Supplemental Digital Content is Available in the Text.A Central Sensitization Inventory cutoff of 40 had good sensitivity and specificity for identifying ≥3 central sensitivity syndromes and other pelvic pain-related comorbidities in endometriosis.

ObjectivePolycystic ovary syndrome (PCOS) is an endocrine disorder affecting approximately one in seven women who experience androgen excess, menstrual cycle irregularities, frequent anovulation and a tendency for central obesity and insulin resistance. Chronic subclinical inflammation is now recognised as being common in the context of PCOS, which led to the postulation that PCOS may fundamentally be an inflammatory process. This study aimed to: (1) evaluate serum C reactive protein (CRP)/albumin ratio as a potential predictive biomarker for PCOS; (2) compare the relationship between CRP/albumin and PCOS to variables classically associated with the syndrome.DesignCase–control study.SettingAdult obstetrics/gynaecology, endocrinology and outpatient clinics; university hospital in Bahrain.Participants200 premenopausal women with a diagnosis of PCOS, and 119 ethnically matched eumenorrheic premenopausal women.Main outcome measuresCRP/albumin ratio, anthropometric measures, insulin resistance, androgen excess.ResultsIndependent of body mass index (BMI), receiver operating characteristic curve for CRP/albumin ratio as a selective biomarker for PCOS was 0.865 (95% CI 0.824 to 0.905), which was more sensitive than CRP alone. Binary regression analysis showed that CRP/albumin ratio outperformed classical correlates, Free Androgen Index and insulin resistance, in predicting PCOS for every BMI category.ConclusionCRP/albumin ratio, a marker for inflammation related to metabolic dysfunction, was found to have a stronger association with PCOS than either androgen excess or insulin resistance. Inflammation is known to be influenced by adiposity, but relative to controls, women with PCOS have higher levels of CRP/albumin irrespective of BMI. These findings support the view that inflammation plays a central role in the pathophysiology of PCOS.

Introduction: Dyspareunia has been traditionally divided into superficial (introital) dyspareunia and deep dyspareunia (pain with deep penetration). While deep dyspareunia can co-exist with a variety of conditions, recent work in endometriosis has demonstrated that coexistence does not necessarily imply causation. Therefore, a reconsideration of the literature is required to clarify the pathophysiology of deep dyspareunia. Aims: To review the pathophysiology of deep dyspareunia, and to propose future research priorities. Methods: Narrative review after appraisal of published frameworks and literature search with the terms (dyspareunia AND endometriosis), (dyspareunia AND deep), (dyspareunia AND (pathophysiology OR etiology)). Main Outcome Variable: Deep dyspareunia (present/absent or along a pain severity scale). Results: Potential etiologies for deep dyspareunia include gynecological, urological, gastrointestinal, nervous system, psychological, and musculoskeletal system related. These etiologies can be classified according to anatomic mechanism (contact with a tender pouch of Douglas, uterus-cervix, bladder, or pelvic floor, with deep penetration). They can also be stratified into four categories (as previously proposed for endometriosis specifically), which can be utilized to personalize management: Type I (primarily gynecologic), Type II (nongynecologic comorbid conditions), Type III (central sensitization and genito-pelvic pain Page 1 of 49 penetration disorder), and Type IV (mixed). Sociocultural and genetic factors and sexual response may also be important for deep dyspareunia. Conclusion: We propose the following eight research priorities for deep dyspareunia: 1) development of deep dyspareunia measurement tools; 2) focus on the population who are avoiding intercourse due to deep dyspareunia; 3) clarification of the role of non-gynecologic comorbidities in the generation of deep dyspareunia; 4) addressing of ethnic and other sociocultural factors; 5) initiation of clinical trials with adequate power for deep dyspareunia outcomes; 6) inclusion of partner variables; 7) elucidation of pathways between psychological factors and deep dyspareunia; and 8) empirical validation of personalized approaches to deep dyspareunia.