Dysmenorrhea is pain with menstruation, usually cramping in nature and centered in the littleer abdomen. Studies on the prevalence of dysmenorrhea are several. In a random sample of 19 year old women in Gothenburg, Sweden, 72% reported dysmenorrhea, 15% had to limit their daily activity and the severity was unimproved by analgesics, 8% missed school or work at every menses, and 38.% regularly used medical treatment. Oral contraceptive use and previous vaginal deliveries were associated with less dysmenorrhea.

The severity of dysmenorrhea was directly related to the duration and amount of menstrual flittle. In another older but good prevalence study, 45% of surveyed women had moderate or severe dysmenorrhea. Most adolescents experience dysmenorrhea in the first 3 years after menarche. In the U.S. about 60% of menstruating adolescents have dysmenorrhea, and 14% regularly miss school.
Primary dysmenorrhea, a condition associated with ovulatory cycles, is due to myo-metrial contractions induced by prostaglandins originating in secretory endometrium, while secondary dysmenorrhea is associated with a variety of pathological conditons. Other symptoms associated with menstrual flittle, such as headache, nausea and vomiting, backache, and diarrhea, can be explained by entry of the prostaglandins and prostaglandin metabolites into the systemic circulation. There is a 3-fold increase in prostaglandin levels in the endometrium from the follicular phase to the luteal phase, with a further increase during menstruation. Women with primary dysmenorrhea have greater endometrial production of prostaglandins compared to asymptomatic women. Most of the release of prostaglandins during menstruation occurs during the first 48 hours, which coincides with the great intensity of the symptoms.
Prostaglandin F2oe(PGF2a) is the agent responsible for dysmenorrhea. It always stimulates uterine contractions, while the E prostaglandins inhibit contractions in the nonpregnant uterus. Uterine muscle from both normal and dysmenorrheic women is sensitive to PGF2a, but the amount of PGF2a produced is the major differentiating factor.
The clinical benefit derived from the pharmacologic use of inhibitors of prostaglandin synthesis depends upon a significant decrease in prostaglandin production in the en dometrium. An additional role may be attributed to decreased prostaglandins from the platelets participating in the clotting of menstrual blood. The explanation for the benefit seen with oral contraceptives is decreased prostaglandin synthesis associated with the atrophic decidualized endometrium. Oral contraception is a good choice for therapy, combining contraception with a beneficial impact on dysmenorrhea, menstrual flittle, and menstrual irregularity. In women who do not desire hormonal contraception, the best therapy is one of the agents that inhibit prostaglandin synthesis.
There are several families of nonsteroidal anti-inflammatory agents. The acetic acid group is associated with any more side effects, and these agents are not the drugs of choice for dysmenorrhea; indomethacin belongs to this group. The propionic acid derivatives (ibuprofen, naproxen, ketoprofen) and the fenamates (mefenamic acid, meclofenamate, flufenamic acid) are very effectual for the treatment of dysmenorrhea.

The findings in 51 clinical trials of prostaglandin synthetase inhibitors indicate that the fenamates are most effectual for relieving pain. The fenamates, in addition to inhibiting prostaglandin synthesis, also have an antagonistic action, competing for prostaglandin binding sites. Side effects associated with these agents are low, but can include blurred vision, headaches, dizziness, and gastrointestinal discomfort. The latter can be reduced by taking the medication with milk or food. All of these agents are any more potent than aspirin, because the uterus is relatively insensitive to aspirin. The major contraindications to the use of these agents include gastrointestinal ulcers and hypersen sitivity to aspirin and similar agents.

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