Authors
Di Wu, Xiuying Chen, Xijun Zhu, Miaomiao Zhang
Published in
Molecular biology reports. Volume 53. Issue 1. Oct 25, 2026. Epub Oct 25, 2026.
Abstract
Primary dysmenorrhea (PD) affects 50-90% of women but remains understudied and inadequately managed. The conventional prostaglandin (PG)-centric model incompletely explains non-steroidal anti-inflammatory drug (NSAID) non-response-which is multifactorial and not mechanistically specific-and lowered pain thresholds outside menstruation. We propose the neuroendocrine-inflammatory framework (NEIF), a testable, hypothesis-generating framework rather than an established pathogenic cascade. NEIF views PD as multilayered: progesterone withdrawal and PG dysregulation; cytokine/NF-κB amplification; oxidative stress; peripheral sensitization; central plasticity; and genetic/epigenetic susceptibility. Evidence strength varies, from direct human and replicated genetic data to correlative, neuroimaging, or preclinical evidence. A speculative NOD-like receptor protein 3 (NLRP3) inflammasome-pyroptosis extension is not a core NEIF level or candidate endotype because direct human PD evidence is absent; it is an evidence-gated validation gap. Candidate biomarkers include menstrual-effluent oxylipins, serum nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF), neuroimaging intermediate phenotypes, and genetic variants; none is clinically qualified. NEIF yields three research-only candidate mechanistic endotypes-PG-predominant, inflammatory-oxidative, and neurogenic-central-not a clinical classification. It reframes PD as systemic and provides testable hypotheses while direct human NLRP3 validation remains desirable but not required for the core framework.
PMID:
42927550
Bibliographic data and abstract were imported from PubMed on 26 Oct 2026.
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