Abstract

Premature ovarian failure (POF) is a human disease characterized by amenorrhea before the age of 40 (or 35), regardless of whether the disease occurs before or after puberty (1). The known causes of POF have included genetic abnormalities, viral infections, and chemical and drug toxicity. However, these factors account for only a small subset of POF patients. For the majority of POF patients, the cause of the disease is unknown, and an immunologic basis has been considered. A recent review estimated that POF occurs in 0.3% of U.S. women of reproductive age, and about 14,000 women are at risk for autoimmune ovarian disease (1). This is likely to be an overestimate since the two classical criteria of organ-specific autoimmunity—serum autoantibodies and inflamed ovaries (oophoritis)—have rarely been documented in POF patients (reviewed in 2). Notwithstanding the uncertain incidence of immunologic POF, the immunologic basis for POF rests on solid grounds. In POF patients antiovarian autoantibodies and oophoritis have been detected;moreover, autoimmune oophoritis occurs as part of the polyendocrine autoimmunity syndromes, along with thyroiditis, insulitis, adrenalitis, myasthenia gravis, and others (1). In addition, autoimmune oophoritis can be readily induced in experimental animals.

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