
Antonio La Marca's lecture answers why luteinising hormone matters already in early folliculogenesis — and does so through two boundary scenarios: hypogonadotropic hypogonadism and polycystic ovarian morphology. Extreme cases make the central mechanism visible: where LH is virtually absent, a healthy follicle does not form.
The starting point is the two-cell, two-gonadotropin theory. LH acts on theca cells to drive androgen synthesis, which granulosa cells convert to estradiol under FSH. Hence the lecture's headline claim: "Without LH, you will never have a healthy ovarian follicle." In young patients with hypogonadotropic hypogonadism — low FSH and LH — stimulation with FSH alone produces no follicular growth, and nothing can be achieved without exogenous LH.
Mechanistically, the early need for LH reflects that theca cells carry LH receptors from the early antral stage and supply the androgen substrate for aromatisation in the granulosa. When that substrate is scarce — because of low LH or reduced receptor sensitivity — the follicle grows suboptimally, and oocyte quality suffers. In older patients and hypo-responders this deficit appears earlier and more strongly, which is precisely why they benefit from extended LH administration.
The two chosen scenarios are opposite in gonadotropic background, yet both highlight LH. In hypogonadotropic hypogonadism, LH deficiency leaves the follicle unable to grow without external support; in polycystic morphology, excessive and chaotic LH signalling disrupts dominant-follicle selection. Contrasting the extremes reveals the fine balance we imitate in a stimulation protocol.
The central theme is Extended LH Administration (ELA); the speaker presented two research lines. In the clinical case discussed, a patient with functional hypothalamic amenorrhea showed a rise in AMH from 0.4 to 1.6 ng/mL over 35 days of LH administration — an illustration that LH influences not only the final stages but the pool of growing follicles.
Multicentre trial data showed that the ELA protocol yields over 20% additional oocytes. The practical message is addressed above all to hypo-responders and patients of advanced reproductive age, in whom an adequate LH level and sensitivity to it become decisive for a proper response and oocyte quality.
The lecture shifts the emphasis from viewing LH as a "trigger hormone" to understanding its role across the whole of stimulation — from early follicle activation to final maturation. For the clinician this means individualising the decision to add LH by patient phenotype, age and presumed receptor sensitivity, rather than following a single template.
What can two extreme clinical scenarios — hypogonadotropic hypogonadism and polycystic ovarian morphology — teach us about LH in early folliculogenesis? Reading the boundary cases is often how the central mechanism becomes visible.
Professor of Obstetrics and Gynecology at the University of Modena and Reggio Emilia and Chair of the Obstetrics and Gynecology Department at the University Hospital of Modena. Internationally recognized for his research on anti-Müllerian hormone (AMH) and ovarian reserve and their application in assisted reproduction.
Author of the lecture "The role of LH in early folliculogenesis: lessons from hypogonadotropic hypogonadism and polycystic ovarian morphology"
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