Abstract

PIP: Uterine hyperactivity causing reduced local blood flow is quite prevalent among nulliparous women in their late teens. This pain called primary dysmenorrhea coincides with the onset of menstruation and stays a few hours to 1-2 days. The uterine agonist prostaglandin PGF2alpha and arginine vasopressin (VP) seem to be involved in dysmenorrhea. Pgf2alpha may induce pain by stimulating afferent nerve fibers. Generally common pain relievers treat dysmenorrhea, but in those instances when they do not, nonsteroid antiinflammatory drugs (NSAIDs) may do so (75% success rate). Yet NSAIDs may not be able to help because of the sizable time lag between ingestion and affecting pain. Moreover pain transpire very quickly and does not always last very long. Nevertheless clinical studies how promise for the NSAID ketoprofen. Plasma levels of ketoprofen reach their peak in 1 hour while it takes naproxen (the reference NSAID) about 2 hours to reach peak plasma levels. Oral contraceptives (OCs), especially those that are gestagen dominated, can also treat primary dysmenorrhea. OCs reduce the strong uterine contractions, blood flow, and sensitivity of the uterus to Pgf2alpha and VP. Calcium channel blocking agents and beta 2 adrenoceptor stimulating drugs may help when other treatments fail, but they have significant side effects. Moreover calcium channel blocking agents are not yet approved in Scandinavia. A double blind cross over comparative study with an intravenous oxytocin analogue shows good promise, but an oral preparation is not yet available. Secondary dysmenorrhea occurs most often in women 30 years old. A bodily condition, such as endometriosis or an IUD, is responsible for it. Many of these conditions stimulate the release of PGs so NSAIDs can generally relieve the pain. Ideally, to relieve suffering though, physicians should treat the condition.