Professional Documents
Culture Documents
CONTENTS
FOREWORD
LIST OF ABBREVIATIONS
1. THYROTOXICOSIS
1.1 Clinical Features
1.2 Laboratory Investigations
1.3 Management
1.3.1
Medical Treatment
1.3.2
Surgery
1.3.3
Radioiodine Therapy
1.4 Management of Complications
1.4.1
Thyrocardiac complications
1.4.2
Hypokalaemic periodic paralysis
1.4.3
Ophthalmopathy
1.4.4
Dermopathy
2. THYROID CRISIS
2.1 Clinical Features
2.2 Management
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3. HYPOTHYROIDISM
3.1 Clinical Features
3.2 Laboratory Investigations
3.3 Management
3.3.1 Overt Hypothyroidism
3.3.2 Subclinical Hypothyroidism
3.3.3 In pregnancy
3.4 Monitoring
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4. MYXOEDEMA COMA
4.1 Management
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5. CONGENITAL HYPOTHYROIDISM
5.1 Clinical Features
5.2 Laboratory Investigations
5.3 Management
5.4 Monitoring
6. THYROIDITIS
6.1 Clinical Features
6.1.1
Hashimotos thyroiditis
6.1.2
Riedels thyroiditis
6.1.3
Subacute (De Quervains) thyroiditis
6.1.4
Postpartum thyroiditis
6.1.5
Painless thyroiditis
6.1.6
Acute pyogenic thyroiditis
6.2 Laboratory Investigations
6.3 Management
7. SINGLE THYROID NODULE
7.1 Diagnosis
7.2 Laboratory Investigations
7.2.1
Fine-needle aspiration cytology (FNAC)
7.2.2
Ultrasound scan
7.2.3
Thyroid scintiscan
7.2.4
Other scans
7.2.5
Thyroid function tests
7.3 Management
8. MULTINODULAR GOITRE
8.1 Clinical Features
8.2 Laboratory Investigations
8.3 Management
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STATEMENT OF INTENT
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REFERENCES
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TASKFORCE
AND
CONTRIBUTORS
Malaysian Endocrine and Metabolic Society
1. Professor Dato Dr Mustaffa Embong
Department of Medicine, School of Medical Sciences,
University Science Malaysia (USM)
2. Assoc Prof Dr Mafauzy Mohamed
Dean, School of Medical Sciences ,USM
3. Assoc Prof Dr Wan Mohamad Wan Bebakar
Head, Department of Medicine, School of Medical Sciences, USM
4. Dr Fuziah Md Zain
Department of Paediatrics, School of Medical Sciences,USM
3. Professor Dato Dr Anuar Zaini Mohd Zain
Dean, Faculty of Medicine, University of Malaya (UM)
6. Professor Dr Amir S Khir
Deputy Dean, Faculty of Medicine, UM
7. Assoc Prof Dr Chan Siew Pheng
Department of Medicine, Faculty of Medicine, UM
8. Assoc Prof Dr Ikram Shah Ismail
Department of Medicine, Faculty of Medicine, UM
9. Assoc Prof Dr Fatimah Harun
Department of Paediatrics, Faculty of Medicine, UM
10. Dr Rokiah Pendek
Department of Medicine, Faculty of Medicine, UM
3. Dr Hisham Abdullah
Consultant Surgeon, Hospital Kuala Lumpur (HKL)
College of Physicians
1. Dato Dr (Mrs) ST Kew
Consultant Physician, Hospital Kuala Lumpur (HKL)
2. Dr Liew Yin Mei
Consultant Physician, Hospital Kuala Lumpur (HKL)
3. Dr Wong Wing Keen
Consultant Physician, Pantai Medical Centre
Malaysian Paediatric Association
1. Assoc Prof Dr Wan Ariffin Abdullah
Department of Paediatrics, Faculty of Medicine, UM
2. Dr Tang Swee Fong
Department of Paediatrics, Faculty of Medicine, HUKM
Malaysian Medical Association
1. Dr Sahathevalingam
2. Dr Radhakrishna
LIST
OF
ABBREVIATIONS
AF
CMZ
CNS
CT
ESR
FNAC
fT4
fT3
IHD
K+
MEN
MNG
MRI
MTC
NSAID
PTU
SSKI
TSH
TRH
T4
T3
Atrial fibrillation
Carbimazole
Central Nervous System
Computerised Tomography
Erythrocyte Sedimentation Rate
Fine-Needle Aspiration Cytology
Free T4
Free T3
Ischaemic Heart Disease
Potassium ion
Multiple Endocrine Neoplasia
Multinodular Goitre
Magnetic Resonance Imaging
Medullary Thyroid Carcinoma
Non-Steroidal Anti-inflammatory Drug
Propylthiouracil
Saturated Solution of Potassium Iodide
Thyroid-stimulating Hormone, Thyrotropin
Thyrotropin-releasing Hormone
Thyroxine
Tri-iodothyronine
1. THYROTOXICOSIS
Thyrotoxicosis is a clinical state due to excess thyroid hormones. Two hormones
tri-iodothyronine (T3) and thyroxine (T4) are produced by the thyroid gland of which
T3 is the active hormone. The causes include:
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30-45 mg/day
300-450 mg/day
Maintenance therapy
(gradual reduction over
3-6 months from initial dose)
5-10 mg/day
50-100 mg/day
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1.3.2 Surgery
Thyroidectomy may be performed in Graves' disease, toxic multinodular
goitre or toxic adenoma.
Indications:
Failed medical treatment i.e. relapse after one or more courses of
antithyroid drugs, non-compliance or development of side-effects.
Those with large goitres, especially with pressure effects.
Patients who prefer surgery.
A relative indication is severe progressive ophthalmopathy.
Surgery should preferably be done by a surgeon proficient in thyroid
surgery.
Pre-operative preparation:
Control thyrotoxic state with medical treatment. Avoid hypothyroidism.
In the last 1-2 weeks, potassium iodide 5 mg tds or Lugol's iodine
5 -10 drops tds may be added to reduce vascularity of the thyroid gland.
1.3.3 Radioiodine Therapy
Radioiodine therapy is safe and appropriate in nearly all types of hyperthyroidism. It should NOT be used in pregnancy and women who are
breast-feeding. In general, radioiodine therapy is not recommended in
children.
Precautions:
Patients need to avoid close contact with young children and pregnant
women for a duration of 10 days after radioiodine therapy.
Women are advised not to become pregnant for at least 4-6 months.
Severe and complicated hyperthyroidism needs to be adequately
controlled before radioiodine treatment.
There is a need to emphasise on long-term follow-up and early detection of
hypothyroidism
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2. THYROID CRISIS
Thyroid crisis is a life threatening exacerbation of the hyperthyroid state with
evidence of decompensation in one or more organ systems. The mortality is 20 - 30 %.
It may be precipitated by stress including concurrent infections, surgery or pregnancy.
2.1 Clinical Features
It is a clinical diagnosis with features of severe thyrotoxicosis, hyperpyrexia
and neuro-psychiatric manifestations such as delirium.
2.2 Management
Rehydration
Treat hyperpyrexia (use fans, tepid sponging and oral paracetamol)
Do NOT use aspirin or NSAIDs
Beta sympathetic blocking agents
Oral propanolol 40 mg qid, or I/V 1-2 mg 4-6 hourly
Iodide
Oral saturated solution of potassium iodide (SSKI) 5 drops 6-hourly
or I/V Sodium Iodide 500 mg 8 hourly
or oral Lugol's iodine 5-10 drops, 6-hourly
Antithyroid Drugs
Carbimazole 15-20 mg 6-hourly
or propylthiouracil 150-200 mg 6-hourly
Corticosteroids
I/V dexamethasone 2 mg 6-hourly
or I/V hydrocortisone 200 mg 6-hourly
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3. HYPOTHYROIDISM
Hypothyroidism is due to deficiency of thyroid hormones resulting in a hypometabolic state. The causes are:
Primary
autoimmune thyroid disease
- thyroid agenesis
post-thyroidectomy
post-radioiodine therapy
Secondary hypopituitarism
Apathy, fatigue
Cold intolerance
Slow speech
Facial puffiness
Weight gain
Constipation
Coarse features
Less common features are:
Menorrhagia
Hoarse voice
Depression
Psychosis
May be asymptomatic.
3.2 Laboratory Investigations
To confirm diagnosis, serum fT4 and TSH should be assayed.
Elevated serum TSH levels are invariably found in primary hypothyroidism.
Serum TSH is useful in assessing adequacy of treatment.
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3.3.3 In pregnancy
There may be a need to increase the dose of L-thyroxine, particularly
during the second and third trimesters.
3.4 Monitoring
The patient should be monitored clinically and biochemically with serum
TSH and fT4 measurements.
Measurements of serum TSH and fT4 should be done 2-3 months after
initiation of therapy to determine the maintenance dose and subsequently
every 6 months to 1 year.
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4. MYXOEDEMA COMA
Myxoedema
coma
be precipitated by stress, infection, or
drugs
(e.g. CNS suppressants). This is not a common condition but urgent treatment is
required because the mortality is high.
4.1 Management
The treatment consists of:
Gradual rewarming with blankets.
Accurate core temperatures should be recorded with a low
reading
Rectal thermometer.
Thyroid hormone replacement with L-thyroxine 300-400 ug given
orally via nasogastric tube or parenterally if available. Alternatively,
doses of tri-iodothyronine 10 ug 8-hourly (IV or orally)
may
be used.
I/V hydrocortisone should be given, 200 mg stat and 100 mg 6-hourly
until patient regains consciousness
Ensure adequate hydration and nutrition;
Use 5-10% dextrose solution to maintain normal blood glucose levels.
Correct electrolyte imbalance (patients tend to be hyponatraemic).
Ensure adequate ventilation.
Patients tend to hypoventilate, resulting in hypercapnoea.
Treat precipitating cause.
Infection may be masked by the hypothyroid state.
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5. CONGENITAL
HYPOTHYROIDISM
An endocrine disorder resulting from inadequate thyroid hormone for the
metabolic needs of a newborn infant. Incidence is between 1:4000 to 1:5000 in
Malaysia. Most infants with the disease have no obvious clinical manifestations at
birth, therefore neonatal screening of thyroid function should be performed on all
newborns. Intellectual impairment can be prevented by early diagnosis and
treatment. The causes include:
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5.3 Management
Treatment should commence as soon as the diagnosis is made.
With early adequate thyroid replacement therapy, patients are expected to
have normal intellectual and physical development.
Starting dose of L-thyroxine is 10-12 ug/kg/day.
The aim is to maintain serum TSH levels within the normal range and fT4
at the upper limit of the normal range adjusted for age.
Treatment should be life-long except in children suspected of having
transient hypothyroidism whereby therapy is stopped at 2 years of age for
re-evaluation.
5.4 Monitoring
Patients should be monitored clinically and biochemically at monthly intervals
for the first 6 months then 3-monthly until one year of age; and thereafter
6 monthly.
Checklist for monitoring include growth parameters (weight, height,
head circumference), developmental milestones and bone age progression.
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6. THYROIDITIS
Thyroiditis is inflammation of the thyroid gland with destruction of the thyroid
tissues to a variable degree. The presentation, functional disturbance and prognosis
depend on the aetiology of the thyroiditis. Presentation may be acute, subacute or
chronic. The causes are:
Autoimmune Infection
Physical
Idiopathic
-
Hashimotos thyroiditis
post-partum thyroiditis
atrophic thyroiditis
viral thyroiditis (De Quervains thyroiditis)
radiation to the neck
painless thyroiditis
Riedels thyroiditis
24
3 Subacute (De Quervain's) thyroiditis usually presents with pain in the region
of thyroid gland which may be mistaken for pharyngitis accompanied in severe
cases by fever. There are also accompanying symptoms and signs of
thyrotoxicosis. On palpation, the gland is slightly to moderately enlarged, firm
and usually exquisitely tender. The disease usually passes through a euthyroid
phase followed by a transient hypothyroid phase prior to full recovery within a
few months in the majority of cases. Rarely, permanent hypothyroidism may
result.
4 Riedels thyroiditis is a rare condition of unknown aetiology presenting with
hypothyroidism and woody hard goitre. The extensive fibrosis may involve the
adjacent structures e.g. trachea and oesophagus and may be associated with
fibrosis elsewhere especially in the retroperitoneal area. Some patients may have
elevated anti-thyroid antibodies but not as high as those of Hashimotos
thyroiditis.
5 Painless thyroiditis is of unknown aetiology and is similar to postpartum
thyroiditis except that this is not associated with pregnancy.
6 Acute pyogenic thyroiditis is rare and is usually a result of dissemination from a
septic focus elsewhere. It usually presents with fever, pain and signs of acute
inflammation in the thyroid gland. Needle aspiration of the thyroid should be
performed for diagnosis and identification of the organism. Rarely, tuberculosis
or anaplastic carcinoma of the thyroid may present similarly.
6.2 Laboratory Investigations
Thyroid function tests to assess functional status are indicated in all patients
with thyroiditis. since some may have subclinical thyroid dysfunction. Repeat
measurements should be performed as thyroid status may change.
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26
The incidence of malignancy in solitary nodule may be as high as 10%. The sudden
appearance of a painful thyroid nodule is usually due to bleeding into a colloid cyst;
this resolves spontaneously.
.
7.1 Diagnosis
The history and physical examination are essential in the initial assessment
of thyroid swelling. The suspicion of malignant disease would be high in
the following:
Age groups of <20 years and >50 years have the highest incidence
of thyroid cancer in a palpable nodule
Male gender
History of rapid increase in size and local pressure symptoms
e.g. dysphagia and hoarseness of voice
History of external neck irradiation during childhood or adolescence
A firm/hard irregular and fixed nodule
Ipsilateral cervical lymphadenopathy (probability of malignancy
increases from about 10% to 70%)
Family history is important Familial medullary thyroid carcinoma has
an autosomal dominant inheritance while papillary thyroid carcinoma is
familial in only 3% of cases
Dominant nodule in a multinodular goitre
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7.2.2
Ultrasound scan is able to accurately indicate whether
there
are multiple nodules and determine changes in size of the
nodule. It can also confirm whether the nodule is cystic where
risk of malignancy is low, solid with a risk of malignancy of
around 20% or mixed with a 30% risk of malignancy.
7.2.3
Thyroid scintiscan with 99mTc or 123I is useful in
differentiating
toxic from cold nodules. The incidence of malignancy in cold
nodules is about 10-20%.
7.2.4
the
should
7.3 Management
In colloid cyst, aspiration may be therapeutic.
Surgery should be considered for recurrence.
Toxic adenoma is treated surgically or with radioiodine.
The use of L-thyroxine to reduce the size of thyroid nodules is seldom
effective.
In papillary and follicular carcinoma, total thyroidectomy followed
by ablative radioiodine and L-thyroxine therapy are potentially curative.
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8.
MULTINODULAR
GOITRE
iodine deficiency
goitrogen ingestion
autoimmune disorders
dyshormonogenesis (usually diffuse in the initial stages)
30
Thyroid scintiscans are not useful except in cases where toxic (hot)
nodules are suspected.
Fine needle aspiration cytology (FNAC) should be performed when
malignancy is suspected.
8.3 Management
No treatment is required when the goitre is small
symptoms. Reassurance is usually adequate.
and
not
causing
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as
STATEMENT OF INTENT
This report is not intended to be construed or to serve as a standard of
medical care.
32
REFERENCES
Treatment of hyperthyroidism and hypothyroidism
1 Larsen PR, Ingbar SH. The thyroid gland. In: Wilson JD, Foster DW, eds. Williams
Textbook of Endocrinology. 8th ed. Philadelphia, PA: WB Saunders Co, 1992:357487.
2 Braverman LE, Utiger RD. Introduction to thyrotoxicosis. In: Braverman LE, Utiger
RD, eds. Werner and Ingbars The Thyroid: A Fundamental and Clinical Text. 6 th
ed. Philadelphia, PA: JB Lippincott Co, 1991:645-647.
3 Haynes RC Jr. Thyroid and antithyroid drugs. In: Gilman AG, Rall TW, Nies AS,
Taylor P, eds. Goodman and Gilmans The Pharmacologic Basis of Therapeutics. 8 th
ed. New York, NY: Pergamon Press, 1990:1361-1383.
4 Franklyn JA. The management of hyperthyroidism. N Engl J Med
1994;330(24):1731-1738.
5 Surks MI. Treatment of hypothyroidism. In: Braverman LE, Utiger RD, eds. Werner
and Ingbars The Thyroid: A Fundamental and Clinical Text. 6 th ed. Philadelphia,
PA: JB Lippincott Co, 1991:1099-1103.
6 Utiger RD. Hypothyroidism. In DeGroot LJ et al, eds. Endocrinology Volume 1, 2nd
ed. Philadelphia, PA: WB saunders Co. 1989:702-721.
7 Griffin JE. Review:hypothyroidism in the elderly. Am J Med Sci 1990;299(5):334345.
8 Barsano CP. Other forms of primary hypothyroidism. In: Braverman LE, Utiger RD
eds. Werner and Ingbars The Thyroid: A Fundamental and Clinical Text. 6th ed.
Philadelphia, PA: JB Lippincott Co, 1991: 956-967.
9 Mandel SJ, Brent GA, Larsen PR. Levothyroxine therapy in patients with thyroid
disease. Ann Intern Med 1993;119:492-502.
10 Roti E, Braverman LE. Thyroid hormone therapy: when to use it when to avoid it.
Drug Therapy 1994;24(4):2-35.
11 Becker DV, Bigos ST, Gaitan E, et al. Optimal use of blood tests for assessment of
thyroid function. Thyroid 1993;3(4):353-354.
12 Hays MT, Nielsen KRK.
Human thyroxine absorption: age effects and
methodological analyses. Thyroid 1994;(4(1):55-64.
13 McEvoy GK. AHFS Drug Information 94. Bethesda, Md: American Hospital
Formulary Service 1994;2101.
33
34
30 Sawin CT. Thyroid dysfunction in older persons. Adv Intern Med 1991;75:223-248.
31 Stall GM, Harris S, Sokoll LJ, Dawson-Hughes B. Accelerated bone loss in
hypothyroid patients overtreated with L-thyroxine. Ann Intern Med 1990;113:265269.
32 Roti E, Minelli R, Gardini E, Braverman LE. The use and misuse of thyroid
hormone. Endocr Rev 1993;14:401-423.
Thyroid nodules
1 AACE Clinical Practice Guidelines for the Evaluation and Treatment of
Hyperthyroidism and Hypothyroidism Endocr Pract 1995;1:54-62.
2 Baskin HJ. Thyroid scans are they necessary? Endocr Pract 1995;1:302-305.
3 Caruso D, Mazzaferri EL. Fine needle aspiration biopsy in the management of
thyroid nodules. Endocrinologist 1991;1:194-202.
4 Cooper DS. Thyroxine suppression therapy for benign nodular disease: clinical
review 66. J Clin Endocrinol Metab 1995;80:331-334.
5 Dworkin HJ, Meier DA, Kaplan M. Advances in the management of patients with
thyroid disease. Semin Nucl Med 1995;25:205-220.
6 Gharib H. Current evaluation of thyroid nodules. Trends Endocrinol Metab
1994;5:365-369.
7 Gharib H, Goellner JR. Fine needle aspiration biopsy of the thyroid: an appraisal.
Ann Intern Med 1993;118:282-289.
8 Gharib H, Zimmerman D, Goellner JR, et al. Fine needle aspiration biopsy:use in
diagnosis and management of pediatric thyroid disease. Endocr Pract 1995;1:9-13.
9 Grant CS, Hay ID, et al. Long-term follow up of patients with benign thyroid FNA
cytologic diagnoses. Surgery 1989; 106:980-986.
10 Hamburger JI, Kaplan MM. Evaluation of thyroid nodules by needle biopsy, In:
Werner and Ingbars The Thyroid. 7th ed. New York:JB Lipincott, 1996.
11 Ledger GA, Khosla S, Lindor NM, et al. Genetic testing in the diagnosis and
management of multiple endocrine neoplasia type II. Ann Intern Med 1995;122:118124.
12 Mazzaferri EL. Thyroid cancer in thyroid nodules: finding a needle in a haystack.
Am J Med 1992;93:359-363.
35
36
10 Gagel RF, Goepfert H, Callender DL. Changing concepts in the pathogenesis and
management of thyroid cracinoma. CA Cancer J Clin 1996;46:261-283.
11 Wells SA, Chi DD, Toshima K, et al. Predictive DNA testing and prophylactic
therapy in patients at risk for multiple endocrine neoplasia type 2A. Ann Surg
1994;120:1377-1381.
Staging and Risk Groups
12 Beahrs OH, Henson DE, Hutter RVP, et al. (American Joint Committee on Cancer).
Manual for Staging of Cancer. 4th ed. Philadelphia PA: JB Lippincott 1992:53-56.
13 Ain KB. Papillary thyroid carcinoma: etiology, assessment and therapy. Endocrinol
Metab Clin North Am 1995;24:711-760.
14 Hay ID. Cytometric DNA ploidy analysis in thyroid cancer. Diagn Oncol
1991;1;181-185.
15 Pyke CM, Hay ID, Goellner Jr, et al. Prognostic significance of calcitonin
immunoreactivity, amyloid staining and flow cytometric DNA measurements in
medullary thyroid carcinoma. Surgery 1991;110:964-970.
16 Byar DP, Green SB, Dor P, et al. A prognostic index for thyroid carcinoma: a study
of the EORTC Thyroid Cancer Cooperative Group. Eur J Cancer1979;15:1033-1041.
17 Hay ID, Grant CS,Taylor WR, et al. Ipsilateral lobectomy versus bilateral lobar
resection in papillary thyroid carcinoma: a retrospective analysis of surgical outcome
using a novel prognsotic scoring system. Surgery 1987;102:1088-1095.
18 Cady B, Rossi R. An expanded view of risk-group definition in differentiated thyroid
carcinoma. Surgery 1988;104:947-953.
19 DeGroot LJ, Kaplan EL, McCormick M, et al. Natural histrory, treatment and course
of papillary thyroid carcinoma. J Clin Endocrinol Metab 1990;71:414-424.
20 Hay ID, Berstralh EJ, Goellner JR, et al. Predicting outcome in papillary thyroid
carcinoma: development of a reliable prognostic scoring system in a cohort of 1,779
patients surgically treated in one institution during 1940 through 1989. Surgery
1993;114:1050-1058.
21 Mazzaferri EL, Jhiang SM. Long-term impact of initial surgical and medical therapy
of papillary and follicular thyroid cancer. Am J Med 1994;97:418-428.
37
22 Shaha AR, Loree TR, Shah JP. Prognostic factors and risk group analysis in
follicular carcinoma of the thyroid. Surgery 1995;118:1131-1138.
23 Loree TR. Therapeutic implications of prognostic factors in differentiated carcinoma
of the thyroid gland. Semin Surg Oncol 1995;11:246-255
Adjuvant Therapy
24 Dulgeroff AJ, Hershman JM. Medical therapy for differentiated thyroid carcinoma.
Endocr Rev 1994;15:500-515.
25 Burman KD. How serious are the risks of thyroid hormone over-replacement?
Thyroid Today 1995;18:1-9.
26 Wong JB, Kaplan MM, Meyer KB, et al. Ablative radioactive iodine therapy for
apparently localized thyroid carcinoma: a decision analtyical perspective. Endocrinol
Metab Clin North Am 1990;19:741-760.
27 Simpson WJ, Pazarella T, Carruthers JJ, et al. Papillary and follicular thyroid cancer:
impact of treatment in 1,578 patients. Int J Radiat Oncol Biol Phys 1988;14:10631075.
28 Brierley JD, Tsang RW. External radiation therapy in the treatment of thyroid
malignancy. Endocrinol Metab Clin North Am 1996;25:141-157.
Long-Term Follow-Up
29 Ozata M, Suzuki S, Miyamoto T, et al. Serum thyroglobulin in the follow-up of
patients with treated differentiated thyroid cancer. J Clin Endocrinol Metab
1994;79:98-105.
30 Spencer CA,Wang CC. Thyroglobulin reassessment: techniques, clinical benefits and
pitfalls. Endocrinol Metab Clin North Am 1995;24:841-863.
31 Galloway RJ, Smallridge RC. Imaging in thyroid cancer. Endocrinol Metab Clin
North Am 1996;25:93-113.
Persistent/Recurrent Disease
1 Mazzaferri EL. Radioactive and other treatments and outcomes. In: Braverman LE,
Utiger RD eds. Werner and Ingbars The Thyroid: A Fundamental and Clinical Text.
7th ed. New York: JB Lippincott Co, 1996: 922-945.
2 Mazzaferri EL. Treating high thyroglobulin with radioiodine a magic bullet or a
shot in the dark? J Clin Endocrinol Metab 1995;80:1485-1487.
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Logo MOH
Logo MEMS
39
Published By
Malaysian Endocrine and Metabolic Society
January 2000
Distributed By
Malaysian Endocrine and Metabolic Society
c/o Department of Medicine, Faculty of Medicine
Hospital Universiti Kebangsaan Malaysia (HUKM)
Jalan Yaakub Latiff, Bandar Tun Razak
56000 Cheras, Kuala Lumpur
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