Objective. The aim of this study was to investigate whether platelet indices-mean platelet volume (MPV), platelet distribution width (PDW), and plateletcrit (PCT) would be useful as noninvasive biomarkers for determining the severity of endometriosis. Methods. A retrospective review of the medical charts of 164 patients diagnosed with endometriosis and who were operated on between 2001 and 2013 was performed. The stage of endometriosis was determined according to revised American Society for Reproductive Medicine criteria. Results. In patients with advanced endometriosis (Stages 3-4), PLT, PCT levels were found to be significantly higher and MPV, PDW values to be significantly lower when compared to initial endometriosis (Stages 1-2). In addition, there was a significant positive correlation between PLT (r: 0.800, P: 0.001) and PCT (r: 0.727, P: 0.002) and the inflammatory marker white blood cell count (WBC). Conclusion. Our finding may not sufficient for employing platelet indices solely in this differential diagnosis, but our finding could provide a suggestion for clinical physicians so that attention is paid to the value of platelet indices and that these may be taken into account when making decisions about the initial or advanced stages of endometriosis. 1. Introduction Endometriosis is one of the most important benign chronic diseases affecting 6–10% of women of reproductive age, being mainly associated with pelvic pain, adhesion formation, and infertility. Endometriosis is characterized by the ectopic presence of endometrial stroma and epithelium [1, 2]. It can be classified into four stages: minimal, mild, moderate, and severe [3]. More advanced endometriosis can be deeply invasive or can present as ovarian endometriotic cysts (endometrioma) [4]. Many theories have been set forth about endometriosis. The implantation theory of Sampson, the coelomic metaplasia theory of Mayer, and the theory of induction constitute the three classic theories that attempt to explain the origin of endometriosis [5, 6]. However, classic theories have failed to establish a definitive pathogenetic mechanism for endometriosis. Recent studies addressing the matter of genetic predisposition have reported that genetic abnormalities may contribute to the development of endometriosis [7]. Besides genetics, growing evidence indicates the significant role played by immunological and inflammatory factors in the development of endometriosis [8]. In particular, chronic pelvic inflammation is a hallmark of endometriosis pathophysiology and thus inflammation is a factor that
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