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

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

weight gain. or abnormalities in cardiac.1-3.7. 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.1 The American Thyroid Association recommends that adults be checked for thyroid dysfunction by measurement of the serum thyrotropin (thyroid stimulating hormone.6 Test Interpretation An increased TSH level (>4. cognitive dysfunction. antithyroid agents. alterations in lipid metabolism.45 mIU/L to 4.6 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. head or neck irradiation.2-5. 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. since thyroid disease symptoms may mimic characteristics associated with aging (eg.12 mIU/L) suggests a diagnosis of primary hypothyroidism. Although many patients with primary hypothyroidism present with typical signs and symptoms suggestive of the condition (see Signs and Symptoms). or reproductive function). although it does occur in individuals of all ages. and alopecia).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).1-4 2 .7 More frequent testing may be appropriate for individuals at higher risk of developing thyroid dysfunction. fatigue. depression. office-based testing of suspected patients by primary care physicians is important to ensure an early and accurate diagnosis.2-4 In the presence of an increased TSH with a normal FT4. patients with subclinical hypothyroidism (mild thyroid failure) may be asymptomatic or have nonspecific signs and symptoms (eg. this diagnosis is confirmed if the patient has a low free thyroxine (FT4) level.8 Because TSH is a more sensitive test than FT4. certain medications. gastrointestinal. although there may be circumstances when patients with chronic autoimmune thyroiditis have normal TSH levels. an endocrinologist should be consulted for evaluation of possible TSH-secreting pituitary tumor or thyroid hormone resistance. patients with subclinical hypothyroidism (mild thyroid failure) will have a normal FT4 with an elevated TSH level.5 Testing Because many signs and symptoms of hypothyroidism are nonspecific and patients with subclinical hypothyroidism (mild thyroid failure) may be asymptomatic. radioactive iodine (131I) therapy.12 mIU/L)* generally excludes the diagnosis of primary hypothyroidism.1-3.5 If the FT4 is high in an individual with a normal or elevated TSH level.8 A normal TSH level in a patient with low FT4 suggests secondary hypothyroidism or a hypothalamic-pituitary disorder. Women older than 40 years of age and elderly individuals of both sexes are affected most frequently. these patients probably should be evaluated by an endocrinologist.6 TSH testing may be particularly useful in elderly patients.3. TSH) concentration beginning at 35 years of age and every 5 years thereafter. A normal TSH level (0.4.1. depression.1-5 Other causes of hypothyroidism include thyroidectomy. or congenital defects.5. The indication for TSH testing is particularly compelling in women. fatigue.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.1.3. memory loss.

PRIMARY HYPOTHYROIDISM DIAGNOSIS ALGORITHM Suspect Hypothyroidism Measure TSH Level TSH >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 .12 mIU/L TSH 0.45-4.12 mIU/L TSH <0.

thyroid disease.0 mIU/L.3 to 3. headache.12 mIU/L. coma Known tracheal compression ▬ ▬ ▬ ▬ Serum sodium <130 mEq/L Pregnancy Postpartum thyroiditis Symptoms suggest secondary or tertiary hypothyroidism (galactorrhea.Signs and Symptoms ▬ History of autoimmune disease ▬ History of Graves disease treatment.0 mIU/L. the normal TSH range that is cited in these algorithms.4 to 4. ICU/CCU patient Age <15 years Cardiac compromised Stupor.7. each laboratory may use different TSH reference ranges.11 though the establishment of a single reference range continues to be controversial. infertility.45 and 4.3 In addition.9 whereas others have proposed a narrower TSH range of 0. physicians should be aware of and act within the normal TSH values used by their laboratories.8 The National Academy of Clinical Biochemistry has proposed a normal TSH range of 0. Serum TSH levels of the reference population in the NHANES III study fell within 0.9. 4 . 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. etc) *Normal TSH reference ranges have been reported in epidemiological studies8 and recommended in various national association guidelines and position statements.

8:457469.291:228-238. Redfern CC. Powe NR. Cooper DS. 1. Laboratory Medicine Practice Guidelines: Laboratory Support for the Diagnosis and Monitoring of Thyroid Disease. Ladenson PW. Demers L. 1998. JAMA. Subclinical thyroid disease: scientific review and guidelines for diagnosis and management. Ortiz E. Solomon DH. 1990. Treatment guidelines for patients with hyperthyroidism and hypothyroidism.160:1573-1575. National Academy of Clinical Biochemistry. Ain KB. Screening for mild thyroid failure at the periodic health examination: a decision and cost-effectiveness analysis. Hypothyroidism. Available at: www. Spencer CA. Pa: WB Saunders Co. JAMA. 2002. Mariash CN. Endocrine Pract. Sawin CT. Ann Intern Med. American Association of Clinical Endocrinologists Thyroid Task Force. 2002. 1989:752-768. et al. AACE medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. 8. Arch Intern Med. eds.263:1529-1532. Philadelphia. Helfand M.273:808-812. J Clin Endocrinol Metab. Singer PA. Utiger RD. 2. 24. 3. and thyroid antibodies in the United States population (1988 to 1994): National Health and Nutrition Examination Survey (NHANES III). Nicoloff JT. Screening for thyroid disease: an update. 2000. American Thyroid Association guidelines for detection of thyroid dysfunction. T4. Chopra IJ. Surks MI. 6. Accessed Oct.References Singer PA. Daniels GH. 2004. American Thyroid Association guidelines for use of laboratory tests in thyroid disorders. Serum TSH. Levy EG. et al.org.nacb.129:144-158. Ladenson PW. 5 . JAMA. et al. JAMA.276:285-292. Hollowell JG. 3rd ed. Flanders WD. 7. In: DeGroot LJ et al. Endocrinology. American College of Physicians. 1995. 2003. Surks MI. 10. et al. Staehling NW. Danese MD.87:489-499. 9. 1996. 4. 5.

and other cardiac changes. accelerated bone turnover. either the dose is inadequate or there are problems with patient compliance or drug interactions.7 Initial and maintenance doses of levothyroxine sodium must be individualized based on the etiology.1.6 µg/kg/d. although a few patients with chronic autoimmune thyroiditis (Hashimoto thyroiditis) spontaneously recover.7 A euthyroid state is usually achieved in adults who require full replacement with a maintenance dosage of levothyroxine sodium that averages 1.7 If TSH remains elevated after initiation of levothyroxine sodium therapy. and the higher the pretreatment TSH level.1-4 Although replacement therapy in patients with subclinical hypothyroidism (mild thyroid failure) can be controversial.5 µg to 25 µg.5 mIU/L to 2.3 Replacement therapy usually must be continued for life.1.PRIMARY HYPOTHYROIDISM MANAGEMENT Overview Thyroid hormone replacement therapy with levothyroxine sodium is the treatment of choice for the routine management of primary hypothyroidism. maintenance dosage is continued and the TSH test repeated annually or whenever the patient becomes symptomatic.4.1-6 There is mounting evidence to suggest that patients with a persistent elevation of serum thyrotropin (thyroid stimulating hormone.11 The fact that dosing requirements may be affected by malabsorptive states or drug interactions should be considered. TSH) may be exposed to greater risk if left untreated.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. as evidenced by normalization of serum TSH levels.5 µg/d to 25 µg/d) and close monitoring to avoid overdosage. the longer it will take. since overdosage may cause decreased bone density.0 mIU/L.2.3 6 .5 µg to 25 µg every 3 to 4 weeks until TSH normalizes to 0.4 Levothyroxine sodium therapy should be initiated in younger healthy adults at the full replacement dose of 1.2 Overdosage of levothyroxine sodium should be avoided.45 mIU/L.2. as well as the age and clinical condition of the patient. tachycardia.2.7 Titration should occur every 6 to 8 weeks until the TSH level reaches 0.2.4.4.7-10 A serum TSH level between 0.4.6 The goal of replacement therapy is to restore the patient to a euthyroid state.1-3 Dosage in older adults should be titrated carefully in increments of 12.2 If noncompliance is excluded.0 mIU/L is considered to be the optimal therapeutic target for levothyroxine sodium therapy.1.0 mIU/L.4.2 Dosage reduction generally is indicated if the TSH level decreases below 0.1. most patients benefit from such therapy.7 After the TSH level has normalized.6 µg/kg/d. the dose should be increased gradually in increments of 12. and other adverse effects including alterations in liver enzymes. and duration of hypothyroidism.2.5 mIU/L to 2.1.5 mIU/L and 2.1.2.7 This usually takes several weeks.7 Older adults or those with known or suspected heart disease require a lower initial dosage (12.1. severity.

Thyroid. Brent GA. Ortiz E. 2000. 2002.273:808-812. Lezotte DC. 6.11(8):757-64. Larsen PR. Nicoloff JT. JAMA. 7. Spencer CA. Braverman LE. 2003. Ladenson PW. Cooper DS. 12. Use of a sensitive thyrotropin assay for monitoring treatment with levothyroxine. Minelli R. Arch Intern Med. McDermott MT. National Academy of Clinical Biochemistry.291:228-238. 11. McDermott MT. 1989. 24. 13. 1993.14:401-423. Crapo LM.160:1573-1575.149:309-312. Chu JW. 2001. 4. Treatment guidelines for patients with hyperthyroidism and hypothyroidism. Ann Intern Med. Endocrine Rev. Surks MI.86:4585-4590. 3.119:492-502. Daniels GH. Laboratory Medicine Practice Guidelines: Laboratory Support for the Diagnosis and Monitoring of Thyroid Disease. JAMA. 1995. Levothyroxine therapy in patients with thyroid disease.8:457469. Ain KB. Subclinical hypothyroidism is mild thyroid failure and should be treated. Endocrine Pract. 5. Gardini E. The treatment of subclinical hypothyroidism is seldom necessary. American Association of Clinical Endocrinologists Thyroid Task Force. Haugen BR. et al. 2. 1993. Watts NB. Levy EG. Subclinical thyroid disease: scientific review and guidelines for diagnosis and management. American Thyroid Association guidelines for detection of thyroid dysfunction. et al. Surks MI. 1990. Available at: www. 7 . Demers L. Mandel SJ. Solomon DH. 9. J Clin Endocrinol Metab. Mariash CN. Arch Intern Med. The use and misuse of thyroid hormone. AACE medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism.263:1529-1532. JAMA. Roti E. J Clin Endocrinol Metab. et al. Singer PA.86:4591-4599. Ridgway EC. 2001. Chopra IJ. 1.nacb. 8. Accessed Oct.References Singer PA. American Thyroid Association guidelines for use of laboratory tests in thyroid disorders. 2001 Aug.org. 2004. et al. Management practices among primary care physicians and thyroid specialists in the care of hypothyroid patients.

5-25 µg/d Increments Continue Dose Decrease Levothyroxine Sodium Dose by 12.45 mIU/L Increase Levothyroxine Sodium Dose by 12.5-25 µg/d Increments Consult Endocrinologist if: − Cardiac status compromised − Stupor. 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. coma − Lithium treatment − Amiodarone treatment − Pre-operative patient.6 µg/kg/d Levothyroxine Sodium 25 to 50 µg/d Levothyroxine Sodium 12.12 mIU/L TSH <0.45-4.12 mIU/L.PRIMARY HYPOTHYROIDISM MANAGEMENT ALGORITHM TSH >4.12 mIU/L TSH 0. ICU/CCU patient − Age <15 years − Sodium < 130 mEq/L − Pregnant − Postpartum thyroiditis Repeat TSH Test Annually or When Symptomatic *Thyroperoxidase antibodies 8 .5 to 25 µg/d 5-6 weeks Repeat TSH Test TSH >4.

1-6. age of the patient. TSH) level and free thyroxine (FT4) estimate are the tests most frequently used for the initial evaluation of possible hyperthyroidism. and duration of the condition.5 Initial Evaluation and Testing Initial evaluation of suspected hyperthyroidism includes a comprehensive medical history and physical examination (to identify goiter. toxic multinodular goiter.1 mIU/L to 0.8 Current studies suggest that TSH values <0.5. toxic adenoma. and the fact that most thyroid function tests (including TSH) give misleading results in patients with acute medical conditions should be considered.3.4 mIU/L have intermediate degrees of suppression of the normal hypothalamic-pituitary axis and may be asymptomatic.45 mIU/L) and an increased FT4 generally confirm a diagnosis of hyperthyroidism. or silent).8.HYPERTHYROIDISM INITIAL DIAGNOSIS Overview Thyrotoxicosis results from excess thyroid hormone and is present in a variety of conditions.6. or effects of certain medications (eg.8.1. or other signs) and appropriate laboratory tests. symptoms of hyperthyroidism and may not even have enlarged thyroid glands.4.5 Elderly patients may have markedly abnormal tests with few.6-9 A decreased TSH level (<0.2. an autonomous thyroid nodule.45 mIU/L to 4.3-6 If results of initial testing indicate hyperthyroidism.4. manifestations and severity depend on the extent of thyroid hormone excess.2.1-5 Thyrotoxicosis may also be associated with excessive pituitary TSH production. further testing using a combination of tests is needed to establish the etiology1. or excessive ingestion of iodine or thyroid hormone.45 mIU/L may represent thyroid hormone excess and in elderly patients may be associated with an increased risk of atrial fibrillation.3-6 Test Interpretation A TSH level of 0.1. these patients probably should be evaluated by an endocrinologist. if any.1 mIU/L generally have symptoms of hyperthyroidism. glucocorticoids or dopamine).3-5 The serum thyrotropin (thyroid stimulating hormone. nodules. this usually should be done in consultation with an endocrinologist.1 Diagnosis of hyperthyroidism in severely ill patients is complex. and osteoporosis.4 A wide range of signs and symptoms is associated with hyperthyroidism (see Signs and Symptoms). and thyroiditis (painful and subacute.1.9 Individuals with TSH levels <0.12 mIU/L generally indicates that the patient is euthyroid.9 A decreased TSH level with normal FT4 suggests that the patient may have subclinical hyperthyroidism or hyperthyroidism resulting from triiodothyronine (T3) toxicosis. tremors.1.10 9 . exophthalmos. although some patients with familial thyroid hormone resistance or a TSH-secreting pituitary tumor may have normal TSH levels with an increased FT4. a trophoblastic tumor. cardiovascular mortality. including hyperthyroidism due to toxic diffuse goiter (Graves disease). those with levels of 0.

HYPERTHYROIDISM INITIAL DIAGNOSIS ALGORITHM Suspect Hyperthyroidism Measure TSH level TSH >4.45 mIU/L. 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 .45-4.12 mIU/L TSH <0.12 mIU/L TSH 0.45 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.

Helfand M. 11 . Franklyn JA. Hollowell JG. thyroid disease.87:489-499. 1. Utiger RD. et al. Werner and Ingbar’s The Thyroid: A fundamental and Clinical Text. Pa: JB Lippincott Co. 7th ed. Ann Intern Med. Flanders WD. or thyroid surgery ▬ Family history of thyroid disease ▬ Goiter ▬ Exophthalmos ▬ Pretibial myxedema ▬ Excessive iodine exposure (contrast dyes.org. Ingbar SH. Braverman LE. Williams Textbook of Endocrinology. 10. 8th ed. 2002. Screening for thyroid disease: an update. The management of hyperthyroidism. Pa: WB Saunders Co. 24. Utiger RD.129:144-158. Foster DW. eds. Laboratory Medicine Practice Guidelines: Laboratory Support for the Diagnosis and Monitoring of Thyroid Disease. Treatment guidelines for patients with hyperthyroidism and hypothyroidism. Cooper DS. N Engl J Med. Roti E. The use and misuse of thyroid hormone. 1996:713-734.nacb. 9. 2002. Introduction to thyrotoxicosis. 2003. Philadelphia.8:457469. 1992:357-487. Nicoloff JT. Endocrine Rev. 4. Spencer CA. et al. Available at: www. Minelli R.Signs and Symptoms ▬ History of autoimmune disease ▬ History of previous Graves disease treatment. JAMA. 5. and thyroid antibodies in the United States population (1988 to 1994): National Health and Nutrition Examination Survey (NHANES III). Redfern CC. Larsen PR. 1994. Levy EG. The thyroid gland. National Academy of Clinical Biochemistry. JAMA. 6. Staehling NW. medications) ▬ ▬ ▬ ▬ ▬ ▬ ▬ ▬ ▬ ▬ Unexplained weight loss Atrial fibrillation/palpitations Depression/dementia Vitiligo Alopecia Coarse or thinning hair Heat intolerance Sweating Hyperdefecation Tremor References Singer PA. T4.273:808-812.14:401-423. In: Wilson JD. 1995. Serum TSH. 1990. 7. 1993. Gardini E. Chopra IJ. American College of Physicians. Solomon DH.263:1529-1532. eds. 3. 2. Demers L. 8. J Clin Endocrinol Metab. Surks MI. American Association of Clinical Endocrinologists Thyroid Task Force. AACE medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. Endocrine Pract. Philadelphia. Accessed Oct. In: Braverman LE. Braverman LE.330:1731-1738. 1998. Mariash CN. American Thyroid Association guidelines for use of laboratory test in thyroid disorders.

toxic adenoma. Singer PA. Larsen PR.5. Laboratory Medicine Practice Guidelines: Laboratory Support for the Diagnosis and Monitoring of Thyroid Disease. 12 .273:808-812. Williams Textbook of Endocrinology.1992:357-487.1. it may also indicate excessive iodine ingestion or factitious T4-induced thyrotoxicosis. JAMA. 24.8:457469. and decreased TSH levels. 2002. Spencer CA. Chopra IJ. Pa: WB Saunders Co. Endocrine Pract. toxic multinodular goiter. Accessed Oct.2. a total T3 (TT3) or free T3 (FT3) test may be indicated. 3. 8th ed.4-6 If the FT4 is normal in a patient with a decreased TSH. 1990.2 Patients with subclinical hyperthyroidism may have a normal FT3.1 There are various thyroid function tests that can be used for the differential diagnosis of conditions associated with hyperthyroidism.263:1529-1532.4-6 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.4. 5. Available at: www.2. or silent). The thyroid gland.2. The management of hyperthyroidism. Ingbar SH. a brain MRI should be considered to investigate hypothalamic-pituitary disease. In: Wilson JD. or silent). If the FT4 is low in a patient with decreased TSH levels.1.1. American Thyroid Association guidelines for use of laboratory tests in thyroid disorders.org. and results of serum thyrotropin (thyroid stimulating hormone. especially in elderly patients. American Association of Clinical Endocrinologists Thyroid Task Force. References 1.1. Levy EG.1. 1995.5 Although a diagnosis of Graves disease is evident if diffuse goiter and ophthalmopathy are present in patients with hyperthyroidism. normal or only slightly increased 123I uptake may be seen. eds. TSH) and free thyroxine (FT4) measurements. including triiodothyronine (T3) radioimmunoassays.nacb.45 mIU/L) in conjunction with a low 123I update generally indicates some form of thyroiditis (painful and subacute.HYPERTHYROIDISM DIFFERENTIAL DIAGNOSIS Overview After an initial diagnosis of hyperthyroidism has been made based on medical history. Franklyn JA. 4. 2003. Cooper DS. National Academy of Clinical Biochemistry.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).330:1731-1738.2.4 Results of 123I uptake tests in conjunction with physical findings usually can differentiate these. normal FT4.6 A high TT3 or FT3 indicates that the patient may have T3 toxicosis. et al. Treatment guidelines for patients with hyperthyroidism and hypothyroidism. 6. a diagnosis of Graves disease in patients without these clinical manifestations can be confirmed by high 123I uptake. Mariash CN.5 A low FT3 indicates that the patient may have euthyroid sick syndrome. or thyrotoxicosis due to some form of thyroiditis (painful and subacute.2. 2. and thyroid scans. radioactive iodine uptake (123I uptake) tests.2.2 It is not feasible or necessary to use all available procedures in every case. Nicoloff JT. 1994. Demers L. Surks MI. AACE medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. further testing is necessary to determine the etiology of the condition so that it can be managed appropriately.6 A diagnosis of toxic nodular goiter or toxic adenoma is suspected in the absence of ophthalmopathy or diffuse goiter. Philadelphia.6 A decreased TSH level (<0.1. JAMA. Solomon DH. N Engl J Med. Foster DW. physical findings.

† PPT . † Postpartum thyroiditis ‡ Erythrocyte sedimentation rate 123 Refer to PPT Diagnosis and Management Algorithm Confirm with High ‡ ESR ESR Normal 13 Consult Endocrinologist. Symptomatic Therapy with Glucocorticoids/ Aspirin. 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 . **If scan shows dominant cold nodule. follow Solitary Thyroid Nodule Algorithm on page 21. TSH <0. No Further Therapy Recommended. Consult Endocrinologist as Needed Consult Endocrinologist for Selection of Appropriate Hyperthyroidism Management Algorithm Toxic Nodular Goiter Refer to Hyperthyroidism Management Algorithm Silent Thyroiditis.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. or Exogenous Thyroid Hormone Subacute Thyroiditis * I uptake may be increased.HYPERTHYROIDISM DIFFERENTIAL DIAGNOSIS ALGORITHM Patient Hyperthyroid. Continue Observation.

5 This is used frequently in patients with severe hyperthyroidism.HYPERTHYROIDISM MANAGEMENT A: 131I THERAPY Overview Radioactive iodine (131I) therapy generally is considered the treatment of choice for Graves disease.12 mIU/L).1. and relatively low 123I uptake.2-4 A high ablative dose more quickly resolves hyperthyroidism.1-5 Radioactive iodine therapy is also used in the management of toxic multinodular goiter and toxic adenoma.3 These patients may require symptomatic therapy (eg.5 The optimum dosage of 131I is controversial.4 Although smaller doses may be used in an attempt to prevent posttreatment hypothyroidism.4. subacute.6 However.5 Thyroid function begins to normalize and goiter size decreases in most patients within 6 to 8 weeks following 131I therapy.2.5 Follow-Up Because of the potential for hypothyroidism following 131I therapy.2. 14 .3 In addition.4 For patients 40 years of age or younger with a first episode of hyperthyroidism. An endocrinologist generally should be consulted concerning the management of patients with hyperthyroidism. 1.2 The principal complication of 131I therapy is hypothyroidism. a small percentage may require a second or third 131I dose 6 to 12 months after the initial dose.1 If thyroid gland failure is indicated by an increased TSH level (>4. levothyroxine sodium (LT4) replacement therapy should be initiated. which occurs in the majority of patients within 6 to 36 months following therapy.4 Patients should be evaluated 4 to 8 weeks after administration of 131I therapy by monitoring serum thyrotropin (thyroid stimulating hormone.2 A single dose is effective in the majority of patients. long-term follow-up is necessary. patients with this form of hyperthyroidism should not be treated with antithyroid drugs or 131I therapy. it is unclear whether this approach effectively decreases the risk and it may increase the failure rate of cure with the first dose.2.3 Radioactive iodine therapy destroys thyroid cells. 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. especially for patients with recurrent hyperthyroidism after antithyroid drug therapy. some clinicians prefer a trial of an antithyroid drug prior to 131I therapy (see Hyperthyroidism Management B: Antithyroid Drugs Algorithm).1.4. 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. beta blockade).5 Radioactive Iodine Therapy The goal of 131I therapy is to destroy enough thyroid tissue to cure hyperthyroidism.2. or silent) is characterized by a low radioactive iodine uptake and is self-limited. which leads to thyroid failure. large goiters. followed by fibrosis and atrophy. minimizing morbidity associated with the condition.1.3. TSH) levels and free thyroxine (FT4) levels.1-4 Because thyroiditis (painful.1.

Levy EG.References 1. Endocrine Pract. Staehling NW.273:808-812. Cooper DS. The thyroid gland. 6. Ingbar SH. 8th ed. Philadelphia. American Association of Clinical Endocrinologists Thyroid Task Force. Williams Textbook of Endocrinology.330:1731-1738 Larsen PR. J Clin Endocrinol Metab. eds. Hollowell JG. 15 . 2. AACE medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. Flanders WD.1996:713-743. Singer PA. In: Wilson JD.87:489-499. et al. Utiger RD. Franklyn JA. Serum TSH. Philadelphia. Treatment guidelines for patients with hyperthyroidism and hypothyroidism. 1994. Werner and Ingbar’s The Thyroid: A Fundamental and Clinical Text. and thyroid antibodies in the United States population (1988 to 1994): National Health and Nutrition Examination Survey (NHANES III). The management of hyperthyroidism. JAMA. 2002.1992:357-487. Cooper DS. et al. 3. 5. Foster DW.8:457469. Pa: WB Saunders Co. Treatment of thyrotoxicosis. Pa: JB Lippincott Co. 1995. eds. 7th ed. 2002. T4. In: Braverman LE. 4. N Engl J Med.

adrenergic blocking agents. or patients with cardiac disease.45 mIU/L.12 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. ‡ Saturated solution of potassium iodide 16 . 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. FT4 High TSH <0. FT4 Normal or Low Refer to Hypothyroidism Management Algorithm Consider use of adjunctive therapy (antithyroid drugs. elderly patients. FT4 Low TSH >4. FT4 Normal TSH and FT4 Normal TSH >4.45 mIU/L. FT4 Normal or Low Consider use of adjunctive therapy (antithyroid drugs. SSKI ) Repeat TSH and FT4 Tests in 1-2 Months Asymptomatic Symptomatic Patient † Hypothyroid TSH <0. administering antithyroid drug 131 treatment 4 to 8 weeks prior to I therapy may be advised. † 131 The most common scenario for any patient prescribed I therapy is hypothyroidism.12 mIU/L.45 mIU/L. adrenergic ‡ blocking agents. FT4 High TSH <0.45 mIU/L.

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.4 Dosage should be adjusted until a maintenance dosage is established that maintains a euthyroid state1. children and younger adults.1.2 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. 1 to 2 years generally is required to decrease the risk of relapse.3. both TSH and free thyroxine (FT4) levels should be monitored. and pregnant women. Permanent remissions of hyperthyroidism following withdrawal of antithyroid drugs may occur.1.5 Optimum duration of antithyroid drug therapy is unclear. thyroid function should be monitored every 3 to 6 months.3. Propylthiouracil may be preferred in severe or life-threatening hyperthyroidism (thyroid storm) because it inhibits the conversion of thyroxine (T4) to triiodothyronine (T3) and.4 Use of serum thyrotropin (thyroid stimulating hormone.4 Antithyroid Drug Therapy Propylthiouracil and methimazole are the antithyroid drugs generally used for management of hyperthyroidism.4. therefore.1-4 Although antithyroid drugs have been used in the management of other forms of hyperthyroidism. methimazole may be preferred because propylthiouracil is associated with a greater propensity for reduced efficacy of ablation.1. although most patients (50% to 80%) have recurrence of the hyperthyroidism.4.1. 9 to 12 months.3-5 A gradual decrease in thyroid hormone levels leads to a euthyroid state. TSH) levels alone to evaluate thyroid function may be misleading.HYPERTHYROIDISM MANAGEMENT B: ANTITHYROID DRUGS Overview Antithyroid drugs are used in the management of Graves disease. and longer durations of therapy may be appropriate. lifelong follow-up is recommended for all patients. including toxic multinodular goiter and toxic adenoma.4 Antithyroid drugs are not indicated for the management of thyroiditis.1-5 In patients who will subsequently undergo 131I therapy. Although a few patients may enter remission after only 4-6 months. thyroid function should be evaluated every 3 months thereafter. these uses are generally temporary and they are not the treatment of choice. primarily in patients with mild first episodes.3.1.3-5 If therapy is discontinued.4.4 Relapse is most likely to occur within the first 3 to 9 months after therapy is discontinued but may occur at any time.3 17 .5 Because the possibility of delayed relapse or hypothyroidism exists.1.3.2.1.1. and then annually. may decrease serum T3 levels more rapidly than methimazole.3 Follow-Up Patients should be monitored and thyroid function evaluated at intervals of 4 to 8 weeks following initiation of antithyroid agent therapy.

2. JAMA.330:1731-1738. The management of hyperthyroidism. Pa: JB Lippincott Co.References 1. Utiger RD. American Association of Clinical Endocrinologists Thyroid Task Force. 8th ed. Larsen PR. eds. Werner and Ingbar’s The Thyroid: A Fundamental and Clinical Text.273:808-812. 18 . 4. 3. In: Wilson JD. Cooper DS. et al. Pa: WB Saunders Co. 7th ed. 1994. Levy EG. Cooper DS.1996:713-734. Philadelphia. In: Braverman LE.8:457469. Foster DW.1992:357-487. Endocrine Pract. AACE medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. The thyroid gland. 5. Franklyn JA. N Engl J Med. Treatment of thyrotoxicosis. eds. Singer PA. 1995. Ingbar SH. Treatment guidelines for patients with hyperthyroidism and hypothyroidism. Philadelphia. Williams Textbook of Endocrinology. 2002.

Then Annually 19 .45 mIU/L. FT4 Normal or Low Continue or Increase Antithyroid Drugs.HYPERTHYROIDISM MANAGEMENT B: ANTITHYROID DRUGS ALGORITHM Hyperthyroidism − Graves Disease Prescribe Antithyroid Drugs 4-8 weeks Measure TSH and FT4 Levels TSH <0. FT4 Normal TSH <0. FT4 High 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.45 mIU/L.45 mIU/L.45 mIU/L. 9-12 Months. FT4 Low TSH >0.

which is an enlargement of the thyroid gland.4 Patients with goitrous autoimmune thyroid disorders usually have measurable titers of thyroid autoantibodies and may be euthyroid or hypothyroid. exposure to environmental or pharmacologic goitrogens.0 mIU/L).2-4 Prolonged administration of levothyroxine sodium therapy in patients who do not respond to such treatment is not justified.1-3 Diffuse goiter may result from iodine deficiency. may be diffuse or nodular. If nodules greater than 1. euthyroid. or hyperthyroid.GOITER WORKUP Overview Goiter. In many patients.3 Patients with nodular goiter should have a thyroid scan and/or ultrasound.4 20 . and a thyroid scan if nodules are present.3 Diffuse goiter in euthyroid and hypothyroid patients younger than 50 years of age with thyroperoxidase antibodies (TPOab.1.6 Patients younger than 50 years of age with no dominant cold nodule may receive levothyroxine sodium therapy. since efficacy has not been proven and risks of overdosage are more serious. measurement of serum thyrotropin (thyroid stimulating hormone.2.0 cm are discovered.1. testing for thyroid autoantibodies to diagnose autoimmune disorders.1-5 The rationale for such therapy is that TSH may act as a cofactor that promotes growth of the thyroid. and may or may not be associated with hypothyroidism or hyperthyroidism. Thyroid stimulating hormone levels should be monitored in patients who do not receive levothyroxine sodium. TSH) and free thyroxine (FT4) levels to determine whether the patient is hypothyroid.1 mIU/L to 1. previously called “antimicrosomal” antibodies) can be treated with levothyroxine sodium.1. the thyroid returns to its original size within in a few months if therapy is discontinued.0 mIU/L or in patients older than 50 years of age. levothyroxine sodium therapy generally is continued with periodic monitoring of TSH levels 2. optimum duration of therapy is not known. or autoimmune processes such as Graves disease or autoimmune thyroiditis (Hashimoto thyroiditis). Nodular goiter responds to levothyroxine sodium therapy less frequently and to a lesser extent than diffuse goiter.2 Nontoxic goiter is often a precursor to toxic multinodular goiter. and effective reduction of TSH levels by levothyroxine sodium may induce regression of nontoxic goiter in some patients.2-5 The goal of therapy is to maintain TSH levels in the lownormal range (0. the physician should consider performing ultrasound-guided fine-needle aspiration (FNA). Management Initial evaluation of goiter includes: a comprehensive physical examination.4 If goiter size decreases or remains stable during therapy.1 Levothyroxine sodium therapy is not used for the treatment of diffuse goiter in patients with baseline TSH levels <1. the toxic form generally is associated with signs and symptoms of hyperthyroidism. since increasing levels may indicate progression of the disease to hypothyroidism.

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

GOITER WORKUP ALGORITHM Goiter Consult With Endocrinologist Measure TSH Levels TSH >4.1-1.12 mIU/L TSH 0.1-1. Refer to Solitary Thyroid Nodule Management Algorithm Levothyroxine Sodium Therapy Goal TSH 0.45 to 4.0 mIU/L Repeat TSH Test in 1 Year Dominant Cold Nodule No Dominant Cold Nodule Perform FNA* Age >50 Age <50 *Fine-needle aspiration.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 0.0 mIU/L Repeat TSH Test in 1 Year 22 .12 mIU/L TSH <0.

Caraballo PJ.26: 777-800. Shaha AR. 31: 699-722.1. the efficacy of LT4 suppressive therapy is controversial. 87: 4154-4159.1-4 Solitary thyroid nodules identified as benign by FNA generally are managed without surgery unless nodule size or patient concerns indicate excision. Management of the single thyroid nodule. Pharmacotherapy for thyroid nodules. reduce nodule size. location. the extent of surgery varies depending on factors such as nodule size. Kaplan BJ. Lawrence W Jr. thyroid nodules.1 mIU/L to 1. 5.2 The principal diagnostic tool used is fine-needle aspiration (FNA) for cytology.6 If effective. hypofunctioning “cold” nodules have a higher probability of being malignant and are usually managed with surgery. Mariani M.4 Some clinicians recommend surgery for all suspicious solitary thyroid nodules. 6. Changing concepts in the diagnosis and management of thyroid nodules. 4. or malignant. TSH) may be a contributing factor to nodule formation. Celani MF. 110:183-93. a reduction in nodule size usually is evident during the first 6 to 12 months of therapy. J Clin Endocrinol Metab. Clar C. suppressive therapy may decrease TSH secretion. and the goal is to maintain the TSH in the low-normal range (0.0 mIU/L). Effectiveness of thyroid hormone suppressive therapy in benign solitary thyroid nodules: a meta-analysis.37:398-401. surgical excision is indicated.1-4 If FNA results indicate that the nodule is malignant or suspicious for malignancy.1-4 References 1. however. 1992.1-4 Randomized. 2002.4 Because thyrotropin (thyroid stimulating hormone.1-4. Castro MR.7 The dosage of levothyroxine sodium used for suppressive therapy ranges from 50 µg to 200 µg daily.1 A history of head or neck irradiation is a major risk factor for the development of thyroid nodules and thyroid cancer. Mariani G. and it is unclear which patients are most likely to respond. Endocrinol Metab Clin North Am. Sheppard MC. and prevent further nodule growth. 3.123:603-608. J Surg Oncol. On the usefulness of levothyroxine suppressive therapy in the medical treatment of benign solitary. while a few recommend a trial of levothyroxine sodium suppressive therapy prior to surgery.5. solid or predominantly solid.80:157-170. and the presence of lymph nodes. Morris JC. 7. 2. 2000. suspicious. 1997. Neises G.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. If results of FNA suggest follicular neoplasm. 2002.1-4 Levothyroxine sodium (LT4) may be used for suppressive therapy of benign nodules. 2002.1-4 Although these scans are not diagnostic. Diagnosis and management of patients with thyroid nodules. Franklyn JA. Gharib H. Richter B. 1990. Endocrinol Metab Clin North Am. controlled studies have suggested that only 25% of benign nodules will decrease in size by 50% in response to LT4 therapy. a thyroid scan can be used to classify the nodule as hyperfunctioning (“hot”) or hypofunctioning (“cold”) depending on its ability to incorporate radioactive isotope. Laryngoscope. Acta Endocrinol (Copenh). A systematic review and meta-analysis. 23 .7 Optimum management of solitary thyroid nodules classified as suspicious by FNA is unclear. Controversies in the management of thyroid nodule.7 The TSH test is used to determine levothyroxine sodium dosage. Clin Endocrinol.1-3 Classification and Management Thyroid nodules generally are classified as benign (colloid or follicular adenomas).

12 mIU/L Refer to Hypothyroidism Differential Diagnosis Algorithm FNA Benign Malignant Suspicious or Follicular Neoplasm Inconclusive or Indeterminate Consider Levothyroxine Sodium Therapy. TSH Goal 0. hoarseness 24 .1-1. 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 <0.45 mIU/L TSH 0.12 mIU/L TSH >4.0 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.

and in up to 25% of women with type 1 diabetes mellitus. subclinical hyperthyroidism. Management Levothyroxine sodium is used as replacement therapy for the management of PPT in patients who have clinical or subclinical hypothyroidism (mild thyroid failure).3.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.6 An endocrinologist generally should be consulted if results of TSH and FT4 testing indicate hyperthyroidism.0 mIU/L is generally considered the optimal therapeutic target for levothyroxine sodium therapy.1.6 A serum TSH level between 0. and thyroid autoantibodies. hypothyroidism.3-6 If symptoms develop.7 After several months of therapy. the dosage is adjusted based on TSH levels. are elevated in a high percentage of patients with PPT.5 mIU/L and 2. dosage of levothyroxine sodium should be decreased and TSH levels tested to determine whether the patient has returned to a euthyroid state.1-6 Postpartum thyroiditis reportedly occurs in 5% to 8% of women.1.5. free thyroxine (FT4) levels are used as an adjunctive test to confirm that the patient is either hypothyroid or hyperthyroid.6 Most women with PPT return to the euthyroid state within 1 year of delivery.* Testing and Test Interpretation Diagnosis of PPT involves serum thyrotropin (thyroid stimulating hormone.6 Women with diabetes mellitus or a familial history of autoimmune thyroid disease appear to be at increased risk for PPT (see Risk Factors). or subclinical hypothyroidism (mild thyroid failure) in a postpartum patient.6 Postpartum thyroiditis is considered to be an autoimmune disorder.3.1.6 Patients with PPT may be symptomatic or asymptomatic. although up to 25% develop permanent primary hypothyroidism.2.6 It may be of benefit to measure these antibodies in all pregnant women in order to identify patients at risk for PPT.1.4. they can occur as early as 1 month or as late as 1 year after delivery.4 25 . however. they generally are evident within 6 months of delivery.3.4-6 Women who develop PPT following pregnancy are at risk for recurrence following subsequent pregnancies.1. TSH) testing and measurement of TPOab levels. including thyroperoxidase antibodies (TPOab).

2. Roman SH. et al. course. 24. 2003. A long-term follow-up of postpartum thyroiditis. Roberts RC.14:401-423. Minelli R. 1987. The use and misuse of thyroid hormone. 26 . 1993. etiology. Gardini E.16:1-11. Demers L.150:1397-1400. Drexler AJ. Stagnaro-Green A. How common is postpartum thyroiditis? A methodologic overview of the literature. Turney SL. Postpartum lymphocytic thyroiditis: prevalence. Arch Intern Med. Roti E. Gerstein HC. Fifty percent or more of women with positive anti-TPO antibodies will develop PPT. 4. and clinical implications.147:221-224. and longterm follow-up.References 1. Accessed Oct. Parkers AB. Nikolai TF. Othman S. Thyroid Today. 7. 1990.79:10-16. Braverman LE. 1990. Spencer CA. clinical.32:559-564. Alvarez-Marfany M. Phillips DIW. J Clin Endocrinol Metab. Laboratory Medicine Practice Guidelines: Laboratory Support for the Diagnosis and Monitoring of Thyroid Disease. Available at: www. Postpartum thyroiditis: prevalence. 3. Clin Endocrinol.org. * Ten percent of women will have positive anti-TPO antibodies with normal TSH levels. National Academy of Clinical Biochemistry. Long-term prospective study of postpartum thyroid dysfunction in women with insulin dependent diabetes mellitus.nacb. 5. Stagnaro-Green A. Robertson C. 1993. Endocrine Rev. Arch Intern Med. 6. 1994.

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 <0.5-2.0 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 . Glucocorticoids.45-4.12 mIU/L TPOab - TSH 0.45-4. Autonomous Thyroid Nodule.12 mIU/L TPOab + or - TSH 0. Dopamine Re-evaluate at 3-6 Months Taper Levothyroxine Sodium Dose Repeat TSH TSH >4.45 mIU/L TPOab + or - Test FT4 Stop Repeat TSH in 3-6 Months Test FT4 TSH >4.12 mIU/L TSH 0. T3* Toxicosis.12 mIU/L TPOab + TSH <0.12 mIU/L FT4 Normal FT4 Low TSH 0.45-4.POSTPARTUM THYROIDITIS DIAGNOSIS AND MANAGEMENT ALGORITHM Suspect PPT Test TSH and TPOab TSH >4.