New concepts in dysmenorrhea

Olavi Ylikorkala, M. Yusoff Dawood
In: American Journal of Obstetrics and Gynecology · 1978 · vol. 130(7) , pp. 833–847 · doi:10.1016/0002-9378(78)90019-4 · W1791445800
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This review explores novel understandings of the pathophysiology and therapeutic strategies for dysmenorrhea, encompassing menstrual pain originating from uterine contractions and associated prostaglandin release.

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Abstract

The etiology of primary dysmenorrhea, which is the most common gynecologic complaint and cause of lost working hours, remains obscure but merits careful scientific investigation. Recent studies suggest that increased endometrial prostaglandin production and release may be responsible for dysmenorrhea. Prostaglandins cause myometrial contractility that, if excessive, leads to uterine ischemia and pain. This hypothesis has led to clinical trials of antiprostaglandin agents such as indomethacin and fenamates, which inhibit the synthesis of prostaglandin through the prostaglandin synthetase system as well as antagonize their action at the cell receptor level. The good response of dysmenorrhea to other conventional forms of therapy such as oral contraceptives and dilatation of the cervix can be partly explained on the basis of a reduced level of prostaglandins in the menstrual fluid with such therapy. There is a definite need for further evaluation of the antiprostaglandin compounds in the treatment of dysmenorrhea so that sound formulations can be evolved for the elimination of this incapacitating disorder.

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dysmenorrhea

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