ptin levels were significantly higher in infertile women with endo metriosis than in patients with pelvic pain and endometri osis or unexplained infertility. Nevertheless, PF leptin levels were inversely correlated with the stage of disease, which could explain our result. PF leptin levels in patients with OE are elevated due to peritoneal endometriotic lesions or OE, the cause is presently unknown. One report showed that patients with superficial endometriomas had significantly higher levels of leptin in the PF than did patients with deep OEs. Another report found that patients with PI at all stages of endometriosis showed higher PF leptin concentrations than patients with no implant, and the presence of OE had no significant main effect on leptin concentration, however, isolated ovarian endometriosis is rare, as it is considered a marker for severe, deeply infiltrating endo metriosis.

Furthermore, many endometriotic lesions, especially diaphragmatic and bowel lesions or atypical, non pigmented PI, may not be visualized during surgery. It is thus extremely difficult to exclude this variable. Thus, peritoneal disease, but not ovarian endometriotic cysts, influences the concentration of leptin in PF in endometriosis, these two types of endometrial lesions selleckchem may have different pathogenic mechanisms and distinct leptin biosynthetic capacities. Alternatively, the leptin may be sequestered into the cystic fluid of the OE. We found increased levels of leptin in the EF compared to the PF of patients with both PI and OE, these variables were not correlated with each other.

The increased levels of lep tin in the EF may be the result of the slight decrease in leptin expression in ovarian tissue affected selleck chemical by endome trioma, this protein may have been secreted into the endo metrioma and diffused in the chocolate fluid. In accordance with previous data, we believe that the concentration of leptin in the PF is influenced by PI, we also suggest that OEs influence leptin concentration in the EF. Our findings show a strong positive correlation be tween the expression of leptin and OBR in OE and PI. A significant positive correlation was observed between leptin and OB RL transcripts in ectopic endometria. Although the difference was not statistically signifi cant, previous data showed a modest positive correlation between the expression of leptin and that of OBR in pa tients with OEs.

Furthermore, these same authors demonstrated that leptin treatment induced OBR ex pression in endometriotic cells. We also demonstrated a significant positive correlation between PF leptin levels and the expression of leptin and OBR in PI, but this cor relation was not observed in OE. In contrast, the expres sion of leptin and its receptor in OE correlated strongly and positively with leptin