Endostatin inhibits the growth of endometriotic lesions but does not affect fertility

Objective: To determine whether endometriosis can be treated with angiogenesis inhibitor endostatin and the effect of this treatment on fertility and reporduction. Design: Pharmacological intervention in a surgically induced model of endometriosis and female mice undergoing mating. Setting: Animal research facility. Animal(s): Eight-week-old, female C57BL/6 and SCID mice. Intervention(s): After implantation of autologous endometrium, mice received endostatin or the vehicle-matched control for 4 weeks. For the reproductive function study, mice receive endostatin or vehicle were matedand reproductive functions were observed. Main Outcome Measure(s): Growth of endometriotric lesions after 4 weeks of treatment, estrous cycling, corpusluteum formation, serum hormone levels, and mating time as fertility meaures; and pregnancy, fetal vitality, number , and outcome of litter as reproductive measures. Result(s): Endostatin suppressed the growth of endometriotic lesions by 47% compared with controls. Estrous cycling and corpus luteum formation were normal in both groups. Female mice recieving endostatin were as fertile as mice recieving vehicle, had normal pregnancies, and delivered the same number of pups. The offspring were healthy without teratogenic stigmata and reproduced normally themselves. Conclusion(s): Antiangiogenic therapy with endostatin may present a promising novel, nontoxic therapeutic option for patients with endometriosis.