
pmid: 17060018
Primary dysmenorrhea or painful menses without identifiable pathology is the most common gynecologic complaint among adolescent females. Sixty to seventy percent of young women report painful periods and 15% of them report an interruption in daily activity due to menstrual pain. Dysmenorrhea is the leading cause of school absenteeism among this population. Painful menses typically presents in the adolescent years about 6-12 months after menarche or when regular ovulatory cycles are established. Symptoms may last up to 72 hours and may include nausea vomiting diarrhea headache fatigue dizziness and syncope as well as cramping. Although dysmenorrhea is frequent problem among adolescents many do not seek help from health care providers. The most common classic explanation for menstrual cramping is the overproduction of prostaglandins (PG) within the endometrium. PGs are inflammatory modulators known to cause myometrial contractions and vasoconstriction. Locally PGs incite uterine contractions and ischemia leading to the cramping pain classic of dysmenorrhea. Through systemic circulation PGs can reach other end organs causing nausea vomiting bloating and headaches. The biochemical production of PGs is directly related to an ovulatory menstrual cycle. Prior to each ovulatory cycle as progesterone is withdrawn arachidonic acid an omega-6 fatty acid is released from endometrial cell wall phospholipids. Free arachidonic acid then sets into motion the cyclo-oxygenase (COX) and lipooxygenase inflammatory cascades that lead to the production of PGs and leukotrienes. Women with dysmenorrhea often have higher levels of PGs in their menstrual fluid when compared to their pain-free counterparts. (excerpt)
Complementary Therapies, Dysmenorrhea, Anti-Inflammatory Agents, Non-Steroidal, Humans, Female
Complementary Therapies, Dysmenorrhea, Anti-Inflammatory Agents, Non-Steroidal, Humans, Female
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