Pain Mechanisms in Peritoneal Diseases Might Be Partially Regulated by Estrogen

To identify factors influencing the differential pain pathogenesis in peritoneal endometriosis (pEM) and peritoneal carcinomatosisin ovarian cancer (pOC), we undertook an experimental study. Tissue samples of 18 patients with pEM, 15 patients with pOC, and15 unaffected peritoneums as controls were collected during laparoscopy or laparotomy. Immunohistochemical stainings wereconducted to identify nerve fibers and neurotrophins in the tissue samples. Additionally, 23 pEM fluids, 25 pOC ascites fluids, and20 peritoneal fluids of patients with myoma uteri as controls were collected. In these fluids, the expression of neurotrophins wasevaluated. The effects of peritoneal fluids and ascites on the neurite outgrowth of chicken sensory ganglia were estimated by usinga neuronal growth assay. An electrochemiluminescence immunoassay was carried out to determine the expression of estrogen inthe peritoneal fluids and ascites. The total and sensory nerve fiber density was significantly higher in pEM than in pOC (P < .001 andP < .01). All neurotrophins tested were present in tissue and fluid samples of pEM and pOC. Furthermore, the neurotrophicproperties of pEM and pOC fluids were demonstrated, leading to sensory nerve fiber outgrowth. Estrogen concentration in theperitoneal fluids of pEM was significantly higher compared to ascites of pOC (P < .001). The total and sensory nerve fiber densityin the tissue samples as well as the estrogen expression in the peritoneal fluid of pEM was considerably higher than that in pOC,representing the most notable difference found in both diseases. This might explain the differential pain perception in pEM andpOC. Therefore, estrogen might be a key factor in influencing the genesis of pain in endometriosis.