ReviewFrontiers in endocrinology2026
Re-assessment of the therapeutic LH window in normogonadotropic IVF patients.
Review in Frontiers in endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Previous research has proposed a luteinizing hormone (LH) threshold and ceiling level, below which oestradiol production is not adequate and above which LH may be detrimental to follicular development. This therapeutic LH window was mainly supported by clinical research in anovulatory patients but observations in normogonadotropic women were controversial. Materials and methods: A literature narrative review from 1985 through 2025. Studies evaluated included i) preclinical studies using Results: In rodents, small amounts of LH/hCG support FSH-induced multiple follicular development in absence of endogenous gonadotropins, while too high LH/hCG exposure consistently induced follicular atresia. In women treatment with too high doses of GnRH agonist or antagonist resulted in undetectable serum LH (well below 1 IU/L), impaired follicular growth, low rises of serum oestradiol, early miscarriage and reduced chance of pregnancy. Too profound suppression was observed in patients treated with a long GnRH agonist protocol, but the incidence depends on the specific agonist, dose and route of administration. Most women treated with the GnRH antagonist protocol, without other pituitary-suppression, remain within the therapeutic LH window (endogenous LH 1-10 IU/L) during the whole stimulation period. In contrast, too much LH/hCG supplementation can compromise clinical outcome, as confirmed in IVF patients treated with r-FSH and a potent r-hCG in a long GnRH agonist protocol. This r-hCG in daily doses of 1 µg or more inhibited the growth of medium-sized follicles which phenomenon has previously also observed in IVF patients treated with u-hCG and in PCOS patients treated with r-LH during ovulation induction. Discussion: Whether commercial combination gonadotropins have inhibitory effects on multiple follicular development is difficult to judge and may depend on the protocol, dose of FSH, dose of LH/hCG, number of treatment days and the potency of the specific LH/hCG preparation. It is concluded that normogonadotropic IVF patients undergoing OS have a clearly defined therapeutic LH window below and above which clinical outcome is compromised.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.