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Hashimoto Thyroiditis Treatment & Management

  • Author: Stephanie L Lee, MD, PhD; Chief Editor: George T Griffing, MD  more...
Updated: Jul 11, 2016

Approach Considerations

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.[10]

Combination therapy

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.[16]

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

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

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.


Surgical Care

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

Long-Term Monitoring

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.

Contributor Information and Disclosures

Stephanie L Lee, MD, PhD Associate Professor, Department of Medicine, Boston University School of Medicine; Director of Thyroid Health Center, Section of Endocrinology, Diabetes and Nutrition, Boston Medical Center; Fellow, Association of Clinical Endocrinology

Stephanie L Lee, MD, PhD is a member of the following medical societies: American College of Endocrinology, American Thyroid Association, Endocrine Society

Disclosure: Nothing to disclose.


Sylvester Odeke, MD, FACE Vidant Medical Group Endocrinology, Diabetes & Metabolism, Greenville, NC

Sylvester Odeke, MD, FACE is a member of the following medical societies: American Association of Clinical Endocrinologists, North Carolina Medical Society, American College of Endocrinology

Disclosure: Nothing to disclose.

Steven B Nagelberg, MD Clinical Professor, Department of Medicine, Division of Endocrinology and Metabolism, Drexel University College of Medicine

Steven B Nagelberg, MD is a member of the following medical societies: Alpha Omega Alpha, American Association of Clinical Endocrinologists, American College of Physicians, American Diabetes Association, American Medical Association, Endocrine Society, Pennsylvania Medical Society

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.


Don S Schalch, MD Professor Emeritus, Department of Internal Medicine, Division of Endocrinology, University of Wisconsin Hospitals and Clinics

Don S Schalch, MD is a member of the following medical societies: American Diabetes Association, American Federation for Medical Research, Central Society for Clinical Research, and Endocrine Society

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

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