ArticleChronic diseases and translational medicine2026
Burden of Liver Disease Among Individuals With Turner Syndrome and Klinefelter Syndrome: A Comprehensive Perspective.
Article in Chronic diseases and translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Burden of Liver Disease Among Individuals With Turner Syndrome and Klinefelter Syndrome: A Comprehensive Perspective.Chronic diseases and translational medicine · 2026Article
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
The liver is increasingly recognized as a major regulator of systemic cardio-renal-metabolic health. Evidence is mounting that sex-chromosome dosage per se itself, independent of gonadal sex hormones, modulates hepatic physiology and liver disease risk. Turner syndrome (TS; monosomy X) and Klinefelter syndrome (KS; 47, XXY and variants) are the two most common sex-chromosome aneuploidies and carry a clinically relevant, yet often under-appreciated, burden of liver disease. Population studies show that individuals with TS have 2- to sixfold higher odds of raised liver enzymes, steatotic liver disease, advanced fibrosis, and even hepatocellular malignancy compared with to sex- and age-matched controls. In KS, the prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) reaches approximately 45%, with testosterone deficiency, visceral adiposity, and systemic inflammation acting as key drivers. Pathogenetic mechanisms converge on vascular dysgenesis and estrogen deficiency in TS, and on hypogonadism-related metabolic derangements in KS, together accelerating steatosis, inflammation, and fibrogenesis. This concise review/Comprehensive perspective reviews discusses historical background, epidemiology, hepatic phenotypes, pathophysiology, and current diagnostic and management recommendations. It also highlights critical knowledge gaps, including the need for prospective cohorts, optimized hormone-replacement protocols, and trials of emerging pharmacological approaches anti-MASH agents. Raising awareness among all stakeholders, endocrinologists, hepatologists, and primary-care physicians is essential for early detection, multidisciplinary management, and improved hepatic and extra-hepatic outcomes in these vulnerable patient populations.
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.