An excess of DRD2 polymorphism 2 was found in exon 7 in women with peritoneal moderate/severe endometriosis. The presence of polymorphism 2 could cause a defect in a post-receptor
signaling mechanism, resulting in a mild increase in serum prolactin levels. Thus, the potential angiogenic role of prolactin may play a role in the implantation of ectopic endometriosis tissue.

Dopamine receptor agonist Quinagolide induced a 69.5% reduction in the size of the lesions, with 35% vanishing completely. Histologic analysis showed tissue degeneration, which was supported by down-regulation of VEGF/VEGFR2, three proangiogenic cytokines (CCL2, RUNX1, and AGGF1) and plasminogen activator inhibitor (PAI) 1, a potent inhibitor of fibrinolysis in the L2 lesions.

By interfering with angiogenesis, enhancing fibrinolysis, and reducing inflammation, quinagolide reduces or eliminates peritoneal endometriotic lesions in women with endometriosis.

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