The Role of Prostaglandins in Primary Dysmenorrhea and the Effectiveness of Anti-Inflammatory Therapy

Primary dysmenorrhea is a recurrent menstrual pain syndrome occurring in the absence of identifiable pelvic pathology. Its most accepted pathophysiological model centers on increased endometrial production of prostaglandin F2α and prostaglandin E2 during menstruation. These mediators intensify uterine contractions, increase intrauterine pressure, reduce uterine blood flow, induce ischemia, and sensitize pain pathways. This article reviews the biological role of prostaglandins, the clinical rationale for NSAID therapy, timing and safety considerations, real-world effectiveness, pharmacovigilance, artificial intelligence, and personalized treatment strategies. The evidence synthesis shows that anti-inflammatory therapy is pathogenetically justified when primary dysmenorrhea is prostaglandin-dominant. However, treatment success depends on early initiation, correct dosing, patient education, safety screening, and reassessment when response is inadequate. Real-world data and AI-based analytics may help identify patients with poor response, detect adverse drug reaction signals, and improve clinical decision support. The article also discusses how Uzbekistan’s developing e-prescription and digital health systems may support safer NSAID use and national evidence generation. A central conclusion is that NSAID therapy should not be evaluated only as a drug effect, but as a complete clinical strategy that includes diagnosis, timing, adherence, contraindication screening, follow-up, and referral criteria. When this strategy is implemented correctly, prostaglandin inhibition remains a rational first-line approach. When it fails, clinicians should consider secondary dysmenorrhea, central sensitization, inadequate exposure, or non-prostaglandin mechanisms rather than repeating empirical analgesic escalation.