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Objective The use of GnRH agonists instead of hCG to trigger ovulation seems to be an effective way to prevent subsequent hCG induced ovarian hyperstimulation in cases of polyfollicular development. But conflicting results are reported on the efficiency of subsequent luteal support using hCG and/or progesterone supplementation. Study design We investigated the efficiency and safety of different luteal support regimes in low dose gonadotropin stimulation non-ivf cycles. A risk for an imminent ovarian hyperstimulation was assumed if preovulatory estradiol levels rose up higher than 700 pg/ml and more than 12 intermediate sized follicles (8–14 mm) were observed. Thirty-six women received 0.5 mg Triptorelin subcutaneously to trigger the ovulation inducing LH surge. After randomization, luteal support regimes started on day 2 after the Triptorelin administration with injections every second day five times in all. Group (a) received 5 × 1000 IU hCG, group (b) received 5 × 500 IU hCG, and group (c) received 5 × 250 mg progesterone, intramuscularly. The monitoring of the ovulation period and the subsequent luteal phase included sonographic measurement of ovarian diameter and estimation of LH, FSH, estradiol and progesterone levels 10 and 34 h as well as 8 days after Triptorelin administration. Results We could prove ovulation in all women and did not find symptoms of ovarian hyperstimulation in any case. Midluteal controls showed extremely low gonadotropins in all groups indicating a long lasting pituitary down regulation after one injection of 0.5 mg Triptorelin. We found high normal sex steroid levels in both hCG groups. The progesterone group displayed a marked luteal phase defect with low levels of progesterone and estradiol in all cases. Conclusion The use of GnRH agonist in cases of polyfollicular development is capable to induce ovulation without a subsequent ovarian enlargement and/or any sign of hyperstimulation syndrome. Luteal support by low dose hCG does not counteract the benefit of GnRH agonist in preventing an ovarian hyperstimulation syndrome, but seems to remedy at least in part the possible deleterious effects of GnRH agonists on luteal functionality.