# Impact of pre-treatment in GnRH-antagonist cycles triggered with GnRH agonist on reproductive outcomes

## TL;DR

Using GnRH agonist as pre-treatment in certain IVF cycles increases the risk of poor oocyte maturation response.

## Contribution

This study identifies that GnRH agonist pre-treatment in GnRH antagonist cycles with agonist triggering is linked to suboptimal reproductive outcomes.

## Key findings

- Pre-treatment with GnRH agonist significantly increased suboptimal maturation response in IVF cycles.
- Basal and pre-trigger LH levels were significantly lower in the pre-treated group.
- Multivariate analysis confirmed GnRH agonist pre-treatment as a significant predictor of suboptimal response.

## Abstract

Pre-treatment (PT) therapies in IVF are known to be used as pre-stimulation
modality to improve cycle outcomes. This study aims to assess whether PT in
GnRH antagonist cycles triggered with GnRH-agonist impact oocyte maturation
response.

Data were retrospectively collected for patients who underwent GnRH
antagonist cycle with agonist triggering with and without PT. The patients
were allocated to groups according to their PT status. The primary outcome
evaluated was suboptimal maturation response. Suboptimal maturation to
trigger was defined as no oocyte upon retrieval when adequate response was
expected.

The study population included 196 patients who underwent GnRH antagonist
cycle with agonist triggering. The study group included 69 patients who
received PT. The control group included 127 patients with no PT. In
univariate analysis, the PT group significantly displayed suboptimal
response compared to the controls (p = 0.008). All the
patients in the study group with suboptimal response (with or without hCG
re-triggering) were treated with GnRH-agonist as PT. Basal and pre-trigger
LH values were significantly lower in the study group compared to controls
(p < 0.001). Multivariate regression analysis
revealed that PT with GnRH agonist was a significant predictor for
suboptimal response.

Pre-treatment, and particularly the use of GnRH-agonist as PT in antagonist
cycles triggered with agonist, increases the risk of suboptimal response to
GnRH-agonist trigger. This might be explained by prolonged pituitary
suppression, which lasts beyond the PT cessation.