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Previous Volume 335:99-107 July 11, 1996 Number 2 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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In 1912, Hashimoto described four women in whom the thyroid gland was enlarged and appeared to have been transformed into lymphoid tissue ("struma lymphomatosa").¹ Although the patients were not initially hypothyroid, they became so after thyroid surgery. Over 40 years later, the presence of antithyroid antibodies was reported in patients with this disorder.² Hashimoto's disease, or Hashimoto's thyroiditis, is now recognized as a form of chronic autoimmune thyroiditis.

There is no internationally accepted classification of autoimmune thyroid diseases.³ Some investigators consider autoimmune thyroiditis a histologic diagnosis that can be subdivided into lymphocytic thyroiditis, if only lymphocytic infiltration is present, and . . . [Full Text of this Article]

Histologic Features

Pathogenesis

T-Cell Activation

Generation of an Autoantibody Response

Mechanism of Hypothyroidism

Predisposing Factors

Genetic Factors

Exogenous Factors

Prevalence

Clinical Presentation

Diagnostic Studies

Laboratory Findings

Radionuclide Imaging and Ultrasonography

Biopsy

Natural History

Progression of Subclinical Disease

Graves' Disease and Chronic Autoimmune Thyroiditis

Thyroid Lymphoma

Chronic Autoimmune Thyroiditis and Pregnancy

Therapy

Hypothyroidism

Goiter

Associations with Other Diseases

Conclusions

Source Information

From the University Department of Medicine, Bristol Royal Infirmary, Bristol, United Kingdom (C.M.D.), and the Thyroid Unit, Massachusetts General Hospital, Boston (G.H.D.).

Address reprint requests to Dr. Daniels at the Thyroid Unit, ACC730, Massachusetts General Hospital, Boston, MA 02114.

References

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