies
The body normally produces antibodies to foreign substances such as bacteria; however,
some people are found to have antibodies against their own thyroid tissue. A condition
known as Hashimoto's Thyroiditis is associated with a high level of these thyroid
antibodies in the blood. Whether the antibodies cause the disease or whether the disease
causes the antibodies is not known; however, the finding of a high level of thyroid
antibodies is strong evidence of this disease. Occasionally, low levels of thyroid
antibodies are found with other types of thyroid disease. When Hashimoto's thyroiditis
presents as a thyroid nodule rather than a diffuse goiter, the thyroid antibodies may not be
present.
Thyroid Needle Biopsy
This has become the most reliable test to differentiate the "cold" nodule that is cancer
from the "cold" nodule that is benign ("hot" nodules are rarely cancerous). It provides
information that no other thyroid test will provide. While not perfect, it will provide
definitive information in 75% of the nodules biopsied. A very extensive discussion of
Thyroid Needle Biopsy is found on another page.
Do I need to stop taking my thyroid pills for these tests?
Since Euthyrox or Synthroid (and most other thyroid pills) behave exactly as normal
human thyroid hormone, they are not rapidly cleared from the body as other medications
are. Most thyroid pills have a half life of 6.7 days which means they must be stopped for
four to five weeks (five half lives) before accurate thyroid testing is possible. An
exception to the long half life of thyroid medication is Cytomel - a thyroid pill with a half
life of only forty-eight hours. Therefore it is possible to change a person's thyroid
replacement to Cytomel for one month to allow time for his regular pills to clear the
body. Cytomel is then stopped for ten days (five half lives) and the appropriate test can
21
then be done. Usually patients, even those who have no remaining thyroid function,
tolerate being off thyroid replacement only ten days quite well.
Normal Laboratory Values

Test
Serum thyroxine
Free thyroxine fraction
Free Thyroxine
Thyroid hormone binding ratio
Free Thyroxine index
Serum Triiodothyronine
Free Triiodothyronine l
Free T3 Index
Radioactive iodine uptake
Serum thyrotropin
Thyroxine-binding globulin
TRH stimulation test Peak
Serum thyroglobulin l
Thyroid microsomal antibody titer
Thyroglobulin antibody titer
Abbreviation
T4
FT4F
FT4
THBR
FT4I
T3
FT3
FT3I
RAIU
TSH
TBG
TSH
Tg
TMAb
TgAb
Typical Ranges
4.6-12 ug/dl
0.03-0.005%
0.7-1.9 ng/dl
0.9-1.1
4-11
80-180 ng/dl
230-619 pg/d
80-180
10-30%
0.5-6 uU/ml
12-20 ug/dl T4 +1.8 ugm
9-30 uIU/ml at 20-30 min
0-30 ng/m
Varies with method
Varies with method
How Your Thyroid Works

Controlling hormones essential to your metabolism
Written by Robert M. Sargis MD, PhD
Your thyroid gland is a small gland, normally weighing less than

one ounce, located in the front of the neck. It is made up of two
halves, called lobes, that lie along the windpipe (trachea) and are
joined together by a narrow band of thyroid tissue, known as the
isthmus.
The thyroid is situated just below your "Adams
apple" or larynx. During development (inside
the womb) the thyroid gland originates in the
back of the tongue, but it normally migrates to the front of the neck
before birth. Sometimes it fails to migrate properly and is located high
in the neck or even in the back of the tongue (lingual thyroid). This is
very rare. At other times it may migrate too far and ends
up in the chest (this is also rare).
The function of the thyroid gland is to take iodine,
found in many foods, and convert it into thyroid
hormones: thyroxine (T4) and triiodothyronine (T3).
Thyroid cells are the only cells in the body which can
absorb iodine. These cells combine iodine and the amino
22
acid tyrosine to make T3 and T4. T3 and T4 are then released into the blood stream and
are transported throughout the body where they control metabolism (conversion of
oxygen and calories to energy).
Every cell in the body depends upon thyroid hormones for regulation of their
metabolism. The normal thyroid gland produces about 80% T4 and about 20% T3,
however, T3 possesses about four times the hormone "strength" as T4.
The thyroid gland is under the control of the pituitary
gland, a small gland the size of a peanut at the base of the
brain (shown here in orange). When the level of thyroid
hormones (T3 & T4) drops too low, the pituitary gland
produces Thyroid Stimulating Hormone (TSH) which
stimulates the thyroid gland to produce more hormones.
Under the influence of TSH, the thyroid will manufacture
and secrete T3 and T4 thereby raising their blood levels.
+The pituitary senses this and responds by decreasing its
TSH production. One can imagine the thyroid gland as a
furnace and the pituitary gland as the thermostat.
Thyroid hormones are like heat. When the heat gets back to the thermostat, it turns the
thermostat off. As the room cools (the thyroid hormone levels drop), the thermostat turns
back on (TSH increases) and the furnace produces more heat (thyroid hormones).
The pituitary gland itself is regulated by another gland, known as the hypothalamus
(shown in the picture above in light blue). The hypothalamus is part of the brain and
produces TSH Releasing Hormone (TRH) which tells the pituitary gland to stimulate
the thyroid gland (release TSH). One might imagine the hypothalamus as the person who
regulates the thermostat since it tells the pituitary gland at what level the thyroid should
be set.
Thyroid Gland, How it Functions,

Symptoms of Hyperthyroidism and
Hypothyroidism
Written by Bridget Brady MD, FACS
23
The thyroid gland is a butterfly-shaped organ located in

the base of your neck. It releases hormones that control metabolismthe way your body
uses energy. The thyroid's hormones regulate vital body functions, including:
Breathing
Heart rate
Central and peripheral nervous systems
Body weight
Muscle strength
Menstrual cycles
Body temperature
Cholesterol levels
Much more!
The thyroid gland is about 2-inches long and lies in front of your throat below the
prominence of thyroid cartilage sometimes called the Adam's apple. The thyroid has two
sides called lobes that lie on either side of your windpipe, and is usually connected by a
strip of thyroid tissue known as an isthmus. Some people do not have an isthmus, and
instead have two separate thyroid lobes.
How the Thyroid Gland Works
The thyroid is part of the endocrine system, which is made up of glands that produce,
store, and release hormones into the bloodstream so the hormones can reach the body's
cells. The thyroid gland uses iodine from the foods you eat to make two main hormones:
Triiodothyronine (T3)
Thyroxine (T4)
It is important that T3 and T4 levels are neither too high nor too low. Two glands in
the brainthe hypothalamus and the pituitary communicate to maintain T3 and T4
balance.
The hypothalamus produces TSH Releasing Hormone (TRH) that signals the pituitary
to tell the thyroid gland to produce more or less of T3 and T4 by either increasing or
decreasing the release of a hormone called thyroid stimulating hormone (TSH).
24
When T3 and T4 levels are low in the blood, the pituitary gland releases more TSH to
tell the thyroid gland to produce more thyroid hormones.
If T3 and T4 levels are high, the pituitary gland releases less TSH to the thyroid gland
to slow production of these hormones.
Why You Need a Thyroid Gland

T3 and T4 travel in your bloodstream to reach almost every cell in the body. The
hormones regulate the speed with which the cells/metabolism work. For example, T3 and
T4 regulate your heart rate and how fast your intestines process food. So if T3 and T4
levels are low, your heart rate may be slower than normal, and you may have
constipation/weight gain. If T3 and T4 levels are high, you may have a rapid heart rate
and diarrhea/weight loss.
Listed below are other symptoms of too much T3 and T4 in your body
(hyperthyroidism):
Anxiety
Irritability or moodiness
Nervousness, hyperactivity
Sweating or sensitivity to high temperatures
Hand trembling (shaking)
Hair loss
Missed or light menstrual periods
The following is other symptoms of too little T3 and T4 in your body

(hypothyroidism):
Trouble sleeping
Tiredness and fatigue
Difficulty concentrating
Dry skin and hair
Depression
Sensitivity to cold temperature
Frequent, heavy periods
25
Joint and muscle pain
5. Sumber : www.mayoclinic.org
Diseases and Conditions

Hypothyroidism (underactive thyroid)
Tests and diagnosis
By Mayo Clinic Staff
Because hypothyroidism is more prevalent in older women, some doctors
recommend that older women be screened for the disorder during routine annual
physical examinations. Some doctors also recommend that pregnant women or
women thinking about becoming pregnant be tested for hypothyroidism.
In general, your doctor may test for an underactive thyroid if you're feeling
increasingly tired, have dry skin, constipation and weight gain, or have had
previous thyroid problems or goiter.
Blood tests
Diagnosis of hypothyroidism is based on your symptoms and the results of blood
tests that measure the level of TSH and sometimes the level of the thyroid
hormone thyroxine. A low level of thyroxine and high level of TSH indicate an
underactive thyroid. That's because your pituitary produces more TSH in an effort
to stimulate your thyroid gland into producing more thyroid hormone.
In the past, doctors weren't able to detect hypothyroidism until symptoms were
fairly advanced. But by using the sensitive TSH test, doctors are able to diagnose
thyroid disorders much earlier often before you experience symptoms.
Because the TSH test is the best screening test, your doctor will likely check TSH
first and follow with a thyroid hormone test if needed. TSH tests also play an
important role in managing hypothyroidism. They help your doctor determine the
right dosage of medication, both initially and over time.
In addition, TSH tests are used to help diagnose a condition called subclinical
hypothyroidism, which usually causes no outward signs or symptoms. In this
condition, you have normal blood levels of triiodothyronine and thyroxine, but
higher than normal levels of TSH.
6. Sumber: https: www.synthroid.com
26
What is TSH?
TSH is short for thyroid-stimulating hormone. TSH is produced by a small gland in the
brain called the pituitary, and can be measured by a common blood test.
TSH & THE THYROID
The hypothalamus, located in the brain, produces thyrotropin-releasing hormone (TRH)

that tells the pituitary gland to make thyroid-stimulating hormone (TSH).
TSH & A THYROID
AFFECTED BY HYPOTHYROIDISM
27
A diseased thyroid is unable to produce enough thyroid hormone.

FOR PEOPLE DIAGNOSED
WITH HYPOTHYROIDISM
*The American Association of Clinical Endocrinologists and the American Thyroid

Association recommend TSH levels between 0.45 and 4.12 mlU/L.
WHAT IS A TSH TEST?

A TSH test is used to check the level of thyroid-stimulating hormone in the blood. Your
TSH level can indicate if your thyroid gland is working properly.
28
While a TSH test is usually used as the initial blood test to detect hypothyroidism, the
doctor may need to order additional tests to diagnose hypothyroidism. The doctor also
may check your level of FT4, or free thyroxine, which is the amount of thyroxine in your
body.
Its important to know that blood tests are not the only way the doctor determines your
hypothyroidism diagnosis. Asking how youre feeling is just as important. Reviewing
your TSH results and discussing all your symptoms helps the doctor see the bigger
picture.
Use
SYNTHROID (levothyroxine sodium tablets, USP) is a prescription, man-made
thyroid hormone that is used to treat a condition called hypothyroidism, except in cases
of temporary hypothyroidism, which is usually associated with an inflammation of the
thyroid gland (thyroiditis). It is meant to replace a hormone that is usually made by your
thyroid gland. Generally, thyroid replacement treatment is to be taken for life.
Important Safety Information
Thyroid hormones, including SYNTHROID, should not be used either alone or

in combination with other drugs for the treatment of obesity or weight loss. In
patients with normal thyroid levels, doses of SYNTHROID used daily for
hormone replacement are not helpful for weight loss. Larger doses may result
in serious or even life-threatening events, especially when used in combination
with certain other drugs used to reduce appetite.
Do not use SYNTHROID if you have hyperthyroidism or over-active thyroid,
uncorrected adrenal problems, are having symptoms of a heart attack, or are allergic
to any of its ingredients.
In women, long-term treatment with SYNTHROID has been associated with
increased bone loss, especially in women who are on high doses or those who are on
high doses after menopause.
Tell your doctor if you are allergic to any foods or drugs, are pregnant or plan to
become pregnant, are breast-feeding or are taking any other drugs, as well as
prescription and over-the-counter products.
Tell your doctor about any other medical conditions you may have, especially heart
disease, diabetes, blood clotting problems, and adrenal or pituitary gland problems.
The dose of other drugs you may be taking to control these conditions may have to
be changed while you are taking SYNTHROID. If you have diabetes, check your
blood sugar levels and/or the glucose in your urine, as ordered by your doctor and
immediately tell your doctor if there are any changes. If you are taking blood
thinners, your blood clotting status should be checked often.
Use SYNTHROID only as ordered by your doctor. Do not stop or change the
amount you take, or how often you take it, unless told to do so by your doctor.
Products such as iron and calcium supplements and antacids can lower your bodys
ability to absorb SYNTHROID, so SYNTHROID should be taken 4 hours before or
after taking these products.
Take SYNTHROID as a single dose, preferably on an empty stomach, one-half to
one hour before breakfast. Your bodys ability to absorb SYNTHROID is improved
when you take it on an empty stomach.
Tell your doctor if you develop any of the following symptoms: rapid or abnormal
heartbeat, chest pain, difficulty catching breath, leg cramps, headache, feeling
nervous, irritability, sleeplessness, shaking, change in appetite, weight gain or loss,
throwing up, diarrhea, increased sweating, unable to tolerate heat, fever, changes in
menstrual periods, swollen red bumps on the skin or skin rash, or any other unusual
medical event.
29
Tell your doctor or dentist that you are taking SYNTHROID before any surgery.
Once your bodys response to SYNTHROID has stabilized, it is important to have
lab tests done, as ordered by your doctor, at least once a year.
This is the most important safety information you should know about
SYNTHROID. For more information, talk with your doctor.
7. Sumber: http://www.medscape.com/viewarticle/705879
How do You Approach the Problem of

TSH Elevation in a Patient on High-dose
Thyroid Hormone Replacement?
John C. Morris
Int J Qual Health Care. 2009;70(5):671-673.
Abstract and Introduction

Abstract
Persistent elevation of TSH levels in patients under treatment for hypothyroidism is a
relatively common clinical problem in endocrinology practice. The most common cause
for this phenomenon is poor patient compliance with their thyroid hormone tablets. In the
compliant patient, however, multiple aetiologies are possible and a methodological and
stepwise approach to the patient's problem will uniformly identify a cause, or at least a
resolution.
Introduction
Thyroid hormone therapy is generally one of the most gratifying and effective hormone
replacements within the clinician's armamentarium. Most patients are satisfactorily
managed with a single tablet of synthetically derived levothyroxine daily. To make that
possible, a wide variety of tablet sizes are available from a number of manufacturers and
feature both brand-name products and several generic preparations. Although the average
dose for effective and optimal replacement varies somewhat from patient to patient, most
hypothyroid patients are managed within a fairly narrow dose window that varies
according to body weight, the average being near 1618 g/kg.[1] Although total body
weight is a convenient measurement upon which to base initial dosing, correct
replacement dosing correlates better with lean body mass than total body weight. [2] In
most patients the circulating concentration of TSH serves as a reflection of thyroid
hormone effect upon the pituitary and thereby as an effective marker of the adequacy of
the replacement dose. However, one of the common clinical problems that I am asked to
review is that of the patient who requires higher doses of levothyroxine for normalization
of their TSH or whose TSH level remains persistently elevated despite these high doses.
For example, a recent patient I was referred was a 40-year-old woman from a
neighbouring community who was diagnosed with hypothyroidism 1 year prior to her
visit. In brief, at that time she expressed symptoms compatible with hypothyroidism, such
30
as severe constipation, fatigue and a modest amount of weight gain, and her thyroid gland
was firm, moderately diffusely enlarged but without nodularity, suggestive of
autoimmune thyroid disease. Laboratory investigation demonstrated marked TSH
elevation (145 mIU/l, normal 0350 mIU/l) and low free thyroxine (39 pmol/l, normal
103232 pmol/l). Her primary care physician started thyroxine replacement at standard
doses and adjusted the dosage upwards on three occasions because of persistently
elevated TSH levels. After taking 300 g of levothyroxine for 6 weeks, she was referred
for further evaluation when her TSH remained elevated (77 mIU/l) and free thyroxine
remained low at 77 pmol/l.
My approach to this patient and those with persistently elevated TSH levels despite doses
of thyroid hormone that should be adequate is outlined below. I recommend following
these steps, although the order of them and the number that may need further pursuit may
vary from one patient to the next, based upon the individual patient's circumstances.
(1) Confirm the diagnosis and laboratory results. Frank primary hypothyroidism by
laboratory definition requires low levels of thyroid hormones (total and free T4 and T3)
and elevated TSH. The finding of a persistently elevated TSH level is not enough to
confirm the diagnosis here, it is also crucial to measure thyroid hormone levels (T4 and
T3). Markedly elevated TSH levels without low or at least low-normal thyroid hormones
suggests other diagnoses or reasons for the discrepant dose requirements such as
heterophilic antibody interference with TSH measurements, TSH secreting pituitary
tumours, or thyroid hormone resistance syndromes. If the thyroid hormone levels are not
low, more investigation and establishing the correct diagnosis are essential. Elevated
thyroid hormone levels that indicate the patient is taking and absorbing the thyroxine
tablets appropriately suggest that investigations including more careful quenching of the
serum samples for heterophilic antibody interference by the laboratory, serial dilution of
the TSH sample, screening of the family members or genetic testing for thyroid hormone
resistance, and pituitary imaging for evidence of pituitary tumours may be helpful.
Measurement of free T4 and/or free T3 by equilibrium dialysis may at times be helpful as
these more direct methods of assay are less susceptible to the effects of thyroxine binding
proteins.
(2) Ask about compliance. The most common reason for unusually high thyroid hormone
dose requirements in my practice is poor compliance with the daily dosing of
levothyroxine. One day's tablet accounts for 14% of the total weekly dose and because of
the long half-life of levothyroxine, missing a day will have an influence on thyroid
hormone and TSH levels that is manifest over several days. Thus, having a discussion
with the patient about compliance should always be the first step in the process. Many
patients will acknowledge forgetting their tablets occasionally if asked in a
nonaccusatory, nonjudgemental manner. What is sometimes difficult here is determining
how often 'occasionally occurs.
(3) Check the patient's medication bottles and tablets. At times the patient's reported dose
may differ from that prescribed and of course errors by the pharmacist also occur,
resulting in tablets inside the bottle that differ from those reported on the label. The
colour coding of thyroxine tablets is helpful for determining the dose the patient is taking,
but many patients, and occasionally their physicians, have colour vision deficiencies
making actual inspection of the tablets an important step in understanding exactly what
the patient is currently ingesting. Confirming records of prescriptions and refill records
with the pharmacy may also be helpful in documenting compliance, or lack thereof.
(4) Review the thyroxine ingestion history. The most efficient and reproducible way of
taking levothyroxine is to ingest the tablets on an empty stomach and avoid ingesting
other medications or food for 3060 min afterwards. A fairly large and still growing
number of medications, supplements and even food items can alter the fraction of an
ingested dose that is absorbed.[3,4] The ingestion of one or more of these items at or near
31
the time of dosing with thyroxine can substantially change the dose requirement in an
individual patient, especially when practised as routine. The most common offenders that
I see are calcium and iron supplements. Some multivitamin preparations may also
influence thyroxine absorption but the effect does not seem as clear or commonly
problematic as that for calcium and iron supplements. A list of medications that may
interfere is included in Table 1 , but this list is certainly incomplete as new offending
medications are reported frequently.
(5) Investigate for malabsorption. Unfortunately, levothyroxine is not fully absorbed after
oral ingestion. On average, only about 7080% of the available tablet dose is absorbed in
euthyroid individuals.[5] Interindividual variability in the efficiency of gastrointestinal
(GI) absorption is fairly large and this variability accounts for most of the range of
requirement seen between compliant patients after adjustment for body size.
Malabsorption syndromes increase the requirement for levothyroxine by further reducing
the fraction of the ingested dose that is absorbed. Patients with short bowel from prior
small bowel bypass or resection commonly require higher than expected T4 doses. If the
patient has frequent, voluminous stools, a malabsorption disorder may be evident and
measurements of stool fat can confirm this diagnosis. However, thyroxine malabsorption
has been reported as the initial finding in patients with otherwise asymptomatic
malabsorptive syndromes, especially coeliac disease.[6] I screen patients that get this far
along the diagnostic pathway with measurement of tissue transglutaminase antibodies
and, if positive, send them for GI evaluation, usually including small bowel biopsy and
stool fat measurements. Correction of the malabsorption will normalize or at least
improve thyroxine absorption in these patients. Helicobacter pylori infection, especially
when accompanied by atrophic gastritis and achlorhydria, has been reported to impair
thyroxine absorption by up to 37% in patients with multinodular goitre. Antibiotic
treatment of the H. pylori infection was also demonstrated to improve absorption and
reduce thyroxine requirement in those patients.[7]
(6) Consider increased turnover or excretion. A number of drugs or clinical conditions
may increase the turnover or excretion of thyroid hormone and thereby increase
considerably the requirement in individuals that are thyroid hormone dependent. Some
examples are phenytoin, carbamazapine and rifampin. Several of the new kinase
inhibitors, such as imatinib and sunitinib, that are entering the clinic for various
malignancies appear to influence thyroxine requirements in this manner and this may be a
class effect, although reports to date are few.[810] In addition, patients with nephrotic
syndrome who excrete large quantities of albumin may have increased thyroxine
requirements due to binding of T4 to the excreted albumin.[11,12] Women experience
increased thyroxine requirements during normal pregnancy, that may reach as much as
50% at its peak.[13]
(7) Perform a thyroxine absorption test. A clinical test to estimate thyroxine absorption
has been proposed that may have utility in patients who have unexpectedly high T4
requirements. This test involves administration of a single large dose of levothyroxine,
usually in the range of 1000 g, then monitoring T4 levels in blood over time.[4]
Although I have occasionally performed this test, I do not find it to be generally helpful
unless it demonstrates completely 'normal results, thereby supporting patient
noncompliance. Unfortunately, there is no well-established standard to which individual
patient results can be compared, especially one done in hypothyroid patients with normal
absorption. In the few circumstances when I have asked a patient to perform the test, the
results indicate that the patient does absorb thyroxine when exposed to a large dose, but
leaves me wondering if it is a normal amount or not, because of the lack of adequate
normal standards. Furthermore, severe hypothyroidism itself may impair absorption,
presumably due to oedema of the small bowel mucosa and this cannot be quantified by
the test. Thus, I have not found that this test helps me very much in the decision-making
process in individual patients.
32
(8) Treat the patient. If an error by the pharmacy or patient, or a compliance-related

cause, is identified, correction of these underlying factors will help to resolve the
situation. In some circumstances compliance issues are best treated by increasing the
tablet size, assuming that compliance will continue at a similar rate. As a 'last resort in
patients with continued poor compliance, evidence supports successful use of thyroxine
administered once weekly. This quantity is roughly equivalent to the entire weekly total
as calculated above, but given as a single oral dose, [14] and administration can be
monitored if needed. Removing interfering drugs or changing ingestion patterns when
present can also be helpful when possible. In many patients the best course is to increase
the patient's T4 dose and titrate upwards until the TSH and T4 levels normalize. Except
in patients with surgical small bowel syndromes, I have not yet seen a patient who
required parenteral administration of thyroid hormone for maintenance. Even relatively
large doses of levothyroxine administered orally are less expensive and better tolerated
that intravenous or intramuscular injections.
The patient described at the beginning of this article was very convincing in her
description of faithfully ingesting her thyroxine tablets and had for several months been
doing so in the absence of other, potentially interfering medications or supplements after
advice from her primary care provider. Although she still described symptoms of
hypothyroidism, I could not elicit symptoms suggestive of malabsorption. Her thyroid
function tests confirmed inadequately replaced primary hypothyroidism in that her TSH
remained elevated at 294 mIU/l and her free and total thyroxine levels were at the lower
end of the normal range, this after ingesting 300 g of thyroxine for approximately 8
weeks. The screens for malabsorption and coeliac disease (transglutaminase antibodies
and stool fat measurement) were negative and urinalysis was normal. I elected to increase
her levothyroxine dose to 400 g daily and 6 weeks later her TSH was below normal (02
mIU/l) and free thyroxine was elevated (257 pmol/l). We reduced the thyroxine dose to
350 g daily and after 8 weeks found that her TSH and free thyroxine levels had returned
to normal. Her fatigue and constipation also improved and she stated that she felt much
better than before.
I have seen a small number of patients (unreported) that appear to have selective
malabsorption of thyroxine. These patients clearly absorb levothyroxine poorly but do not
have evidence of generalized malabsorption or of coeliac disease and respond well to
increasing the levothyroxine to levels well above those considered usual, in the range of
400600 g per day. At present I am not aware of a physiological explanation for these
findings but I suspect one will be forthcoming with further investigation into thyroxine
transport and absorption. The patient described above may be a representative.
8. Sumber: http://www.medscape.com/viewarticle/722086_5
The Challenges and Complexities of

Thyroid Hormone Replacement
Shayri M. Kansagra, BS; Christopher R. McCudden, PhD; Monte S. Willis, MD, PhD
33
Lab Med. 2010;41(6):229-348.
T4/T3 Combination Compared with T4 Monotherapy

The recent resurgence into hypothyroidism treatment research derives from the
experience of clinicians who found that some patients remain symptomatic while on
prescribed T4 replacement therapy. For example, 1 survey conducted in the United
Kingdom revealed that patients treated with T4 had significantly more psychological
morbidity compared with euthyroid controls. [37] This was supported by findings in animal
models, where hypothyroid rats realized normal thyroid hormone levels on a combination
of T3 and T4 (in the ratio normally secreted by the rat thyroid gland) but not with T4
monotherapy.[38] This led to a landmark study by Bunevicius and colleagues who
assessed whether T4/T3 combination therapy had any advantages over T4 monotherapy
for hypothyroidism (Table 1).[19] To compare therapies, they used a crossover study
design with 33 patients on different regimens of monotherapy and combination therapy
over 2 different 5-week periods. [19] Combination therapy was achieved by replacing 50
g of the patient's usual T4 dose (ranging from 100300 g/day) with 12.5 g of T3.[19]
Patients who received combination therapy had lower total and free T4 levels and higher
T3 levels than patients who received T4 monotherapy. It was reported that cognitive
performance and mood were significantly improved or normalized after treatment. [19]
These findings prompted a series of papers aimed at assessing the potential advantages of
combination therapy over monotherapy for hypothyroidism. [19,3943]
Following the landmark paper, Bunevicius and colleagues performed a second crossover
trial in women who had undergone a subtotal thyroidectomy as a treatment for Graves'
disease (Table 1).[44] In this study, T4 therapy consisted of either the patient's regular
dose of T4 or combination therapy, which was achieved by replacing 50 g of the usual
T4 dose with 10 g of T3. After a period of 5 weeks, the patients were crossed over
blindly to the opposite treatment. In patients who received combination therapy, the
severity of symptoms of hypothyroidism and hyperthyroidism had a tendency to
decrease, as indicated by patient scores on a standard symptom scale. Mental status also
tended to improve with combination therapy compared with monotherapy, based on
apparent improvement in mood (indicated by Visual Analogue Scale [VAS] scores).
However, there was no difference in cognitive performance improvement (indicated by
improved scores on the Digit Symbol and Digit Span tests of the Wechsler Adult
Intelligence Scale). Although this study was small (n=13), the authors concluded its
findings were consistent with those of their earlier study in terms of demonstrating a
relationship between T4/T3 combination therapy and improved mental function. [44]
Lab Med. 2010;41(6):229-348. 2010 American Society for Clinical Pathology
Table 1. Summary of Major Studies to Date Which Compared Combined T3/T4 Therapies to Single T4 Monotherapies for
Hypothyroidism
Bunevicius, et Bunevicius Clyde, et al
al 1999[7]
2002[32]
2003[28]
Number of
study
33
participants
(n)/cohort
10
46
Sawka, et al
2003[29]
Walsh, et al 2003[31]
Siegmund, et al
2004[30]
Rodriguez, et alEscobarSaravanan
2005[33]
Morreale 2005[34] 2005[35]
40
110
23
27
Patients with
chronic
Women with
Patients with
autoimmune sub-total
Ages 2465 with depressive
thyroiditis or thyroidprimary
symptoms and
thyroid cancer ectomy for
hypothyroidism primary
treated by near- Graves'
hypothyroidism
total
disease
thyroidectomy
28
85% autoimmune or
idiopathic
Hypothyroidism due
hypothyroidism.
to
Women with
Primary
Remaining had post- surgery/radioiodine
overt primary
hypothyroidism
surgical hypo(21) or auto-immune
hypothyroidism
thyroidism,Graves' thyroiditis (2)
disease, and
Hashimoto's
697
Family practice
patients 1875
with T4 dose >
100 mcg/day and
no T4 adjustments
in the past 3
months. Thyroid
CA and
Secondary
34

Hypothyroidism
excluded.
disease.
Randomized
control,
Study design
crossoverdesign
Treatment
Original T4
dosage at
baseline vs
original dosage
minus 50 mcg
T4 replaced by
12.5 mcg of T3
per day.
Length of
study periods 5
(in weeks)
Double blind,
Randomized
cross-over
control trial
study
Randomized
control trial
Double blind,
randomized control
trial with cross-over
Design
Double blind,
Double blind,
randomized
Double blind,
randomized control
control trial with randomized
trial with cross-over
cross-over
cross-over trial
design
design
Double blind,
randomized crossover trial
Original T4
Original T4
dosage at
dosage at
Original T4 dose
Original T4 dosage
baseline vs
Original T4 dosage
baseline vs
at baseline vs
vs original does
original
vs original dose
original dosage half of original
minus 5% T4
dosage minus
minus 50 mcg T4
minus 50 mcg T4 T4 dosage plus
replaced by T3 in
50 mcg T4
plus 10 mcg T3 once
replaced with 7.5 12.5 mcg of T3
that amount once a
replaced by
a day.
mcg T3 given twice a day.
day.
10 mcg T3
twice a day.
per day.
100 mcg T4e vs

Original T4
75 mcg T4 plus 5
dosage vs
Original T4
mcg T3. All pts
original dose
dosage vs original
received 87.5
minus 50 mcg
dose minus 50
mcg thyroxine
T4 replaced by
mcg T4 plus 10
plus 7.5 mcg T3
10 mcg T3 once
mcg T3 per day.
per day during
a day.
the last 8 weeks.
16
15
10
12
12
All material on this website is protected by copyright, Copyright 1994-2015 by WebMD LLC. This
website also contains material copyrighted by 3rd parties.
9. Sumber: http://emedicine.medscape.com/article/122393-medication
Hypothyroidism
Author: Philip R Orlander, MD; Chief Editor: George T Griffing, MD
Practice Essentials
Hypothyroidism is a common endocrine disorder resulting from deficiency of thyroid
hormone. In the United States and other areas of adequate iodine intake, autoimmune
thyroid disease (Hashimoto disease) is the most common cause of hypothyroidism;
worldwide, iodine deficiency remains the foremost cause.
The image below depicts the hypothalamic-pituitary-thyroid axis.
35
The hypothalamic-pituitary-thyroid
axis. Levels of circulating thyroid hormones are regulated by a complex feedback system
involving the hypothalamus and pituitary gland.
Signs and symptoms

Hypothyroidism commonly manifests as a slowing in physical and mental activity but
may be asymptomatic. Symptoms and signs are often subtle and neither sensitive nor
specific.
The following are symptoms of hypothyroidism:
Fatigue, loss of energy, lethargy

Weight gain
Decreased appetite
Cold intolerance
Dry skin
Hair loss
Sleepiness
Muscle pain, joint pain, weakness in the extremities
Depression
Emotional lability, mental impairment
Forgetfulness, impaired memory, inability to concentrate
Constipation
Menstrual disturbances, impaired fertility
Decreased perspiration
Paresthesia and nerve entrapment syndromes
Blurred vision
Decreased hearing
Fullness in the throat, hoarseness
The following are symptoms more specific to Hashimoto thyroiditis:
Feeling of fullness in the throat

Painless thyroid enlargement
Exhaustion
Transient neck pain, sore throat, or both
36
Physical signs of hypothyroidism include the following:
Weight gain
Slowed speech and movements
Dry skin
Jaundice
Pallor
Coarse, brittle, straw-like hair
Loss of scalp hair, axillary hair, pubic hair, or a combination
Dull facial expression
Coarse facial features
Periorbital puffiness
Macroglossia
Goiter (simple or nodular)
Hoarseness
Decreased systolic blood pressure and increased diastolic blood pressure
Bradycardia
Pericardial effusion
Abdominal distention, ascites (uncommon)
Hypothermia (only in severe hypothyroid states)
Nonpitting edema (myxedema)
Pitting edema of lower extremities
Hyporeflexia with delayed relaxation, ataxia, or both
Myxedema coma is a severe form of hypothyroidism that most commonly occurs in

individuals with undiagnosed or untreated hypothyroidism who are subjected to an
external stress. Features are as follows:
Altered mental status

Hypothermia
Bradycardia
Hypercarbia
Hyponatremia
Cardiomegaly, pericardial effusion, cardiogenic shock, and ascites may be present
See Clinical Presentation for more detail.
Diagnosis
Third-generation thyroid-stimulating hormone (TSH) assays are generally the most
sensitive screening tool for primary hypothyroidism.[1] If TSH levels are above the
reference range, the next step is to measure free thyroxine (T4) or the free thyroxine
index (FTI), which serves as a surrogate of the free hormone level. Routine measurement
of triiodothyronine (T3) is not recommended.
Results in patients with hypothyroidism are as follows:
Elevated TSH with decreased T4 or FTI

Elevated TSH (usually 4.5-10.0 mIU/L) with normal free T4 or FTI is considered
mild or subclinical hypothyroidism
Abnormalities in the complete blood count and metabolic profile that may be found in
patients with hypothyroidism include the following[2] :
Anemia
Dilutional hyponatremia
Hyperlipidemia
37
Reversible increases in creatinine [2]

Elevations in transaminases and creatinine kinase
No universal screening recommendations exist for thyroid disease for adults. The
American Thyroid Association recommends screening at age 35 years and every 5 years
thereafter, with closer attention to patients who are at high risk, such as the following[3] :
Pregnant women
Women older than 60 years
Patients with type 1 diabetes or other autoimmune disease
Patients with a history of neck irradiation
See Workup for more detail.
Management
Monotherapy with levothyroxine (LT4) remains the treatment of choice for
hypothyroidism. Aspects of LT4 treatment are as follows:
Otherwise young and healthy patients can be started on LT4 at anticipated full
replacement doses
In elderly patients and those with known ischemic heart disease, begin with one
fourth to one half the expected dose and adjust the dose in small increments after no
less than 4-6 weeks
For most cases of mild to moderate hypothyroidism, a starting LT4 dose of 50-75 g
daily will suffice
Clinical benefits begin in 3-5 days and level off after 4-6 weeks
Achieving a TSH level within the reference range may take several months
LT4 dosing changes should be made every 6-8 weeks until the patients TSH is in
target range
After dose stabilization, patients can be monitored with annual clinical evaluations and
TSH monitoring. Patients should be monitored for symptoms and signs of
overtreatment, which include the following:
Tachycardia
Palpitations
Atrial fibrillation
Nervousness
Tiredness
Headache
Increased excitability
Sleeplessness
Tremors
Possible angina
In patients who continue to have symptoms (eg, weight gain, fatigue) despite
normalization of their TSH level, consideration should be given to causes other than
hypothyroidism. In some cases, however, the persistence of symptoms results from
impaired conversion of T4 to T3 in the brain; these patients may benefit from
combination LT4/liothyronine (LT3) therapy.[4]
The updated guidelines on hypothyroidism issued by the American Thyroid Association
in 2014 maintain the recommendation of levothyroxine as the preparation of choice for
hypothyroidism, with the following considerations:[5, 6]
38
If levothyroxine dose requirements are much higher than expected, consider

evaluating for gastrointestinal disorders such as Helicobacter pylori related
gastritis, atrophic gastritis, or celiac disease; if such disorders are detected and
effectively treated, re-evaluation of thyroid function and levothyroxine dosage is
recommended.
Initiation or discontinuation of estrogen and androgens should be followed by
reassessment of serum TSH at steady state, since such medications may alter
levothyroxine requirement.
Serum TSH should be reassessed upon initiation of agents such as tyrosine kinase
inhibitors that affect thyroxine metabolism and thyroxine or triiodothyronine
deiodination.
Serum TSH monitoring is advisable when medications such as phenobarbital,
phenytoin, carbamazepine, rifampin, and sertraline are started.
When deciding on a starting dose of levothyroxine, the patients weight, lean body
mass, pregnancy status, etiology of hypothyroidism, degree of TSH elevation, age,
and general clinical context, including the presence of cardiac disease, should be
considered. The serum TSH goal appropriate for the clinical situation should also be
considered.
Thyroid hormone therapy should be initiated as an initial full replacement or as
partial replacement with gradual increments in the dose titrated upward using serum
TSH as the goal.
Dose adjustments should be made upon significant changes in body weight, with
aging, and with pregnancy; TSH assessment should be performed 4-6 weeks after
any dosage change.
Reference ranges of serum TSH levels are higher in older populations (eg, >65
years), so higher serum TSH targets may be appropriate.
Updated recommendations concerning hypothyroidism treatment in pregnant women are

as follows:[5, 6]
Pregnant women with overt hypothyroidism should receive levothyroxine

replacement therapy with the dose titrated to achieve a TSH concentration within the
trimester-specific reference range.
Serial serum TSH levels should be assessed every 4 weeks during the first half of
pregnancy to adjust levothyroxine dosing to maintain TSH within the trimesterspecific range.
Serum TSH should be reassessed during the second half of pregnancy.
In women already taking levothyroxine, 2 additional doses per week of the current
levothyroxine dose, given as one extra dose twice weekly with several days
separation, may be started as soon as pregnancy is confirmed.
Treatment of myxedema coma is as follows:
Intravenous (IV) LT4 at a dose of 4 g/kg of lean body weight, or approximately

200-250 g, as a bolus in a single or divided dose, depending on the patients risk of
cardiac disease
After 24 hours, 100 g LT4 IV, then 50 g/day IV
Stress doses of IV glucocorticoids
Subsequent adjustment of the LT4 dose can be based on clinical and laboratory
findings
39
10. Sumber: http://www.ncbi.nlm.nih.gov/books/NBK83492/
Screening and Treatment of

Subclinical Hypothyroidism or
Hyperthyroidism
Introduction
Background
A mildly elevated thyroid stimulating hormone (TSH also called thyrotropin)
concentration is the most common thyroid function test abnormality encountered in
everyday practice. Most patients who have a mildly elevated TSH have a normal free
thyroxine (T4) level. The treatment of such patients is controversial, particularly when
they have few or no symptoms and no other clinical evidence of thyroid disease. Less
frequently, clinicians encounter patients who have a low or undetectable serum TSH and
normal triiodothyronine (T3) and free T4 levels. The management of these patients is also
unclear.
The main purpose of this review is to compare the effectiveness of different strategies for
managing individuals who have mildly elevated serum TSH concentrations and those
who have mildly diminished TSH concentrations with normal free T3 and/or free T4. We
also address the evidence for whether the primary care clinician should screen for thyroid
function in patients who have no specific indication for thyroid testing and who come to
the clinician for other reasons. For the purposes of this review, we considered overt
thyroid disease to be a well-defined clinical entity that has clear signs and symptoms, and
thus, outside the scope of our review.
This topic was also the focus of a 2004 U.S. Preventive Services Task Force review. 1
Description of Condition
Disorders of the thyroid gland are among the most common endocrine conditions that
U.S. clinicians evaluate and treat. Hyperthyroidism or hypothyroidism affects about five
percent of adults in the United States. 2
The thyroid gland is involved in metabolic homeostasis in adults. It accomplishes this
through secretion of two hormones, thyroxine (T4) and triiodothyronine (T3), and is
regulated by thyroid stimulating hormone (TSH), which is secreted by the anterior
pituitary. Hypothyroidism is the under-secretion of thyroid hormones, while
hyperthyroidism is the over-secretion of these hormones.
Symptoms of overt hypothyroidism are subtle and nonspecific and may include fatigue,
feeling cold, weight gain, hair loss, poor concentration, dry skin, and constipation (Table
1). If overt hypothyroidism is allowed to progress due to lack of treatment or undertreatment, then myxedema coma, a life-threatening condition, can occur. Myxedema
coma is generally seen in the elderly and may be precipitated by factors that impair
respiration; it is marked by hypothermia, hypoventilation, decreased level of
consciousness, and sometimes seizures and death. 3
40
Table 1. Symptoms and signs of overt thyroid dysfunction

Hypothyroidism
Hyperthyroidism
Symptoms Coarse, dry skin and hair Nervousness and irritability
Cold intolerance
Heat intolerance
Constipation
Increased frequency of stools
Deafness
Muscle weakness
Diminished sweating
Increased sweating
Physical tiredness
Fatigue
Hoarseness
Blurred or double vision
Paresthesias
Erratic behavior
Periorbital puffiness
Restlessness
Heart palpitations
Restless sleep
Decrease in menstrual cycle
Increased appetite
Signs
Slow cerebration
Distracted attention span
Slow movement
Tremors
Slowing of ankle jerk
Tachycardia
Weight gain
Weight Loss
Goiter
Goiter
Symptoms and signs of overt thyroid dysfunction.

Symptoms of overt hyperthyroidism may include palpitations, heat intolerance, and
sweating, weight loss, hyperactivity, and fatigue. Thyroid storm is a life-threatening
condition that results from an acute illness superimposed on undiagnosed or under-treated
hyperthyroidism. It is accompanied by fever, delirium, seizures, and coma.3
Subclinical thyroid dysfunction includes subclinical hypo- and hyperthyroidism. Since
the development of sensitive TSH assays, these conditions have been defined as follows
(Table 2):
High or low serum thyroid stimulating hormone (TSH) levels

Normal free T4 and T3 levels
The absence of signs and symptoms of overt thyroid dysfunction.3
Table 2. Classification of thyroid dysfunction: Biochemical definition

Thyroid
hormones
Condition
TSH
Overt hyperthyroidism
< 0.1 mIU/L or undetectable Elevated T4

or T3
Overt hypothyroidism
> 4.5 mIU/L
Subclinical hyperthyroidism TSH < 0.1 mIU/L
Comments
Low T4
Normal
and T3
T4
Clearly low serum TSH
41

Condition
TSH
Thyroid
hormones
Comments
0.1 mIU/L <= TSH < 0.4 mIU/L
Normal
and T3
T4
4.5 mIU/L < TSH < 10 mIU/L
Normal T4
Mildly elevated TSH
TSH >= 10 mIU/L
Normal T4
Markedly elevated TSH
Low but detectable
Subclinical hypothyroidism
Abbreviation: TSH=thyroid stimulating hormone.
For the purposes of this report, the term subclinical thyroid dysfunction is used to
define the state of having an abnormal TSH in the context of normal free T4 and T3
levels. It includes those with sub-clinical thyroid disease, i.e. those who have a high risk
of disease progression or other adverse consequences, but also those whose prognosis is
not well understood.
Patients with subclinical hypothyroidism are further categorized into those with mildly
elevated TSH (4.510 mIU/L), and those with markedly increased serum TSH levels
(>10 mIU/L).4Similarly, TSH levels below the lower reference limit can be classified as
low but detectable (serum TSH 0.1-0.4mIU/L) and clearly low serum TSH (less than
0.1mIU/L).
Although widely used in the literature, these thresholds are arbitrary. For example,
longitudinal studies have demonstrated that the risk of progression to overt
hypothyroidism increases as the initial serum TSH level increases, but do not support the
common notion of a threshold at either 4.5 mIU/L or at 10 mIU/L.1 Nevertheless, because
many guidelines and studies use these thresholds, we use them in this report.
The biochemical definition has several limitations. First, the term subclinical usually
implies that symptoms and signs are absent, whereas, in actual practice, the more
common situation is that patients have nonspecific symptoms such as cold intolerance or
feeling tired. As Cooper has noted, Although subclinical hypothyroidism is the term
most frequently used, it is not necessarily apt, since on close questioning many patients
disclose mild nonspecific symptoms. Mild hypothyroidism may be a more appropriate
term for this very common syndrome, which is defined by an isolated elevated serum
TSH level in the setting of normal serum thyroid hormone levels, in the presence or
absence of symptoms.5 Importantly, the presence of such symptoms does not mean they
are related to the finding of an abnormal TSH test. In epidemiologic studies, individuals
who had one or two nonspecific symptoms, such as cold intolerance or feeling a little
tired, were no more likely to have subclinical thyroid dysfunction, or be at increased
health risk, than were asymptomatic individuals in the general population.6-10
Second, the biochemical, TSH-based definition of subclinical thyroid dysfunction does
not take into account clinical factors that affect the natural history. Subclinical
hypothyroidism can be caused by recent hospitalization for severe illness; previously
treated Graves disease or nodular thyroid disease; thyroiditis and recovery from
thyroiditis; or untreated adrenal insufficiency. The lack of clinical context has caused
confusion about the applicability of evidence from patients with overt thyroid disease to
asymptomatic, otherwise healthy individuals who have an abnormal TSH level. For
example, a frequently cited randomized trial of treatment for subclinical hypothyroidism
recruited patients who had undergone treatment for Graves disease.11 Such patients
42
predictably and rapidly progress to symptomatic hypothyroidism if not treated. While the
study demonstrated quite convincingly that early treatment can prevent symptoms in
patients who have undergone thyroid ablation, patients who have no history of thyroid
disease and no clinical findings or symptoms attributable to the thyroid are unlikely to
progress as rapidly, so treatment has much less effect on symptoms in the short term. The
vast majority of patients identified by screening in the clinic or population-based settings
are in the latter group.
Third, there is no consensus on what TSH level should be used as the cut off to diagnose
subclinical hypothyroidism or hyperthyroidism. Differences among assays make it
difficult to establish a universal upper limit.12 Most studies define an abnormal TSH test
result as the upper and lower limits of the assays 95 percent reference range,
approximately 0.1 to 4.5 mIU/L.
This method, although widely used in laboratory medicine, is not appropriate for
identifying a threshold for diagnosing or treating subclinical hypothyroidism.13 As for
other clinical measures, such as blood pressure, bone density, or serum lipid levels, the
threshold should depend on the risk associated with a particular level as well as the
balance of benefits and harms of treatment. Some have argued that the threshold for
subclinical hypothyroidism should be raised above the upper limit of the reference range.
The rationale is that otherwise healthy individuals who have a TSH in the range 4.5
mIU/L to 8 mIU/L or 9 mIU/L have not been shown to benefit from detection and
treatment. Other experts argue that, because a TSH within the upper end of the usual
reference range (2.5 to 4.5 mIU/L) confers some additional risk of progressing to overt
hypothyroidism over time, the threshold for diagnosing subclinical hypothyroidism
should be lowered to 2.5 mIU/L.14-16 Approximately 9.7 percent of the U.S. adult
population, representing 20.6 million Americans, has a TSH in this range and would be
identified as having subclinical hypothyroidism if this change were made.4
The appropriate level for decisionmaking can only be decided by better evidence about
the adverse consequences in untreated individuals and the benefits and harms of
treatment at different TSH thresholds.1,4,13,17 Because it depends on the risk of
complications in a particular population, the appropriate TSH cutoff for defining
subclinical hypothyroidism might vary with age, gender, and race.18
Fourth, although the definition of subclinical thyroid dysfunction requires a normal free
T4 level, the definition is not necessarily applicable to the individual patient. Some
experts argue that if a patients TSH level is mildly elevated, then even if their thyroid
hormone levels are within the normal range, they are not truly normal for that
individual.19 Put differently, while higher levels of thyroid-stimulating hormone increase
thyroid hormone production, the additional production does not fully compensate for the
underlying deficiency. According to this view, subclinical hypothyroidism represents
early thyroid failure, that is, less than full compensation for the diminished function of
the thyroid gland.
Prevalence and Course of Mild Thyroid Dysfunction

Using the upper limit of the reference range as a cut off, approximately 5 percent of
women and 3 percent of men have subclinical thyroid dysfunction (i.e., TSH > 4
mIU/L).1 Approximately one in four of these individuals has a markedly elevated TSH
concentration (>10 mIU/L). Such patients are likely to progress to overt hypothyroidism
over 20 years.20
The other 75 percent of individuals with subclinical hypothyroidism have mildly elevated
TSH levels (4 mIU/L < TSH 10 mIU/L). In this group, age, sex, geographic region, and
the presence of thyroid auto-antibodies are strong predictors of the rate of progression to
43
overt hypothyroidism. From one-third to two-thirds of these individuals have antithyroid

antibodies. Depending on age, sex, and TSH level, 50 percent to 70 percent of these
individuals will progress to overt disease over 20 years. In those who do not have
antithyroid antibodies, the risk of progression is lower.20
In general, prevalence increases with age, is higher among whites compared with blacks,
and higher in women compared with men.21 Estimates of the prevalence of subclinical
hypothyroidism vary based on demographic factors and differences in the defined upper
normal limit for TSH. A systematic review and meta-analysis of good-quality crosssectional studies1 estimated that the prevalence in women ranged from 1.2 percent among
non-Hispanic, African-American women to 5.8 percent in non-Hispanic, white women
and from 4 percent in women age 18-44 to over 17 percent in women over 75 years. In
the NHANES sample, estimates ranged from 1.8 percent among non-Hispanic, AfricanAmerican men to 2.4 percent among Mexican-American men.22 In a population-based
epidemiological study in Whickham, England, the prevalence ranged from 1 percent
among men 18-65 to 6.2 percent among men 65 or older.23
Strategies for Detecting and Managing Subclinical

Thyroid Dysfunction
Screening Strategies
Screening can be defined as the application of a test to detect a potential disease or
condition in a person who has no known signs or symptoms of that condition at the time
the test is done.24 In case-finding, testing for thyroid dysfunction is performed among
patients who come to their clinicians for unrelated reasons. When the test is abnormal, the
patient is called back for a detailed thyroid-directed history and confirmatory testing.
Subclinical hypothyroidism is diagnosed if the TSH remains elevated and the free T4
remains normal for a period of 3-6 months. While hypothyroidism and hyperthyroidism
are distinctly different disorders, with different symptoms and potential complications,
screening for both subclinical hypo- and hyperthyroidism is accomplished through testing
of serum TSH, with testing of serum free T4 if the TSH is high, and of T3 as well as free
T4 if the TSH falls below the normal range.3
Management Strategies
Subclinical Hypothyroidism
For patients with subclinical hypothyroidism, the alternative management strategies are
treatment with thyroid replacement hormone versus watchful waiting. A detailed strategy
for routine treatment is described elsewhere.12 Treatment strategies vary, but all begin
with repeat testing to confirm that the TSH is still elevated. If the TSH is >10 mIU/L on
repeat testing, treatment with levothyroxine is initiated. If the TSH is mildly elevated
(above the reference range but below 10 mIU/L), some experts recommend routine
treatment. Others recommend measurement of serum thyroid peroxidase antibodies and
treatment with levothyroxine if antibody levels are high. All guidelines recommend
levothyroxine rather than triiodothyronine or both as the drug of choice. The preference
for levothyroxine is based on the results of randomized trials of levothyroxine alone
versus combination therapy for patients with overt hypothyroidism that show no clear
benefit of combination therapy over levothyroxine alone.25
Watchful waiting encompasses two different strategiesexpectant management or
active surveillance. Expectant management means closely watching a patients
condition and treating if symptoms develop or laboratory results change. Active
surveillance means repeating thyroid function tests and taking a thyroid-directed history
44
at a particular interval; then, if symptoms or laboratory results change, beginning

treatment. The appropriate time-interval for retesting individuals with subclinical thyroid
dysfunction is unknown.
A recent British guideline26 offered the following typical strategy for active surveillance:
If screening is performed, and a high serum TSH concentration and normal free T4 is
found, repeat measurement 3-6 months later after excluding nonthyroidal illness and
drug interference
If the TSH is mildly elevated (above the reference range but below 10 mIU/L), obtain
serum thyroid peroxidase antibodies
If antibody levels are high, repeat measurement of TSH annually. If they are low,
repeat measurement of TSH every 3 years. Initiate treatment if the TSH level is
greater than 10 mIU/L or the patient develops clinical findings of hypothyroidism.
Practice styles vary widely. A well-conducted chart review study of 500 patients with
subclinical hypothyroidism seen at the Mayo Clinic in 1995-1996 found that clinicians
treated 38.7 percent of patients who had a TSH between 5.1 and 10.0 mIU/L.27
Unfortunately, more recent data and primary care-based practice patterns are not
available.
Subclinical Hyperthyroidism
For subclinical hyperthyroidism, some experts 21,28 recommend repeating thyroid function
tests after 3 months and, if the TSH remains suppressed, obtaining ultrasonography and a
24-hour Radioactive Iodine Uptake (RAIU) thyroid scan. These guidelines recommend
antithyroid treatment if the patient has a persistent TSH level less than 0.1 mIU/L and is
found to have Graves or nodular thyroid disease. Treatments include medications, such as
propylthiouracil, or ablation with radioactive iodine or surgery. The guideline
recommended against routine treatment in those whose TSH was between 0.1 and 0.45
mIU/L.
Guidelines on Early Detection and Treatment

A review of the history of guidelines for subclinical thyroid dysfunction provides insight
into the reason for practice variation (see also Appendix E). In 1990 and again in 1998,
the American College of Physicians found it is reasonable to screen women older than
50 years of age for unsuspected but symptomatic thyroid disease. The guideline
specified that the goal of routine testing was to find overt, but overlooked, thyroid
dysfunction, not subclinical hypothyroidism. Because the clinical significance of mildly
elevated TSH test results was uncertain, the guideline recommended obtaining a free T4
test only when the TSH level was undetectable or 10 mIU/L or more. The ACP guideline
panel used a systematic review of the literature to arrive at its recommendations.10These
guidelines expired in 2003.
In 1999, the American Association of Clinical Endocrinologists recommended screening
asymptomatic women over the age of 60.29In 2000, the American Thyroid Association
recommended screening all patients over 35 years of age every 5 years (more frequently
if the patient is at increased risk).30 These organizations used a consensus process to
develop guidelines and did not use systematic reviews in arriving at their
recommendations.
In 2003, the Institute of Medicine (IOM) published a volume entitled Medicare
Coverage of Routine Screening for Thyroid Disease, which examined the issue of
screening for thyroid dysfunction in the Medicare population and concluded that there is
insufficient evidence to recommend periodic, routine screening for thyroid dysfunction
among asymptomatic persons using serum TSH levels.31 In 2004, the USPSTF
45
determined that the evidence was poor that treatment of screen-detected adults, in either
the general population or in specific high-risk groups, improves clinically important
outcomes and concluded that there was insufficient evidence to recommend for or against
screening for thyroid disease in adults. These groups used essentially identical systematic
reviews to arrive at their recommendations.1,31 The USPSTF issued an I
recommendation, indicating that the evidence was insufficient to recommend for or
against routine screening for thyroid disease in adults.32The conclusions about the
evidence were:
There is fair evidence that the thyroid stimulating hormone (TSH) test can detect
subclinical thyroid dysfunction in people without symptoms of thyroid dysfunction,
but poor evidence that treatment improves clinically important outcomes in adults
with screen-detected thyroid disease
Although the yield of screening is greater in certain high-risk groups (e.g., postpartum
women, people with Downs syndrome, and the elderly), there is poor evidence that
screening these groups leads to clinically important benefits
There is the potential for harm caused by false positive screening tests; however, the
magnitude of harm is not known
There is good evidence that overtreatment with levothyroxine occurs in a substantial
proportion of patients, but the long-term harmful effects of overtreatment are not
known. As a result, the balance of benefits and harms of screening asymptomatic
adults for thyroid disease could not be determined.
In 2004, a panel sponsored by the American Association of Clinical Endocrinologists, the

American Thyroid Association, and the Endocrine Society evaluated data regarding the
management of subclinical thyroid dysfunction.21 Unlike the older AACE and ATA
guidelines, the panel used a systematic review of the evidence to arrive at its
recommendations.33 The panel adopted the strength of evidence rating of the USPSTF in
its assessment. The panel found insufficient evidence to support population-based
screening and recommended against population-based screening for thyroid disease,
though it did advocate aggressive case-finding in those considered high-risk, including
pregnant women and women older than 60. They also recommended against routine
treatment of patients with subclinical hypothyroidism with serum TSH levels of 4.5 10.0 mIU/L. Specifically, the panel found insufficient evidence to support routine
treatment of individuals who have a mildly elevated TSH (Table 3). The findings about
the evidence regarding the complications of subclinical hypothyroidism and the effects of
treatment agreed with those of the IOM and USPSTF.
Table 3. Evidence for the association of subclinical hypothyroidism (TSH

4.5-10 mIU/L) and adverse health outcomes and quality of evidence for
risks and benefits of treatment: Findings of the American Association of
Clinical Endocrinologists, the American Thyroid Association, and the
Endocrine Society Panel
Strength of evidence for Strength of evidence
association with complications regarding benefits
and
harms
of
treatment
overt Gooda
Not applicabled
Complication
Progression
to
hypothyroidism
Adverse cardiac end points Insufficientb
Elevation
in
serum Insufficientc
cholesterol and
LDL-C
levels
Cardiac dysfunction
Insufficientc
No evidence
Insufficient
Insufficient
46
Complication
Symptoms
hypothyroidism
Psychiatric symptoms
Strength of evidence for Strength of evidence

association with complications regarding benefits
and
harms
of
treatment
of No evidence
Insufficient
No evidence
Insufficient
(Adapted from JAMA 200421)

a Good: Evidence includes consistent results from well-designed, well-conducted
studies in representative populations that directly assess effects on health
outcomes.
b Insufficient: Evidence is insufficient to assess the effects on health outcomes
because of limited number or power of studies, important flaws in their design or
conduct, gaps in the chain of evidence, or lack of information on important health
outcomes.
c Data did not distinguish between serum TSH concentrations between 4.5-10
mIU/L and > 10 mIU/L.
d Thyroid hormone therapy normalizes serum TSH at any TSH concentration.
Evidence for the association of subclinical hypothyroidism (TSH 4.5-10 mIU/L) and
adverse health outcomes and quality of evidence for risks and benefits of treatment:
Findings of the American Association of Clinical Endocrinologists, the American
Thyroid (more...)
In 2005, the three professional societies that sponsored the evidence-based panel issued a
consensus statement rejecting its recommendations.34 While acknowledging that the
independent review panel found insufficient evidence to recommend treatment of patients
with subclinical hypothyroidism in the range of 4.5-10.0 mIU/L, the counter argued that
lack of definitive evidence for a benefit does not equate to evidence for lack of benefit
and recommended that most patients with TSH levels between 4.5 and 10.0 mIU/L
should be considered for treatment. Their rationale for recommending screening despite
gaps in the evidence about treatment is discussed in detail in the next section of this
report (Rationale for Screening and Treatment).
In 2006, three British professional associations (Association for Clinical Biochemistry,
the British Thyroid Association, and the British Thyroid Foundation) published
guidelines for using thyroid function tests.26 The guideline panel found that screening
for thyroid dysfunction in a healthy adult population is not warranted. It recommended
against routine treatment of patients who have a TSH concentration above the reference
range but below 10 mIU/L but said that a therapeutic trial of thyroxine [should be
considered] on an individual patient basis. The British panel noted that that there was
growing evidence against the use of thyroxine in elderly patients, in whom an elevated
TSH concentration may reflect an adaptive mechanism to prevent excessive
catabolism. Like the ACP and AACE guidelines, the British panel recommended
aggressive case-finding in women with non-specific symptoms. The panel used
systematic reviews in their process for developing guidelines.35
In 2007, The American College of Obstetricians and Gynecologists (ACOG)
recommended against routine screening in pregnant women. It stated that there is no
evidence that identifying and treating pregnant women with subclinical hypothyroidism
improved either maternal or infant outcomes.36
Rationale for Screening and Treatment

47
Subclinical Hypothyroidism
Although there is wide agreement that the long-term benefits of early treatment of
subclinical thyroid dysfunction have not been proven, there is disagreement about what to
do until better evidence is available. This disagreement reflects differing views of the
clinical relevance of research about the complications of subclinical thyroid dysfunction.
Proponents argue that thyroid dysfunction is common and associated with significant
morbidity. Additionally, a serum TSH test is relatively inexpensive, accurate, readily
available, and generally a very acceptable test for patients to undergo.30,34Symptoms of
overt thyroid dysfunction also can be vague and at times difficult to diagnose, and
therefore, thyroid screening may allow the diagnosis of overt disease earlier in the
clinical course, thus reducing morbidity.30,34,37 For subclinical hypothyroidism, treatment
with levothyroxine is noninvasive and inexpensive. Finally, proponents argue that the
potential harms of screening are small in relation to the potential benefits: Because the
potential harm of early detection and treatment appear to be so minor and preventable, it
seems prudent to err on the side of early detection and treatment until there is sufficient
data to address these issues definitively.34
Since 2005, the most important, widely cited argument for early treatment of thyroid
dysfunction is the association of untreated subclinical hypothyroidism with other risk
factors for heart disease and with incident coronary disease or heart failure later in life.
Subclinical hypothyroidism may be a risk factor for atherosclerosis and myocardial
infarction, but epidemiologic studies of this question have had mixed results.38-42 Four
recent meta-analyses have evaluated the association of subclinical thyroid disorder on
cardiac mortality or all-cause mortality.
One meta-analysis included six cohort studies and found that those with subclinical
hypothyroidism had a relative risk (RR) of 1.53 (1.31-1.79) of having coronary artery
disease (CAD) at baseline.43 Subclinical hypothyroidism was associated with a RR of
1.188 (1.024-1.379) of developing CAD in followup (included studies followup ranged
from 4 to 20 years), but was not found to be associated with all-cause mortality.43 The
second review (of 14 cohort and two case-control studies) found no association with
subclinical hyperthyroidism and circulatory or all-cause mortality.44 With regard to
subclinical hypothyroidism, the association with circulatory mortality was not statistically
significant, but a hazard ratio of 1.25 (1.3-1.53) was found for all-cause mortality.44 The
third review, which included 10 population-based prospective studies and two studies of
convenience samples of cardiac patients or patients with a history of stroke or hip
replacement, found no overall statistically significant association between either
subclinical hypothyroidism or subclinical hyperthyroidism and total mortality or coronary
morbidity or mortality.45 A statistically significant, but small, increased risk for heart
disease was found for individuals younger than 65.45 The last meta-analysis included 15
studies (six population-based cross-sectional studies and nine longitudinal cohort studies)
with 2,531 subclinical hypothyroid participants and 26,491 euthyroid individuals.46 Five
studies provided longitudinal data on the risk of coronary events; in these, overall there
was no difference in incident ischemic heart disease (IHD) in subclinical hypothyroid
participants and euthyroid participants (OR 1.27 [0.951.69]). In a subgroup analysis, in
studies of subjects younger than 65 years, the odds ratio was 1.68 (1.272.23), but for
older subjects, there was no relationship between subclinical hypothyroidism and incident
IHD (OR 1.02 [0.851.22]).46
The epidemiological studies included in these reviews had serious limitations. Many
included individuals who had known thyroid disease, ischemic heart disease, or TSH
levels within the reference range. Many included subjects who underwent treatment with
levothyroxine during the followup period. In general, the studies did not adequately
control for potential confounders, such as lipid levels and blood pressure.
48
The most recent research addresses some of the limitations of previous studies.40,47One of
these, from the Cardiovascular Health Study, found no relationship between an elevated
TSH level and cardiovascular outcomes among 3, 233 individuals aged 65 years or older
enrolled in 1989-1990 and followed an average of 12.5 years.40 The other was an
reanalysis of the Wickham Study, a survey of 2,779 adults sampled from a mixed urban
and rural area of England conducted between July 1972 and June 1974. The goal of the
study was to assess the prevalence of thyroid disease in a cross-section of the community.
Personal and family history of thyroid disease and thyroid-related symptoms was
collected along with history of diabetes and cardiovascular-related diseases, and fasting
blood samples included assessment of levels of TSH, T4, T3, and cholesterol.23 Unlike
the earlier report from the Whickham study,48 the new analysis included only subjects
who had mildly elevated TSH levels, excluded subjects who had known thyroid disease
or ischemic heart disease, stratified subjects according to whether they were treated with
thyroxine during the followup period, and adjusted for several cardiovascular risk factors
as well as socioeconomic status. After adjustment for baseline age, gender, social class,
body weight, history of cerebrovascular disease, diabetes mellitus, smoking, systolic and
diastolic blood pressure, serum cholesterol levels, and levothyroxine use during followup
as covariates, subclinical hypothyroidism was associated with a higher risk of coronary
events over 20 years (hazard ratio 1.76 [1.152.71]) When levothyroxine use during
followup was not controlled for, the relationship was weaker (hazard ratio 1.53 [0.97
2.45]). Among the 91 subjects who had subclinical hypothyroidism, two of 20 who were
treated with levothyroxine during the course of the study died, versus 22 of 71 who did
not receive levothyroxine. Despite the low number of events, the authors reported a
hazard ratio of 0.20 (0.050.89) for all-cause mortality after adjustment for age, gender,
and total serum cholesterol.
While it is stronger than previous evidence, this analysis also had weaknesses. First, the
description of the methods for ascertaining cardiac events is not clear. Specifically, it is
not clear what events were considered in addition to documented myocardial infarction or
death from coronary disease. In the context of risk factor epidemiology, for a broadly
defined composite endpoint, the hazard ratios are low, making it more likely that
confounding or methodological factors account for the observed differences. Second, the
study did not control for the use of lipid-lowering medications during the followup
period. It is possible that the better outcomes of subjects treated with levothyroxine could
be due to other interventions introduced by their clinicians. Finally, the study was
conducted between 1972 and 1974, before the era of statins and other aggressive cardiac
risk management techniques. It is possible that the association between subclinical
hypothyroidism and subsequent cardiovascular outcomes would become negligible in the
context of current cardiac disease management.
The 2004 USPSTF review by Helfand found that evidence regarding mildly elevated
TSH levels and hyperlipidemia and atherosclerosis was inconsistent.1 In the recent
reanalysis of the Whickham study data, subjects with subclinical hypothyroidism had
higher baseline systolic blood pressure (146.9 26.4 mm Hg vs.139.5 24.7 mm Hg) and
total cholesterol levels (6.2 1.3 mmol/L [239.8 50.3 mg/dL]) vs. 5.9 1.2 [228.2
46.4 mg/dL]) and were slightly less likely to smoke than euthyroid subjects (see
Appendix A for lipid conversion factors). After adjustment for age, gender, weight,
smoking, and relevant medications, however, systolic blood pressure was associated with
subclinical hypothyroidism, but total cholesterol was not. In other cross-sectional studies,
subclinical hypothyroidism was weakly associated with total and LDL cholesterol, blood
pressure, abnormalities of cardiac function, and subcutaneous fat.49,50
Recently, two prospective studies have demonstrated a correlation between subclinical
hypothyroidism and congestive heart failure (CHF). In the Health, Aging, and Body
Composition Study cohort, 338 of 2,730 individuals, ages 70 to 79 were found to have
subclinical hypothyroidism.41 After a 4 year followup, a total of 178 individuals had a
CHF event.41 While those with a TSH of 4.5 to 6.9 did not have a statistically significant
49
higher rate of CHF events compared to those without subclinical hypothyroidism, those
with a TSH of 7 to 9.9 had a hazard ratio of 2.58 (95% CI, 1.19-5.60) and those with a
TSH >10 had a hazard ratio of 3.26 (95% CI, 1.37-7.77).41 Additionally, of the 2,555
without a history of CHF, those with a TSH of > 7 had a hazard ratio of 2.33 (95% CI,
1.1.0-4.96) of developing a incident CHF event.41 In the Cardiovascular Health Study
cohort, 474 of 3044 subjects older than 65 years who had no history of CHF had
subclinical hypothyroidism, 46 of whom had a TSH of > 10.51 After a median of 12 years
of followup, those with a TSH >10 had a hazard ratio of 1.88 (95% CI,1.05-3.34) of
developing a CHF event, while those with a TSH of 4.5 to 9.9 were not more likely to
have a CHF event.51
These two relatively large prospective cohort studies do indicate that an isolated TSH
might be a risk factor for the development of CHF, particularly for individuals with a
TSH of > 10. This association deserves further study. However, it is still unknown if
thyroid replacement therapy would modify this potential risk.
Subclinical Hyperthyroidism
Cross-sectional studies have shown untreated subclinical hyperthyroidism to be
associated with tachycardia, increased left ventricular mass leading to diastolic
dysfunction, atrial arrhythmias, and a decline in bone mass density increasing the risk of
fractures.1,21 Only atrial fibrillation and disease progression have been associated with
subclinical hyperthyroidism in longitudinal studies.1 In a recent longitudinal study of 102
women who had a TSH between 0.1 to 0.4 mIU/L, three progressed to overt
hyperthyroidism and 24 reverted to a normal TSH.52
In summary, progression to overt disease is the best established complication of
subclinical thyroid dysfunction. Epidemiologic data suggest that subclinical
hypothyroidism is associated with cardiovascular disease in subjects younger than 65
years, but the magnitude of risk is low. Evidence about the relationship of a mildly
elevated TSH to symptoms and to other cardiac risk factors, including the metabolic
syndrome, is weak. Subclinical hyperthyroidism is less common and less studied, and
thus, its natural history and effects are less clear.
Scope of Review
The main question addressed in this review was whether individuals who have mildly
abnormal TSH values will either benefit from or be harmed by screening and potential
subsequent treatment. We also addressed the question of whether the primary care
clinician should screen for thyroid function in patients seen in general medical practice
who have no specific indication for thyroid testing and who come to the clinician for
other reasons. For the purposes of this review, we considered overt thyroid disease to be a
well-defined clinical entity that has clear signs and symptoms, and thus, outside the scope
of our review.
In order for a condition to be a good candidate for screening in the general population,
several conditions need to be met. First, the condition needs to be relatively prevalent,
having a significant impact on the health of the population or an easily identified special
population. Second, there needs to be a test that is readily available to the general
population that is of reasonable cost and accuracy and is acceptable to individuals to
undergo. Finally, there needs to be an intervention that is of reasonable cost and
tolerability that when administered in a timely fashion will alter the disease state to
prevent morbidity and/or morality.
The Helfand (2004) review established that subclinical thyroid disease is quite prevalent;
may be responsible for morbidity; and that the serum TSH test is a readily available,
50
reliable, and acceptable test to detect the condition with a sensitivity above 98 percent
and specificity greater than 92 percent.1 However, in 2004, it remained unclear whether,
if detected, treating patients with subclinical thyroid disease would reduce morbidity.
As evidence of prevalence, test yield, and test performance have already been adequately
established,1 this current review focuses on whether new evidence demonstrates that
treatment improves clinically important outcomes in adults with screen-detected thyroid
disease.
Key Questions and Analytic Framework

We reviewed published studies to answer the following key questions:
Key Question 1
Does screening for subclinical thyroid dysfunction reduce morbidity or mortality?
Key Question 2
What are the harms of screening? Specifically, how frequently and how severely do
patients screened for subclinical thyroid dysfunction experience adverse psychological
impacts or other harms of work-up from screening?
Key Question 3
Does treatment of patients with subclinical hypothyroidism
hyperthyroidism detected by screening affect outcomes?
or
subclinical
Key Question 4
What are the harms of treatment of subclinical hypothyroidism and subclinical
hyperthyroidism? Specifically, what are the consequences of over-treatment, including
effects on bone mineral density and incidence of atrial fibrillation, and how frequently do
they occur?
We developed the final analytic framework shown in Figure 1 to guide the literature
review. The analytic framework shows the populations, classification, intermediate
outcomes, and health outcomes we examined in the review. We defined the target
population as community-living, non-pregnant adults, without a history of thyroid disease
or symptoms of overt hypothyroidism or hyperthyroidism, who might be representative
of those seen in primary care settings.
51
Analytic framework. Note: A. fibrillation=atrial fibrillation; CAD=coronary artery

disease; CHF=congestive heart failure; DEXA=dual-energy x-ray absorptiometry;
NNS=number needed to screen; NNT=number needed to treat; S=subclinical;
TSH=thyroid stimulating (more...)
In the framework, Arrow 1 represents studies directly comparing the effects of screening
versus not screening on important health outcomes (Key Question 1). Arrow 2,
corresponding to Key Question 2, represents evidence about the potential harms of
screening. Arrow 3 represents studies comparing different strategies (treatment vs.
monitoring) for managing individuals who are found to have borderline high or low TSH
levels (Key Question 3). Arrow 4 represents studies of the harms of treatment. Outcomes
of interest for subclinical hypothyroidism were cardiovascular morbidity and mortality,
measures of well-being including but not limited to cognition and memory, weight
change, blood pressure changes, and changes in lipid levels. For subclinical
hyperthyroidism, outcomes of interest were cardiovascular morbidity and mortality,
osteoporotic fractures, measures of well-being including but not limited to cognition and
memory, weight changes, blood pressure changes, changes in bone mineral density, and
changes in lipid levels.
Copyright Notice
Bookshelf ID: NBK83492
52

11. Sumber: http://www.todaysgeriatricmedicine.com/archive/110612p6.shtml
Elevated TSH Levels:

To Treat or Not to Treat?
By Juliann Schaeffer
Aging Well
Vol. 5 No. 6 P. 6
Physicians are accustomed to checking thyroid-stimulating hormone (TSH) in
older adults with symptoms of an over- or underactive thyroid, as its a fairly
accurate and routine measure of thyroid function. But a new study suggests that
for many patients, treatment for mild TSH elevations may no longer be
warranted.
As increasing numbers of people live into their 80s and 90s, it is important to
know how to manage their health, including thyroid function, says Anne
Cappola, MD, ScM, an associate professor of medicine at the Perelman School
of Medicine at the University of Pennsylvania and lead study author. We sought
to describe what happens to thyroid function in older people over time and to
determine the relationship between thyroid function and mortality in this
population.
The study, accepted for publication in The Endocrine Societys Journal of
Clinical Endocrinology & Metabolism, questions the assertion that slightly
elevated TSH levels are linked to an increase in mortality and suggests that
such elevations may actually be a normal part of healthful aging.
Study Particulars
The study first examined 5,888 men and women aged 65 and older between
1989 and 1992. Then in 2005, researchers reexamined 843 surviving
participants thyroid function for any changes in physical and cognitive function.
Study participants ranged in age from 77 to 102, with a mean age of 85.
We found that levels of TSH gradually increase during the aging process, which
means that more older people are outside of standard reference ranges and
could be labeled with the diagnosis of subclinical hypothyroidism, Cappola
says. However, older people [mean age of 85] with subclinical hypothyroidism
did not have a higher death rate and, if anything, there was a suggestion that
having subclinical hypothyroidism was protective.
In addition, higher levels of thyroid hormone itself were associated with a higher
risk of death, she adds. Gradual increases in TSH have been shown in
younger populations, and it was gratifying to be able to extend these longitudinal
53
findings into our older population. Based on our work and those of other groups,
we hypothesized that subclinical hypothyroidism would not be associated with
mortality. Ours is the largest study in older people to show this.
Cappola says elevated TSH levels are relatively common in older adults, seen
in approximately 15% of US adults aged 65 and older, and its more common in
women than in men, she says, noting that previous research suggests it
becomes more common in patients in their 70s and tends to run in families.
When to Treat
Cappola notes that older adults with only a mild elevation in TSH are unlikely to
see their levels progress to a dangerous level. We have shown in previous
studies that the mildly elevated TSH level tends to persist or revert to normal
and rarely progresses to a dangerous level. Others have shown an annual rate
of progression of 2% to 4%, she says.
What are considered mild vs. extreme in TSH increases? According to Cappola,
her research regarded mildly elevated TSH levels as those in the 4.5 to 7 mU/L
range, while very elevated TSH levels were considered to be those greater than
20 mU/L. The 7 to 10 and 10 to 20 mU/L ranges are somewhat gray zones,
she says, but most would treat persistently elevated TSH levels in this range,
regardless of the patients age. The treatment is thyroid hormone replacement
with levothyroxine.
While Cappola stresses that very elevated TSH levels are a separate matter
altogether and still need to be treated, she notes that milder increases havent
yet shown to be a risk to older adults health. There are serious risks to not
treating very elevated TSH levels, she explains. Our research group is looking
for risks to leaving mildly elevated TSH levels untreated in older adults, and we
have not found any so far.
An important point is that for elderly patients, and increasingly as the patient
ages, doctors need to think carefully about both the indications and ramifications
of any treatment, notes Rosemary Laird, MD, MHSA, AGSF, medical director of
the Health First Aging Institute and past president of the Florida Geriatrics
Society.
Certainly, with subclinical disease there is no perceived loss of quality of life, so
treatment of any kind should be carefully considered. For clinicians, these
results support watchful waiting and serial reassessment for most older adults
with only mildly elevated TSH levels. It even suggests some evidence of
potential harm from higher levels of thyroid hormone, so all the more reason to
carefully choose ones response to mildly elevated TSH, she posits.
We can also use this [studys findings] as a reminder that geriatric care needs
to be care that is individually tailored and reactive to an individuals overall
quality of life and life expectancy, since both of these foundational pieces of
information make the difference in clinical decision making, Laird adds.
54
It is Cappolas hope that these findings take hold in the clinical community,
prompting geriatricians and primary care physicians to think twice before
treating their much older patients for such mild elevations that, in her opinion
and from recent evidence, prove unlikely to do any harm on their own while
focusing instead on those with more aggressive leaps in TSH.
Our study shows that a gradual increase in TSH occurs during healthy aging
and that mild increases in TSH are not harmful in the oldest old, she says.
Beyond that, we found that higher levels of thyroid hormone are associated with
increased mortality. These findings raise concern for reflexively treating older
people with mild elevations in TSH with thyroid hormone replacement.
Juliann Schaeffer is an associate editor at Great Valley Publishing Company.
12. Sumber: https://labtestsonline.org/understanding/analytes/tsh/tab/test/
The Test
1.
2.
3.
4.
How is it used?
When is it ordered?
What does the test result mean?
Is there anything else I should know?
How is it used?
The thyroid-stimulating hormone (TSH) test is often the test of choice for evaluating
thyroid function and/or symptoms of a thyroid disorder, including hyperthyroidism or
hypothyroidism.
TSH is produced by the pituitary gland, a tiny organ located below the brain and behind
the sinus cavities. It is part of the body's feedback system to maintain stable amounts of
the thyroid hormones thyroxine (T4) and triiodothyronine (T3) in the blood and to help
control the rate at which the body uses energy.
A TSH test is frequently ordered along with or preceding a free T4 test. Other thyroid
tests that may be ordered include a free T3 test and thyroid antibodies (if autoimmunerelated thyroid disease is suspected). Sometimes TSH, free T4 and free T3 are ordered
together as a thyroid panel.
TSH testing is used to:
Diagnose a thyroid disorder in a person with symptoms

Screen newborns for an underactive thyroid
Monitor thyroid replacement therapy in people with hypothyroidism
Monitor anti-thyroid treatment in people with hyperthyroidism
Help diagnose and monitor infertility problems in women
Help evaluate the function of the pituitary gland (occasionally)
55
Screen adults for thyroid disorders, although expert opinions vary on who can
benefit from screening and at what age to begin
When is it ordered?
A health practitioner may order a TSH test when someone has symptoms of
hyperthyroidism or hypothyroidism and/or when a person has an enlarged thyroid gland
(goiter).
Signs and symptoms of hyperthyroidism may include:
Increased heart rate

Anxiety
Weight loss
Difficulty sleeping
Tremors in the hands
Weakness
Diarrhea (sometimes)
Light sensitivity, visual disturbances
The eyes may be affected: puffiness around the eyes, dryness, irritation, and, in some
cases, bulging of the eyes.
Signs and symptoms of hypothyroidism may include:
Weight gain
Dry skin
Constipation
Cold intolerance
Puffy skin
Hair loss
Fatigue
Menstrual irregularity in women
TSH may be ordered at regular intervals when an individual is being treated for a known
thyroid disorder. When a person's dose of thyroid medication is adjusted, the American
Thyroid Association recommends waiting 6-8 weeks before testing the level of TSH
again.
TSH screening is routinely performed in the United States on newborns soon after birth
as part of each state's newborn screening program.
In 2004, the U.S. Preventive Services Task Force found insufficient evidence to
recommend for or against routine screening for thyroid disease in asymptomatic adults.
However, the American Thyroid Association and the American Association of Clinical
Endocrinologists released clinical practice guidelines in 2012 that recommend that
screening for hypothyroidism should be considered in people over the age of 60.
Because the signs and symptoms of both hypothyroidism and hyperthyroidism are so
similar to those seen in many common disorders, health practitioners often need to rule
out thyroid disease even though the patient has another problem.
What does the test result mean?

A high TSH result may mean that:
The person tested has an underactive thyroid gland that is not responding adequately
to the stimulation of TSH due to some type of acute or chronic thyroid dysfunction
56
A person with hypothyroidism or who has had their thyroid gland removed is
receiving too little thyroid hormone replacement medication and the dose may need
to be adjusted
A person with hyperthyroidism is receiving too much anti-thyroid medication and
the dose needs adjusting
There is a problem with the pituitary gland, such as a tumor producing unregulated
levels of TSH
A low TSH result may indicate:
An overactive thyroid gland (hyperthyroidism)

Excessive amounts of thyroid hormone medication in those who are being treated for
an underactive (or removed) thyroid gland
Insufficient anti-thyroid medication in a person being treated for hyperthyroidism;
however, it may take a while for TSH production to resume after successful antithyroid treatment. This is why the American Thyroid Association recommends
monitoring this treatment with tests for thyroid hormones (T4 and T3) as well as
TSH levels.
Damage to the pituitary gland that prevents it from producing adequate amounts of
TSH
Whether high or low, an abnormal TSH indicates an excess or deficiency in the amount
of thyroid hormone available to the body, but it does not indicate the reason why. An
abnormal TSH test result is usually followed by additional testing to investigate the
cause of the increase or decrease.
The following table summarizes some examples of typical test results and their potential
meaning.
High
Normal
High
Low
Low
Normal
High or
normal
Low or
normal
Free or
total T3
Normal
Low or
normal
Normal
High or
normal
Low or
normal
High
High
TSH
Low
Low
Normal
Free T4
Probable Interpretation
Mild (subclinical) hypothyroidism
Hypothyroidism
Mild (subclinical) hyperthyroidism
Hyperthyroidism
Non-thyroidal illness; pituitary
(secondary) hypothyroidism
Thyroid hormone resistance syndrome
(a mutation in the thyroid hormone
receptor decreases thyroid hormone
function)
Is there anything else I should know?

It is important to note that TSH, free T4, and free T3 tests are a "snapshot" of what is
occurring within a dynamic system. An individual person's thyroid testing results may
vary and may be affected by:
Increases, decreases, and changes (inherited or acquired) in the proteins that bind
T4 and T3
Pregnancy
Estrogen and other drugs
Liver disease
57
Systemic illness
Resistance to thyroid hormones
Many medications including aspirin and thyroid-hormone replacement therapy

may affect thyroid gland function test results and their use should be discussed with the
health practitioner prior to testing.
Illnesses not directly related to the thyroid, "nonthyroidal illnesses," can affect thyroid
hormones levels. In particular, the level of T3 can be low in nonthyroidal illness (NTI).
Typically, the thyroid hormone levels return to normal after a person recovers from the
nonthyroidal illness. Historically, this condition was referred to as "euthyroid sick
syndrome" but that term is controversial because there is some question as to whether
those affected have a thyroid gland that is functioning normally (euthyroid).
When a health practitioner adjusts a person's thyroid hormone replacement dosage, it is
important to wait at least one to two months before checking the TSH again so that the
new dose can have its full effect.
Extreme stress and acute illness may affect TSH test results. It is generally
recommended that thyroid testing be avoided in hospitalized patients or deferred until
after a person has recovered from an acute illness.
Results may be low during the first trimester of pregnancy.
Candesartan
COMMON BRAND NAME(S): Atacand
GENERIC NAME(S): CANDESARTAN CILEXETIL
1. Sumber : https://en.wikipedia.org/wiki/Candesartan
Candesartan
Candesartan
58
Systematic (IUPAC) name

2-ethoxy-1-({4-[2-(2H-1,2,3,4-tetrazol-5-yl)phenyl]phenyl}methyl)-1H1,3-benzodiazole-7-carboxylic acid
Clinical data
Atacand
Trade names
monograph
AHFS/Drugs.com
a601033
MedlinePlus
Pregnancy
category
Legal status
AU:
(Prescription only)
Routes of
oral
administration
Pharmacokinetic data
15% (candesartan
Bioavailability
cilexetil)
Candesartan cilexetil:
intestinal wall;
Metabolism
candesartan: hepatic
(CYP2C9)
9 hours
Biological half-life
Renal 33%, faecal 67%
Identifiers
Excretion
CAS Registry
Number
139481-59-7
ATC code
C09CA06
PubChem
CID: 2541
587
IUPHAR/BPS
DB00796
DrugBank
2445
ChemSpider
S8Q36MD2XX
UNII
KEGG
D00626
ChEBI
CHEBI:3347
ChEMBL
Formula
CHEMBL1016
Chemical data
C24H20N6O3
Molecular mass
SMILES[show]
InChI[show]
440.45 g/mol
59
(what is this?) (verify)

Candesartan (rINN) /kndsrtn/ is an angiotensin II receptor antagonist used mainly for
the treatment of hypertension. The prodrug candesartan cilexetil is marketed by
AstraZeneca and Takeda Pharmaceuticals, commonly under the trade names Blopress,
Atacand, Amias, and Ratacand. It is available in generic form.[1]
Contents
o
o
1 Clinical use
1.1 Prehypertension
1.2 Combination with diuretic
2 Chemistry and pharmacology
3 Development history
4 See also
5 References
6 External links
Clinical use
Main article: Angiotensin II receptor antagonist
As with other angiotensin II receptor antagonists, candesartan is indicated for the treatment
of hypertension. Results from the CHARM study (early 2000s) demonstrated the morbidity
and mortality reduction benefits of candesartan therapy in congestive heart failure.[2] Thus,
while ACE inhibitors are still considered first-line therapy in heart failure, candesartan can be
used in combination with an ACE to achieve improved mortality and morbidity vs. an ACE
alone and additionally is an alternative in patients intolerant of ACE inhibitor therapy.
Prehypertension
In a four-year randomized controlled trial, candesartan was compared to placebo to see
whether it could prevent or postpone the development of full-blown hypertension in people
with so-called prehypertension. During the first two years of the trial, half of participants
were given candesartan, and the others received placebo; candesartan reduced the risk of
developing hypertension by nearly two-thirds during this period. In the last two years of the
study, all participants were switched to placebo. By the end of the study, candesartan had
significantly reduced the risk of hypertension, by more than 15%. Serious side effects were
actually more common among participants receiving placebo than in those given
candesartan.[3]
Combination with diuretic

Candesartan is also available in a combination formulation with a low dose of the thiazide
diuretic hydrochlorothiazide, to achieve an additive antihypertensive effect.
Candesartan/hydrochlorothiazide combination preparations are marketed under various trade
names including Atacand HCT, Hytacand, Blopress Plus, Advantec and Ratacand Plus.
60
Candesartan cilexetil
Chemistry and pharmacology

Candesartan is marketed as the cyclohexyl 1-hydroxyethyl carbonate (cilexetil) ester, known
as candesartan cilexetil. Candesartan cilexetil is metabolised completely by esterases in the
intestinal wall during absorption to the active candesartan moieity.
The use of a prodrug form increases the bioavailability of candesartan. Despite this, absolute
bioavailability is relatively poor at 15% (candesartan cilexetil tablets) to 40% (candesartan
cilexetil solution). Its IC50 is 15 g/kg.
Development history
The compound known as TCV-116 (candesartan) was studied by Japanese scientists using
standard laboratory rats. Animal studies were published showing the effectiveness of the
compound in 1992-1993, with a pilot study on humans published in the summer of 1993. [4][5]
See also
Discovery and development of angiotensin receptor blockers
References
http://www.sandoz.com/cs/www.sandoz.comv4/assets/media/shared/documents/Candesartan_PR.pdf
Pfeffer M, Swedberg K, Granger C, Held P, McMurray J, Michelson E, Olofsson B,
Ostergren J, Yusuf S, Pocock S (2003). "Effects of candesartan on mortality and morbidity in
patients with chronic heart failure: the CHARM-Overall programme". Lancet 362 (9386):
75966. doi:10.1016/S0140-6736(03)14282-1. PMID 13678868.
Julius S, Nesbitt SD, Egan BM; et al. (July 2006). "Feasibility of treating
prehypertension with an angiotensin-receptor blocker". New England Journal of Medicine
354 (16): 168597. doi:10.1056/NEJMoa060838. PMID 16537662.
Mizuno, K.; et al. (1992). "Hypotensive activity of TCV-116, a newly developed
angiotensin II receptor antagonist, in spontaneously hypertensive rats.". Life Sci. 51 (20):
PL183187. PMID 1435062.
Ogihara, T.; et al. (JulAug 1993). "Pilot study of a new angiotensin II receptor
antagonist, TCV-116: effects of a single oral dose on blood pressure in patients with
essential hypertension.". Clin Ther. 15 (4): 68491. PMID 8221818.
2. Sumber: http://www.webmd.com/drugs/2/drug-8183/candesartan-oral/details
candesartan
COMMON BRAND NAME(S): Atacand
GENERIC NAME(S): CANDESARTAN CILEXETIL
I want to save to My MedicineYES
61
WARNINGS:
This drug can cause serious (possibly fatal) harm to an unborn baby if used during pregna...
Uses
Candesartan is used to treat high blood pressure (hypertension). Lowering high blood
pressure helps prevent strokes, heart attacks, and kidney problems. Candesartan belongs to a
class of drugs called angiotensin receptor blockers (ARBs). It works by relaxing blood
vessels so blood can flow more easily.
This medication is also used to treat heart failure.
This medication is not recommended for use in children younger than 1 year due to
increased risk of side effects.
OTHER USES: This section contains uses of this drug that are not listed in the approved
professional labeling for the drug but that may be prescribed by your health care
professional. Use this drug for a condition that is listed in this section only if it has been so
prescribed by your health care professional.
This drug may also be used to help protect the kidneys from damage due to diabetes.
How to use candesartan

Read the Patient Information Leaflet if available from your pharmacist before you start
taking candesartan and each time you get a refill. If you have any questions, ask your doctor
or pharmacist.
Take this medication by mouth with or without food as directed by your doctor, usually
once or twice daily.
The dosage is based on your medical condition and response to treatment. In children, the
dosage is also based on weight.
Use this medication regularly to get the most benefit from it. To help you remember, take it
at the same time(s) each day. It is important to continue taking this medication even if you
feel well. Most people with high blood pressure do not feel sick. For the treatment of high
blood pressure, it may take up to 6 weeks before you get the full benefit of this drug.
Tell your doctor if your condition does not improve or if it worsens (such as your blood
pressure readings remain high or increase).
What conditions does candesartan treat?
conditions
What conditions does candesartan treat?
candesartan oral is used to treat the following:
High Blood Pressure, Chronic Heart Failure
candesartan oral may also be used to treat:
62
Kidney Disease from Diabetes, Diastolic Heart Failure, Nondiabetic Proteinuric

Nephropathy
3. Sumber: http://drugs.webmd.boots.com/drugs/drug-71-Candesartan.aspx
CANDESARTAN
Brand Name(s) : Amias
CANDESARTAN WARNINGS
Candesartan should be used with caution in:
patients with kidney disease or who have had a kidney transplant, patients with liver or
heart disease, with renal artery stenosis, those with abnormally low blood pressure,
patients who are about to have anaesthetics and surgery (including dental surgery),
obstructive hypertrophic cardiomyopathy, primary hyperaldosteronism,
hyperkalaemia, severe congestive heart failure.
It should not be used in:
women who are more than 3 months pregnant (it is also better to avoid candesartan in
early pregnancy), patients who are allergic to candesartan or to any of the ingredients
in the medicine; severe liver disease or biliary obstruction (a problem with the
drainage of the bile from the gall bladder).
Also see list of precautions and interactions

STORAGE
Do not store above 30 C
CANDESARTAN USES
Candesartan is used to lower blood pressure by relaxing your blood vessels, making it
easier for your heart to pump your blood around your body.
It is an angiotensin II receptor antagonist, sometimes known as an angiotensin receptor
blocker (ARB).
It is used to lower your blood pressure.
63
In general this drug is used to treat high blood pressure (hypertension). It is also used to
treat heart failure when combined with a specific type of medicines called angiotensinconverting-enzyme inhibitors (ACE inhibitors) or when ACE inhibitors are considered not
suitable
Benefits of being on this drug can include lowering of blood pressure and treating heart
failure
Listed below are the typical uses of Candesartan.
Treatment of high blood pressure in adult patients

Treatment of heart failure with reduced heart muscle function in addition to an
angiotensin converting enzyme (ACE) inhibitor or when ACE inhibitors cannot be
used, in adult patients.
On occasion your doctor may prescribe this medicine to treat a condition not on the above
list.
HOW TO USE/TAKE
How often do I take it?
Take this medication orally usually once a day, with or without food.
Use this medication regularly in order to get the most benefit from it.
Remember to use it at the same time each day - unless specifically told otherwise by
your doctor.
It may take up to 4 weeks before the full benefit of this drug takes effect.
Certain medical conditions may require different dosage instructions as directed by
your doctor.
What dose?
Dosage is based on your age, gender, medical condition, response to therapy, and use of
certain interacting medicines.
Do I need to avoid anything?
When driving vehicles or operating machines it should be taken into account that
dizziness or weariness may occur during treatment. Consult your doctor or pharmacist
for more details.
When can I stop?
It is important to continue taking this medication even if you feel well, unless your doctor
tells you to stop.
CANDESARTAN SIDE EFFECTS
Vertigo,
headache,
nausea,
hepatitis,
blood disorders,
back pain,
joint pain (arthralgia),
muscle pain (myalgia),
rash,
64
urticaria,
pruritus,
dizziness,
cold or flu-like symptoms/respiratory infections,
hypotension (low blood pressure).
changes in kidney function and potassium and sodium levels
swelling of the face, lips, tongue and/or throat,
jaundice (yellow skin and/or eyes),
hepatitis (inflamed liver),
changes in red blood cell levels and decreased levels of white blood cells.
If any of these persist or you consider them severe then contact your doctor or pharmacist.
Stop taking candesartan and tell your doctor immediately if you develop any of the
following symptoms: swollen face, lips, tongue, eyes and or throat; jaundice.
Remember that your doctor has prescribed this medication because he or she has judged
that the benefit to you is greater than the risk of side effects. Many people using this
medication do not have serious side effects.
A serious allergic reaction to this drug is unlikely, but seek immediate medical attention if
it occurs. Symptoms of a serious allergic reaction include: rash, itching/swelling (especially
of the face/tongue/throat), dizziness, trouble breathing.
This is not a complete list of possible side effects. If you notice other effects not listed
above, contact your doctor or pharmacist.
The Yellow Card Scheme allows you to report suspected side effects from any type of
medicine (which includes vaccines, herbals and over the counter medicines) that you are
taking. It is run by the medicines safety watchdog called the Medicines and Healthcare
products Regulatory agency (MHRA). Please report any suspected side effect on the
Yellow Card Scheme website.
CANDESARTAN PRECAUTIONS
This medication should not be used if you have certain medical conditions. Before using
this medicine, consult your doctor or pharmacist if you have: severe liver disease or biliary
obstruction; are pregnant or are planning to become pregnant; breastfeeding.
Before using this medication, tell your doctor or pharmacist your medical history,
especially any of the following: kidney disease or kidney transplant; liver disease; renal
artery stenosis; abnormally low blood pressure; obstructive hypertrophic cardiomyopathy;
primary hyperaldosteronism; hyperkalaemia (high potassium levels); severe congestive
heart failure; intolerance to any of the ingredients.
Before having surgery, tell your doctor or dentist that you are taking this medication.
Does alcohol intake affect this drug?
If you are being treated for heart failure, your doctor may recommend that you avoid
alcohol.
The elderly. Candesartan can be used in the elderly.

Pregnancy and breastfeeding - please ensure you read the detailed information below
PREGNANCY
65
Candesartan is not safe to take if you are, or are planning to become, pregnant.
It is sensible to limit use of medication during pregnancy whenever possible. However, your
doctor may decide that the benefits outweigh the risks in individual circumstances and after
a careful assessment of your specific health situation.
If you have any doubts or concerns you are advised to discuss the medicine with your doctor
or pharmacist.
BREAST FEEDING
Candesartan is not safe to take if you are breastfeeding.
It is sensible to limit use of medication during breastfeeding whenever possible. However,
your doctor may decide that the benefits outweigh the risks in individual circumstances and
after a careful assessment of your specific health situation.
If you have any doubts or concerns you are advised to discuss the medicine with your doctor
or pharmacist.
CANDESARTAN INTERACTIONS
Your doctor or pharmacist may already be aware of any possible drug interactions and may
be monitoring you for them. Do not start, stop, or change the dosage of any medicine before
checking with them first.
This drug should not be used with the following medications because very serious, possibly
fatal interactions may occur: none known.
Before using this medication, tell your doctor or pharmacist of all prescription and nonprescription/herbal products you may use, especially of:
Lithium for mania and depression

Potassium sparing diuretics (e.g. amiloride, triamteren, spironolactone)
Potassium supplements
Salt substitutes containing potassium
heparin
ACE inhibitors (such as enalapril, captopril, lisinopril or ramipril)
Diuretics (water tablets)
Non-steroidal anti-inflammatory painkillers (such as ibuprofen, naproxen or
diclofenac)
COX-2 inhibitors (such as celecoxib or etoricoxib)
More than 3 g of aspirin
This information does not contain all possible interactions. Therefore, before using
Candesartan, tell your doctor or pharmacist of all the products you use.
66

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