Johns Hopkins Medical Institutions
Autoimmune Disease Research Center


Endocrine Diseases
Addison's Disease
Autoimmune Hypoparathyroidism
Autoimmune Hypophysitis
Autoimmune Oophoritis
Autoimmune Orchitis
Graves' Disease
Hashimoto's Thyroiditis
Polyglandular Autoimmune Syndrome Type 1 (PAS-1)
Polyglandular Autoimmune Syndrome Type 2 (PAS-2)
Polyglandular Autoimmune syndrome Type 3 (PAS 3)
Type 1 Diabetes Mellitus
Hashimoto's Thyroiditis
Prepared by: Daniela Cihakova MD, PhD

Definition: Hashimoto’s thyroiditis is a chronic inflammatory autoimmune disease of the thyroid gland.

Description: The thyroid produces two hormones, T3 and T4, which control metabolism of almost all cells in a body. The pituitary gland secrets a hormone called TSH (thyroid stimulating hormone), which increases thyroid gland hormone production. Hashimoto's thyroiditis occurs when inflammation caused by an autoimmune process destroys the thyroid gland, leading to an insufficient production of thyroid hormones. The disease is named after its discoverer, Hakaru Hashimoto. Hashimoto's thyroiditis is the most common form of thyroiditis.

Symptoms: Usually painless, diffuse and gradual enlargement of the thyroid gland, which can be notice as enlargement of neck. Rarely, it can be accompanied with shortness of breath (dyspnea) or difficulty swallowing (dysphagia) due to the pressure of the growing goiter.

The thyroid hormone deficiency may have no symptoms. However, the common symptoms are:
  • fatigue,
  • depression,
  • sensitivity to cold,
  • weight gain,
  • muscle weakness,
  • coarsening of the skin,
  • dry or brittle hair,
  • constipation,
  • muscle cramps,
  • increased menstrual flow, and
  • increased risk of miscarriage


Diagnosis:
  1. Serologic tests for antibodies and hormones level in blood:
    • Subclinical hypothyroidism -normal FT4, but elevated TSH (Thyroid Stimulating Hormone)
    • Clinical primary hypothyroidism – low FT4, low T3 and elevated TSH
  2. Needle biopsy and serologic tests for antibodies.
  3. Cholesterol and triacylglycerids can be increased.
  4. Clinical signs: presence of goiter; facial pallor; bradycardia; hypertension; delayed relaxation of deep-tendon reflexes; and edema (myxedema) of the skin of the hands, feet, and eyelids.


Incidence: 0.3–1.5 cases per 1,000 per year. The number of diagnosed Hashimoto’s thyroiditis is increasing over time, mainly due to better diagnostic techniques and an active search among family members of known patients. The female-to-male ratio is 20:1. The disease is most common in middle aged women, but it can affect all age groups, including children.

Treatment: Currently, there is no treatment capable of stopping the autoimmune process leading to Hashimoto's thyroiditis. Hypothyroidism, which is a result of the thyroid gland destruction, can be treated by a lifelong thyroide hormone replacement. Under the hormone replacement therapy, the size of the goiter usually decreases. If not, surgery may be required.

Pathogenesis: At this stage, we have circumstantial and indirect evidence that Hashimoto’s thyroiditis is an autoimmune disease.

Circumstantial evidence:
  • 25 percent of patients with Hashimoto's thyroiditis may develop polyglandular syndromes (such as pernicious anemia, diabetes, or adrenal insufficiency) or other autoimmune diseases (such as Sjogren’s syndrome).
  • Positive family history of Hashimoto’s thyroiditis or others autoimmune diseases.
  • High serum of IgG antibodies.
  • The thyroid gland has a diffuse lymphocyte infiltration, fibrosis, and parenchymal atrophy.
  • Presence of specific antibodies against thyroglobulin (TG) and thyroid peroxidase (TPO). Presence of these antibodies is not enough for a diagnosis of Hashimoto’s thyroiditis, since 10 percent of women in the population have these antibodies.

Indirect evidence:
  • Mouse model: Experimental autoimmune thyroiditis (EAT) can be induced in genetically susceptible animals by immunization with mouse thyroglobulin (MTg) in an adjuvant. Adoptive transfer of immunized donor spleen cells into naive recipients cause the disease as well.

Links to other Resources:

www.thyroid-info.com

www.thyroid.org

www.thyroidfoundation.org

www.jhsph.edu
 
 

 
JHU Autoimmunity Home JHU Pathology Home Feedback JHU Bloomberg School of Public Health


Johns Hopkins Medicine
Web site designed by Alberto Fenu and Patrizio Caturegli

Disclaimer Last Modified: 09/10/2001
© Copyright 2000 | All Rights Reserved | Johns Hopkins University School of Medicine & Johns Hopkins Health System
720 Rutland Avenue, Baltimore, Maryland 21205 USA