Dysmenorrhea; causes, symptoms and treatment


Dysmenorrhea; causes, symptoms and treatment
Dysmenorrhea, the painful cramping sensation in the lower abdomen often accompanied by other symptoms such as sweating, tachycardia, headaches, nausea, vomiting and diarrhea, occurs just before or during the menses. It is classified as primary dysmenorrhea that usually begins at or shortly after menarche and is usually not accompanied by pelvic pathologic conditions, and secondary dysmenorrhea, that in contrast, arises later and usually is associated with other pelvic pathologies.

Primary dysmenorrhea is believed to affect approximately 50% of menstruating women, and in 10% it is severe enough to limit daily activity. Although the pathogenesis is unclear, the association with uterine hypercontractility, cramping, and other prostaglandin-induced symptoms as well as the demonstration of elevated prostaglandin (PG) Fand PGE2 levels in the secretory endometrium, have led to the theory that prostaglandin-induced uterine hypercontractility and vasoconstriction, and the resulting uterine ischemia are associated with the pathogenesis of the symptoms. NSAIDs are the mainstay of treatment, and are effective in alleviating the symptoms in more than 72% of the women. In those patients for whom NSAIDs are either contraindicated or ineffective, the oral contraceptives are of proven value. If the patient also requires contraception, oral contraceptive therapy may be the treatment of choice. When used for dysmenorrhea, the exact mode of action of OCs is unclear. They may act by reducing the MBL consequent upon reduction in endometrial growth  thus affecting a reduction in prostaglandin output in menstrual blood and ensuing uterine tonicity. However, the role of oral contraceptive therapy in symptom control is limited by the dearth of large randomized controlled studies; the existing studies being limited to crosssectional comparisons. Furthermore, the efficacy of low-dose oral preparations in symptom relief has also not been established, although there are indications of its effectiveness . In women who fail to respond to NSAIDs or OCPs, it is important to consider secondary causes of dysmenorrhea.

Secondary dysmenorrhea may occur at any age. The pain is usually secondary to some pathological process, the most important of which is endometriosis. Other causes include cervical stenosis, chronic PID, pelvic congestion, conditionedbehavior, and stress and tension.

Endometriosis is an important cause of morbidity and subfertility in women in their reproductive years. Hormonal contraceptive preparations play a limited role in the symptom alleviation in women with endometriosis. Given the dearth of randomized placebo-controlled trials, there is little evidence to support the use of ovulation suppression therapy in patients with endometriosis. However, there is promising evidence from case series that the LNG-IUS may have a role to play in reducing the size of rectovaginal endometriotic deposits and alleviating pain in patients with the disorder. LNG-IUS may also have a role to play in symptom alleviation in the related disorder, adenomyosis.

Adenomyosis is an ill-understood disorder and is usually suspected on the basis of menorrhagia, dysmenorrhea and an enlarged uterus. The final diagnosis is, however, histological, following hysterectomy or endometrial resection. The diagnosis may be suspected on the basis of clinical symptoms of pelvic pain, menorrhagia, and enlarged uterus. Magnetic resonance imaging may be helpful in providing confirmatory evidence. Although the treatment is primarily surgical, and the diagnosis is often confirmed from histological examination of the surgical specimen, there is some evidence to suggest the use of LNG-IUS and mifepristone (an antiprogestin) in the management of the symptoms. Although the exact mode of action of mifepristone (Mifegyn®, Exelgyn Laboratories, Oxon, UK) is unclear, it may be related to its contraceptive action. In particular, when administered in the follicular phase of the cycle, mifepristone has an inhibitory effect on follicular development and ovulation. In the secretory phase of the menstrual cycle, it has an adverse influence on endometrial development and function. Despite the inconsistent effect on the inhibition of ovulation, mifepristone appears to have a favorable contraception effectiveness when administered weekly, chiefly due to its effect on endometrial receptivity. Furthermore, a high dose of mifepristone (200 mg) administered immediately following ovulation is highly effective in preventing implantation, and thus may be useful as a postcoital contraceptive, with reported failure rates of 3–16%.

Mifepristone has been demonstrated to relieve pain in women with symptomatic endometriosis and also to decrease the size of uterine leiomyomata by about 50%.The applicability of the drug for non-contraceptive uses will have to await larger randomized studies exploring its long-term safety and efficacy.

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