luteal GnRH antagonist severe early OHSS treatment, ganirelix luteal phase ovarian hyperstimulation syndrome, OHSS management GnRH antagonist live birth rates, Lainas luteal antagonist OHSS pregnancy outcomes, severe early OHSS outpatient management without hospitalization, GnRH antagonist peri-implantation period IVF safety, OHSS-free clinic tertiary prevention strategy, polycystic ovaries high risk OHSS IVF fresh transfer, prospective cohort OHSS antagonist neonatal outcomes, ovarian hyperstimulation syndrome regression luteal antagonist
PMID 5536562 5536562
Cite this article
Hack, M., Brish, M., Serr, D. M., Insler, V., & Lunenfeld, B. (1970). Outcome of pregnancy after induced ovulation. Follow-up of pregnancies and children born after gonadotropin therapy. JAMA, 211(5), 791-797.
Hack M, Brish M, Serr DM, Insler V, Lunenfeld B. Outcome of pregnancy after induced ovulation. Follow-up of pregnancies and children born after gonadotropin therapy. JAMA. 1970;211(5):791-797.
Hack, M., et al. "Outcome of pregnancy after induced ovulation. Follow-up of pregnancies and children born after gonadotropin therapy." JAMA, vol. 211, no. 5, 1970, pp. 791-797.
Infertility affects 1 in 6 people globally (and up to a third of physicians) and is recognized by the World Health Organization and the American Medical Association as a disease. Since 1978, the development of assisted reproductive technology (ART), which is defined as fertility treatments in which gametes or embryos are handled in vitro, has made it possible to overcome otherwise insurmountable barriers to conception and has led to the birth of more than 10 million children worldwide.
EndometriosisOvarian Cancer RiskLong-term Health Outcomes
Endometriosis has been associated with an increased risk of ovarian cancer; however, the associations between endometriosis subtypes and ovarian cancer histotypes have not been well-described. To evaluate the associations of endometriosis subtypes with incidence of ovarian cancer, both overall and by histotype. DESIGN, SETTING, Population-based cohort study using data from the Utah Population Database. The cohort was assembled by matching 78 893 women with endometriosis in a 1:5 ratio to women without endometriosis. Endometriosis cases were identified via electronic health records and categorized as superficial endometriosis, ovarian endometriomas, deep infiltrating endometriosis, or other. Estimated adjusted hazard ratios (aHRs), adjusted risk differences (aRDs) per 10 000 women, and 95% CIs for overall ovarian cancer, type I ovarian cancer, and type II ovarian cancer comparing women with each type of endometriosis with women without endometriosis. Models accounted for sociodemographic factors, reproductive history, and past gynecologic operations. In this Utah-based cohort, the mean (SD) age at first endometriosis diagnosis was 36 (10) years. There were 597 women with ovarian cancer. Ovarian cancer risk was higher among women with endometriosis compared with women without endometriosis (aHR, 4.20 [95% CI, 3.59-4.91]; aRD, 9.90 [95% CI, 7.22-12.57]), and risk of type I ovarian cancer was especially high (aHR, 7.48 [95% CI, 5.80-9.65]; aRD, 7.53 [95% CI, 5.46-9.61]). Ovarian cancer risk was highest in women with deep infiltrating endometriosis and/or ovarian endometriomas for all ovarian cancers (aHR, 9.66 [95% CI, 7.77-12.00]; aRD, 26.71 [95% CI, 20.01-33.41]), type I ovarian cancer (aHR, 18.96 [95% CI, 13.78-26.08]; aRD, 19.57 [95% CI, 13.80-25.35]), and type II ovarian cancer (aHR, 3.72 [95% CI, 2.31-5.98]; aRD, 2.42 [95% CI, -0.01 to 4.85]). Ovarian cancer risk was markedly increased among women with ovarian endometriomas and/or deep infiltrating endometriosis. This population may benefit from counseling regarding ovarian cancer risk and prevention and could be an important population for targeted screening and prevention studies.