Introduction
Dysmenorrhea is defined as severe pelvic pain, which may occur during or just before the menstrual cycle. It is commonly associated with nausea, vomiting, sweating, tachycardia, diarrhea, lethargy, dizziness, and breast tenderness. Dysmenorrhea has been classified as primary or secondary. Primary dysmenorrhea is any degree of cramping during menstruation without any attributable pathology and typically affects teenage women who have just established ovulatory cycles. In contrast, secondary dysmenorrhea is due to a pathologic process such as endometriosis, adenomyosis or pelvic masses. For the most part, it develops after menarche and is seen in older women. Dysmenorrhea has been reported to range in prevalence from 3% to 90%. Furthermore, about 15% of women with dysmenorrhea have severe symptoms, which preclude daily activities such as work, school, and child care.
The endometrium of the uterus produces prostaglandin PGF-2α, resulting in contractions of the uterus and smooth muscle in the gastrointestinal tract. In fact, the intensity of the menstrual cramps and associated symptoms of nausea, vomiting, and diarrhea are directly proportional to the amount of PGF-2α released [1].
The treatment of primary dysmenorrhea is directed at blocking the production of prostaglandins with prostaglandin synthetase inhibitors (PGSI). PGSI inhibit cyclo-oxygenase (COX), the enzyme that converts arachidonic acid to endoperoxides. The endoperoxides are then converted to prostaglandins. Nonsteroidal anti-inflammatory drugs (NSAIDs), one class of PGSI, include medications such as ibuprofen, naproxen, and ketoprofen. NSAIDs have been shown to be significantly more effective for pain relief than placebo [2]. In addition to inhibiting endometrial prostaglandin production, NSAIDs have direct analgesic properties at the central nervous system level. Adverse effects of NSAIDs include gastrointestinal symptoms, central nervous system symptoms, hematologic abnormalities, bronchospasm, fluid retention, edema, and toxic effects on the liver and kidney. However, when a 3-day regimen is used in young and healthy women with primary dysmenorrhea, these adverse effects are rare. The fenamates, such as mefenamic acid, belong to a similar class of PGSI and have also been shown to be effective in relieving menstrual-associated pain (Table 56.1).
Table 56.1 Common PGSI used for treating dysmenorrhea
| Generic name | Trade name | Dosing |
| Naproxen sodium | Naprosyn | 250–500 mg every 6 hours |
| Ibuprofen | Motrin | 400–800 mg every 6–8 hours |
| Ketoprofen | Orudis | 25–200 mg every 6–8 hours |
| Mefenamic acid | Ponstel | 250–500 mg every 6–8 hours |
| Meclofenamate sodium | Meclamen | 100 mg every 8 hours |
Other effective treatments include oral contraceptives (OCPs), which prevent ovulation, decrease the production of prostaglandins, and decrease the flow during menstruation. A Cochrane analysis from 2001 gleaned data from four randomized controlled trials and concluded that combined OCPs with medium-dose estrogen and first-/second-generation progestogens were more effective than placebo in relieving primary dysmenorrhea [3]. The relief of pain and reduction in circulating prostaglandins, however, are only confined to the affected cycles; there is no carry-over effect after stopping the OCP.
Alternative pharmacologic treatments for primary dysmenorrhea include rose tea, fennel seeds, vitamin B6, vitamin E, and fish oil (omega-3 fatty acids), which have all been shown to be more effective than placebo in decreasing perceived menstrual pain [4-7].
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