“…As stated before, GH adjuvant therapy was clinically widely used in poor ovarian responders (7, 8, 10, 11, 14, 16, 19, 60–63, 67–76), poor quality of embryos (16, 17, 67, 70, 74, 77), improper endometrial reaction (5, 12, 56, 78, 79) and repeated implantation failure (1, 63, 80–82). When it is used in patients with repeat implantation failure which is defined as failure of pregnancy despite implantation of a high-quality embryo at least three times or of over 10 embryos on repeat implantation failure (1, 63, 80–82), the mechanism of this action is, as stated before, related to GH stimulating proliferation and differentiation of granulosa cells, increasing production of estradiol in both early and late follicular development for animal and human ovaries, enhancing effect of FSH on the development of ovarian follicles and improving endometrial thickness (82, 98–100). A recent randomized controlled clinical trial performed in China of GH co-treatment on controlled ovarian stimulation in normal ovarian response women showed significantly ( P < 0.05) higher two pronuclei rate (33.92 vs. 30.92%) and higher quality embryo rate (63.4 vs. 59.33%) besides significantly increased number of embryos available (3.79 ± 2.74 vs. 2.90 ± 2.12, P < 0.001) and higher endometrial thickness on hCG day (11.96 ± 2.24 vs. 11.62 ± 2.81, P = 0.036) in 781 patients receiving GH of 1IU/4IU administered daily since day two of the previous cycle or day two in accordance with controlled ovarian stimulation until hCG trigger in comparison with the control group without GH adjuvant therapy (79).…”