Aim: This study aims to assess the impacts of various trigger day progesterone (P) and luteinizing hormone (LH) levels on live birth rates (LBRs) in fresh in vitro fertilization (IVF) cycles, considering their elevation from stimulation and premature luteinization.
Methods: This retrospective cohort study included the first ovarian stimulation cycles with GnRH antagonist protocol of 1253 patients who underwent intracytoplasmic sperm injection and fresh embryo transfer at a tertiary clinic's IVF center between 2010 and 2016. Participants were divided into four groups based on trigger day serum P and LH levels, using the 90th percentile thresholds for P (1.7 ng/mL) and LH (5.2 IU/L). The primary outcome measure was LBR.
Results: The LBRs observed in the respective groups were as follows: P < 1.7 ng/mL and LH <5.2 IU/L (21.3%, 214/1005); P < 1.7 ng/mL and LH ≥5.2 IU/L (19.1%, 22/115); P ≥ 1.7 ng/mL and LH <5.2 IU/L (19.3%, 23/119); and P ≥ 1.7 ng/mL and LH ≥5.2 IU/L (28.6%, 4/14). There were no statistically significant differences between the groups (p = 0.782). Additionally, a multivariate generalized additive model, adjusted for female age, body mass index, infertility duration, number of embryos transferred, and embryo transfer day, found that the interaction between LH and P levels did not significantly predict LBRs (p = 0.533). However, univariate analysis identified an optimal trigger day P range between 0.58 and 1.69 ng/mL for achieving higher LBRs, demonstrating a non-linear relationship. Furthermore, total FSH and LH dosages during stimulation had a statistically significant combined effect on trigger day P levels (p = <0.001), with the addition of LH leading to lower P levels compared to cycles stimulated with recombinant FSH alone.
Conclusions: The relationship and interaction between trigger day LH and P levels do not significantly influence LBRs, as variations in LH do not alter the effect of P, suggesting that the impact of P elevation on LBRs is independent of its cause, whether from ovarian stimulation or premature luteinization.
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http://dx.doi.org/10.1111/jog.16181 | DOI Listing |
Front Endocrinol (Lausanne)
January 2025
Department of Reproductive Health and Infertility, Zigong Maternal and Child Health Hospital, Zigong, Sichuan, China.
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Department of Obstetrics and Gynecology, Health Sciences University, Tepecik Education and Research Hospital, Izmir, Turkey.
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Methods: This retrospective cohort study included the first ovarian stimulation cycles with GnRH antagonist protocol of 1253 patients who underwent intracytoplasmic sperm injection and fresh embryo transfer at a tertiary clinic's IVF center between 2010 and 2016. Participants were divided into four groups based on trigger day serum P and LH levels, using the 90th percentile thresholds for P (1.
Glia
January 2025
Kentucky Spinal Cord Injury Research Center, University of Louisville, School of Medicine, Louisville, Kentucky, USA.
Cellular stressors inhibit general protein synthesis while upregulating stress response transcripts and/or proteins. Phosphorylation of the translation factor eIF2α by one of the several stress-activated kinases is a trigger for such signaling, known as the integrated stress response (ISR). The ISR regulates cell survival and function under stress.
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