ReviewEndocrine2025
Polycystic ovary syndrome and idiopathic central precocious puberty: two sides of the same coin?
Review in Endocrine, 2025. 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeSeveral studies have reported an association between central precocious puberty (CPP) and a higher prevalence of polycystic ovary syndrome (PCOS), raising the hypothesis that CPP may act as an early-life indicator of increased PCOS risk. This review investigates the shared genetic, epigenetic, and environmental factors potentially underlying CPP and PCOS, with the aim of clarifying their connection and supporting advances in early detection and management.
methodsA comprehensive literature review was conducted using the PubMed/MEDLINE database, prioritizing research from the past two decades, supplemented by key studies from earlier years. This research included studies on genetic and epigenetic factors, endocrine-disrupting chemicals (EDCs), and metabolic influences related to CPP and PCOS. Both original research and review articles were selected, focusing on the identification of pathophysiological mechanisms and risk factors linking these disorders.
resultsGenome-wide association studies (GWAS) have linked genetic variants in the kisspeptin and neurokinin B signaling pathways to increased gonadotropin-releasing hormone (GnRH) secretion, triggering early puberty. Moreover, increased GnRH pulsatility contributes to elevated luteinizing hormone (LH) levels, altered LH/follicle-stimulating hormone (FSH) ratios, and ovarian hyperandrogenism—key pathophysiological features of PCOS. Additionally, epigenetic modifications, particularly changes in DNA methylation at CpG sites, have been observed in both CPP and PCOS. A hyperandrogenic intrauterine environment and inadequate fetal growth contribute to prenatal epigenetic alterations, while postnatal factors such as obesity, insulin resistance, and exposure to EDCs further influence epigenetic modifications. Although insulin resistance and hyperandrogenism are central features linking CPP to PCOS, the precise mechanisms underlying these associations remain complex and not yet fully elucidated.
conclusionsIdentifying shared genetic and environmental factors influencing early puberty onset and PCOS highlights the importance of close clinical monitoring in early life, though preventive interventions remain unproven. Further research is needed to clarify these mechanisms, which will support the development of more precise prevention and treatment strategies in clinical practice.
Indexed as
Identifiers
41091301What 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.