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  • Title: Dysmenorrhea.
    Author: Dawood MY.
    Journal: J Reprod Med; 1985 Mar; 30(3):154-67. PubMed ID: 3158737.
    Abstract:
    Dysmenorrhea affects over 50% of menstruating women and causes extensive personal and public health problems, a high degree of absenteeism and severe economic loss. In primary dysmenorrhea there is no macroscopically identifiable pelvic pathology, while in secondary dysmenorrhea gross pathology is present in the pelvic structures. With primary dysmenorrhea the pain is suprapubic and spasmodic, and associated symptoms may be present. Characteristically dysmenorrhea starts at or shortly after menarche. The pain lasts for 48-72 hours during the menstrual flow and is most severe during the first or second day of menstruation. It is now clear that in many women with primary dysmenorrhea the pathophysiology is due to increased and/or abnormal uterine activity because of the excessive production and release of uterine prostaglandins. Treatment with many of the prostaglandin synthetase inhibitors (nonsteroidal antiinflammatory drugs) will produce significant relief from dysmenorrhea and a concomitant decrease in menstrual fluid prostaglandins. For dysmenorrheic women who desire oral contraception, this agent will relieve the dysmenorrhea by suppressing endometrial growth, thus resulting in a decrease in the menstrual flow as well as in menstrual fluid prostaglandins. For those not requiring oral contraception the drug of choice for primary dysmenorrhea remains a prostaglandin inhibitor. Laparoscopy need be resorted to only if a pelvic abnormality is detected on examination or if treatment with prostaglandin inhibitors for up to six months is not significantly effective. In secondary dysmenorrhea, relief is obtained when the pelvic pathology--such as ovarian cysts, uterine fibroids, adhesions, cervical stenosis, congenital malformation of the uterus and endometriosis--is treated. In women using IUDs the dysmenorrhea is readily controlled with prostaglandin inhibitors since the underlying pathophysiology is excessive prostaglandin production and release.
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