ALGORITHMS

FOR DIAGNOSIS & MANAGEMENT OF THYROID DISORDERS

ELLIOT G. LEVY, MD
Clinical Professor Department of Medicine and Endocrinology University of Miami Miami, Florida

E. CHESTER RIDGWAY, MD
Professor of Medicine Head, Division of Endocrinology, Metabolism, and Diseases University of Colorado Health Sciences Center Denver, Colorado

LEONARD WARTOFSKY, MD
Chairman and Program Director Internal Medicine Department of Medicine The Washington Hospital Center Washington, DC

TABLE OF CONTENTS

INTRODUCTION ............................................................................................................ 1

PRIMARY HYPOTHYROIDISM DIAGNOSIS ...................................................................... 2

PRIMARY HYPOTHYROIDISM MANAGEMENT ................................................................ 6

HYPERTHYROIDISM INITIAL DIAGNOSIS ....................................................................... 9

HYPERTHYROIDISM DIFFERENTIAL DIAGNOSIS ............................................................ 12 HYPERTHYROIDISM MANAGEMENT A: 131I THERAPY .................................................. 14

HYPERTHYROIDISM MANAGEMENT B: ANTITHYROID DRUGS ...................................... 17

GOITER WORKUP .......................................................................................................... 20

SOLITARY THYROID NODULE ....................................................................................... 23

POSTPARTUM THYROIDITIS DIAGNOSIS AND MANAGEMENT ........................................ 25

the attributes of the patient. and accurate interpretations of appropriate laboratory tests. the benefits and risks of treatment. consultation with an endocrinologist is recommended at specific points in the algorithms. An endocrinologist should always be consulted when thyroid disorders are suspected in children because of important differences in the management of pediatric patients. These algorithms are concise. Appropriate management of thyroid disorders is based on an accurate diagnosis based on clinical presentation. ophthalmopathy associated with Graves disease). These algorithms are not intended to represent in-depth standards of treatment and do not obviate the need for consultation with an endocrinologist. the large number and variety of available tests and their interpretation in various clinical circumstances can be confusing. patient history. In addition. Diagnosis of thyroid dysfunction can be difficult for various reasons. as the natural history of a thyroid disorder evolves. there are changes in symptoms associated with the underlying thyroid dysfunction. Although some thyroid disorders have clinical manifestations that are distinctive (eg. In fact. Patients with subclinical hypothyroidism (mild thyroid failure) or subclinical hyperthyroidism may be asymptomatic. and the available medication from managed care formularies. improvements have been made in laboratory tests to assess thyroid function.INTRODUCTION Thyroid disorders occur in a significant proportion of the general population and increasingly are being diagnosed and managed by primary care physicians. physical examination for anatomic changes in the thyroid gland and signs of hypothyroidism or hyperthyroidism. including the etiology of the dysfunction. practical guides that can be used by primary care physicians and other specialists for the evaluation and management of patients with certain thyroid diseases. The following diagnosis and management algorithms were developed to provide an overview of critical aspects of the initial evaluation and management of patients with thyroid disorders. 1 . Nonetheless. and may be difficult to recognize. its treatment and management must be individualized based on many factors. Once thyroid dysfunction is diagnosed. nonspecific. Over the last decade. many clinical features of hypothyroidism or hyperthyroidism are subtle.

2-5. depression.5 Diagnosis of hypothyroidism in severely ill patients is complex. a thyroid peroxidase antibody (TPOab) test is useful for establishing thyroid autoimmunity as the cause of subclinical hypothyroidism (mild thyroid failure). but it can also be justified in men over 60 years of age as a relatively costeffective measure in the context of a periodic health examination. fatigue.7.5. or reproductive function). fatigue.1-5 Other causes of hypothyroidism include thyroidectomy.8 A normal TSH level in a patient with low FT4 suggests secondary hypothyroidism or a hypothalamic-pituitary disorder. although there may be circumstances when patients with chronic autoimmune thyroiditis have normal TSH levels.8 Because TSH is a more sensitive test than FT4. an endocrinologist should be consulted for evaluation of possible TSH-secreting pituitary tumor or thyroid hormone resistance.5 If the FT4 is high in an individual with a normal or elevated TSH level. TSH) concentration beginning at 35 years of age and every 5 years thereafter. cognitive dysfunction. gastrointestinal. office-based testing of suspected patients by primary care physicians is important to ensure an early and accurate diagnosis. Although many patients with primary hypothyroidism present with typical signs and symptoms suggestive of the condition (see Signs and Symptoms). memory loss. antithyroid agents.1 The American Thyroid Association recommends that adults be checked for thyroid dysfunction by measurement of the serum thyrotropin (thyroid stimulating hormone.12 mIU/L) suggests a diagnosis of primary hypothyroidism.1-3. or congenital defects.3.1-4 2 .6 Test Interpretation An increased TSH level (>4. alterations in lipid metabolism.PRIMARY HYPOTHYROIDISM DIAGNOSIS Overview Adult primary hypothyroidism is caused most frequently by chronic autoimmune thyroiditis (Hashimoto thyroiditis) and is present in 5-10% of the adult US population. radioactive iodine (131I) therapy.12 mIU/L)* generally excludes the diagnosis of primary hypothyroidism. head or neck irradiation. although it does occur in individuals of all ages.45 mIU/L to 4. Women older than 40 years of age and elderly individuals of both sexes are affected most frequently. weight gain. patients with subclinical hypothyroidism (mild thyroid failure) will have a normal FT4 with an elevated TSH level. these patients probably should be evaluated by an endocrinologist. and the fact that most thyroid function tests (including the TSH test) often give misleading results in patients with other acute medical conditions should be considered.1.2-4 In the presence of an increased TSH with a normal FT4. A normal TSH level (0. certain medications. or abnormalities in cardiac.3. since thyroid disease symptoms may mimic characteristics associated with aging (eg.1. depression. patients with subclinical hypothyroidism (mild thyroid failure) may be asymptomatic or have nonspecific signs and symptoms (eg.5 Testing Because many signs and symptoms of hypothyroidism are nonspecific and patients with subclinical hypothyroidism (mild thyroid failure) may be asymptomatic.6 A comprehensive medical diagnosis confirmed by thyroid function tests prior to treatment is important to avoid the inappropriate use of thyroid hormone replacement therapy in patients who are not clinically hypothyroid.6 TSH testing may be particularly useful in elderly patients.7 More frequent testing may be appropriate for individuals at higher risk of developing thyroid dysfunction. The indication for TSH testing is particularly compelling in women.1-3. and alopecia). this diagnosis is confirmed if the patient has a low free thyroxine (FT4) level.4.

45 mIU/L Measure FT4 Level Patient Euthyroid Patient may be Hyperthyroid FT4 High FT4 Normal FT4 Low Refer to Hyperthyroidism Diagnosis Algorithms Consult Endocrinologist for Possible TSH-Secreting Pituitary Tumor or Thyroid Hormone Resistance Test TPOab to Establish Presence of Thyroid Autoimmunity Patient Hypothyroid Refer to Hypothyroidism Management Algorithm Refer to Hypothyroidism Management Algorithm 3 .PRIMARY HYPOTHYROIDISM DIAGNOSIS ALGORITHM Suspect Hypothyroidism Measure TSH Level TSH >4.12 mIU/L TSH 0.12 mIU/L TSH <0.45-4.

4 . thyroid disease. physicians should be aware of and act within the normal TSH values used by their laboratories.0 mIU/L. each laboratory may use different TSH reference ranges. infertility.Signs and Symptoms ▬ History of autoimmune disease ▬ History of Graves disease treatment.3 to 3. the normal TSH range that is cited in these algorithms.45 and 4.7. coma Known tracheal compression ▬ ▬ ▬ ▬ Serum sodium <130 mEq/L Pregnancy Postpartum thyroiditis Symptoms suggest secondary or tertiary hypothyroidism (galactorrhea.8 The National Academy of Clinical Biochemistry has proposed a normal TSH range of 0.3 In addition. etc) *Normal TSH reference ranges have been reported in epidemiological studies8 and recommended in various national association guidelines and position statements.11 though the establishment of a single reference range continues to be controversial. or thyroid surgery ▬ Family history of thyroid disease ▬ History of head/neck irradiation ▬ Elevated cholesterol ▬ Elevated creatine phosphokinase (CPK) ▬ Hyponatremia (serum sodium <130 mEq/L) ▬ Depression/dementia ▬ Lithium treatment ▬ ▬ ▬ ▬ ▬ ▬ ▬ ▬ ▬ ▬ ▬ ▬ ▬ Cardiomegaly Pericardial effusion Bradycardia Low voltage on ECG Cold intolerance Fatigue Infertility Irregular menses Weight gain Vitiligo Alopecia Coarse or thinning hair Hoarse voice Consult Endocrinologist if: ▬ ▬ ▬ ▬ ▬ Pre-operative patient.0 mIU/L. headache.12 mIU/L.9.4 to 4. Serum TSH levels of the reference population in the NHANES III study fell within 0.9 whereas others have proposed a narrower TSH range of 0. ICU/CCU patient Age <15 years Cardiac compromised Stupor.

3rd ed. 1989:752-768. American Thyroid Association guidelines for use of laboratory tests in thyroid disorders. Ortiz E. 5. American Association of Clinical Endocrinologists Thyroid Task Force. Arch Intern Med. Accessed Oct. National Academy of Clinical Biochemistry. Laboratory Medicine Practice Guidelines: Laboratory Support for the Diagnosis and Monitoring of Thyroid Disease. Solomon DH. 2004. 7. Ain KB. Powe NR. Available at: www. In: DeGroot LJ et al. 1996. 1990. Sawin CT. 10. et al. Levy EG. 2002. Mariash CN. Subclinical thyroid disease: scientific review and guidelines for diagnosis and management.291:228-238. Philadelphia. Danese MD. 2002. Demers L. 2003. Hollowell JG. Flanders WD. Spencer CA. Screening for thyroid disease: an update. Cooper DS. 4. Daniels GH.References Singer PA. Ann Intern Med. Surks MI.8:457469. 3. Endocrine Pract.87:489-499. 2. et al. et al. Treatment guidelines for patients with hyperthyroidism and hypothyroidism.org. Serum TSH. JAMA. 2000. American College of Physicians. Ladenson PW. Ladenson PW. JAMA. Singer PA. 24. 6. 1998. Hypothyroidism. Screening for mild thyroid failure at the periodic health examination: a decision and cost-effectiveness analysis. Surks MI.276:285-292. T4. Utiger RD. J Clin Endocrinol Metab. American Thyroid Association guidelines for detection of thyroid dysfunction. 1. AACE medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism.273:808-812. Pa: WB Saunders Co. JAMA.160:1573-1575. 8. JAMA. Redfern CC. Chopra IJ. 1995. and thyroid antibodies in the United States population (1988 to 1994): National Health and Nutrition Examination Survey (NHANES III).nacb.263:1529-1532. Helfand M. 9. Staehling NW.129:144-158. et al. Endocrinology. Nicoloff JT. 5 . eds.

4. tachycardia. the longer it will take. as evidenced by normalization of serum TSH levels.1.2 Overdosage of levothyroxine sodium should be avoided.5 mIU/L to 2.7 Initial and maintenance doses of levothyroxine sodium must be individualized based on the etiology.7 Older adults or those with known or suspected heart disease require a lower initial dosage (12. the dose should be increased gradually in increments of 12.PRIMARY HYPOTHYROIDISM MANAGEMENT Overview Thyroid hormone replacement therapy with levothyroxine sodium is the treatment of choice for the routine management of primary hypothyroidism.6 µg/kg/d.6 µg/kg/d. accelerated bone turnover.7 This usually takes several weeks.1-4 Although replacement therapy in patients with subclinical hypothyroidism (mild thyroid failure) can be controversial. either the dose is inadequate or there are problems with patient compliance or drug interactions.3 Replacement therapy usually must be continued for life.1-3 Dosage in older adults should be titrated carefully in increments of 12. and duration of hypothyroidism.0 mIU/L is considered to be the optimal therapeutic target for levothyroxine sodium therapy.2. since overdosage may cause decreased bone density.4. maintenance dosage is continued and the TSH test repeated annually or whenever the patient becomes symptomatic.1.2.7-10 A serum TSH level between 0. although a few patients with chronic autoimmune thyroiditis (Hashimoto thyroiditis) spontaneously recover. and the higher the pretreatment TSH level.1-6 There is mounting evidence to suggest that patients with a persistent elevation of serum thyrotropin (thyroid stimulating hormone.6 The goal of replacement therapy is to restore the patient to a euthyroid state.5 µg/d to 25 µg/d) and close monitoring to avoid overdosage. and other cardiac changes.5 µg to 25 µg every 3 to 4 weeks until TSH normalizes to 0.1.7 If TSH remains elevated after initiation of levothyroxine sodium therapy.1.4.4.45 mIU/L.4.2 If noncompliance is excluded.3 6 .7 After the TSH level has normalized.1. as well as the age and clinical condition of the patient.5 µg to 25 µg.2.2.5 mIU/L and 2.4 Dosage and Dosage Adjustment TSH is the test of choice for monitoring long-term thyroid hormone replacement therapy because it is sensitive to small alterations in levothyroxine sodium dosage and generally correlates well with thyroid hormone responsiveness.7 A euthyroid state is usually achieved in adults who require full replacement with a maintenance dosage of levothyroxine sodium that averages 1.2.2.0 mIU/L.11 The fact that dosing requirements may be affected by malabsorptive states or drug interactions should be considered.1. most patients benefit from such therapy. severity.1.7 Titration should occur every 6 to 8 weeks until the TSH level reaches 0.0 mIU/L.2 Dosage reduction generally is indicated if the TSH level decreases below 0. and other adverse effects including alterations in liver enzymes.5 mIU/L to 2.4 Levothyroxine sodium therapy should be initiated in younger healthy adults at the full replacement dose of 1. TSH) may be exposed to greater risk if left untreated.

Watts NB. Ridgway EC.References Singer PA. Ain KB. 8. 11. Larsen PR. 6. 9. et al.86:4585-4590. 13.149:309-312. Braverman LE. Mariash CN. Ann Intern Med. Crapo LM. 1993. JAMA. National Academy of Clinical Biochemistry. Surks MI. 7 .119:492-502. McDermott MT. Ortiz E. 12.291:228-238. Laboratory Medicine Practice Guidelines: Laboratory Support for the Diagnosis and Monitoring of Thyroid Disease. et al. Minelli R. 24.nacb. Management practices among primary care physicians and thyroid specialists in the care of hypothyroid patients. American Association of Clinical Endocrinologists Thyroid Task Force. Cooper DS. et al. 1990. J Clin Endocrinol Metab. The treatment of subclinical hypothyroidism is seldom necessary. J Clin Endocrinol Metab. Thyroid. Levy EG.org. Solomon DH. 1. Arch Intern Med. American Thyroid Association guidelines for use of laboratory tests in thyroid disorders. The use and misuse of thyroid hormone. Endocrine Rev. Roti E. 2001 Aug. 1995. Ladenson PW. Surks MI. Nicoloff JT. Treatment guidelines for patients with hyperthyroidism and hypothyroidism. Mandel SJ. JAMA. 3. JAMA. Levothyroxine therapy in patients with thyroid disease. Accessed Oct.14:401-423. 2001.8:457469. McDermott MT. Chu JW.86:4591-4599.11(8):757-64. 1993. 5. 2. American Thyroid Association guidelines for detection of thyroid dysfunction. 1989. Lezotte DC. Demers L. AACE medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. Subclinical hypothyroidism is mild thyroid failure and should be treated. 2002.273:808-812. et al. 4. 2001. Available at: www. 2004. Daniels GH.263:1529-1532. Brent GA. 7. Subclinical thyroid disease: scientific review and guidelines for diagnosis and management. Spencer CA. Endocrine Pract. 2000. Singer PA.160:1573-1575. Chopra IJ. 2003. Gardini E. Use of a sensitive thyrotropin assay for monitoring treatment with levothyroxine. Haugen BR. Arch Intern Med.

45 mIU/L Increase Levothyroxine Sodium Dose by 12.45-4.PRIMARY HYPOTHYROIDISM MANAGEMENT ALGORITHM TSH >4. ICU/CCU patient − Age <15 years − Sodium < 130 mEq/L − Pregnant − Postpartum thyroiditis Repeat TSH Test Annually or When Symptomatic *Thyroperoxidase antibodies 8 . coma − Lithium treatment − Amiodarone treatment − Pre-operative patient.6 µg/kg/d Levothyroxine Sodium 25 to 50 µg/d Levothyroxine Sodium 12. TPOab* + normal or low FT4 Age 15-40 Age >40-60 Age >60 or Known/Suspected Heart Disease Normal FT4 Low FT4 Levothyroxine Sodium 25 to 75 µg/d Levothyroxine Sodium 1.5-25 µg/d Increments Consult Endocrinologist if: − Cardiac status compromised − Stupor.12 mIU/L TSH 0.12 mIU/L TSH <0.12 mIU/L.5-25 µg/d Increments Continue Dose Decrease Levothyroxine Sodium Dose by 12.5 to 25 µg/d 5-6 weeks Repeat TSH Test TSH >4.

8 Current studies suggest that TSH values <0. an autonomous thyroid nodule. symptoms of hyperthyroidism and may not even have enlarged thyroid glands.HYPERTHYROIDISM INITIAL DIAGNOSIS Overview Thyrotoxicosis results from excess thyroid hormone and is present in a variety of conditions. and osteoporosis.2.45 mIU/L to 4. or effects of certain medications (eg.3-5 The serum thyrotropin (thyroid stimulating hormone.3-6 If results of initial testing indicate hyperthyroidism. including hyperthyroidism due to toxic diffuse goiter (Graves disease). exophthalmos.45 mIU/L may represent thyroid hormone excess and in elderly patients may be associated with an increased risk of atrial fibrillation. manifestations and severity depend on the extent of thyroid hormone excess.1-6.1 Diagnosis of hyperthyroidism in severely ill patients is complex. nodules.1. tremors.1. cardiovascular mortality.5 Initial Evaluation and Testing Initial evaluation of suspected hyperthyroidism includes a comprehensive medical history and physical examination (to identify goiter.2. a trophoblastic tumor.1 mIU/L to 0.3.5 Elderly patients may have markedly abnormal tests with few. although some patients with familial thyroid hormone resistance or a TSH-secreting pituitary tumor may have normal TSH levels with an increased FT4. and the fact that most thyroid function tests (including TSH) give misleading results in patients with acute medical conditions should be considered.4.10 9 .5.9 A decreased TSH level with normal FT4 suggests that the patient may have subclinical hyperthyroidism or hyperthyroidism resulting from triiodothyronine (T3) toxicosis. if any. TSH) level and free thyroxine (FT4) estimate are the tests most frequently used for the initial evaluation of possible hyperthyroidism.6. and duration of the condition.1.4 A wide range of signs and symptoms is associated with hyperthyroidism (see Signs and Symptoms).12 mIU/L generally indicates that the patient is euthyroid. toxic adenoma. and thyroiditis (painful and subacute. age of the patient. glucocorticoids or dopamine).4 mIU/L have intermediate degrees of suppression of the normal hypothalamic-pituitary axis and may be asymptomatic. this usually should be done in consultation with an endocrinologist.1-5 Thyrotoxicosis may also be associated with excessive pituitary TSH production.8.1. or other signs) and appropriate laboratory tests. these patients probably should be evaluated by an endocrinologist. toxic multinodular goiter.6-9 A decreased TSH level (<0. those with levels of 0. or silent).4.1 mIU/L generally have symptoms of hyperthyroidism.8.3-6 Test Interpretation A TSH level of 0.45 mIU/L) and an increased FT4 generally confirm a diagnosis of hyperthyroidism. or excessive ingestion of iodine or thyroid hormone.9 Individuals with TSH levels <0. further testing using a combination of tests is needed to establish the etiology1.

Normal FT4 Consult Endocrinologist if FT4 Level is High Consult Endocrinologist to Investigate Hyperthyroidism Etiology Consult Endocrinologist to Investigate Pituitary Disease Consult Endocrinologist for Subclinical Hyperthyroidism Refer to Hyperthyroidism Differential Diagnosis Algorithm Refer to Hyperthyroidism Differential Diagnosis Algorithm 10 .12 mIU/L TSH <0.12 mIU/L TSH 0.45 mIU/L.45 mIU/L Refer to Hypothyroidism Diagnosis Algorithm Patient Euthyroid Measure FT4 Measure FT4 Levels if a TSH Secreting Pituitary Tumor of Thyroid Hormone Resistance is Suspected FT4 High FT4 Low TSH <0.45-4.HYPERTHYROIDISM INITIAL DIAGNOSIS ALGORITHM Suspect Hyperthyroidism Measure TSH level TSH >4.

or thyroid surgery ▬ Family history of thyroid disease ▬ Goiter ▬ Exophthalmos ▬ Pretibial myxedema ▬ Excessive iodine exposure (contrast dyes. Accessed Oct. Foster DW. 3. 2002. Levy EG.Signs and Symptoms ▬ History of autoimmune disease ▬ History of previous Graves disease treatment. 10. Franklyn JA. The management of hyperthyroidism. Minelli R.org. Gardini E. Werner and Ingbar’s The Thyroid: A fundamental and Clinical Text. Philadelphia. eds.14:401-423. medications) ▬ ▬ ▬ ▬ ▬ ▬ ▬ ▬ ▬ ▬ Unexplained weight loss Atrial fibrillation/palpitations Depression/dementia Vitiligo Alopecia Coarse or thinning hair Heat intolerance Sweating Hyperdefecation Tremor References Singer PA. National Academy of Clinical Biochemistry. Solomon DH. Larsen PR. JAMA. Ann Intern Med. Redfern CC. 8th ed. 24. 5. Braverman LE.129:144-158. Utiger RD. 1994.8:457469. 1993. Available at: www. Mariash CN. Endocrine Pract. Williams Textbook of Endocrinology.nacb. 2002. Introduction to thyrotoxicosis. Surks MI. 4. T4. The use and misuse of thyroid hormone. Cooper DS. J Clin Endocrinol Metab. Flanders WD. 2003. Utiger RD. N Engl J Med. 9. et al. 1996:713-734. Philadelphia. 7. 11 . 1992:357-487. and thyroid antibodies in the United States population (1988 to 1994): National Health and Nutrition Examination Survey (NHANES III). Hollowell JG. Pa: WB Saunders Co. Chopra IJ. Ingbar SH. Braverman LE. In: Wilson JD. et al.87:489-499. Serum TSH. AACE medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism.273:808-812. 7th ed. American College of Physicians. JAMA. Nicoloff JT. 2. Screening for thyroid disease: an update.263:1529-1532. Treatment guidelines for patients with hyperthyroidism and hypothyroidism. Demers L. 8. The thyroid gland. 1998. In: Braverman LE. thyroid disease. 1. 6. Helfand M. 1990. Pa: JB Lippincott Co. Laboratory Medicine Practice Guidelines: Laboratory Support for the Diagnosis and Monitoring of Thyroid Disease. Roti E. Endocrine Rev. American Association of Clinical Endocrinologists Thyroid Task Force. American Thyroid Association guidelines for use of laboratory test in thyroid disorders. 1995. Spencer CA. eds. Staehling NW.330:1731-1738.

Accessed Oct. 2002. 1990.330:1731-1738. et al. Singer PA. 1995. Solomon DH. 12 . a total T3 (TT3) or free T3 (FT3) test may be indicated. including triiodothyronine (T3) radioimmunoassays. Larsen PR.2.nacb.2. JAMA. Cooper DS. American Association of Clinical Endocrinologists Thyroid Task Force.HYPERTHYROIDISM DIFFERENTIAL DIAGNOSIS Overview After an initial diagnosis of hyperthyroidism has been made based on medical history. References 1. N Engl J Med.1. The thyroid gland.45 mIU/L) in conjunction with a low 123I update generally indicates some form of thyroiditis (painful and subacute. toxic multinodular goiter. 6. physical findings.1992:357-487. and thyroid scans. and decreased TSH levels. 2003. Chopra IJ.4-6 A thyroid scan can be used to distinguish toxic nodular goiter and toxic adenoma from Graves disease and to assess the functional status of thyroid nodules.1. Ingbar SH. 8th ed. a diagnosis of Graves disease in patients without these clinical manifestations can be confirmed by high 123I uptake. Treatment guidelines for patients with hyperthyroidism and hypothyroidism.2. toxic adenoma.1.1. Pa: WB Saunders Co. radioactive iodine uptake (123I uptake) tests.4.263:1529-1532. Mariash CN. it may also indicate excessive iodine ingestion or factitious T4-induced thyrotoxicosis.1.2 It is not feasible or necessary to use all available procedures in every case. If the FT4 is low in a patient with decreased TSH levels. 5.2. In: Wilson JD.1 There are various thyroid function tests that can be used for the differential diagnosis of conditions associated with hyperthyroidism.org. 4.2. Available at: www.4 Results of 123I uptake tests in conjunction with physical findings usually can differentiate these.2.3 Tests and Test Interpretation The most probable causes of hyperthyroidism in a patient with decreased serum TSH levels and increased FT4 are toxic diffuse goiter (Graves disease).5. a brain MRI should be considered to investigate hypothalamic-pituitary disease. Philadelphia. Foster DW.6 A high TT3 or FT3 indicates that the patient may have T3 toxicosis. Franklyn JA. Nicoloff JT. JAMA.2 Patients with subclinical hyperthyroidism may have a normal FT3.6 A diagnosis of toxic nodular goiter or toxic adenoma is suspected in the absence of ophthalmopathy or diffuse goiter. 24. further testing is necessary to determine the etiology of the condition so that it can be managed appropriately.4-6 If the FT4 is normal in a patient with a decreased TSH. Endocrine Pract. or thyrotoxicosis due to some form of thyroiditis (painful and subacute.5 A low FT3 indicates that the patient may have euthyroid sick syndrome.5 Although a diagnosis of Graves disease is evident if diffuse goiter and ophthalmopathy are present in patients with hyperthyroidism.273:808-812. 1994. Spencer CA. American Thyroid Association guidelines for use of laboratory tests in thyroid disorders. especially in elderly patients.6 A decreased TSH level (<0. Williams Textbook of Endocrinology. normal FT4. Demers L. or silent). Laboratory Medicine Practice Guidelines: Laboratory Support for the Diagnosis and Monitoring of Thyroid Disease. 3.1. 2. Levy EG. AACE medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. National Academy of Clinical Biochemistry. and results of serum thyrotropin (thyroid stimulating hormone.8:457469. eds. Surks MI. The management of hyperthyroidism. normal or only slightly increased 123I uptake may be seen. or silent). TSH) and free thyroxine (FT4) measurements.

† PPT . Beta-Blockers to Normalize Pulse Consult Endocrinologist to Rule Out Malignancy Differential Diagnosis − Excessive levothyroxine sodium treatment − Euthyroid sick syndrome − Graves disease − Multinodular goiter − Hyperfunctioning nodule − Glucocorticoid treatment − Dopamine treatment − Partial panhypopituitarism . Symptomatic Therapy with Glucocorticoids/ Aspirin. Continue Observation. † Postpartum thyroiditis ‡ Erythrocyte sedimentation rate 123 Refer to PPT Diagnosis and Management Algorithm Confirm with High ‡ ESR ESR Normal 13 Consult Endocrinologist. or Exogenous Thyroid Hormone Subacute Thyroiditis * I uptake may be increased.HYPERTHYROIDISM DIFFERENTIAL DIAGNOSIS ALGORITHM Patient Hyperthyroid. follow Solitary Thyroid Nodule Algorithm on page 21. Consult Endocrinologist as Needed Consult Endocrinologist for Selection of Appropriate Hyperthyroidism Management Algorithm Toxic Nodular Goiter Refer to Hyperthyroidism Management Algorithm Silent Thyroiditis. No Further Therapy Recommended. TSH <0.45 mIU/L Measure FT4 Levels High Normal Test l Uptake 123 Measure T3 or FT3 Levels High Normal Low High Normal Low Painful Thyroid? Diffuse Goiter Nodular Goiter* T3 Toxicosis Consult Endocrinologist to Investigate Subclinical Hyperthyroidism Graves Disease Thyroid Scan** No Consult Endocrinologist for Selection of Appropriate Hyperthyroidism Management Algorithm Yes Euthyroid Sick Syndrome. **If scan shows dominant cold nodule.

and relatively low 123I uptake. early hypothyroidism is only transient in some cases and periodic monitoring of TSH and FT4 is recommended in the first post-treatment year to confirm the need for life-long LT4 therapy.4.1 If thyroid gland failure is indicated by an increased TSH level (>4.1. long-term follow-up is necessary. which leads to thyroid failure.5 The optimum dosage of 131I is controversial. levothyroxine sodium (LT4) replacement therapy should be initiated. TSH) levels and free thyroxine (FT4) levels. or silent) is characterized by a low radioactive iodine uptake and is self-limited.2.HYPERTHYROIDISM MANAGEMENT A: 131I THERAPY Overview Radioactive iodine (131I) therapy generally is considered the treatment of choice for Graves disease. which occurs in the majority of patients within 6 to 36 months following therapy.5 Thyroid function begins to normalize and goiter size decreases in most patients within 6 to 8 weeks following 131I therapy.4 For patients 40 years of age or younger with a first episode of hyperthyroidism.1-4 Because thyroiditis (painful. large goiters.12 mIU/L).5 Radioactive Iodine Therapy The goal of 131I therapy is to destroy enough thyroid tissue to cure hyperthyroidism.1. followed by fibrosis and atrophy.3.3 Radioactive iodine therapy destroys thyroid cells.2.5 Follow-Up Because of the potential for hypothyroidism following 131I therapy.1-5 Radioactive iodine therapy is also used in the management of toxic multinodular goiter and toxic adenoma.1.4 Although smaller doses may be used in an attempt to prevent posttreatment hypothyroidism. 14 . beta blockade). subacute.2 A single dose is effective in the majority of patients.1. 1.5 This is used frequently in patients with severe hyperthyroidism.2 The principal complication of 131I therapy is hypothyroidism.2. some clinicians prefer a trial of an antithyroid drug prior to 131I therapy (see Hyperthyroidism Management B: Antithyroid Drugs Algorithm). elderly patients and patients with cardiac disease may require 4 to 8 weeks of antithyroid drugs prior to 131I therapy to immediately control the hyperthyroidism and to reduce the risk of exacerbation of hyperthyroidism.6 However.3 These patients may require symptomatic therapy (eg. a small percentage may require a second or third 131I dose 6 to 12 months after the initial dose. minimizing morbidity associated with the condition. especially for patients with recurrent hyperthyroidism after antithyroid drug therapy.2-4 A high ablative dose more quickly resolves hyperthyroidism. An endocrinologist generally should be consulted concerning the management of patients with hyperthyroidism. patients with this form of hyperthyroidism should not be treated with antithyroid drugs or 131I therapy.2.3 In addition.4 Patients should be evaluated 4 to 8 weeks after administration of 131I therapy by monitoring serum thyrotropin (thyroid stimulating hormone. it is unclear whether this approach effectively decreases the risk and it may increase the failure rate of cure with the first dose.4.

J Clin Endocrinol Metab. American Association of Clinical Endocrinologists Thyroid Task Force. 7th ed. Pa: WB Saunders Co. Ingbar SH. 1995. 2002. In: Braverman LE. Staehling NW. Cooper DS. 15 .273:808-812. et al. T4. JAMA. et al. 3. Williams Textbook of Endocrinology. AACE medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. Utiger RD. Philadelphia. 4. 6.References 1. 2002. Werner and Ingbar’s The Thyroid: A Fundamental and Clinical Text. 2.87:489-499. The management of hyperthyroidism. eds. Foster DW.1992:357-487. Treatment guidelines for patients with hyperthyroidism and hypothyroidism. Serum TSH. 8th ed. N Engl J Med. In: Wilson JD. Levy EG. 5.1996:713-743. Singer PA.8:457469. Treatment of thyrotoxicosis. Hollowell JG. Philadelphia. 1994. Franklyn JA. Endocrine Pract. Pa: JB Lippincott Co. and thyroid antibodies in the United States population (1988 to 1994): National Health and Nutrition Examination Survey (NHANES III). The thyroid gland. Flanders WD. eds. Cooper DS.330:1731-1738 Larsen PR.

FT4 Low TSH >4. adrenergic blocking agents. † 131 The most common scenario for any patient prescribed I therapy is hypothyroidism. ‡ Saturated solution of potassium iodide 16 .12 mIU/L.45 mIU/L.45 mIU/L. administering antithyroid drug 131 treatment 4 to 8 weeks prior to I therapy may be advised. adrenergic ‡ blocking agents. or patients with cardiac disease. FT4 Normal or Low Consider use of adjunctive therapy (antithyroid drugs.45 mIU/L. SSKI) 131 Repeat TSH and FT4 Tests in 1-2 Months Repeat TSH and FT4 Tests in 4-6 Months Patient † Hypothyroid I Repeat Therapy in 6-12 Months Reevaluate Treatment Options in the Clinical Assessment *For cases involving severe thyrotoxicosis.45 mIU/L. elderly patients. FT4 High TSH <0. FT4 High TSH <0. FT4 Normal TSH and FT4 Normal TSH >4. SSKI ) Repeat TSH and FT4 Tests in 1-2 Months Asymptomatic Symptomatic Patient † Hypothyroid TSH <0. FT4 Normal TSH and FT4 Normal TSH Low or Normal.HYPERTHYROIDISM MANAGEMENT A: 131 I THERAPY ALGORITHM Hyperthyroidism − Graves Disease − Toxic Nodular Goiter l Therapy* 4-8 weeks 131 Measure TSH and FT4 Levels TSH <0.12 mIU/L. FT4 Normal or Low Refer to Hypothyroidism Management Algorithm Consider use of adjunctive therapy (antithyroid drugs.

may decrease serum T3 levels more rapidly than methimazole. both TSH and free thyroxine (FT4) levels should be monitored.1. children and younger adults.5 Antithyroid drugs interfere with thyroid hormone synthesis and some data suggest that they may also have immunologic effects that alter the underlying cause of Graves hyperthyroidism. and then annually.4 Antithyroid Drug Therapy Propylthiouracil and methimazole are the antithyroid drugs generally used for management of hyperthyroidism.1.3 Follow-Up Patients should be monitored and thyroid function evaluated at intervals of 4 to 8 weeks following initiation of antithyroid agent therapy.1. lifelong follow-up is recommended for all patients.3.3 17 . methimazole may be preferred because propylthiouracil is associated with a greater propensity for reduced efficacy of ablation. primarily in patients with mild first episodes. TSH) levels alone to evaluate thyroid function may be misleading. Although a few patients may enter remission after only 4-6 months. thyroid function should be evaluated every 3 months thereafter.3-5 If therapy is discontinued.1. 1 to 2 years generally is required to decrease the risk of relapse.4.HYPERTHYROIDISM MANAGEMENT B: ANTITHYROID DRUGS Overview Antithyroid drugs are used in the management of Graves disease.5 Because the possibility of delayed relapse or hypothyroidism exists.1.3-5 A gradual decrease in thyroid hormone levels leads to a euthyroid state. Propylthiouracil may be preferred in severe or life-threatening hyperthyroidism (thyroid storm) because it inhibits the conversion of thyroxine (T4) to triiodothyronine (T3) and.3. these uses are generally temporary and they are not the treatment of choice.2. and pregnant women. although most patients (50% to 80%) have recurrence of the hyperthyroidism.3.1.5 Optimum duration of antithyroid drug therapy is unclear.4 Dosage should be adjusted until a maintenance dosage is established that maintains a euthyroid state1.2 Antithyroid drugs also are used prior to radioactive iodine (131I) therapy in the treatment of Graves disease in elderly patients and patients with cardiac disease to immediately control the hyperthyroidism and to reduce the risk of exacerbation of hyperthyroidism.4 Relapse is most likely to occur within the first 3 to 9 months after therapy is discontinued but may occur at any time.4 Use of serum thyrotropin (thyroid stimulating hormone. therefore. Permanent remissions of hyperthyroidism following withdrawal of antithyroid drugs may occur.3. and longer durations of therapy may be appropriate.4 Antithyroid drugs are not indicated for the management of thyroiditis. thyroid function should be monitored every 3 to 6 months.1-4 Although antithyroid drugs have been used in the management of other forms of hyperthyroidism.4.1.4.1. including toxic multinodular goiter and toxic adenoma. 9 to 12 months.1-5 In patients who will subsequently undergo 131I therapy.

8th ed. Levy EG. 18 . Cooper DS. Werner and Ingbar’s The Thyroid: A Fundamental and Clinical Text. Larsen PR. The management of hyperthyroidism. AACE medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. Pa: WB Saunders Co. et al. Endocrine Pract.1992:357-487.References 1. 3. Treatment of thyrotoxicosis. 2002. American Association of Clinical Endocrinologists Thyroid Task Force. 1995.8:457469. eds. eds. Pa: JB Lippincott Co. Ingbar SH. The thyroid gland. 5. Cooper DS. In: Braverman LE. Philadelphia.273:808-812. Utiger RD. Foster DW. 7th ed. 4. Treatment guidelines for patients with hyperthyroidism and hypothyroidism.330:1731-1738. N Engl J Med. Franklyn JA. Williams Textbook of Endocrinology. JAMA. Philadelphia. 1994. 2. Singer PA.1996:713-734. In: Wilson JD.

9-12 Months.45 mIU/L. FT4 Normal TSH <0.45 mIU/L. FT4 High TSH <0.45 mIU/L.45 mIU/L. FT4 Low TSH >0.HYPERTHYROIDISM MANAGEMENT B: ANTITHYROID DRUGS ALGORITHM Hyperthyroidism − Graves Disease Prescribe Antithyroid Drugs 4-8 weeks Measure TSH and FT4 Levels TSH <0. Consider Using 131 I Therapy Algorithm Asymptomatic Hypothyroid Symptoms 4-8 weeks Continue Dose or Re-evaluate Treatment Options Reduce Dose 4-8 weeks Discontinue Drugs Monitor 3-6 Months. Then Annually 19 . FT4 Normal or Low Continue or Increase Antithyroid Drugs.

6 Patients younger than 50 years of age with no dominant cold nodule may receive levothyroxine sodium therapy. the thyroid returns to its original size within in a few months if therapy is discontinued.0 mIU/L). since increasing levels may indicate progression of the disease to hypothyroidism.4 20 .4 If goiter size decreases or remains stable during therapy. and a thyroid scan if nodules are present.1-5 The rationale for such therapy is that TSH may act as a cofactor that promotes growth of the thyroid.GOITER WORKUP Overview Goiter.2-5 The goal of therapy is to maintain TSH levels in the lownormal range (0.1. since efficacy has not been proven and risks of overdosage are more serious. which is an enlargement of the thyroid gland. levothyroxine sodium therapy generally is continued with periodic monitoring of TSH levels 2.2.1 Levothyroxine sodium therapy is not used for the treatment of diffuse goiter in patients with baseline TSH levels <1. Thyroid stimulating hormone levels should be monitored in patients who do not receive levothyroxine sodium.2-4 Prolonged administration of levothyroxine sodium therapy in patients who do not respond to such treatment is not justified.3 Diffuse goiter in euthyroid and hypothyroid patients younger than 50 years of age with thyroperoxidase antibodies (TPOab. and may or may not be associated with hypothyroidism or hyperthyroidism. Nodular goiter responds to levothyroxine sodium therapy less frequently and to a lesser extent than diffuse goiter. testing for thyroid autoantibodies to diagnose autoimmune disorders. TSH) and free thyroxine (FT4) levels to determine whether the patient is hypothyroid.1 mIU/L to 1. or hyperthyroid. previously called “antimicrosomal” antibodies) can be treated with levothyroxine sodium. or autoimmune processes such as Graves disease or autoimmune thyroiditis (Hashimoto thyroiditis).0 mIU/L or in patients older than 50 years of age.4 Patients with goitrous autoimmune thyroid disorders usually have measurable titers of thyroid autoantibodies and may be euthyroid or hypothyroid.1-3 Diffuse goiter may result from iodine deficiency.1. and effective reduction of TSH levels by levothyroxine sodium may induce regression of nontoxic goiter in some patients.0 cm are discovered. euthyroid.2 Nontoxic goiter is often a precursor to toxic multinodular goiter.3 Patients with nodular goiter should have a thyroid scan and/or ultrasound. If nodules greater than 1. the physician should consider performing ultrasound-guided fine-needle aspiration (FNA). optimum duration of therapy is not known.1. exposure to environmental or pharmacologic goitrogens. may be diffuse or nodular. the toxic form generally is associated with signs and symptoms of hyperthyroidism. measurement of serum thyrotropin (thyroid stimulating hormone. Management Initial evaluation of goiter includes: a comprehensive physical examination. In many patients.

Berghout A. Ann Intern Med. Smits NJ. Philadelphia. Clinical manifestations and management of nontoxic diffuse and nodular goiter. Roti E. 3. 21 . Mandel SJ. Drexhage HA. Pa: WB Saunders Co. 4. Endocrine Rev. Minelli R. 1993. Marqusee E. Pa: JB Lippincott Co. Larsen PR. Utiger RD. 2. Usefulness of ultrasonography in the management of nodular thyroid disease. In: Braverman LE. 6. 5. 8th ed. Comparison of placebo with L-thyroxine alone or with carbimazole for treatment of sporadic non-toxic goiter. The use and misuse of thyroid hormone. 6th ed. Brent GA. Foster DW. Philadelphia. 1993. Touber JL. Werner and Ingbar’s The Thyroid: A Fundamental Clinical Text.14:401-423. Williams Textbook of Endocrinology. In: Wilson JD. Wiersinga WM. Gerber H.119:492-502. Ann Intern Med. Larsen PR.1991:1114-1118. eds.References 1. 1990. 2000. eds. Braverman LE. Gardini E.1992:357-487. Frates MC. et al.133:696-700. Benson CB. Studer H.336:193-197. Levothyroxine therapy in patients with thyroid disease. Ingbar SH. The thyroid gland. Lancet.

45 to 4.0 mIU/L Repeat TSH Test in 1 Year 22 .1-1.0 mIU/L Repeat TSH Test in 1 Year Dominant Cold Nodule No Dominant Cold Nodule Perform FNA* Age >50 Age <50 *Fine-needle aspiration. Refer to Solitary Thyroid Nodule Management Algorithm Levothyroxine Sodium Therapy Goal TSH 0.GOITER WORKUP ALGORITHM Goiter Consult With Endocrinologist Measure TSH Levels TSH >4.45 mIU/L Patient Hypothyroid Measure TPOab Levels Refer to Hyperthyroidism Diagnosis Algorithms Refer to Hypothyroidism Diagnosis Algorithm Positive Negative Age >50 Age <50 Perform Thyroid Scan and/or Ultrasound Levothyroxine Sodium Therapy Goal TSH 0.1-1.12 mIU/L TSH <0.12 mIU/L TSH 0.

Shaha AR. 5.1-4. 2002. reduce nodule size.1-4 Levothyroxine sodium (LT4) may be used for suppressive therapy of benign nodules. TSH) may be a contributing factor to nodule formation. Richter B. Endocrinol Metab Clin North Am. suspicious. Kaplan BJ. Mariani G. while a few recommend a trial of levothyroxine sodium suppressive therapy prior to surgery. Celani MF. 87: 4154-4159. and it is unclear which patients are most likely to respond.1-4 If FNA results indicate that the nodule is malignant or suspicious for malignancy.37:398-401.1-4 Solitary thyroid nodules identified as benign by FNA generally are managed without surgery unless nodule size or patient concerns indicate excision.7 Optimum management of solitary thyroid nodules classified as suspicious by FNA is unclear.6 If effective. Gharib H. 23 . a thyroid scan can be used to classify the nodule as hyperfunctioning (“hot”) or hypofunctioning (“cold”) depending on its ability to incorporate radioactive isotope. 6. and the goal is to maintain the TSH in the low-normal range (0.1 A history of head or neck irradiation is a major risk factor for the development of thyroid nodules and thyroid cancer. J Clin Endocrinol Metab. 1997.1. Mariani M. 2. A systematic review and meta-analysis. Changing concepts in the diagnosis and management of thyroid nodules. 1992.1-4 Although these scans are not diagnostic. Pharmacotherapy for thyroid nodules. Diagnosis and management of patients with thyroid nodules. Management of the single thyroid nodule. If results of FNA suggest follicular neoplasm. On the usefulness of levothyroxine suppressive therapy in the medical treatment of benign solitary. and the presence of lymph nodes. controlled studies have suggested that only 25% of benign nodules will decrease in size by 50% in response to LT4 therapy. surgical excision is indicated. the extent of surgery varies depending on factors such as nodule size. Caraballo PJ. location.2 The principal diagnostic tool used is fine-needle aspiration (FNA) for cytology. 2002. 2000. Clar C.SOLITARY THYROID NODULE Overview Clinically apparent solitary thyroid nodules occur in up to 4% to 7% of the general population and are more common in women than in men.1-4 Randomized. Endocrinol Metab Clin North Am. J Surg Oncol. Castro MR. 110:183-93. Lawrence W Jr.7 The dosage of levothyroxine sodium used for suppressive therapy ranges from 50 µg to 200 µg daily. Acta Endocrinol (Copenh). Sheppard MC. Controversies in the management of thyroid nodule. 3. suppressive therapy may decrease TSH secretion. Effectiveness of thyroid hormone suppressive therapy in benign solitary thyroid nodules: a meta-analysis. hypofunctioning “cold” nodules have a higher probability of being malignant and are usually managed with surgery. Franklyn JA.4 Some clinicians recommend surgery for all suspicious solitary thyroid nodules.4 Because thyrotropin (thyroid stimulating hormone. Neises G.0 mIU/L).7 The TSH test is used to determine levothyroxine sodium dosage. 4. thyroid nodules. Laryngoscope. however.26: 777-800. 31: 699-722. Morris JC. the efficacy of LT4 suppressive therapy is controversial. or malignant. solid or predominantly solid.1-3 Classification and Management Thyroid nodules generally are classified as benign (colloid or follicular adenomas). a reduction in nodule size usually is evident during the first 6 to 12 months of therapy.1 mIU/L to 1. 2002.123:603-608.5. and prevent further nodule growth.1-4 References 1. 1990. Clin Endocrinol.80:157-170. 7.

0 mIU/L Follow up After 1 Year Perform Surgery Perform Scan Repeat FNAB Cold Nodule Hot Nodule Nodule Growth No Change Nodule Decrease Perform Surgery Evaluate for Hyperthyroidism Perform Surgery Consider Discontinuing Levothyroxine Sodium but Resuming for Nodule Regrowth Continue Observation and Levothyroxine Sodium Consider Repeating FNA Risk Factors − History of head or neck irradiation − Family history of thyroid cancer. pheochromocytoma − Lymphadenopathy − Rapid growth − Male − Age <20 or >60 − Pain in nodule.45-4.SOLITARY THYROID NODULE ALGORITHM Solitary Thyroid Nodule Consult With Endocrinologist Measure TSH Levels Refer to Hyperthyroidism Differential Diagnosis Algorithm for Hot Nodule TSH <0.1-1. hoarseness 24 .12 mIU/L TSH >4.45 mIU/L TSH 0. TSH Goal 0.12 mIU/L Refer to Hypothyroidism Differential Diagnosis Algorithm FNA Benign Malignant Suspicious or Follicular Neoplasm Inconclusive or Indeterminate Consider Levothyroxine Sodium Therapy.

* Testing and Test Interpretation Diagnosis of PPT involves serum thyrotropin (thyroid stimulating hormone.0 mIU/L is generally considered the optimal therapeutic target for levothyroxine sodium therapy. and in up to 25% of women with type 1 diabetes mellitus.1.7 After several months of therapy. dosage of levothyroxine sodium should be decreased and TSH levels tested to determine whether the patient has returned to a euthyroid state.3.5 mIU/L and 2.6 Women with diabetes mellitus or a familial history of autoimmune thyroid disease appear to be at increased risk for PPT (see Risk Factors).6 It may be of benefit to measure these antibodies in all pregnant women in order to identify patients at risk for PPT.6 Postpartum thyroiditis is considered to be an autoimmune disorder.2. although up to 25% develop permanent primary hypothyroidism. are elevated in a high percentage of patients with PPT. they generally are evident within 6 months of delivery. or subclinical hypothyroidism (mild thyroid failure) in a postpartum patient. including thyroperoxidase antibodies (TPOab). Management Levothyroxine sodium is used as replacement therapy for the management of PPT in patients who have clinical or subclinical hypothyroidism (mild thyroid failure).1. and thyroid autoantibodies. however.1.3. TSH) testing and measurement of TPOab levels.4 25 .4. hypothyroidism.6 Most women with PPT return to the euthyroid state within 1 year of delivery.6 An endocrinologist generally should be consulted if results of TSH and FT4 testing indicate hyperthyroidism.6 Patients with PPT may be symptomatic or asymptomatic.3-6 If symptoms develop.5.3.4-6 Women who develop PPT following pregnancy are at risk for recurrence following subsequent pregnancies.1. free thyroxine (FT4) levels are used as an adjunctive test to confirm that the patient is either hypothyroid or hyperthyroid.6 A serum TSH level between 0. subclinical hyperthyroidism. the dosage is adjusted based on TSH levels.POSTPARTUM THYROIDITIS DIAGNOSIS AND MANAGEMENT Overview Postpartum thyroiditis (PPT) is a form of transient thyroiditis characterized by the development of hyperthyroidism or hypothyroidism in postpartum women who were euthyroid during pregnancy.1.1-6 Postpartum thyroiditis reportedly occurs in 5% to 8% of women. they can occur as early as 1 month or as late as 1 year after delivery.

1990. Roberts RC. Long-term prospective study of postpartum thyroid dysfunction in women with insulin dependent diabetes mellitus. Roti E. A long-term follow-up of postpartum thyroiditis. Stagnaro-Green A. Endocrine Rev. 5. Braverman LE. Postpartum lymphocytic thyroiditis: prevalence. Roman SH.79:10-16.150:1397-1400. Demers L. 1994. course. J Clin Endocrinol Metab.16:1-11. Laboratory Medicine Practice Guidelines: Laboratory Support for the Diagnosis and Monitoring of Thyroid Disease.nacb. Parkers AB. Phillips DIW. Clin Endocrinol. 24. Drexler AJ.References 1. Available at: www. Arch Intern Med. Alvarez-Marfany M. 3. Robertson C. Stagnaro-Green A. etiology. Gerstein HC. Turney SL. Gardini E. 1990. Othman S.14:401-423. National Academy of Clinical Biochemistry. Postpartum thyroiditis: prevalence. 2. Arch Intern Med.147:221-224. How common is postpartum thyroiditis? A methodologic overview of the literature. 1993. Minelli R.32:559-564. Nikolai TF. Spencer CA. and clinical implications. 26 . 1993. 2003. and longterm follow-up. Fifty percent or more of women with positive anti-TPO antibodies will develop PPT. The use and misuse of thyroid hormone. Thyroid Today. * Ten percent of women will have positive anti-TPO antibodies with normal TSH levels. Accessed Oct. et al. clinical. 1987. 7.org. 4. 6.

T3* Toxicosis.45-4.0 mIU/L Gradually Discontinue Therapy After 1 Year *Triiodothyronine Risk Factors − Prior PPT episode − Family history of autoimmune disease or thyroid disease − Positive TPOab − Diabetes mellitus − Goiter − Depression − Signs and symptoms of thyroid disease 27 .12 mIU/L FT4 Normal FT4 Low TSH 0.12 mIU/L TSH <0.12 mIU/L TPOab + or - TSH 0.12 mIU/L TPOab - TSH 0. Glucocorticoids. Dopamine Re-evaluate at 3-6 Months Taper Levothyroxine Sodium Dose Repeat TSH TSH >4.45 mIU/L FT4 High FT4 Normal FT4 Low Patient Subclinical Hypothyroid (Mild Thyroid Failure) Levothyroxine Sodium to Normalize TSH Patient Hypothyroid Consult Endocrinologist to Investigate Hyperthyroidism Etiology Consult Consult Endocrinologist Endocrinologist to Investigate to Investigate Pituitary Subclinical Disease or Hyperthyroidism Euthyroid Sick Possible Syndrome Causes: Excessive Levothyroxine Sodium Medication.12 mIU/L TSH 0.5-2.POSTPARTUM THYROIDITIS DIAGNOSIS AND MANAGEMENT ALGORITHM Suspect PPT Test TSH and TPOab TSH >4.45-4. Autonomous Thyroid Nodule.45 mIU/L TPOab + or - Test FT4 Stop Repeat TSH in 3-6 Months Test FT4 TSH >4.45-4.12 mIU/L TPOab + TSH <0.

Sign up to vote on this title
UsefulNot useful