Hashimoto Thyroiditis Treatment & Management
- Author: Stephanie L Lee, MD, PhD; Chief Editor: George T Griffing, MD more...
The treatment of choice for Hashimoto thyroiditis (or hypothyroidism from any cause) is thyroid hormone replacement. The drug of choice is orally administered levothyroxine sodium, usually for life.
Tailor and titrate the dose of levothyroxine sodium to meet the individual patient's requirements. The goal of therapy is to restore a clinically and biochemically euthyroid state. The standard dose is 1.6-1.8 mcg/kg lean body weight per day, but the dose is patient dependent. The free T4 and TSH levels are within reference ranges in the biochemically euthyroid state, with the TSH level in the lower half of the reference range.
Patients younger than 50 years who have no history or evidence of cardiac disease can usually be started on full replacement doses.
Start patients older than age 50 years and younger patients with cardiac disease on a low dose of 25 mcg (0.025 mg) per day, with clinical and biochemical reevaluation in 6-8 weeks. Carefully titrate the dose upward to achieve a clinical and biochemical euthyroid state. Rarely, it may not be possible to achieve a euthyroid state in a patient with baseline cardiac dysrhythmic disease without worsening his or her cardiac status. In such cases, the astute clinician is content to achieve the clinically euthyroid state and to accept a slightly elevated TSH level.
Elderly patients usually require a smaller replacement dose of levothyroxine, sometimes less than 1 mcg/kg lean body weight per day.
Elderly patients and patients on androgens for various reasons usually require decreased levothyroxine replacement dosing.
Patients who have undergone bowel resection and have short-bowel syndrome (or malabsorption for any reason) often require increased doses of levothyroxine to maintain the euthyroid state.
In their previously described study of 830 patients with Hashimoto thyroiditis, Tagami et al found that, following treatment with small doses of levothyroxine in 32 of the study's patients with subclinical hypothyroidism, significant decreases occurred in the patients' total cholesterol, LDL, and non-HDL levels, as well as in their LDL/HDL ratios.
One popular treatment, more so among patients than physicians, is the combined use of liothyronine (T3) and levothyroxine in an effort to mimic more closely thyroid hormone physiology. However, a literature review found that out of 9 controlled clinical trials, only 1 indicated that combined therapy seemed to improve the mood, quality of life, and psychometric performance of patients more than did levothyroxine alone.
Until investigators can demonstrate a definite advantage to the administration of levothyroxine plus liothyronine, the use of levothyroxine alone should remain the treatment of choice for replacement therapy in hypothyroidism.
Consultation with an endocrinologist is recommended
Pregnancy induces a state of increased need for levothyroxine. In women with hypothyroidism and in women with inadequate thyroid reserve from Hashimoto thyroiditis or partial thyroidectomy, this is manifested by an increase in the level of TSH and a decrease in the level of free T4.
The increase in the levothyroxine requirement is thought to be due to increased levels of thyroid hormone–binding protein, increased use by the fetus, and increased metabolism of thyroxine by the fetoplacental unit. The increase usually resolves and levothyroxine requirements return to prepregnancy levels 6-8 weeks postpartum.
Note that total T4 and T3 levels may actually be increased in pregnancy. This phenomenon is thought to be due to the estrogen-induced sialylation (increased sialic acid content) of the thyroxine-binding globulin (TBG). This leads to decreased clearance of the TBG by the liver and to increased levels and binding capacity of the TBG. Increased TBG synthesis is also thought to play a contributory role. The pregnancy-induced increased need for T4 occurs in the first trimester, usually within the first 8 weeks, and persists throughout pregnancy. Patients with hypothyroidism may require up to a 45-50% increase in the levothyroxine dose.
Patients with hypothyroidism are best followed up by monitoring the TSH and free T4 levels. Upon becoming pregnant, patients should have the TSH and free T4 levels checked within 4-8 weeks and then every 6-8 weeks while dose adjustments are being made. Patients who are adequately dosed and who are in a clinically and biochemically euthyroid state should have thyroid function tests (TSH and free T4) every 8 weeks. Dose adjustments should be made to keep the free T4 and TSH within reference ranges.
Patients who are diagnosed with Hashimoto thyroiditis or hypothyroidism from any cause during pregnancy should be started on a levothyroxine dose close to their replacement requirement, and the TSH level should be normalized as soon as possible. Untreated hypothyroidism carries increased maternal and fetal complications.
A transient reduction in serum TSH levels occurs toward the end of the first trimester, owing to high circulating levels of human chorionic gonadotropin (hCG); this phenomenon is often confused with hyperthyroidism.
The incidence of fetal loss is increased in patients who are TPO antibody positive.
Myxedema coma is a state of extreme hypothyroidism with a very high mortality rate (approaching 60%). Patients with this condition usually present with an acute precipitating condition, most often in the following settings:
Long-standing, undiagnosed hypothyroidism
Discontinuation of T4 replacement therapy
Failure to institute T4 replacement after radioactive iodine ablation of the thyroid in Graves disease or after total thyroidectomy
Myxedema coma typically manifests in winter (or during extremely cold weather) in an elderly woman who has long-standing hypothyroidism. Hospitalized patients may have a history of sedating medication use. Typical clinical findings include hypothermia, obtundation or coma, hypoventilation, bradycardia, hyponatremia, hypoglycemia, and hypotension. Besides having an elevated TSH level, these patients may have undetectable free T4 levels.
The usual precipitating causes include infection, cardiovascular accident, pulmonary infection, congestive cardiac failure, and drugs, such as narcotics, sedatives, anesthetic agents, antidepressants, and tranquilizers (all of which depress the respiratory drive).
Therapy should be conducted in an acute care unit, where patients may require the following:
Ventilatory support for hypoventilation and carbon dioxide retention
Electrocardiographic monitoring and a Swan-Ganz catheter for hemodynamic monitoring
Judicious rewarming to avoid excessive vasodilatation, which would increase oxygen consumption and could lead to worsening of hypotension and vascular collapse
Steroids, preferably hydrocortisone in stress doses
Treatment of infection or any other precipitating causes
Fluid restriction with or without hypertonic saline and Lasix to promote water diuresis
Levothyroxine is administered intravenously in a loading dose of 4 mcg/kg of lean body weight; this is about 300-600 mcg, which should be administered by rapid IV injection. The daily maintenance dose is 50-100 mcg/d, administered intravenously until the patient can take it orally.
Indications for surgery include the following:
A large goiter with obstructive symptoms, such as dysphagia, voice hoarseness, and stridor, caused by extrinsic obstruction of airflow - Evaluate patients with these symptoms with a barium swallow study and pulmonary function tests, including flow volume loops and a neck computed tomography (CT) scan
Presence of a malignant nodule - As found by cytologic examination via fine-needle aspiration
Presence of a lymphoma diagnosed on fine-needle aspiration - Thyroid lymphoma responds very well to radiotherapy and is the treatment modality of choice in this situation
Cosmetic reasons - For large, unsightly goiters
Upon the initiation of the levothyroxine replacement therapy, check thyroid function tests, specifically TSH, initially every 6-8 weeks as dose adjustments are made. After the attainment of the clinical euthyroid state and a normal TSH level, patients and the TSH levels may be checked every 6-12 months.
More frequent follow-up and TSH checks may need to be performed when patients start taking medications, such as ferrous sulfate, calcium supplementation, and multivitamins, that have the potential to impair the absorption of levothyroxine and therefore to affect the TSH level. Patients need to be advised to separate these medications from levothyroxine by at least 4 hours.
Follow-up care should include clinical evaluation for symptoms of hypothyroidism or iatrogenic hyperthyroidism.
Physical examination should routinely include weight measurement, pulse and blood pressure determinations, and thyroid examination for the presence of nodules.
Baloch ZW, LiVolsi VA. Fine-needle aspiration of the thyroid: today and tomorrow. Best Pract Res Clin Endocrinol Metab. 2008 Dec. 22(6):929-39. [Medline].
Fava A, Oliverio R, Giuliano S, et al. Clinical evolution of autoimmune thyroiditis in children and adolescents. Thyroid. 2009 Feb 18. [Medline].
Hadj-Kacem H, Rebuffat S, Mnif-Feki M, et al. Autoimmune thyroid diseases: genetic susceptibility of thyroid-specific genes and thyroid autoantigens contributions. Int J Immunogenet. 2009 Apr. 36(2):85-96. [Medline].
Duntas LH. Environmental factors and autoimmune thyroiditis. Nat Clin Pract Endocrinol Metab. 2008 Aug. 4(8):454-60. [Medline].
Tomer Y, Huber A. The etiology of autoimmune thyroid disease: a story of genes and environment. J Autoimmun. 2009 Mar 21. [Medline].
Jørgensen KT, Rostgaard K, Bache I, et al. Autoimmune diseases in women with Turner's Syndrome. Arthritis Rheum. 2010 Feb 25. 62(3):658-666. [Medline].
Wiebolt J, Achterbergh R, den Boer A, et al. Clustering of additional autoimmunity behaves differently in Hashimoto's patients compared with Graves' patients. Eur J Endocrinol. 2011 May. 164(5):789-94. [Medline].
Vestgaard M, Nielsen LR, Rasmussen AK, et al. Thyroid peroxidase antibodies in pregnant women with type 1 diabetes: impact on thyroid function, metabolic control and pregnancy outcome. Acta Obstet Gynecol Scand. 2008. 87(12):1336-42. [Medline].
Mazokopakis EE, Papadomanolaki MG, Tsekouras KC, et al. Is vitamin D related to pathogenesis and treatment of Hashimoto's thyroiditis?. Hell J Nucl Med. 2015 Sep-Dec. 18(3):222-7. [Medline].
Tagami T, Tamanaha T, Shimazu S, et al. Lipid Profiles in the Untreated Patients with Hashimoto Thyroiditis and the Effects of Thyroxine Treatment on Subclinical Hypothyroidism with Hashimoto Thyroiditis. Endocr J. 2009 Dec 22. [Medline]. [Full Text].
Vanderpump MP, French JM, Appleton D. The prevalence of hyperprolactinaemia and association with markers of autoimmune thyroid disease in survivors of the Whickham Survey cohort. Clin Endocrinol (Oxf). 1998 Jan. 48(1):39-44. [Medline].
Vanderpump MP, Tunbridge WM, French JM. The incidence of thyroid disorders in the community: a twenty-year follow-up of the Whickham Survey. Clin Endocrinol (Oxf). 1995 Jul. 43(1):55-68. [Medline].
Kim KW, Park YJ, Kim EH, et al. Elevated risk of papillary thyroid cancer in Korean patients with Hashimoto's thyroiditis. Head Neck. 2011 May. 33(5):691-5. [Medline].
Kahaly GJ, Diana T, Glang J, et al. Thyroid Stimulating Antibodies Are Highly Prevalent in Hashimoto's Thyroiditis and Associated Orbitopathy. J Clin Endocrinol Metab. 2016 May. 101(5):1998-2004. [Medline].
Huber A, Menconi F, Corathers S, et al. Joint genetic susceptibility to type 1 diabetes and autoimmune thyroiditis: from epidemiology to mechanisms. Endocr Rev. 2008 Oct. 29(6):697-725. [Medline]. [Full Text].
Escobar-Morreale HF, Botella-Carretero JI, Escobar del Rey F, et al. REVIEW: Treatment of hypothyroidism with combinations of levothyroxine plus liothyronine. J Clin Endocrinol Metab. 2005 Aug. 90(8):4946-54. [Medline]. [Full Text].
Bozkurt NC, Karbek B, Ucan B, Sahin M, Cakal E, Ozbek M, et al. The Association Between Severity of Vitamin D Deficiency and Hashimoto's Thyroiditis. Endocr Pract. 2013 Jan 21. 1-14. [Medline].
Tomer Y, Blackard JT, Akeno N. Interferon alpha treatment and thyroid dysfunction. Endocrinol Metab Clin North Am. 2007 Dec. 36 (4):1051-66; x-xi. [Medline]. [Full Text].
Dorr HG, Bettendorf M, Binder G, Karges B, Kneppo C, Schmidt H, et al. Levothyroxine Treatment of Euthyroid Children with Autoimmune Hashimoto Thyroiditis: Results of a Multicenter, Randomized, Controlled Trial. Horm Res Paediatr. 2015 Aug 7. [Medline].
Pyzik A, Grywalska E, Matyjaszek-Matuszek B, Rolinski J. Immune disorders in Hashimoto's thyroiditis: what do we know so far?. J Immunol Res. 2015. 2015:979167. [Medline].
Caturegli P, De Remigis A, Rose NR. Hashimoto thyroiditis: clinical and diagnostic criteria. Autoimmun Rev. 2014 Apr-May. 13 (4-5):391-7. [Medline].