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Expert Opin Pharmacother. 2008 Oct;9(15):2661-72. doi: 10.1517/14656566.9.15.2661 .

Dysmenorrhea in adolescents and young adults: from pathophysiology to pharmacological treatments and management strategies.

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Warren Alpert Medical School of Brown University, Hasbro Children's Hospital/Rhode Island Hospital, Division of Adolescent Medicine, Department of Pediatrics, 593 Eddy Street, Providence, RI 02903, USA.



Dysmenorrhea is the most common gynecologic complaint among adolescent and young adult females. Dysmenorrhea is usually primary and is associated with normal ovulatory cycles and with no pelvic pathology. In approximately 10% of females with severe dysmenorrhea symptoms, pelvic abnormalities such as endometriosis or uterine anomalies may be found.


To review the current knowledge regarding the pathophysiology of dysmenorrhea, as well as review pharmacological treatments and strategies for management of dysmenorrhea in adolescent and young adult females.


Review of original articles on dysmenorrhea that have been published in the medical literature.


Potent prostaglandins and potent leukotrienes play an important role in generating primary dysmenorrhea symptoms. Non-steroidal anti-inflammatory drugs (NSAIDs) are the most common pharmacologic treatment for dysmenorrhea. A loading dose of NSAIDs (typically twice the regular dose) should be used as initial treatment for dysmenorrhea, followed by a regular dose until symptoms abate. Adolescents and young adults with symptoms that do not respond to treatment with NSAIDs for three menstrual periods should be offered hormonal treatment such as combined estrogen/progestin oral contraceptive pills (OCPs) for three menstrual cycles. If dysmenorrhea does not improve within 6 months of treatment with NSAID and OCPs, a laparoscopy is indicated to look for endometriosis. The goal of pharmacological treatment for endometriosis is to block its abnormal positive feedback loop. The abnormal loop consists of high local levels of estrogen in the lesions, which induce transcription of COX-2 and synthesis of prostaglandin E(2.) This results in further expression and activity of aromatase and a further increase in estrogen.

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