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Hashimoto Thyroiditis
Author: Stephanie L Lee, MD, PhD; Chief Editor: George T Griffing, MD more...
Updated: Jun 3, 2014

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 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 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 (antithyroglobulin) 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 thyroid
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.

Background
Hashimoto thyroiditis (or Hashimotos thyroiditis) is characterized by the destruction of thyroid cells by various celland 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

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 receptorblocking 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, cedliac disease and type 1 diabetes mellitus.[7, 8]
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.[9]

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.[10, 11]

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.

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.[12] These cancers are
not clearly more aggressive than other papillary thyroid carcinomas.

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.

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 separateby at least 4 hoursingestion of levothyroxine from ingestion of
cholestyramine, ferrous sulfate, sucralfate, calcium carbonate, aluminum hydroxide (and other antacids), and ironcontaining multivitamins, all of which impair the absorption of levothyroxine.
For patient education information, see the Thyroid and Metabolism Center, as well as Thyroid Problems.

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, and The 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, American College of Endocrinology, and North Carolina Medical Society

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, Pennsylvania Medical Society, and The Endocrine Society
Disclosure: Nothing to disclose.
Chief Editor
George T Griffing, MD Professor 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, American College of Medical Practice Executives, American College of Physician
Executives, American College of Physicians, American Diabetes Association, American Federation for Medical
Research, American Heart Association, Central Society for Clinical Research, International Society for Clinical
Densitometry, Southern Society for Clinical Investigation, and The Endocrine Society
Disclosure: Nothing to disclose.
Additional Contributors
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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