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Hashimoto Thyroiditis

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

Practice Essentials

Hashimoto thyroiditis is part of the spectrum of autoimmune thyroid diseases (AITDs) and is characterized by the destruction of thyroid cells by various cell- and antibody-mediated immune processes. This condition is the most common cause of hypothyroidism in the United States in individuals older than 6 years.

Signs and symptoms

Hypothyroidism typically has an insidious onset with subtle signs and symptoms that may progress to more advanced or even florid signs and symptoms over months to years. The presentation of patients with hypothyroidism may also be subclinical, diagnosed based on routine screening of thyroid function. Such patients may have nonspecific symptoms that are difficult to attribute to thyroid dysfunction. They frequently do not improve with thyroid hormone supplementation..

Early nonspecific symptoms may include the following:

  • Fatigue
  • Constipation
  • Dry skin
  • Weight gain

More advanced/florid symptoms may include the following:

  • Cold intolerance
  • Voice hoarseness and pressure symptoms in the neck from thyroid enlargement
  • Slowed movement and loss of energy
  • Decreased sweating
  • Mild nerve deafness
  • Peripheral neuropathy
  • Galactorrhea
  • Depression, dementia, and other psychiatric disturbances
  • Memory loss
  • Joint pains and muscle cramps
  • Hair loss
  • Menstrual irregularities
  • Sleep apnea and daytime somnolence

See Autoimmune Disorders: Making Sense of Nonspecific Symptoms, a Critical Images slideshow, to help identify several diseases that can cause a variety of nonspecific symptoms.

See Clinical Presentation for more detail.

Diagnosis

Physical findings are variable and depend on the extent of the hypothyroidism and other factors, such as age. Examination findings may include the following:

  • Puffy face and periorbital edema typical of hypothyroid facies
  • Cold, dry skin, which may be rough and scaly
  • Peripheral edema of hands and feet, typically nonpitting
  • Thickened and brittle nails (may appear ridged)
  • Bradycardia
  • Elevated blood pressure (typically diastolic hypertension)
  • Diminished deep tendon reflexes and the classic prolonged relaxation phase
  • Macroglossia
  • Slow speech
  • Ataxia

Testing

Laboratory studies and potential results for patients with suspected Hashimoto thyroiditis include the following:

  • Serum thyroid-stimulating hormone (TSH) levels: Sensitive test of thyroid function; levels are invariably raised in hypothyroidism due to Hashimoto thyroiditis and in primary hypothyroidism from any cause
  • Free T4 levels: Needed to correctly interpret the TSH in some clinical settings; low total T4 or free T4 level in the presence of an elevated TSH level further confirms diagnosis of primary hypothyroidism
  • T3 levels: Low T3 level and high reverse T3 level may aid in the diagnosis of nonthyroidal illness
  • Thyroid autoantibodies: Presence of typically anti-TPO (anti-thyroid peroxidase) and anti-Tg (anti-thyroglobulin) antibodies delineates the cause of hypothyroidism as Hashimoto thyroiditis or its variant; however, 10-15% of patients with Hashimoto thyroiditis may be antibody negative

The following tests are not necessary for the diagnosis of primary hypothyroidism but may be used to evaluate complications of hypothyroidism in some patients, as indicated:

  • Complete blood count: Anemia in 30-40% of patients with hypothyroidism
  • Total and fractionated lipid profile: Possibly elevated total cholesterol, LDL, and triglyceride levels in hypothyroidism
  • Basic metabolic panel: Decreased glomerular filtration rate, renal plasma flow, and renal free water clearance in hypothyroidism; may result in hyponatremia
  • Creatine kinase levels: Frequently elevated in severe hypothyroidism
  • Prolactin levels: May be elevated in primary hypothyroidism

Imaging tests

Features of Hashimoto thyroiditis are usually identifiable on an ultrasonogram; however, a thyroid ultrasonogram is usually not necessary for diagnosing the condition. This imaging modality is useful for assessing thyroid size, echotexture, and, most importantly, whether thyroid nodules are present.

Chest radiography and echocardiography are not usually performed and are not necessary in routine diagnosis or evaluation of hypothyroid patients.

Procedures

Hashimoto thyroiditis is a histologic diagnosis. Therefore, perform fine-needle aspiration of any dominant or suspicious thyroid nodules to exclude malignancy or the presence of a thyroid lymphoma in fast-growing goiters.[1]

See Workup for more detail.

Management

Pharmacotherapy

The treatment of choice for Hashimoto thyroiditis (or hypothyroidism from any cause) is thyroid hormone replacement. The drug of choice is individually tailored and titrated levothyroxine sodium administered orally, usually for life.

Surgery

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
  • Presence of a malignant nodule, as demonstrated by cytologic examination
  • Presence of a lymphoma diagnosed on fine-needle aspiration
  • Cosmetic reasons (eg, large, unsightly goiters)

See Treatment and Medication for more detail.

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Background

Hashimoto thyroiditis (or Hashimoto’s thyroiditis) is characterized by the destruction of thyroid cells by various cell- and antibody-mediated immune processes. It is the most common cause of hypothyroidism in the United States after age 6 years. Hashimoto thyroiditis is part of the spectrum of autoimmune thyroid diseases (AITDs). (See Etiology, Presentation, and Workup.)

By strict criteria, Hashimoto thyroiditis is a histologic diagnosis first described by Hakaru Hashimoto, a Japanese surgeon working in Berlin, Germany. His report, published in 1912, was based on the examination of 4 postoperative cases. He is also credited with introducing the term struma lymphomatosa in reference to the syndrome.

Other variants of AITD include the following conditions:

  • Atrophic thyroiditis
  • Juvenile thyroiditis [2]
  • Postpartum thyroiditis
  • Silent thyroiditis
  • Focal thyroiditis
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Etiology

The initiating process in Hashimoto thyroiditis is not well understood.[3, 4, 5, 6] The thyroid gland is typically goitrous but may be atrophic or normal in size. Antibodies binding to and blocking the thyroid-stimulating hormone (TSH) receptor, thyrotropin receptor blocking antibodies (TBII) have also been described and may contribute to impairment in thyroid function. The result is inadequate thyroid hormone production and secretion, although initially, preformed thyroxine (T4) and triiodothyronine (T3) may "leak" into the circulation from damaged cells.

Patients with Hashimoto thyroiditis have antibodies to various thyroid antigens, the most frequently detected of which include anti-thyroid peroxidase (anti-TPO), antithyroglobulin (anti-Tg), and to a lesser extent, TSH receptor-blocking antibodies (TBII). Nevertheless, a small percentage of patients with Hashimoto thyroiditis (approximately 10-15%) may be serum antibody negative.

Other antithyroid antibodies found in AITD (including Hashimoto thyroiditis) include thyroid-stimulating antibody and cytotoxic antibody.

Hashimoto thyroiditis has a markedly higher clustering of other autoimmunity diseases, including pernicious anemia, adrenal insufficiency, celiac disease, and type 1 diabetes mellitus.[7, 8]

A study by Mazokopakis et al indicated that an association may exist between vitamin D deficiency and the development of Hashimoto thyroiditis. The study, which included 218 patients with Hashimoto thyroiditis, found serum 25-hydroxy vitamin D levels to be negatively correlated with anti-TPO levels in all patients, with the anti-TPO levels being significantly greater in the 186 patients who were vitamin D deficient. After receiving oral vitamin D3 supplementation of 1200-4000 IU daily for 4 months, serum anti-TPO levels in the vitamin D deficient patients were determined to be significantly reduced.[9]

In a study of 830 patients with Hashimoto thyroiditis, Tagami et al reported slight, but significant, increases in TSH serum levels and decreases in free T4 serum levels, with increasing patient age. In addition, TSH levels were positively correlated with levels of total cholesterol, triglycerides, low-density lipoprotein (LDL), high-density lipoprotein (HDL), and non-HDL, as well as with the ratio of LDL to HDL. Free T4 levels, on the other hand, were negatively correlated with these lipid parameters.[10]

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Epidemiology

Occurrence in the United States

Hashimoto thyroiditis is the most common cause of hypothyroidism in the United States after age 6 years, with the incidence estimated to be 1.3% in a series of 5000 children aged 11-18 years. In adults, the incidence is estimated to be 3.5 per 1000 per year in women and 0.8 per 1000 per year in men. Incidence may be as high as 6% in the Appalachian region.

In the Colorado Thyroid Disease Prevalence Study, involving 25,862 adults, the prevalence of elevated TSH in symptomatic and asymptomatic adults was 9.5%, with a greater percentage of those involved being women. The prevalence of hypothyroidism and of thyroid disease in general increases with age.

International occurrence

Worldwide, the most common cause of hypothyroidism is iodine deficiency. However, Hashimoto thyroiditis remains the most common cause of spontaneous hypothyroidism in areas of adequate iodine intake. The annual incidence of Hashimoto thyroiditis worldwide is estimated to be 0.3-1.5 cases per 1000 persons.[11, 12]

Sex- and age-related demographics

The incidence of Hashimoto thyroiditis is estimated to be 10-15 times higher in females. The most commonly affected age range in Hashimoto thyroiditis is 30-50 years, with the peak incidence in men occurring 10-15 years later. The overall incidence of hypothyroidism increases with age in men and women.

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Prognosis

With early diagnosis, timely institution of levothyroxine replacement therapy, informed patient follow-up care, and attention to other attendant complications, the prognosis in Hashimoto thyroiditis is excellent, with patients leading a normal life. Untreated myxedema coma has a poor prognosis and a high mortality rate.

Morbidity related to Hashimoto thyroiditis typically results from failure to make the diagnosis of hypothyroidism or to institute L-thyroxine replacement therapy in adequate doses, or from failure on the part of the patient to take the replacement medication.

The increased prevalence of lipid disorders in association with untreated hypothyroidism has the potential to increase morbidity from coronary artery disease.

The risk for papillary thyroid carcinoma is increased in patients with Hashimoto thyroiditis.[13] These cancers are not clearly more aggressive than other papillary thyroid carcinomas.

A study by Kahaly et al indicated that a strong link exists between the presence of TSH receptor-stimulating antibodies (TSAbs) in patients with Hashimoto thyroiditis and the development of thyroid-associated orbitopathy (TAO). The study, which included 700 patients with Hashimoto thyroiditis, found higher serum levels of TSAbs in those with TAO than in those without this condition, while patients with active and severe TAO had higher TSAb levels than did patients with mild and inactive TAO. Healthy controls were negative for TSAbs.[14]

Therapeutic complications

Complications of overreplacement with levothyroxine sodium Include the following:

  • Accelerated bone loss
  • Reduction in bone mineral density
  • Osteoporosis
  • Increased heart rate
  • Increased cardiac wall thickness
  • Increased contractility

The last three problems above increase the risk of cardiac arrhythmias (especially atrial fibrillation), particularly in the elderly population.

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Patient Education

Patients should know that thyroid replacement therapy in Hashimoto thyroiditis is, except in very rare cases, lifelong. Patients must be informed about the importance of compliance with their replacement therapy and must be instructed to report any symptoms suggestive of hyperthyroidism caused by overreplacement.

Patients must be instructed to separate—by at least 4 hours—ingestion of levothyroxine from ingestion of cholestyramine, ferrous sulfate, sucralfate, calcium carbonate, aluminum hydroxide (and other antacids), and iron-containing multivitamins, all of which impair the absorption of levothyroxine.

For patient education information, see the Thyroid and Metabolism Center, as well as Thyroid Problems.

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Contributor Information and Disclosures
Author

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.

Coauthor(s)

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.

Acknowledgements

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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