New concepts in dysmenorrhea

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.

PIP: Recent studies are reviewed on the etiology of primary dysmenorrhea as well as on proper treatment, based on physiology, of this disorder. These studies suggested that increased endometrial prostaglandin production and release may cause dysmenorrhea. Since prostaglandins cause myometrial contractility, then if production and release of prostaglandins are excessive, uterine ischemia and pain result. Studies of therapeutic value of prostaglandin synthetase inhibitors show good results; agents such as indomethacin and the fenamates inhibit the synthesis of prostaglandin through the synthetase system as well as antagonize prostaglandins' conventional action at the cell receptor level. Other more conventional forms of therapy for dysmenorrhea have also garnered good results, these include ingestion of oral contraceptives and dilatation of the cervix, and their effectiveness can be explained partly on the basis of a reduced level of prostaglandins in the menstrual fluid. The need for further evaluation of antiprostaglandin compounds is promoted.