Clinical diagnostic criteria for premenstrual syndrome and guidelines for their quantification for research studies.

Premenstrual syndrome (PMS) encompasses a variety of symptoms appearing during the luteal phase of the menstrual cycle. Although PMS is widely recognized, the etiology remains unclear and it lacks definitive, universally accepted diagnostic criteria. To address these issues an international multidisciplinary group of experts evaluated the current definitions and diagnostic criteria of PMS and premenstrual dysphoric disorder (PMDD). Following extensive correspondence, a consensus meeting was held with the aim of producing updated diagnostic criteria for PMS and guidelines for clinical and research applications. This report presents the conclusions and recommendations of the group. It is hoped that the criteria proposed by the group will become widely accepted and eventually be incorporated into the next edition of the World Health Organization's International Classification of Diseases (ICD-11). It is also hoped that the proposed guidelines for quantification of criteria will be used by clinicians and investigators to facilitate diagnostic uniformity in the field as well as adequate treatment modalities when warranted.

Human epicardial adipose tissue is a source of inflammatory mediators.

BACKGROUND: Inflammatory mediators that originate in vascular and extravascular tissues promote coronary lesion formation. Adipose tissue may function as an endocrine organ that contributes to an inflammatory burden in patients at risk of cardiovascular complications. In this study, we sought to compare expression of inflammatory mediators in epicardial and subcutaneous adipose stores in patients with critical CAD. METHODS AND RESULTS: Paired samples of epicardial and subcutaneous adipose tissues were harvested at the outset of elective CABG surgery (n=42; age 65+/-10 years). Local expression of chemokine (monocyte chemotactic protein [MCP]-1) and inflammatory cytokines (interleukin [IL]-1beta, IL-6, and tumor necrosis factor [TNF]-alpha) was analyzed by TaqMan real-time reverse transcription-polymerase chain reaction (mRNA) and by ELISA (protein release over 3 hours). Significantly higher levels of IL-1beta, IL-6, MCP-1, and TNF-alpha mRNA and protein were observed in epicardial adipose stores. Proinflammatory properties of epicardial adipose tissue were noted irrespective of clinical variables (diabetes, body mass index, and chronic use of statins or ACE inhibitors/angiotensin II receptor blockers) or plasma concentrations of circulating biomarkers. In a subset of samples (n=11), global gene expression was explored by DNA microarray hybridization and confirmed the presence of a broad inflammatory reaction in epicardial adipose tissue in patients with coronary artery disease. The above findings were paralleled by the presence of inflammatory cell infiltrates in epicardial adipose stores. CONCLUSIONS: Epicardial adipose tissue is a source of several inflammatory mediators in high-risk cardiac patients. Plasma inflammatory biomarkers may not adequately reflect local tissue inflammation. Current therapies do not appear to eliminate local inflammatory signals in epicardial adipose tissue.