Hypothyroidism overview

DefinitionEtiologyEpidemiologyPathophysiologyClinical Presentation
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A clinical state defined as decreased production of thyroid hormone, by the thyroid gland resulting in deficiency of circulating hormone which regulates essential functions; such as heart rate, digestion, physical growth, and if left untreated, leads to multiple organ and tissues damage.


Thyroid hormone resistance: Mutation within thyroid hormone receptors (TRB) leads to poor hormone recognition by tissues and causes a condition similar to low thyroid production state.



Primary hypothyroidism:

  • Indicates decreased thyroidal secretion of thyroid hormone by factors affecting the thyroid gland itself

Secondary hypothyroidism:

  • Decreased thyroidal secretion of thyroid hormone can also be caused by insufficient stimulation of the thyroid gland by thyroid-stimulating hormone (TSH), due to factors directly interfering with pituitary TSH release.

Tertiary hypothyroidism:

  • Indicates decreased thyroidal secretions due to indirect reduction in thyroid releasing hormone (TRH) release from the hypothalamus.


Note: Clinically it is difficult to differentiate between the secondary and tertiary hypothyroidism so they are often collectively referred to as "central hypothyroidism"


Myxedema coma:

A severe state of hypothyroidism which, if left untreated, leads to severe stress and infections.


  • Myxedema coma is a potentially lethal but rare condition, occurring with severe hypothyroidism


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Various functional or structural disorders are involved which may cause hypothyroidism, and are categorized as follows:


Primary hypothyroidism:

  • Deficient thyroid hormone production by thyroid gland. Usually inherited. Accounts for approximately 90-95% of hypothyroidism


Central hypothyroidism:

  • Inadequate stimulation of the normal gland from defect at the level of pituitary or hypothalamus


Peripheral (extrathyroidal) hypothyroidism:

  • Symptoms exhibiting hypothyroid state, despite normal structure and function of the thyroid gland and due to peripheral tissue resistance to thyroid hormone


Causes of Hypothyroidism

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  • Predominant age: >40 years
  • Predominant gender: Female > Male, 5:1-10:1


  • 5-10/1,000 in general population
  • Common in elderly
  • >65 years of age, increases to
    • 6-10% of women
    • 2-3% of men

Hashimoto's thyroiditis:

  • Annual incidence
    • Women: 400 per 100,000
    • Men: 100 per 100,000
  • Mean age at diagnosis: 60 years
  • Commonest cause of hypothyroidism


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  • Hypothyroidism results from dysfunction in the normal homeostasis in the formation and regulation of the active form of thyroid hormone T3
  • Thyroid hormone deficiency may stem from a variety of causes including destruction/atrophy of the thyroid gland (primary hypothyroidism), pituitary insufficiency (secondary hypothyroidism) or from abnormalities of the hypothalamic-pituitary axis (tertiary hypothyroidism)


1-Image-Normal Regulation Hypothyroidism-Pathophisiology-Hypothyroid


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In primary hypothyroidism, in response to a drop in T4 secretion from the thyroid gland, TSH secretion from the pituitary is increased. Thus, an elevated TSH is the primary marker of primary hypothyroidism.


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Clinical Presentation:

Clinically the disease varies from one patient to the other depending upon cause, duration and severity of the hypothyroid state. Since thyroid hormones influence most organs, tissues and cells of the body, there can be a wide spectrum of sign and symptoms in this disorder (see figure).


1-Image-Symptoms-Clinical features-Hypothyroid


Note: An endocrinologist would most likely recognize the subtle manifestations and would be more skilled to do physical thyroid gland examination. Consultation is recommended for:

  • Patients of age ≤18 years
  • Patients who do not respond to treatment
  • Pregnant patients
  • Cardiac patients
  • Structural changes in the thyroid gland
  • Presence of other endocrine diseases


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Differential Diagnosis:
  • Sick euthyroid syndrome
  • Thyroiditis
  • Depression
  • Hypochondriasis
  • Nephrotic syndrome
  • Chronic nephritis
  • Addison disease
  • Hypopituitarism
  • Neurasthenia
  • Chronic fatigue syndrome
  • Fibromyalgia
  • Congestive heart failure (CHF)
  • Primary amyloidosis
  • Dementia from other causes
  • Infertility
  • Menopause
  • Ovarian insufficiency
  • Obesity
  • Sleep disorders


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Investigation and Workup:

History and Physical:

History and physical examination will provide definitive information in severe cases, but the disease can often be asymptomatic or have non-specific signs and symptoms. However; biochemical proof of thyroid hormone deficiency is necessary for diagnosis.


Laboratory studies:

  • Common tests of thyroid function include TSH, free T4, anti-thyroid peroxidase (anti-TPO) antibodies (see figure)
  • Serum thyrotropin hormone (TSH) measurement is the first-line diagnostic test
  • An elevated TSH level should be confirmed by a repeated measurement, along with measurement of serum free T4 estimates
  • Many patients with primary hypothyroidism have normal circulating levels of T3
  • Free T4 assays can be unreliable in the setting of severe illness

1-Image-Common Tests of Thyroid Function-Investigations- Hypothyroidism


Interpretation of test results:

Although most laboratories report the upper range of normal for TSH is 4.5 mIU/L, evidence suggests that the true upper limit of normal may be as low as 2.5 mu/L.


Ref: Wartofsky, L. The evidence for a narrower thyrotropin reference range is compelling. The Journal of Clinical Endocrinology & Metabolism, 90:5483-5488, 2005.


Overt primary hypothyroidism:

  • TSH: Increased
  • Serum free thyroxine (T4): Decreased


Subclinical hypothyroidism:

  • TSH: Elevated (usually <10 mlU/L)
  • Serum free T4: Normal


Secondary or tertiary hypothyroidism:

  • TSH: Low or normal
  • Serum free T4: Decreased
  • Impaired TSH response to TRH


Antithyroid antibodies:

Anti-Thyroid peroxidase (TPO) antibodies

  • Useful to establish an autoimmune etiology of hypothyroidism in selected cases
  • Useful in predicting progression of subclinical to overt hypothyroidism


Imaging Studies

Ultrasound (thyroid):

  • Detect nodules and infiltrative disease
  • Useful in follow-up for size of thyroid and nodules

MRI of the pituitary gland/hypothalamus:

  • When central hypothyroidism is suspected


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a) Management of Hypothyroidism

Goals: Restore and maintain euthyroid state as reflected by TSH levels.


Agent of choice:

  • Levothyroxine once daily, on an empty stomach
  • Recommend: High quality (same brand) of levothyroxine to be prescribed throughout the therapy, reason being bioequivalence and brand interchangeability has not been proven among different brands


Treatment: Is individualized considering age, weight and cardiac status (see figure below)


Monitor treatment: Every 6 to 8 weeks until TSH is normalized, then at 6 months initially followed by annual assessments.


Drugs that interfere with thyroid hormone absorption:

  • Iron
  • Calcium carbonate
  • Cholestyramine
  • Lithium
  • Aluminum hydroxide gel
  • Sucralfate
  • Dietary soy


Medical conditions that may interfere with thyroid hormone absorption:

  • GI malabsorptive disorders
  • Previous small-bowel bypass surgery


1-Image-Levo dosing-Treatment-Hypothyroidism


b) Management of subclinical hypothyroidism:

Individuals having a mild increase in TSH (usually <10 mUI/L), with normal free T4 and T3, and who may or may not be symptomatic; ~3-20% of these cases, may progress to (overt hypothyroidism)


Treatment is indicated in patients with:

- TSH >10 mIU/ml


- TSH above normal (4.5 to 10 mUl/L) with a goiter or

anti-TPO antibodies, pregnancy, infertility, signs or symptoms



  • Starting dosage: 25-50 mcg/d (see figure)
  • Monitor TSH in 6-8 weeks and the dose should be adjusted accordingly
  • Target TSH value is between 0.3-3.0 mIU/ml
  • Once the disease is stabilized annually asses the patient

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c) Management of Hypothyroidism during Pregnancy:

Hypothyroidism in pregnancy is associated with:

  • Preeclampsia
  • Anemia
  • Postpartum hemorrhage
  • Cardiac ventricular dysfunction
  • Spontaneous abortion
  • Low birth weight
  • Impaired cognitive development
  • Fetal mortality/ still births


➣ Increased dosage requirements should be anticipated

during pregnancy

  • Especially in the first and second trimesters


➣ Women with a history of treated hypothyroidism who are

contemplating pregnancy should be rendered euthyroid

with a goal TSH no higher than 2.5mUI/L before



➣ Patients with hypothyroidism should increase the

levothyroxine dose by 30% to 50% by four to six weeks



➣ For previously diagnosed women, serum TSH levels

should be measured:

  • Every 4 weeks during the first half of pregnancy
  • At least once between 26 and 32 weeks gestation
  • At 6 weeks postpartum


➣ Levothyroxine dose should be adjusted:

  • To maintain a serum TSH less than 2.5 mIU/L, in the first trimester and <3.0 mUI/L in the second and third trimesters
  • The dose of levothyroxine may be returned to preconception levels immediately postpartum



  • DeGroot L, Abalovich M, Alexander E, et al. Management of thyroid dysfunction during pregnancy or postpartum: An Endocrine Society clinical practice guideline. Journal of Clinical Endocrinology & Metabolism, 2012; 97:2543-2565
  • Stagnaro-Green A, Abalovich M, Alexander E, et al. Guidelines of the American Thyroid Association for the diagnosis and management of thyroid disease during pregnancy and postpartum. Thyroid. 2011; 21:1-45


d) Hypothyroidism and concurrent diseases:

Diabetes mellitus:

  • Approximately 10% of type1 diabetes mellitus patients will develop chronic thyroiditis in their lifetime
  • Patients with diabetes should always be examined for goiter and regular TSH level monitoring should be done
  • Approximately 25% of women with type1 diabetes mellitus will develop postpartum thyroiditis



Typically patients seek medical attention for infertility or previous miscarriages, when investigated by careful history, examination and labs will demonstrate clinical or subclinical hypothyroidism.


  • Patients with increased TSH levothyroxine replacement therapy will normalize the fertility issues



In patients with depression, clinical and subclinical hypothyroidism should always be considered.


  • Appropriate levothyroxine doses should be initiated in patients with elevated TSH levels

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e) Management of myxedema coma: (Endocrine



  • Myxedema coma is an endocrine emergency and should be treated aggressively
  • Any precipitating factors should be treated
  • Administer mechanical ventilation if necessary
  • Parenteral hydrocortisone (50 mg every 6 hours)
    • Until coexisting adrenal insufficiency excluded
  • Intravenous Hypertonic saline and glucose
    • For severe Hyponatremia or hypoglycemia
  • Passive correction of hypothermia
    • Active correction can cause vasodilatation and hypotension


Preferred treatment:

  • Levothyroxine
    • 500 mcg IV, as a one-time loading dose
    • Subsequent daily dose: 50-100 mcg

Alternative treatment 1:

  • Tri-iodothyronine, T3
    • IV or via nasogastric tube, 10-25 mcg every 8-12 hours
    • Excess T3 may provoke arrhythmias

Alternative treatment 2:

  • Combined Levothyroxine (T4) and Tri-iodothyronine (T3)
    • Initial IV bolus levothyroxine (200 mcg) Tri-iodothyronine (25 mcg)
    • Subsequent daily doses of levothyroxine (50-100 mcg) and T3 (10 mcg every 8 h) until the patient responds


Thyroid agents

  • ➣ Levothyroxine



  • Exact mechanism of action is unknown
  • It is generally believed that they exerts its many actions through control of DNA transcription and, ultimately, protein synthesis
  • Levothyroxine (T4) is a synthetic form of thyroxine, an endogenous hormone secreted by the thyroid gland. T4 is metabolically deiodinated to active metabolite, L-triiodothyronine (T3) in peripheral tissues




  • Usual initial dose ~1.7 mcg/kg/day PO once daily; usual doses are ≤200 mcg/day; may titrate dose by 12.5-25 mcg (every 6-8 weeks); Max. 300 mcg/day


Age >50 years or <50 year with cardiac disease

  • Usual initial dose is 25-50 mcg/day; may titrate dose at 6-8 weeks intervals, as needed


Age >50years with cardiac disease

  • Usual initial dose is 12.5-25 mcg/day; may titrate dose at 4-6 weeks interval, as needed


Subclinical hypothyroidism

  • Start with 25-50 mcg/day; may titrate dose at 6-8 week intervals as needed


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Clinical Trials:
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Pipeline Agents:

Pending new data.


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Physician Resources:

1. Tips for patient care

Risk factor management:

  • Advise patient to report signs of infection or potential heart problems (palpitations, dyspnea)
  • Hypothyroidism could increase the risk of infertility and miscarriage
  • If suspecting the presence of adrenal insufficiency, it should be confirmed or ruled out and should be treated prior to treatment of hypothyroidism
  • Generally, routine surgery in a hypothyroid patient should be deferred until euthyroidism is restored
  • Diabetic patients may need readjustment of hypoglycemic agents with institution of thyroxine
  • High-bulk diet may help avoid constipation
  • Educate patient about myxedema coma



  • Monitor TSH levels every 6 to 8 weeks until normalized, then at 6 months, followed by annual assessments
  • An elevated TSH level should be confirmed by a repeated measurement, along with measurement of serum free T4
  • If treatment in subclinical hypothyroidism is not initiated, then monitor with annual TSH and free T4 measurement
  • Follow cardiac status closely in elderly patients



  • Advise patient to establish prescribed routine for pill-taking
  • Educate about importance of drug therapy compliance
  • Appreciate lower starting doses of drugs in elderly and debilitated patients
  • Consider concurrent risk factors and disease states with the prescribed therapy
  • Levothyroxine is usually the first choice of treatment
  • Thyroid hormone has a narrow toxic-to-therapeutic ratio
    • Must be titrated on the basis of laboratory tests and clinical responses
  • Avoid over-replacement with thyroid hormone


Social and Stress factors:

  • Ensure patient and family are well informed about disease and its treatment
  • Individuals with hypothyroid should be regularly screened for subclinical psychological distress and psychiatric disorders



  • Iron supplements frequently decreases levothyroxine absorption; caution required especially when iron supplements are prescribed due to increase demand of iron during pregnancy
  • Thyroid hormone replacement can precipitate adrenal crises in patients with untreated adrenal insufficiency
  • Relapses will occur if treatment is interrupted


Activities (physical, mental, others):

  • Stress on the importance of staying active and having a regular exercise routine
  • Advise patients to keep themselves mentally active


Myxedema coma:

  • Myxedema coma is a medical emergency
  • Untreated hypothyroidism may progress to myxedema coma
  • Identify and treat the precipitating factors of myxedema coma, such as hypoglycemia, infection, medications, cold exposure
  • A random cortisol level should be drawn prior to therapy
  • Administer hydrocortisone until coexisting adrenal insufficiency is ruled out
  • Deterioration of the patient's mental status is one of the key manifestation of myxedema coma


Hypothyroidism and Pregnancy:

  • Hypothyroidism in pregnancy is safely and easily treated with synthetic thyroid hormone
  • Uncontrolled hypothyroidism during pregnancy can lead to, e.g.
    • Congestive heart failure, preeclampsia, miscarriage, Low birth weight
    • Cognitive and developmental disabilities in the new born
  • Levothyroxine requirements will likely increase during pregnancy. Monitor TSH level every 4-6 weeks during the first half of pregnancy and at least once between 26 and 32 weeks gestation
  • Women with hypothyroidism should achieve good control prior to conception (TSH not more than 2.5mlU/L)
  • After delivery, most patients need to decrease the thyroxine dosage they received during pregnancy
  • There is an increased risk of developing permanent primary hypothyroidism in women with a history of postpartum thyroiditis


2. Scales and Table


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Core Resources:

  • American Association of clinical endocrinologist Medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism, 2006 amended version. Endocrine practice Vol 8 No.6
  • Braverman LE, Utiger RD, eds. Werner and Ingbar's The Thyroid. 9th ed. Philadelphia: Lippincott Williams & Wilkins; 2005
  • Compendium of Pharmaceuticals and Specialties (CPS). Canadian Pharmacist association. Toronto: Webcom Inc. 2012
  • Day RA, Paul P, Williams B, et al (eds). Brunner & Suddarth's Textbook of Canadian Medical-Surgical Nursing. 2nd ed. Philadelphia: Lippincott Williams and Wilkins; 2010
  • Foster C, Mistry NF, Peddi PF, Sharma S, eds. The Washington Manual of Medical Therapeutics. 33rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2010
  • Gray J, ed. Therapeutic Choices. Canadian Pharmacists Association. 6th ed. Toronto: Webcom Inc. 2011
  • Katzung BG, Masters SB, Trevor AJ, eds. Basic and Clinical Pharmacology. 1th ed. New York: McGraw-Hill; 2009
  • Longo D, Fauci A, Kasper D, et al (eds). Harrison's Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2011
  • Management of thyroid dysfunction during pregnancy and postpartum. An endocrine society clinical practice guidelines. 2007 J Clin Endocrinol Metab:92; S1-S47
  • McPhee SJ, Papadakis MA, eds. Current Medical Diagnosis & Treatment. 49th ed. New York: McGraw-Hill; 2010
  • Pagana KD, Pagana TJ eds. Mosby's Diagnostic and Laboratory Test Reference. 9th ed. St. Louis: Elsevier-Mosby; 2009
  • Skidmore-Roth L. ed. Mosby's drug guide for nurses. 9th ed. St. Louis: Elsevier-Mosby; 2011
  • Skidmore-Roth L, ed. Mosby's nursing drug reference. 24th ed. St. Louis: Elsevier-Mosby; 2011


Online Pharmacological Resources:

  • e-Therapeutics
  • Lexicomp
  • RxList
  • Epocrates


Journals/Clinical Trials:

  • Abalovich M, et al: Management of thyroid dysfunction during pregnancy and postpartum: an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2007;92:S1-S47
  • American Association of Clinical Endocrinologists medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. Endocr Pract. 2002;8:457-469
  • American College of Physicians. Clinical guideline, part 1. Screening for thyroid disease. Ann Intern Med. 1998;129:141-3
  • Alexander EK, Marqusee E, Lawrence J, et al. Timing and magnitude of increases in levothyroxine requirements during pregnancy in women with hypothyroidism. N Engl J Med. 2004;351:241-9
  • Asssessment of iodine deficiency disorders and monitoring there elimination. A guide for programme managers. (3rd edition). World Health Organization 2007
  • Aoki Y, Belin RM, Clickner R, et al. Serum TSH and total T4 in the United States population and their association with participant characteristics: National Health and Nutrition Examination Survey (NHANES 1999-2002). Thyroid. 2007;17:1211-23
  • Bunevicius R, Kazanavicius G, Zalinkevicius R, et al. Effects of thyroxine as compared with thyroxine plus triiodothyronine in patients with hypothyroidism. N Engl J Med. 1999;340:424-429
  • Cappola AR, Fried LP, Arnold AM, et al. Thyroid status, cardiovascular risk, and mortality in older adults. JAMA 2006; 295:1033-1041
  • Cinemre H, Bilir C, Gokosmanoglu F, et al. Hematologic effects of levothyroxine in iron-deficient subclinical hypothyroid patients: a randomized, double-blind, controlled study. J Clin Endocrinol Metab. Jan 2009;94:151-6
  • Clyde PW, Harari AE, Getka EJ, Shakir KM. Combined levothyroxine plus liothyronine compared with levothyroxine alone in primary hypothyroidism: a randomized controlled trial. JAMA. 2003; 290:2952-8
  • Cooper DS. Subclinical hypothyroidism. N Engl J Med 2001;345:260-265
  • Cooper DS, Doherty GM, Haugen BR, Kloos RT, Lee SL, Mandel SJ, et al. Management guidelines for patients with thyroid nodules and differentiated thyroid cancer. Thyroid 2006;16:109-142
  • Delange F, de Benoist B, Pretell E, et al: Iodine deficiency in the world: Where do we stand at the turn of the century? Thyroid 2001;11:437-447
  • Eskes SA, Endert E, Fliers E, et al. Prevalence of Growth Hormone Deficiency in Hashimoto's Thyroiditis. J Clin Endocrinol Metab. 2010;95:2266-70
  • Escobar-Morreale HF, et al: REVIEW: Treatment of hypothyroidism with combinations of levothyroxine plus liothyronine. J Clin Endocrinol Metab 2005;90:4946-4954
  • Garber JR, Hennessy JV, et al: Clinical Upate. Managing the challenges oh hypothyroidism. J Fam Pract 2006;55:S1-8
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  • Gyamfi C, Wapner RJ, D'Alton ME. Thyroid dysfunction in pregnancy: the basic science and clinical evidence surrounding the controversy in management. Obstet Gynecol. Mar 2009;113:702-7
  • Haddow JE, Palomaki GE, Allan WC, Williams JR, Knight GJ, Gagnon J, et al. Maternal thyroid deficiency during pregnancy and subsequent neuropsychological development of the child. N Engl J Med. 1999;341:549-55
  • Hollowell JG, Staehling NW, Flanders WD, et al. Serum TSH, T(4), and thyroid antibodies in the United States population (1988 to 1994): National Health and Nutrition Examination Survey (NHANES III). J Clin Endocrinol Metab.2002;87:489-99
  • Helfand M. Screening for subclinical thyroid dysfunction in non-pregnant adults: a summary of the evidence for the U.S. Preventive Services Task Force. Ann Intern Med. 2004;140:128-141
  • Helfand M, Redfern CC. Clinical guideline, part 2. Screening for thyroid disease: an update. American College of Physicians. Ann Intern Med.1998;129:144-158
  • Ito M, Arishima T, Kudo T, Nishihara E, et al. Effect of levo-thyroxine replacement on non-high-density lipoprotein cholesterol in hypothyroid patients. J Clin Endocrinol Metab. 2007;92:608-611
  • Kajantie E, Phillips DI, Osmond C, et al. Spontaneous hypothyroidism in adult women is predicted by small body size at birth and during childhood. J Clin Endocrinol Metab. 2006;91:4953-4956
  • Kreisman SH, Hennessey JV. Consistent reversible elevations of serum creatinine levels in severe hypothyroidism. Arch Intern Med. 1999;159:79-82
  • Ladenson PW. Recognition and management of cardiovascular disease related to thyroid dysfunction. Am J Med. 1990;88:638-641
  • Ladenson PW, Singer PA, Ain KB, Bagchi N, Bigos ST, Levy EG, et al. American Thyroid Association Guidelines For Detection Of Thyroid Dysfunction. Arch Internal Med. 2000;160:1573-1575
  • LeBeau SO, Mandel SJ. Thyroid disorders during pregnancy. Endocrinol Metab Clin North Am. 2006;35:117-136, vii
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  • Roos A, Linn-Rasker SP, et al. The starting dose of levothyroxine in primary hypothyroidism treatment: A prospective, randomized, double-blind trial. Arch Int Med 2005; 165:1714-1720
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  • Supit EJ, Peiris AN. Interpretation of laboratory thyroid function tests for the primary care physician. South Med J 2002;95:481-485
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Ronald M. Goldenberg, MD, FRCPC, FACE, Staff Endocrinologist, North York General Hospital, ON Canada; Endocrinologist & Medical Co-Director, LMC Endocrinology Centres, Toronto, ON Canada
.......................................... PHARMACY EDITOR:
William Semchuk, M.Sc., Pharm.D.,FCSHP Manager, Clinical Pharmacy Services, Regina Qu’Appelle Health Region 14, Regina, SK Canada

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