Abstract

Estrogenic therapy for dysmenorrhea has been endorsed by many investigators. The rationale for its use, however, still is based on theory. Some clinicians believe that menstrual pain is a manifestation of an estrogenic deficiency; others claim that an excess of progestin is the exciting cause. Estrogenic therapy is used generally by those who hold either of these views, either as complemental therapy or as a contraphysiologic approach designed to over-ride corpus luteum function. There is another group of workers who employ progesterone on the basis that the pain results from an excess of estrogen and presumably from a deficit in progestin production.

Systems of therapy based on these theories have been described as yielding varying degrees of relief but, as yet, no satisfactory explanations have been offered of the pharmacologic actions which produce desirable symptomatic responses. The alleviation of symptoms is usually regarded as proof of the correctness of whichever theoretical basis was postulated.

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