DYSMENORRHEA: CLINICAL MANIFESTATIONS, PATHOGENESIS AND CONTEMPORARY TREATMENT STRATEGIES
This review analyzes dysmenorrhea's clinical features, prostaglandin-driven pathogenesis, and contemporary treatments, emphasizing a combined approach of pathophysiological reasoning, real-world evidence, and artificial intelligence for improved care.
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This IMRAD-based analytical review synthesizes dysmenorrhea evidence from PubMed-indexed reviews, Cochrane sources, WHO menstrual health materials, ACOG/ESHRE guidance, and regulatory sources (FDA/EMA) to summarize clinical phenotypes, prostaglandin-centered pathogenesis, differential diagnosis, and contemporary treatment strategies, with an implementation perspective for Uzbekistan. It finds that primary dysmenorrhea is mainly driven by increased endometrial production of prostaglandin F2α and prostaglandin E2, leading to myometrial hypercontractility, vasoconstriction, ischemia, and pain, while secondary dysmenorrhea requires evaluation for conditions including endometriosis and adenomyosis. A major caveat is that the paper is an analytical narrative review that synthesizes existing guidance and evidence rather than reporting new primary studies. Relevance to endometriosis: the paper explicitly frames secondary dysmenorrhea evaluation around endometriosis and cites ACOG guidance on dysmenorrhea and endometriosis in adolescents, though its main focus is dysmenorrhea pathogenesis and management strategies broadly, including when secondary causes are suspected.
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