VASCULAR ENDOTHELIAL GROWTH-FACTOR (VEGF) IN ENDOMETRIOSIS

Angiogenesis is likely to be involved in the pathogenesis of endometri osis, According to the transplantation theory, when the exfoliated end ometrium is attached to the peritoneal layer the establishment of a ne w blood supply is essential for the survival of the endometrial implan t and development of endometriosis, From the known angiogenic factors, vascular endothelial growth factor (VEGF) has emerged as a pivotally important regulator of normal angiogenesis and pathological neovascula rization, The VEGF protein was evaluated immunohistochemically in the eutopic endometrium of 10 women without endometriosis (group I) at lap aroscopy and the eutopic endometrium and peritoneal endometriotic lesi ons of 43 women with endometriosis (group II). VEGF histological score s were 9.7 +/- 4.3 and 4.0 +/- 2.6 respectively in the epithelium and stroma of the eutopic endometrium of group I women, and 10.3 +/- 2.3 a nd 3.6 +/- 2.3 respectively in women of group II. In red lesions, the VEGF scores were 11.1 +/- 3.0 in the epithelium and 5.1 +/- 3.0 in the stroma, and in black lesions were 8.6 +/- 2.7 and 1.6 +/- 1.6, respec tively. Significantly lower;values were observed in black lesions as c ompared with eutopic endometrium and red lesions, the values of which were similar. Scores were also evaluated according to the phase of the cycle. In eutopic as well as ectopic endometrium, no significant cycl ic variations were observed throughout the cycle. However, VEGF conten t was found to be higher in the eutopic glandular epithelium of women with endometriosis during the late secretory phase, possibly suggestin g a more likely tendency to implant. In contrast, significantly higher VEGF content was noted in red lesions as compared with black lesions, During all phases of the cycle, the VEGF content in stromal cells of red lesions was higher than in black lesions. Similarities in VEGF con tent were observed in the glandular epithelium of the eutopic endometr ium of women with endometriosis and red lesions, suggesting that endom etriosis probably arises from the peritoneal seeding of viable endomet rial cells during retrograde menstruation and that red lesions can be considered as the first stage of implantation. After the attachment ph ase, the high VEGF levels could provoke an increase in the subperitone al vascular network and facilitate implantation and viability in the r etroperitoneal space. Lower VEGF levels in black lesions explain the d ecrease in both stromal vascularization, followed by fibrosis and inac tivation of the implant.