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Hypothyroidism Treatment & Management

  • Author: Philip R Orlander, MD; Chief Editor: George T Griffing, MD  more...
 
Updated: Jul 12, 2016
 

Approach Considerations

The treatment goals for hypothyroidism are to reverse clinical progression and correct metabolic derangements, as evidenced by normal blood levels of thyroid-stimulating hormone (TSH) and free thyroxine (T4). Thyroid hormone is administered to supplement or replace endogenous production. In general, hypothyroidism can be adequately treated with a constant daily dose of levothyroxine (LT4).

Thyroid hormone can be started at anticipated full replacement doses in individuals who are young and otherwise healthy. In elderly patients and those with known ischemic heart disease, treatment should begin with one fourth to one half the expected dosage, and the dosage should be adjusted in small increments after no less than 4-6 weeks. For most cases of mild to moderate hypothyroidism, a starting levothyroxine dosage of 50-75 µg/day will suffice.

Clinical benefits begin in 3-5 days and level off after 4-6 weeks. Achieving a TSH level within the reference range may take several months because of delayed readaptation of the hypothalamic-pituitary axis. In patients receiving treatment with LT4, dosing changes should be made every 6-8 weeks until the patient’s TSH is in target range.

In patients with central (ie, pituitary or hypothalamic) hypothyroidism, T4 levels rather than TSH levels are used to guide treatment. In most cases, the free T4 level should be kept in the upper third of the reference range.

After dosage stabilization, patients can be monitored with annual or semiannual clinical evaluations and TSH monitoring. Patients should be monitored for symptoms and signs of overtreatment, which include the following:

  • Tachycardia
  • Palpitations
  • Atrial fibrillation
  • Nervousness
  • Tiredness
  • Headache
  • Increased excitability
  • Sleeplessness
  • Tremors
  • Possible angina

The updated guidelines on hypothyroidism issued by the American Thyroid Association in 2014 maintain the recommendation of levothyroxine as the preparation of choice for hypothyroidism, with the following considerations:[5, 6]

  • If levothyroxine dose requirements are much higher than expected, consider evaluating for gastrointestinal disorders such as Helicobacter pylori –related gastritis, atrophic gastritis, or celiac disease; if such disorders are detected and effectively treated, re-evaluation of thyroid function and levothyroxine dosage is recommended.
  • Initiation or discontinuation of estrogen and androgens should be followed by reassessment of serum TSH at steady state, since such medications may alter levothyroxine requirement.
  • Serum TSH should be reassessed upon initiation of agents such as tyrosine kinase inhibitors that affect thyroxine metabolism and thyroxine or triiodothyronine deiodination.
  • Serum TSH monitoring is advisable when medications such as phenobarbital, phenytoin, carbamazepine, rifampin, and sertraline are started.
  • When deciding on a starting dose of levothyroxine, the patient’s weight, lean body mass, pregnancy status, etiology of hypothyroidism, degree of TSH elevation, age, and general clinical context, including the presence of cardiac disease, should be considered. The serum TSH goal appropriate for the clinical situation should also be considered.
  • Thyroid hormone therapy should be initiated as an initial full replacement or as partial replacement with gradual increments in the dose titrated upward using serum TSH as the goal.
  • Dose adjustments should be made upon significant changes in body weight, with aging, and with pregnancy; TSH assessment should be performed 4-6 weeks after any dosage change.
  • Reference ranges of serum TSH levels are higher in older populations (eg, >65 years), so higher serum TSH targets may be appropriate.

A meta-analysis of randomized, controlled trials of T4-triiodothyronine (T3) combination therapy versus T4 monotherapy for treatment of clinical hypothyroidism found no difference in effectiveness between combination therapy and monotherapy with respect to side effects such as bodily pain, depression, fatigue, body weight, anxiety, quality of life, and total low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol and triglyceride levels.[38]

A study of athyrotic patients found a high heterogeneity in these patients’ ability to produce T3 when treated with levothyroxine. Approximately 20% of these athyrotic patients did not maintain normal free T4 or free T3 values despite a normal TSH.[39] However, it is unclear whether more physiologic treatments offer any benefit, even in subgroups of hypothyroid patients.

In patients who continue to have symptoms (eg, weight gain and fatigue) despite normalization of the TSH level, one should consider causes other than hypothyroidism, rather than simply increasing the thyroid hormone dose on the basis of symptoms alone (see DDx). In some cases, however, symptom persistence is the result of a polymorphism of the deiodinase 2 enzyme, which converts T4 to T3 in the brain; these patients may benefit from combined LT4-liothyronine (LT3) therapy, using a physiologic LT4-to-LT3 ratio in the range of 10-14:1.[4]

Most patients with hypothyroidism can be treated in an ambulatory care setting. Patients who require long-term continuous tube feeding routinely require intravenous (IV) LT4 replacement because the absorption of oral agents is impaired by the contents of tube feeds. Alternatively, tube feeds can be withheld for 1 hour while the patient receives an oral preparation of LT4. It should be noted that oral and IV preparations of LT4 are not equivalent; consequently, great care must be taken in switching between these formulations.

Patients with severe hypothyroidism requiring hospitalization (eg, myxedema) may require aggressive management. Overreplacement or aggressive replacement with any thyroid hormone may precipitate tachyarrhythmias or, very rarely, thyroid storm and should be balanced against the need for urgent replacement. Risk is higher with T3 therapy.

Surgery is rarely needed in patients with hypothyroidism; it is more commonly required in the treatment of hyperthyroidism. However, surgery is indicated for large goiters that compromise tracheoesophageal function.

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Hypothyroidism in Pregnancy

The updated guidelines on hypothyroidism issued by the American Thyroid Association in 2014 concerning hypothyroidism treatment in pregnant women are as follows:[5, 6]

  • Pregnant women with overt hypothyroidism should receive levothyroxine replacement therapy with the dose titrated to achieve a TSH concentration within the trimester-specific reference range.
  • Serial serum TSH levels should be assessed every 4 weeks during the first half of pregnancy to adjust levothyroxine dosing to maintain TSH within the trimester-specific range.
  • Serum TSH should be reassessed during the second half of pregnancy.
  • In women already taking levothyroxine, 2 additional doses per week of the current levothyroxine dose, given as one extra dose twice weekly with several days’ separation, may be started as soon as pregnancy is confirmed.

Hypothyroidism in pregnancy can produce an array of obstetric complications. Even mild disease may have adverse effects on the offspring. Adverse effects of hypothyroidism in pregnancy include the following:

  • Preeclampsia
  • Anemia
  • Postpartum hemorrhage
  • Cardiac ventricular dysfunction
  • Increased risk of spontaneous abortion
  • Low birth weight
  • Impaired cognitive development in the fetus [40]
  • Fetal mortality

Despite the possibility of poor fetal outcomes, routine screening for thyroid dysfunction is not performed in the United States and remains a controversial topic. A study reviewing the records of pregnant women screened between June 2005 and May 2008 found that only 23% of these women were tested for hypothyroidism.[41] The study also found a 15% prevalence of hypothyroidism among pregnant women, a figure that is significantly higher than the 2-3% frequently cited in older literature.[41]

Increased thyroid hormone dosage requirements should be anticipated during pregnancy, especially in the first and second trimesters. Studies have suggested that in pregnant women with hypothyroidism, the LT4 dose should be increased by 30% at the confirmation of pregnancy and subsequently adjusted in accordance with TSH levels.

In addition, iodine demands are higher with pregnancy and lactation. Iodine needs rise from approximately 150 µg/day in the nonpregnant woman to 240-290 µg/day with pregnancy and lactation. Guidelines from the American Thyroid Association recommend that all pregnant and lactating women ingest a minimum of 250 mg iodine daily—optimally, in the form of potassium iodide, to ensure consistent delivery.[42]

For pregnant women with previously diagnosed hypothyroidism, serum TSH levels should be measured every 3-4 weeks during the first half of pregnancy and every 6-10 weeks thereafter. The LT4 dose should be adjusted so as to keep the serum TSH below 2.5 mIU/L. TSH and free T4 levels should be measured 3-4 weeks after every dosage adjustment.[43]

Autoimmune thyroid disease without overt hypothyroidism has been associated with a higher miscarriage rate. Negro et al showed that euthyroid Caucasian women with positive anti−thyroid peroxidase (anti-TPO) antibodies who were treated with LT4 during the first trimester had lower miscarriage rates than those who were not treated. These women also had lower rates of premature delivery, comparable to rates in women without thyroid antibodies.[44]

In a meta-analysis of 3 studies involving 220 women with subclinical hypothyroidism or thyroid autoimmunity who were undergoing assisted reproduction technologies, Velkeniers et al concluded that treatment with LT4 should be recommended to improve pregnancy outcomes.[45] In pooled analyses, LT4 treatment resulted in a significantly higher delivery rate and a significantly lower miscarriage rate.

Such findings, if confirmed by sufficient data, would provide an indication for treating euthyroid pregnant women who have thyroid antibodies.

LT4 should not be taken with prenatal vitamin preparations containing iron and calcium. After delivery, the LT4 dose can be reduced to the prepregnancy level, and TSH should be checked in 6 weeks.

In a study of 77 pregnant women with newly diagnosed subclinical (64 women) or overt (13 women) hypothyroidism, Abalovich et al determined the specific levothyroxine (LT4) dosages required to return these patients to a euthyroid state. The investigators found that the most successful dosages, as follow, varied according to baseline levels of thyroid stimulating hormone (TSH)[46, 47] :

  • Subclinical hypothyroidism (TSH 4.2 mIU/L or less): 1.2 µg/kg/day
  • Subclinical hypothyroidism (TSH > 4.2-10 mIU/L): 1.42 µg/kg/day
  • Overt hypothyroidism: 2.33 µg/kg/day

These dosages proved appropriate in 89% and 77% of patients with subclinical or overt hypothyroidism, respectively, and were recommended by the study's authors for pregnant patients with hypothyroidism that has been newly diagnosed during pregnancy.

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Subclinical Hypothyroidism

Significant controversy persists regarding the treatment of patients with mild hypothyroidism.[48] Some have argued that treatment of these patients improves symptoms, prevents progression to overt hypothyroidism, and may have cardioprotective benefits. Reviews by the US Preventive Services Task Force[37] and an independent expert panel[49] found inconclusive evidence to recommend aggressive treatment of patients with TSH levels of 4.5-10 mIU/L.

The Endocrine Society recommends T4 replacement in pregnant women with subclinical hypothyroidism.[50] The American College of Obstetricians and Gynecologists does not recommend it as a routine measure.[51]

Ultrasonography may have prognostic value in subclinical hypothyroidism. In an Italian study, progression to overt hypothyroidism occurred more often in patients whose ultrasonographic thyroid scan showed diffuse hypoechogenicity (an indication of chronic thyroiditis).[52]

In nonpregnant patients, following subclinical hypothyroidism and treating on a case-by-case basis is reasonable. Treatment of subclinical hypothyroidism has been shown to reduce total cholesterol, non-HDL cholesterol, and apolipoprotein B levels[53] and to decrease arterial stiffness and systolic blood pressure.[54] In patients with concomitant subclinical hypothyroidism and iron deficiency anemia, iron supplementation may be ineffective if LT4 is not given.[55]

Guidelines from the American Association of Clinical Endocrinologists (AACE) recommend treatment in patients with TSH levels higher than 10 mIU/L and in patients with TSH levels of 5-10 mIU/L in conjunction with goiter or positive anti-TPO antibodies; these patients have the highest rates of progression to overt hypothyroidism. An initial LT4 dosage of 50-75 µg/day can be used, which can be titrated every 6-8 weeks to achieve a target TSH of between 0.3 and 3 mIU/L.[36]

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Myxedema Coma

In patients with myxedema coma, an effective approach consists of the following:

  • Give 4 µg of LT4 per kilogram of lean body weight (approximately 200-250 µg) as an IV bolus in a single or divided dose, depending on the patient’s risk of cardiac disease
  • 24 hours later, give 100 µg IV
  • Subsequently, give 50 µg/day IV, along with stress doses of IV glucocorticoids
  • Adjust the dosage on the basis of clinical and laboratory findings

If adrenal insufficiency is suspected (eg, in a patient with hypothyroidism secondary to panhypopituitarism), that diagnosis should be investigated. If adrenal insufficiency is confirmed, stress doses of IV glucocorticoids should be given before hypothyroidism is treated. If the patient’s condition is critical and there is no time to complete the workup for adrenal insufficiency before the necessary use of IV LT4, the patient must be given stress-dose glucocorticoids to prevent the catastrophic complication of adrenal crisis.

Use of IV LT3 is controversial and based on expert opinion. It is associated with a higher frequency of adverse cardiac events and is generally reserved for patients who are not improving clinically on LT4. LT3 can be given initially as a 10 µg IV bolus, which is repeated every 8-12 hours until the patient can take maintenance oral doses of T4.

Advanced age, high-dose T4 therapy, and cardiac complications have the highest associations with mortality in myxedema coma (see Hypothyroidism and Myxedema Coma in Emergency Medicine).[56]

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Complications of Treatment

Thyroid hormone replacement can precipitate adrenal crises in patients with untreated adrenal insufficiency by enhancing hepatic corticosteroid metabolism. If adrenal insufficiency is suspected, it should be confirmed or ruled out; if confirmed, it should be treated before treatment of hypothyroidism.

Aggressive replacement of thyroid hormone may compromise cardiac function in patients with existing cardiac disease. In these patients, administer smaller initial doses of LT4, and titrate the dosage upward in small increments.

Subclinical hyperthyroidism is a more common complication of treatment with LT4. The relationship of overtreatment to osteoporosis and fracture is not consistent and is best studied in postmenopausal women.

A large population-based nested case-control study demonstrated a 2-fold to 3-fold increase in fractures in LT4 users older than 70 years; the increase was dose-related.[57] Because thyroid function studies were not performed, the relation between subclinical hyperthyroidism and osteoporosis requires further evaluation. However, this study does support careful dose titration, especially in elderly patients.

Nonetheless, patients at risk for osteoporosis (eg, women who are estrogen-deficient) and individuals receiving a long-term suppressive dose of LT4 (eg, patients with differentiated thyroid cancer) should be closely monitored. It should be noted that patients with thyroid cancer are usually on a higher dose of LT4. The desired TSH depends on the staging of the cancer and on the evidence (or lack of evidence) of active disease. In patients with stage IV thyroid cancer, it is desirable to keep the TSH below 0.1 mIU/L in the long term.

Patients should be advised that in rare cases, vision may temporarily worsen when hormone therapy is initiated. Pseudotumor cerebri may occur, albeit uncommonly. Patients with depression may develop mania, and psychosis may be exacerbated in patients with severe psychological illness.

Because most brain growth occurs in the first 2 years of life, untreated hypothyroidism in infants can cause irreversible mental retardation. Older infants are spared nervous system damage but continue to have slowed physical and linear bone growth. They also have delayed dental development.

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Diet and Activity

No specific diets are required for hypothyroidism. Subclinical hypothyroidism has been seen in increased frequency in patients with greater iodine intake. The World Health Organization (WHO) recommends a daily dietary iodine intake of 150 µg for adults, 200 µg for pregnant and lactating women, and 50-120 µg for children.

Patients who have hypothyroidism have generalized hypotonia and may be at risk for ligamentous injury, particularly from excessive force across joints. Thus, patients should exercise caution with certain activities, such as contact sports and heavy physical labor.

Patients with uncontrolled hypothyroidism may have difficulty maintaining concentration in low-stimulus activities and may have slowed reaction times. Patients should use caution when engaging in an activity that poses a risk of injury (eg, operating presses or heavy equipment and driving).

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Consultations

Indications for referral to an endocrinologist include any of the following[1] :

  • A nodular thyroid, suspicious thyroid nodules, or compressive symptoms (eg, dysphagia)
  • Pregnancy (or planned pregnancy)
  • Underlying cardiac disorders or other endocrine disorders
  • Age younger than 18 years
  • Secondary or tertiary hypothyroidism
  • Unusual constellation of thyroid function test results
  • Inability to maintain TSH in the target range
  • Unresponsiveness to treatment

Some patients with subacute or postpartum thyroiditis can develop thyrotoxicosis (or symptoms consistent with hyperthyroidism) before developing hypothyroidism. These patients also may benefit from consultation with an endocrinologist.

Suspected myxedema coma is a medical emergency with a high risk of mortality, and it necessitates requires initiation of IV LT4 and glucocorticoid therapy before laboratory confirmation. An urgent endocrinology consultation should be obtained.

Rarely, an increase in size of a goiter in a patient with autoimmune thyroid disease could indicate a lymphoma. These patients should be evaluated by an endocrinologist.

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Long-Term Monitoring

Once an appropriate therapeutic dosage is arrived at, patients can be monitored annually or semiannually with laboratory evaluation and physical examination. In addition, monitor patients for signs of excess dosing (eg, nervousness, palpitations, diarrhea, excessive sweating, heat intolerance, chest pain, or insomnia). Monitor pulse rate, blood pressure, and vital signs. In children, sleeping pulse rate and basal temperature can be used as guides to the adequacy of the clinical response to treatment.

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Contributor Information and Disclosures
Author

Philip R Orlander, MD Director and Professor, Division of Endocrinology, Assistant Dean for Educational Programs, Vice-Chair of Medicine for Education, Program Director, Internal Medicine Residency Program, University of Texas Health Science Center at Houston

Philip R Orlander, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, American Diabetes Association, Endocrine Society, Texas Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Jeena M Varghese, MD Assistant Professor, Division of Endocrinology, University of Texas Health Science Center at Houston

Jeena M Varghese, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, American Thyroid Association, Endocrine Society

Disclosure: Nothing to disclose.

Lance M Freeman, MD Fellow, Division of Endocrinology, University of Texas Health Science Center at Houston

Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD Professor Emeritus of Medicine, St Louis University School of Medicine

George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, International Society for Clinical Densitometry, Southern Society for Clinical Investigation, American College of Medical Practice Executives, American Association for Physician Leadership, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical and Translational Research, Endocrine Society

Disclosure: Nothing to disclose.

Acknowledgements

Anu Bhalla Davis, MD Assistant Professor, Department of Internal Medicine, Division of Diabetes, Endocrinology, and Metabolism, University of Texas Medical School at Houston

Disclosure: Nothing to disclose.

Shikha Bharaktiya, MD Physician in Endocrinology, Diabetes, and Metabolism, Endocrinology Clinics of Texas, PA

Disclosure: Nothing to disclose.

Arthur B Chausmer, MD, PhD, FACP, FACE, FACN, CNS Professor of Medicine (Endocrinology, Adj), Johns Hopkins School of Medicine; Affiliate Research Professor, Bioinformatics and Computational Biology Program, School of Computational Sciences, George Mason University; Principal, C/A Informatics, LLC

Arthur B Chausmer, MD, PhD, FACP, FACE, FACN, CNS is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Endocrinology, American College of Nutrition, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Medical Informatics Association, American Society for Bone and Mineral Research, Endocrine Society, and International Society for Clinical Densitometry

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Walter R Woodhouse, MD, MSA Associate Clinical Professor, Department of Family Practice, Medical College of Ohio

Walter R Woodhouse, MD, MSA is a member of the following medical societies: American Academy of Family Physicians, American Academy of Pain Medicine, and Society of Teachers of Family Medicine

Disclosure: Nothing to disclose.

Frederick H Ziel, MD Associate Professor of Medicine, University of California, Los Angeles, David Geffen School of Medicine; Physician-In-Charge, Endocrinology/Diabetes Center, Director of Medical Education, Kaiser Permanente Woodland Hills; Chair of Endocrinology, Co-Chair of Diabetes Complete Care Program, Southern California Permanente Medical Group

Frederick H Ziel, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Endocrinology, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Diabetes Association, American Federation for Medical Research, American Medical Association, American Society for Bone and Mineral Research, California Medical Association, Endocrine Society, andInternational Society for Clinical Densitometry

Disclosure: Nothing to disclose.

References
  1. Garber JR, Cobin RH, Gharib H, et al. Clinical practice guidelines for hypothyroidism in adults: cosponsored by the American Association of Clinical Endocrinologists and the American Thyroid Association. Thyroid. 2012 Dec. 22(12):1200-35. [Medline].

  2. Kreisman SH, Hennessey JV. Consistent reversible elevations of serum creatinine levels in severe hypothyroidism. Arch Intern Med. 1999 Jan 11. 159(1):79-82. [Medline].

  3. Ladenson PW, Singer PA, Ain KB, et al. American Thyroid Association guidelines for detection of thyroid dysfunction. Arch Intern Med. 2000 Jun 12. 160(11):1573-5. [Medline].

  4. McDermott MT. Does combination T4 and T3 therapy make sense?. Endocr Pract. 2012 Sep-Oct. 18(5):750-7. [Medline].

  5. [Guideline] 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. [Medline]. [Full Text].

  6. Melville NA. New ATA guidelines stick with levothyroxine for hypothyroidism. Medscape Medical News from WebMD. October 02, 2014. Available at http://www.medscape.com/viewarticle/832682. Accessed: February 19, 2015.

  7. Stuckey BG, Kent GN, Ward LC, Brown SJ, Walsh JP. Postpartum thyroid dysfunction and the long-term risk of hypothyroidism: results from a 12-year follow-up study of women with and without postpartum thyroid dysfunction. Clin Endocrinol (Oxf). 2010 Sep. 73(3):389-95. [Medline].

  8. Wolter P, Dumez H, Schoffski P. Sunitinib and hypothyroidism. N Engl J Med. 2007 Apr 12. 356(15):1580; author reply 1580-1. [Medline].

  9. Smit JW, Stokkel MP, Pereira AM, Romijn JA, Visser TJ. Bexarotene-induced hypothyroidism: bexarotene stimulates the peripheral metabolism of thyroid hormones. J Clin Endocrinol Metab. 2007 Jul. 92(7):2496-9. [Medline].

  10. Denny JC, Crawford DC, Ritchie MD, et al. Variants near FOXE1 are associated with hypothyroidism and other thyroid conditions: using electronic medical records for genome- and phenome-wide studies. Am J Hum Genet. 2011 Oct 7. 89(4):529-42. [Medline]. [Full Text].

  11. Vono-Toniolo J, Rivolta CM, Targovnik HM, Medeiros-Neto G, Kopp P. Naturally occurring mutations in the thyroglobulin gene. Thyroid. 2005 Sep. 15(9):1021-33. [Medline].

  12. Park SM, Chatterjee VK. Genetics of congenital hypothyroidism. J Med Genet. 2005 May. 42(5):379-89. [Medline]. [Full Text].

  13. Paschke R, Ludgate M. The thyrotropin receptor in thyroid diseases. N Engl J Med. 1997 Dec 4. 337(23):1675-81. [Medline].

  14. Macchia PE, Lapi P, Krude H, et al. PAX8 mutations associated with congenital hypothyroidism caused by thyroid dysgenesis. Nat Genet. 1998 May. 19(1):83-6. [Medline].

  15. Everett LA, Glaser B, Beck JC, et al. Pendred syndrome is caused by mutations in a putative sulphate transporter gene (PDS). Nat Genet. 1997 Dec. 17(4):411-22. [Medline].

  16. Cetani F, Barbesino G, Borsari S, et al. A novel mutation of the autoimmune regulator gene in an Italian kindred with autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy, acting in a dominant fashion and strongly cosegregating with hypothyroid autoimmune thyroiditis. J Clin Endocrinol Metab. 2001 Oct. 86(10):4747-52. [Medline].

  17. Woeber KA. Iodine and thyroid disease. Med Clin North Am. 1991 Jan. 75(1):169-78. [Medline].

  18. Yamada M, Mori M. Mechanisms related to the pathophysiology and management of central hypothyroidism. Nat Clin Pract Endocrinol Metab. 2008 Dec. 4(12):683-94. [Medline].

  19. Nebesio TD, McKenna MP, Nabhan ZM, Eugster EA. Newborn screening results in children with central hypothyroidism. J Pediatr. 2010 Jun. 156(6):990-3. [Medline].

  20. Doeker BM, Pfaffle RW, Pohlenz J, Andler W. Congenital central hypothyroidism due to a homozygous mutation in the thyrotropin beta-subunit gene follows an autosomal recessive inheritance. J Clin Endocrinol Metab. 1998 May. 83(5):1762-5. [Medline].

  21. Bonomi M, Busnelli M, Beck-Peccoz P, et al. A family with complete resistance to thyrotropin-releasing hormone. N Engl J Med. 2009 Feb 12. 360(7):731-4. [Medline].

  22. Katakami H, Kato Y, Inada M, Imura H. Hypothalamic hypothyroidism due to isolated thyrotropin-releasing hormone (TRH) deficiency. J Endocrinol Invest. 1984 Jun. 7(3):231-3. [Medline].

  23. Niimi H, Inomata H, Sasaki N, Nakajima H. Congenital isolated thyrotrophin releasing hormone deficiency. Arch Dis Child. 1982 Nov. 57(11):877-8. [Medline]. [Full Text].

  24. 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 Dec. 17 (12):1211-23. [Medline].

  25. Kajantie E, Phillips DI, Osmond C, Barker DJ, Forsen T, Eriksson JG. Spontaneous hypothyroidism in adult women is predicted by small body size at birth and during childhood. J Clin Endocrinol Metab. 2006 Dec. 91(12):4953-6. [Medline].

  26. Sawin CT, Castelli WP, Hershman JM, McNamara P, Bacharach P. The aging thyroid. Thyroid deficiency in the Framingham Study. Arch Intern Med. 1985 Aug. 145(8):1386-8. [Medline].

  27. Winther KH, Cramon P, Watt T, et al. Disease-Specific as Well as Generic Quality of Life Is Widely Impacted in Autoimmune Hypothyroidism and Improves during the First Six Months of Levothyroxine Therapy. PLoS One. 2016 Jun 3. 11(6):e0156925. [Medline]. [Full Text].

  28. Zamfirescu I, Carlson HE. Absorption of levothyroxine when coadministered with various calcium formulations. Thyroid. 2011 May. 21(5):483-6. [Medline]. [Full Text].

  29. Piantanida E, Gallo D, Veronesi G, et al. Masked hypertension in newly diagnosed hypothyroidism: a pilot study. J Endocrinol Invest. 2016 May 19. [Medline].

  30. 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 Feb. 87(2):489-99. [Medline].

  31. Negro R, Formoso G, Mangieri T, Pezzarossa A, Dazzi D, Hassan H. Levothyroxine treatment in euthyroid pregnant women with autoimmune thyroid disease: effects on obstetrical complications. J Clin Endocrinol Metab. 2006 Jul. 91(7):2587-91. [Medline].

  32. Liu Y. Clinical significance of thyroid uptake on F18-fluorodeoxyglucose positron emission tomography. Ann Nucl Med. 2009 Jan. 23(1):17-23. [Medline].

  33. Clinical guideline, part 1. Screening for thyroid disease. American College of Physicians. Ann Intern Med. 1998 Jul 15. 129(2):141-3. [Medline].

  34. Helfand M, Redfern CC. Clinical guideline, part 2. Screening for thyroid disease: an update. American College of Physicians. Ann Intern Med. 1998 Jul 15. 129(2):144-58. [Medline].

  35. American Academy of Family Physicians. Summary of Policy Recommendations for Periodic Health Examinations. Reprint no. 510. Leawood, KS: American Academy of Family Physicians; 2002.

  36. [Guideline] Baskin HJ, Cobin RH, Duick DS, et al. American Association of Clinical Endocrinologists medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. Endocr Pract. 2002 Nov-Dec. 8(6):457-69. [Medline].

  37. Screening for thyroid disease: recommendation statement. Ann Intern Med. 2004 Jan 20. 140(2):125-7. [Medline].

  38. Grozinsky-Glasberg S, Fraser A, Nahshoni E, Weizman A, Leibovici L. Thyroxine-triiodothyronine combination therapy versus thyroxine monotherapy for clinical hypothyroidism: meta-analysis of randomized controlled trials. J Clin Endocrinol Metab. 2006 Jul. 91(7):2592-9. [Medline].

  39. Gullo D, Latina A, Frasca F, Le Moli R, Pellegriti G, Vigneri R. Levothyroxine monotherapy cannot guarantee euthyroidism in all athyreotic patients. PLoS One. 2011. 6(8):e22552. [Medline].

  40. Haddow JE, Palomaki GE, Allan WC, et al. Maternal thyroid deficiency during pregnancy and subsequent neuropsychological development of the child. N Engl J Med. 1999 Aug 19. 341(8):549-55. [Medline].

  41. Blatt AJ, Nakamoto JM, Kaufman HW. National status of testing for hypothyroidism during pregnancy and postpartum. J Clin Endocrinol Metab. 2012 Mar. 97(3):777-84. [Medline].

  42. [Guideline] 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 Oct. 21(10):1081-125. [Medline]. [Full Text].

  43. LeBeau SO, Mandel SJ. Thyroid disorders during pregnancy. Endocrinol Metab Clin North Am. 2006 Mar. 35(1):117-36, vii. [Medline].

  44. Negro R, Formoso G, Mangieri T, Pezzarossa A, Dazzi D, Hassan H. Levothyroxine treatment in euthyroid pregnant women with autoimmune thyroid disease: effects on obstetrical complications. J Clin Endocrinol Metab. 2006 Jul. 91(7):2587-91. [Medline].

  45. Velkeniers B, Van Meerhaeghe A, Poppe K, Unuane D, Tournaye H, Haentjens P. Levothyroxine treatment and pregnancy outcome in women with subclinical hypothyroidism undergoing assisted reproduction technologies: systematic review and meta-analysis of RCTs. Hum Reprod Update. 2013 May-Jun. 19(3):251-8. [Medline].

  46. Busko M. Optimal levothyroxine doses for hypothyroidism in pregnancy. Medscape Medical News from WebMD. December 9, 2013. Available at http://www.medscape.com/viewarticle/817459. Accessed: January 5, 2014.

  47. Abalovich M, Vazquez A, Alcaraz G, et al. Adequate levothyroxine doses for the treatment of hypothyroidism newly discovered during pregnancy. Thyroid. 2013 Nov. 23(11):1479-83. [Medline].

  48. Cooper DS, Biondi B. Subclinical thyroid disease. Lancet. 2012 Mar 24. 379(9821):1142-54. [Medline].

  49. Surks MI, Ortiz E, Daniels GH, et al. Subclinical thyroid disease: scientific review and guidelines for diagnosis and management. JAMA. 2004 Jan 14. 291(2):228-38. [Medline].

  50. [Guideline] De Groot L, Abalovich M, Alexander EK, et al. Management of thyroid dysfunction during pregnancy and postpartum: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2012 Aug. 97(8):2543-65. [Medline]. [Full Text].

  51. Gyamfi C, Wapner RJ, D'Alton ME. Thyroid dysfunction in pregnancy: the basic science and clinical evidence surrounding the controversy in management. Obstet Gynecol. 2009 Mar. 113(3):702-7. [Medline].

  52. Rosario PW, Bessa B, Valadao MM, Purisch S. Natural history of mild subclinical hypothyroidism: prognostic value of ultrasound. Thyroid. 2009 Jan. 19(1):9-12. [Medline].

  53. Ito M, Arishima T, Kudo T, et al. Effect of levo-thyroxine replacement on non-high-density lipoprotein cholesterol in hypothyroid patients. J Clin Endocrinol Metab. 2007 Feb. 92(2):608-11. [Medline].

  54. Peleg RK, Efrati S, Benbassat C, Fygenzo M, Golik A. The effect of levothyroxine on arterial stiffness and lipid profile in patients with subclinical hypothyroidism. Thyroid. 2008 Aug. 18(8):825-30. [Medline].

  55. Cinemre H, Bilir C, Gokosmanoglu F, Bahcebasi T. Hematologic effects of levothyroxine in iron-deficient subclinical hypothyroid patients: a randomized, double-blind, controlled study. J Clin Endocrinol Metab. 2009 Jan. 94(1):151-6. [Medline].

  56. Wartofsky L. Myxedema coma. Endocrinol Metab Clin North Am. 2006 Dec. 35(4):687-98, vii-viii. [Medline].

  57. Turner MR, Camacho X, Fischer HD, et al. Levothyroxine dose and risk of fractures in older adults: nested case-control study. BMJ. 2011 Apr 28. 342:d2238. [Medline]. [Full Text].

  58. Busko M. Subclinical hypothyroidism in pregnancy usually transient. Medscape Medical News from WebMD. December 20, 2013. Available at http://www.medscape.com/viewarticle/818195. Accessed: December 30, 2013.

  59. Shields BM, Knight BA, Hill AV, Hattersley AT, Vaidya B. Five-year follow-up for women with subclinical hypothyroidism in pregnancy. J Clin Endocrinol Metab. 2013 Dec. 98(12):E1941-5. [Medline].

 
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The hypothalamic-pituitary-thyroid axis. Levels of circulating thyroid hormones are regulated by a complex feedback system involving the hypothalamus and pituitary gland.
 
 
 
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