Highlights & Basics
- Primary hypothyroidism usually presents with nonspecific symptoms of fatigue, depression, constipation, and mild weight gain.
- Commonly, disease is subclinical.
- Physical exam may show dry skin, thick tongue, eyelid edema, and bradycardia.
- Elevated thyroid-stimulating hormone and low free thyroxine confirms the diagnosis.
- Treatment is with levothyroxine; starting dose depends on age and presence of co-existing cardiac disease.
- Over-treatment is uncommon but can lead to iatrogenic hyperthyroidism.
Quick Reference
History & Exam
Key Factors
nonspecific symptoms
Other Factors
lethargy
constipation
weight gain
depression
menstrual irregularity
dry or coarse skin
change in voice
bradycardia
hypertension
delayed relaxation of tendon reflexes
cold sensitivity
coarse hair
eyelid edema
goiter
Diagnostics Tests
1st Tests to Order
serum thyroid-stimulating hormone (TSH)
Other Tests to consider
free serum thyroxine (T4)
antithyroid peroxidase antibodies
CBC
fasting blood glucose
serum cholesterol
Treatment Options
ongoing
confirmed overt primary hypothyroidism
healthy with age ≤65 years
pre-existing coronary artery disease or age >65 years
subclinical hypothyroidism with TSH >10 mIU/L
low-dose levothyroxine
Definition
Vignette
Common Vignette
Other Presentations
Epidemiology
Etiology
Pathophysiology
Diagnostic Approach
Clinical evaluation
Diagnostic testing
Risk Factors
History & Exam
Tests
Differential Diagnosis
Central or secondary hypothyroidism
Differentiating Signs/Symptoms
- Symptoms include those of primary hypothyroidism (fatigability, cold intolerance, weight gain) with or without other symptoms of hypopituitarism, including hypogonadism and secondary adrenal insufficiency.
- Signs on physical exam indicate hypothyroidism, including skin changes, hair loss, and bradycardia. There may be other signs of a sellar or parasellar mass such as papilledema and visual field deficits (a bitemporal hemianopsia).[31]
Differentiating Tests
- Diagnostic evaluation of central hypothyroidism includes serum thyroid-stimulating hormone (TSH) and free thyroxine (T4). In central hypothyroidism, free T4 is low and TSH may be low, normal, or slightly elevated. MRI may reveal sellar or parasellar pathology.
Depression
Differentiating Signs/Symptoms
- Many of the symptoms of hypothyroidism, which are nonspecific, can be caused by depressive disorders. Both disorders are quite common in primary care practice. The symptoms of hypothyroidism respond to thyroid hormone replacement therapy; however, 5% to 10% of patients with well controlled levothyroxine-treated hypothyroidism have persistent symptoms.[1] Depressive disorders generally respond to treatment with antidepressants and/or behavior therapy.
Differentiating Tests
- Hypothyroidism is diagnosed by an elevated thyroid-stimulating hormone, which is normal in depression.
Alzheimer dementia
Differentiating Signs/Symptoms
- In older patients the two conditions may be indistinguishable. Cognitive dysfunction in hypothyroidism responds to thyroid replacement therapy.[1]
Differentiating Tests
- Patients with Alzheimer dementia have normal thyroid-stimulating hormone. Computed tomography of the head may show signs of atrophy.
Anemia
Differentiating Signs/Symptoms
- Hypothyroid and anemic patients often have fatigue and dyspnea on exertion. Primary hypothyroidism is associated with concurrent autoimmune conditions such as pernicious anemia.[1]
Differentiating Tests
- Thyroid-stimulating hormone (TSH) is elevated in primary hypothyroidism and the anemia is usually normocytic. In other forms of anemia, the TSH is not elevated and the red cells indices are variable (e.g., macrocytosis in pernicious anemia, microcytosis in iron deficiency anemia).
Screening
Treatment Approach
Levothyroxine therapy
- Treatment is indicated in all symptomatic patients with overt primary hypothyroidism
- Many experts also recommend treating subclinical hypothyroidism (asymptomatic with a normal serum free thyroxine [T4]) if thyroid-stimulating hormone (TSH) is >10 mIU/L, as the theoretical risk of progression to overt hypothyroidism is high.[2] [8] [46] Observational data indicate that the risk of coronary heart disease and its resultant mortality is higher in individuals with subclinical hypothyroidism if TSH is >10 mIU/L.[47] Despite the lack of good evidence, some experts recommend treating the following groups of patients with subclinical hypothyroidism and TSH <10 mIU/L:
- Women who are trying to conceive and have a history of infertility or ovulatory dysfunction.
- Adults younger than age 70 years who have goiter, antithyroid peroxidase antibodies, or symptoms of hypothyroidism.[43]
- Patients ages over 65 years without heart disease are less tolerant of full replacement initial doses.[45] A low starting dose is also recommended in these patients with titration in small increments every 4-6 weeks.
- The main complication of treatment is over-replacement of thyroid hormone, which increases the risk of osteoporosis and atrial fibrillation.[1]
- Pregnancy increases thyroid hormone requirements and the required dose of levothyroxine may increase accordingly. It may be necessary to increase the dose of levothyroxine by 25% to 30% in the first trimester.[29] TSH should be measured every 4-6 weeks in pregnant women on levothyroxine therapy until mid-gestation, then once in each of the second and third trimesters.[29] [49]
- Iron, cholestyramine, calcium, and sucralfate decrease levothyroxine absorption.[1] [8] Anticonvulsants (e.g., phenytoin, phenobarbital, and carbamazepine) increase its protein-binding capacity. Rifampin and sertraline increase its metabolism.[1] [8] Concomitant use of these drugs may cause an increase in dosage requirements.
- Some patients achieve a normal TSH but still have symptoms. This should be acknowledged and alternative causes considered. Although there is no good evidence that combination therapy with levothyroxine and liothyronine is indicated, this is an area of ongoing research.[50]
- The dose is increased or decreased in small increments to normalize TSH, which is the chemical goal of therapy. Some experts advocate consistently using one preparation of brand-name levothyroxine, arguing that it provides a more reliable dose than generic preparations.[8]
Treatment Options
confirmed overt primary hypothyroidism
healthy with age ≤65 years
levothyroxine
Primary Options
- levothyroxine
1.6 micrograms/kg/day orally, adjust dose in increments of 12.5 to 25 micrograms to normalize TSH
- levothyroxine
Comments
- The main complication of treatment is over-replacement of thyroid hormone, which increases the risk of osteoporosis and atrial fibrillation.[1]
- Pregnancy increases thyroid hormone requirements and the required dose of levothyroxine may increase. Thyroid-stimulating hormone (TSH) should be measured every 4-6 weeks in pregnant women on levothyroxine therapy until mid-gestation, then once in each of the second and third trimesters.[29] [49] It may be necessary to increase the dose of levothyroxine by 25% to 30% in the first trimester of pregnancy.[29] Nephrotic syndrome and malabsorption (e.g., celiac disease) can increase levothyroxine requirements.[1] [45] Concomitant use of iron, cholestyramine, calcium, sucralfate, anticonvulsants (e.g., phenytoin, phenobarbital, and carbamazepine), rifampin, and sertraline may cause an increase in dosage requirements.[1] [8]
pre-existing coronary artery disease or age >65 years
low-dose levothyroxine
Primary Options
- levothyroxine
25-50 micrograms orally once daily, adjust dose in increments of 12.5 to 25 micrograms every 4-6 weeks
- levothyroxine
Comments
- Levothyroxine therapy may exacerbate angina in patients with coronary artery disease.[45] A lower starting dose of levothyroxine is recommended, with titration in small increments every 4-6 weeks to a full therapeutic dose and close attention to the development of ischemic symptoms.[45] Patients ages over 65 years even without heart disease are also less tolerant of full replacement initial doses.[45] A low starting dose is recommended in these patients with titration in small increments every 4-6 weeks.
- The main complication of treatment is over-replacement of thyroid hormone, which increases the risk of osteoporosis and atrial fibrillation.[1]
- Nephrotic syndrome and malabsorption (e.g., celiac disease) can increase levothyroxine requirements.[1] [45] Concomitant use of iron, cholestyramine, calcium, sucralfate, anticonvulsants (e.g., phenytoin, phenobarbital, and carbamazepine), rifampin, and sertraline may cause an increase in dosage requirements.[1] [8]
subclinical hypothyroidism with TSH >10 mIU/L
low-dose levothyroxine
Primary Options
- levothyroxine
1 microgram/kg/day orally (usual dose 50-75 micrograms/day), adjust dose in increments of 25 to 50 micrograms to normalize TSH
- levothyroxine
Comments
- In cases where the thyroid-stimulating hormone (TSH) is only mildly elevated, the patient is not symptomatic and the serum free thyroxine (T4) is normal, the diagnosis is subclinical hypothyroidism.[2] Many experts recommend treating these patients if TSH is >10 mIU/L, as the theoretical risk of progression to overt hypothyroidism is high.[2] [8] [46] There is also some evidence that there is an increased risk of coronary heart disease.[47] Despite the lack of good evidence, some experts recommend treating adults aged under 70 years (who have goiter, antithyroid peroxidase antibodies, or symptoms of hypothyroidism) with subclinical hypothyroidism and TSH <10mIU/L.[43]
- Treatment is recommended for pregnant women if the TSH is greater than the pregnancy-specific reference range and they are thyroid peroxidase antibody (TPOAb) positive. If they are TPOAb negative, treatment is recommended if the TSH is >10 mlU/L.[29]
- Patients should be started on a low dose of levothyroxine. The dose is adjusted in small increments to normalize TSH, which is the chemical goal of therapy. Due to the long half-life of levothyroxine (1 week), TSH should be measured 4-6 weeks after initiation of therapy or dosage change.[8]
- The main complication of treatment is over-replacement of thyroid hormone, which increases the risk of osteoporosis and atrial fibrillation.[1]
- Pregnancy increases thyroid hormone requirements and the required dose of levothyroxine may increase. TSH should be measured every 4-6 weeks in pregnant women on levothyroxine therapy until mid-gestation, then once in each of the second and third trimesters.[29] [49] It may be necessary to increase the dose of levothyroxine by 25% to 30% in the first trimester of pregnancy.[29] Nephrotic syndrome and malabsorption (e.g., celiac disease) can increase levothyroxine requirements.[1] [8] Concomitant use of iron, cholestyramine, calcium, sucralfate, anticonvulsants (e.g., phenytoin, phenobarbital, and carbamazepine), rifampin, and sertraline may cause an increase in dosage requirements.[1] [8]
Prevention
Primary Prevention
Follow-Up Overview
Prognosis
Monitoring
Complications
Citations
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American Association of Clinical Endocrinologists; American Thyroid Association. Clinical practice guidelines for hypothyroidism in adults: cosponsored by the American Association of Clinical Endocrinologists and the American Thyroid Association. Endocr Pract. 2012 Nov-Dec;18(6):988-1028.[Abstract][Full Text]
Alexander EK, Pearce EN, Brent GA, et al. 2017 guidelines of the American Thyroid Association for the diagnosis and management of thyroid disease during pregnancy and the postpartum. Thyroid. 2017 Mar;27(3):315-89.[Abstract][Full Text]
Jonklaas J, Bianco AC, Bauer AJ, et al. Guidelines for the treatment of hypothyroidism: prepared by the American Thyroid Association Task Force on Thyroid Hormone Replacement. Thyroid. 2014 Dec;24(12):1670-751.[Abstract][Full Text]
1. Chaker L, Bianco AC, Jonklaas J, et al. Hypothyroidism. Lancet. 2017 Sep 23;390(10101):1550-62.[Abstract][Full Text]
2. Cooper DS, Biondi B, Cappola AR. Subclinical hypothyroidism: a review. JAMA. 2019 Jul 9;322(2):153-60. [Abstract]
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7. Vanderpump MP, Tunbridge WM, French JM, et al. The incidence of thyroid disorders in the community: a twenty-year follow-up of the Whickham survey. Clin Endocrinol. 1995 Jul;43(1):55-68.[Abstract]
8. American Association of Clinical Endocrinologists; American Thyroid Association. Clinical practice guidelines for hypothyroidism in adults: cosponsored by the American Association of Clinical Endocrinologists and the American Thyroid Association. Endocr Pract. 2012 Nov-Dec;18(6):988-1028.[Abstract][Full Text]
9. Zimmermann MB, Andersson M. Global endocrinology: global perspectives in endocrinology: coverage of iodized salt programs and iodine status in 2020. Eur J Endocrinol. 2021 Jun 10;185(1):R13-21. [Abstract][Full Text]
10. Han X, Ding S, Lu J, et al. Global, regional, and national burdens of common micronutrient deficiencies from 1990 to 2019: a secondary trend analysis based on the Global Burden of Disease 2019 study. EClinicalMedicine. 2022 Feb;44:101299.[Abstract][Full Text]
11. Dold S, Zimmermann MB, Jukic T, et al. Universal salt iodization provides sufficient dietary iodine to achieve adequate iodine nutrition during the first 1000 days: a cross-sectional multicenter study. J Nutr. 2018 Apr 1;148(4):587-98.[Abstract][Full Text]
12. Lazarus JH. The importance of iodine in public health. Environ Geochem Health. 2015 Aug;37(4):605-18.[Abstract]
13. Caldwell KL, Pan Y, Mortensen ME, et al. Iodine status in pregnant women in the National Children's Study and in US women (15-44 years), National Health and Nutrition Examination Survey 2005-2010. Thyroid. 2013 Aug;23(8):927-37.[Abstract][Full Text]
14. Pearce EN, Farwell AP, Braverman LE. Thyroiditis. N Engl J Med. 2003 Jun 26;348(26):2646-55.[Abstract]
15. Ragusa F, Fallahi P, Elia G, et al. Hashimotos' thyroiditis: epidemiology, pathogenesis, clinic and therapy. Best Pract Res Clin Endocrinol Metab. 2019 Dec;33(6):101367.[Abstract]
16. Rizzo LFL, Mana DL, Serra HA. Drug-induced hypothyroidism. Medicina (B Aires). 2017;77(5):394-404.[Abstract][Full Text]
17. Gabora K, Piciu A, Bădulescu IC, et al. Current evidence on thyroid related adverse events in patients treated with protein tyrosine kinase inhibitors. Drug Metab Rev. 2019 Nov;51(4):562-9.[Abstract]
18. Keely EJ. Postpartum thyroiditis: an autoimmune thyroid disorder which predicts future thyroid health. Obstet Med. 2011 Mar;4(1):7-11.[Abstract][Full Text]
19. Zimmermann MB, Boelaert K. Iodine deficiency and thyroid disorders. Lancet Diabetes Endocrinol. 2015 Apr;3(4):286-95.[Abstract]
20. Lisco G, De Tullio A, Triggiani D, et al. Iodine Deficiency and Iodine Prophylaxis: An Overview and Update. Nutrients. 2023 Feb 16;15(4):.[Abstract][Full Text]
21. Rayman MP. Multiple nutritional factors and thyroid disease, with particular reference to autoimmune thyroid disease. Proc Nutr Soc. 2019 Feb;78(1):34-44.[Abstract][Full Text]
22. Leung AM, Braverman LE. Consequences of excess iodine. Nat Rev Endocrinol. 2014 Mar;10(3):136-42.[Abstract][Full Text]
23. Kahaly GJ, Frommer L. Polyglandular autoimmune syndromes. J Endocrinol Invest. 2018 Jan;41(1):91-8.[Abstract]
24. Trohman RG, Sharma PS, McAninch EA, et al. Amiodarone and thyroid physiology, pathophysiology, diagnosis and management. Trends Cardiovasc Med. 2019 Jul;29(5):285-95.[Abstract][Full Text]
25. Kyritsi EM, Kanaka-Gantenbein C. Autoimmune thyroid disease in specific genetic syndromes in childhood and adolescence. Front Endocrinol (Lausanne). 2020 Aug 19;11:543.[Abstract][Full Text]
26. Siskind SM, Lee SY, Pearce EN. Investigating hypothyroidism. BMJ. 2021 Apr 27;373:n993.[Abstract][Full Text]
27. Carlé A, Pedersen IB, Knudsen N, et al. Hypothyroid symptoms and the likelihood of overt thyroid failure: a population-based case-control study. Eur J Endocrinol. 2014 Nov;171(5):593-602.[Abstract]
28. Canaris GJ, Steiner JF, Ridgway EC. Do traditional symptoms of hypothyroidism correlate with biochemical disease? J Gen Intern Med. 1997 Sep;12(9):544-50.[Abstract][Full Text]
29. Alexander EK, Pearce EN, Brent GA, et al. 2017 guidelines of the American Thyroid Association for the diagnosis and management of thyroid disease during pregnancy and the postpartum. Thyroid. 2017 Mar;27(3):315-89.[Abstract][Full Text]
30. Wopereis DM, Du Puy RS, van Heemst D, et al. The relation between thyroid function and anemia: a pooled analysis of individual participant data. J Clin Endocrinol Metab. 2018 Oct 1;103(10):3658-67.[Abstract][Full Text]
31. Persani L, Cangiano B, Bonomi M. The diagnosis and management of central hypothyroidism in 2018. Endocr Connect. 2019 Feb;8(2):R44-54.[Abstract][Full Text]
32. LeFevre ML, U.S. Preventive Services Task Force. Screening for thyroid dysfunction: US Preventive Services Task Force recommendation statement. Ann Intern Med. 2015 May 5;162(9):641-50.[Abstract][Full Text]
33. Rastogi MV, LaFranchi SH. Congenital hypothyroidism. Orphanet J Rare Dis. 2010 Jun 10;5:17.[Abstract][Full Text]
34. Kopel J. A global perspective on newborn congenital hypothyroidism screening. Proc (Bayl Univ Med Cent). 2020 Jan;33(1):137-9.[Abstract][Full Text]
35. Rose SR, Wassner AJ, Wintergerst KA, et al. Congenital hypothyroidism: screening and management. Pediatrics. 2023 Jan 1;151(1):e2022060419. [Abstract][Full Text]
36. Rugge JB, Bougatsos C, Chou R. Screening and treatment of thyroid dysfunction: an evidence review for the US Preventive Services Task Force. Ann Intern Med. 2015 Jan 6;162(1):35-45.[Abstract][Full Text]
37. Vissenberg R, van den Boogaard E, van Wely M, et al. Treatment of thyroid disorders before conception and in early pregnancy: a systematic review. Hum Reprod Update. 2012 Jul;18(4):360-7.[Abstract]
38. Spencer L, Bubner T, Bain E, et al. Screening and subsequent management for thyroid dysfunction pre-pregnancy and during pregnancy for improving maternal and infant health. Cochrane Database Syst Rev. 2015 Sep 21;2015(9):CD011263.[Abstract][Full Text]
39. Reid SM, Middleton P, Cossich MC, et al. Interventions for clinical and subclinical hypothyroidism pre-pregnancy and during pregnancy. Cochrane Database Syst Rev. 2013 May 31;(5):CD007752.[Abstract][Full Text]
40. Negro R, Schwartz A, Gismondi R, et al. Universal screening versus case finding for detection and treatment of thyroid hormonal dysfunction during pregnancy. J Clin Endocrinol Metab. 2010 Apr;95(4):1699-707.[Abstract]
41. American College of Obstetricians and Gynecologists. Thyroid disease in pregnancy: ACOG practice bulletin, Number 223. Obstet Gynecol. 2020 Jun;135(6):e261-74.[Abstract]
42. Birtwhistle R, Morissette K, Dickinson JA, et al. Recommendation on screening adults for asymptomatic thyroid dysfunction in primary care. CMAJ. 2019 Nov 18;191(46):E1274-80.[Abstract][Full Text]
43. British Columbia Ministry of Health. Thyroid function tests in the diagnosis and monitoring of thyroid function disorder. October 2018 [internet publication].[Full Text]
44. Toward Optimized Practice Clinical Practice Guideline Working Group Canada. Clinical practice guideline: investigation and management of primary thyroid dysfunction. April 2014 [internet publication].[Full Text]
45. Jonklaas J, Bianco AC, Bauer AJ, et al. Guidelines for the treatment of hypothyroidism: prepared by the American Thyroid Association Task Force on Thyroid Hormone Replacement. Thyroid. 2014 Dec;24(12):1670-751.[Abstract][Full Text]
46. Villar HC, Saconato H, Valente O, et al. Thyroid hormone replacement for subclinical hypothyroidism. Cochrane Database Syst Rev. 2007 Jul 18;2007(3):CD003419.[Abstract][Full Text]
47. Rodondi N, den Elzen WP, Bauer DC, et al. Subclinical hypothyroidism and the risk of coronary heart disease and mortality. JAMA. 2010 Sep 22;304(12):1365-74.[Abstract]
48. Roos A, Linn-Rasker SP, van Domburg RT, et al. The starting dose of levothyroxine in primary hypothyroidism treatment: a prospective, randomized, double-blind trial. Arch Intern Med. 2005 Aug 8-22;165(15):1714-20.[Abstract][Full Text]
49. Lee SY, Pearce EN. Assessment and treatment of thyroid disorders in pregnancy and the postpartum period. Nat Rev Endocrinol. 2022 Mar;18(3):158-71.[Abstract][Full Text]
50. Okosieme O, Gilbert J, Abraham P, et al. Management of primary hypothyroidism: statement by the British Thyroid Association Executive Committee. Clin Endocrinol (Oxf). 2016 Jun;84(6):799-808.[Abstract][Full Text]
51. Thayakaran R, Adderley NJ, Sainsbury C, et al. Thyroid replacement therapy, thyroid stimulating hormone concentrations, and long term health outcomes in patients with hypothyroidism: longitudinal study. BMJ. 2019 Sep 3;366:l4892.[Abstract][Full Text]
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53. Wilson SA, Stem LA, Bruehlman RD. Hypothyroidism: diagnosis and treatment. Am Fam Physician. 2021 May 15;103(10):605-13.[Abstract][Full Text]
Key Articles
Other Online Resources
Referenced Articles
Guidelines
Diagnostic
Summary
Includes information on the diagnosis and management of thyroid disease in pregnant women.Published by
American College of Obstetricians and Gynecologists
Published
2020
Summary
The Task Force recommends against screening asymptomatic nonpregnant adults ages 18 years and older for thyroid dysfunction in primary care settings. However, this does not apply to individuals with risk factors for thyroid dysfunction.Published by
Canadian Task Force on Preventive Health Care
Published
2019
Summary
Concise, well presented, and organized guideline that clearly outlines information on the detection of thyroid dysfunction in adults (individuals 19 years of age and over), screening recommendations, an abbreviated list of risk factors, and diagnostic strategies.Published by
British Columbia Ministry of Health
Published
2018
Summary
Guidelines providing recommendations to clinicians on the treatment of thyroid disease during pregnancy and postpartum.Published by
American Thyroid Association
Published
2017
Summary
This guideline addresses the testing and monitoring of patients with suspected thyroid disease, including primary hypothyroidism.Published by
Toward Optimized Practice Clinical Practice Guideline Working Group (Canada)
Published
2014
Summary
A thyroid-stimulating hormone assay should be considered if you suspect primary hypothyroidism.Free thyroxine can be obtained to assess degree of hypothyroidism or diagnose subclinical hypothyroidism.Additional tests include thyroid antibodies.Thyroid imaging (ultrasound or scan) not necessary unless there is suspicion of a structural abnormality.Published by
American Association of Clinical Endocrinologists; American Thyroid Association
Published
2012
Treatment
Summary
Concise, well presented, and organized guideline that clearly outlines information on treatment for thyroid function disorders, special considerations for pregnant women, and monitoring.Published by
British Columbia Ministry of Health
Published
2018
Summary
Guidelines providing recommendations to clinicians on the treatment of thyroid disease during pregnancy and postpartum.Published by
American Thyroid Association
Published
2017
Summary
Detailed guideline on the treatment of hypothyroidism, emphasizing that levothyroxine therapy remains the best evidence-based therapy.This guideline also offers extensive information on levothyroxine preparations, dosage, absorption, metabolism, as well as monitoring of therapy, patient satisfaction, and other therapies for hypothyroidism.Published by
American Thyroid Association
Published
2014
Summary
Consistently use one high-quality brand name levothyroxine to treat hypothyroidism.Monitor treatment by aiming to normalize thyroid-stimulating hormone (TSH) value.Recheck TSH 6 weeks after initiating therapy or changing dosage. In stable patients check TSH every 6 to 12 months.Treat subclinical hypothyroidism if TSH is over 10 milli-international units/L.Published by
American Association of Clinical Endocrinologists; American Thyroid Association
Published
2012