B ACKGROUND
To evaluate the effect of triggering ovulation by inducing with GnRH-a versus hCG for IUI cycles.
O BJECTIVES
• Prospective randomized control trial
• Infertility subjects in Vietnam undergoing IUI after either a natural cycle or stimulated cycles with hMG were randomly assigned to receive ovulation triggering by hCG or GnRH agonist.
• Insemination was performed 36 hours after ovulation trigger followed by 200mg vaginal progesterone in both groups.
• Statistical analysis was performed using SPSS. Data was nonparametric and baseline comparisons were made with the Mann-Whitney U test.
• Clinical pregnancy rates were calculated by Chi square tests. Both logistic regression and GEE models were utilized to account for potential confounders, which can occur despite randomization, and to estimate mean effect sizes.
M ATERIALS & M ETHODS
R ESULTS
C ONCLUSIONS
• Ovulation trigger with hCG is associated with significantly increased clinical pregnancy rates in patients undergoing ovulation induction with IUI in comparison to GnRH agonist trigger.
• Given the low risk of OHSS in patients undergoing ovulation induction, hCG trigger is more beneficial for pregnancy outcomes in ovulation induction cycles.
Minh Tam Le
1, D.N. Nguyen
1, J.R.Zolton
2, N.T. Cao
1, V.Q.H. Nguyen
1, Q.V. Truong
1, A.H. DeCherney
2, M.J. Hill, DO
21Hue University of Medicine and Pharmacy, Hue, Vietnam 2Eunice Kennedy Shriver National Institute of Child Health and Human Development, NIH, Bethesda, MD
GnRH agonist versus hCG trigger in ovulation induction with intrauterine insemination:
a randomized controlled trial
Variable hCG GnRH agonist P value
Age (years) 35 (28-41) 30 (29-36) 0.58
BMI (kg/m
2) 22 (18.8-24.5) 20.8 (19.8-21.8) 0.34
AMH 4.2 (0.7-12.5) 5.6 (3.8-10.6) 0.57
Male-factor
infertility 80% 78% 0.85
Tubal factor 7% 5% 0.75
Ovulatory disorder 47% 42% 0.27
Endometriosis 5% 5% 1
PCOS 36% 33% 0.63
DOR 12% 16% 0.43
Unexplained 17% 14% 0.67
Table 1 Patient demographics
• 90 subjects were randomized to hCG trigger and 79 to GnRH-a. Patient demographics and stimulation characteristics were similar (Tables 1
& 2).
• Clinical pregnancy rate (Table 2) was higher in the hCG trigger group (30.0%) versus the GnRH agonist trigger group (13.9%) (P=0.01; OR 0.37 95% CI =0.17- 0.84). Adjusting for age, AMH, and hMG use, the GEE estimation of the mean pregnancy rate was 32.0% versus 10.8%
(P =0.02).
• In regression models adjusting for the same confounders, the unadjusted likelihood of pregnancy was decreased with GnRH agonist (OR 0.37, 95% CI 0.17-0.82, P=0.01), similar to the adjusted model (OR 0.27, 95%CI 0.09-0.81, P=0.02).
The use of gonadotropin-releasing hormone agonists (GnRH-a) versus human chorionic gonadotropin (hCG) for ovulation induction may be another choice for triggering and may decrease the risk of ovarian hyperstimulation syndrome. The endogenous LH surge by GnRH-a may also more closely mimic natural conditions. However, GnRH-a may result in pituitary down-regulation, inadequate corpus luteum function, and subsequently progesterone deficiency in the luteal phase.
Variable hCG GnRH agonist P value
hMG cycles 18% 28% 0.14
Endometrial
thickness (mm) 8 (6.7-7.9) 8 (6.7-9) 0.15 hMG (IU) 225 (187-600) 300 (225-450) 0.67 Clinical pregnancy
(unadjusted) 30.0% 13.9% 0.01
Clinical pregnancy
(adjusted)* 32.0% 10.8% 0.02
Table 2: Stimulation characteristics and outcome
*Adusted for age, AMH, and hMG use
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