Evidence map›Paper›PMID 42309239›Full record

ArticleJHEP reports : innovation in hepatology2026

Refined liver MRI-derived cT1 thresholds capturing hepatic fat fraction enhance mortality risk prediction.

Minsun Kwak, Abdelrahman M Attia, Mohammad Saeid Rezaee-Zavareh, Yufeng Wang, Lixia Wang, Walid S Ayoub, Alexandar Kuo, Paul Martin, Hirsh D Trivedi, Aarshi Vipani and 6 more

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In one paragraph

Article in JHEP reports : innovation in hepatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors.

Minsun KwakKarsh Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, California, USA; Department of Internal Medicine, Healthcare Research Institute, Healthcare System Gangnam Center, Seoul National University Hospital, Seoul, Republic of Korea.
Abdelrahman M AttiaKarsh Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Mohammad Saeid Rezaee-ZavarehMiddle East Liver Diseases (MELD) Center Teheran, Iran.
Yufeng WangBiomedical Imaging Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Lixia WangBiomedical Imaging Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Walid S AyoubKarsh Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Alexandar KuoKarsh Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Paul MartinKarsh Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Hirsh D TrivediKarsh Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, California, USA; Division of Gastroenterology & Hepatology, Dell Medical School at University of Texas, Austin, Texas, USA.
Aarshi VipaniKarsh Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Yun WangKarsh Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Stephen PandolKarsh Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Debiao LiBiomedical Imaging Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Shelly C LuKarsh Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Hyun-Seok KimKarsh Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Ju Dong YangKarsh Division of Gastroenterology and Hepatology, Cedars-Sinai Medical Center, Los Angeles, California, USA; Comprehensive Transplant Center, Cedars-Sinai Medical Center, Los Angeles, CA, USA; Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA. Electronic address: judong.yang@csmc.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimsCorrected T1 (cT1), measured by liver MRI, enables non-invasive assessment of hepatic water content. Although a threshold of ≥800 ms has been proposed to identify individuals at risk of metabolic dysfunction-associated steatohepatitis (MASH) and adverse outcomes, it identifies only a small proportion of individuals (∼5%) and may fail to capture risk below this threshold. We aimed to evaluate whether cT1 values below 800 ms are associated with mortality and whether hepatic steatosis, assessed by MRI-derived proton density fat fraction (PDFF), modifies this association.

methodsWe analyzed 29,597 UK Biobank participants with liver MRI-derived cT1 measurements. Participants were categorized into three groups (<700, 700-799, and ≥800 ms) based on penalized spline analysis. Outcomes included all-cause mortality, cause-specific mortality, and liver-related events. Cox proportional hazards models were adjusted for demographic, lifestyle, and cardiometabolic factors.

resultsApproximately 40% of participants had cT1 values of 700-799 ms, and 5% had cT1 values ≥800 ms. Over a median follow-up of 5.3 years, participants with cT1 values of 700-799 ms had higher risks of all-cause mortality (adjusted hazard ratio [aHR] 1.21; 95% CI 1.02-1.43) and cardiovascular mortality (aHR 1.54; 95% CI 1.04-2.28) than those with cT1 values <700 ms. Risks were even higher among participants with cT1 values ≥800 ms. Clinically significant hepatic steatosis (PDFF ≥10%) significantly modified the association between cT1 and all-cause mortality (p for interaction <0.05). Higher cT1 was associated with increased all-cause mortality only among participants with PDFF <10% (aHR 1.25 [95% CI 1.06-1.49] for cT1 700-799 ms and 2.20 [95% CI 1.40-3.48] for cT1 ≥800 ms, compared with cT1 <700 ms), but not among those with PDFF ≥10%.

conclusioncT1 values between 700 and 799 ms were independently associated with an increased risk of mortality. Notably, this association was modified by the presence of clinically significant hepatic steatosis as assessed by PDFF. IMPACT AND IMPLICATIONS: Using liver MRI to measure cT1, we demonstrated that cT1 values of 700-799 ms, below the conventional threshold of 800 ms, were independently associated with an increased risk of all-cause and cardiovascular mortality. We also found that this association was present only among participants with PDFF <10%, indicating that clinically significant hepatic steatosis modifies the relationship between cT1 and mortality. These findings suggest that lower cT1 thresholds may improve risk stratification and that the prognostic significance of cT1 should be interpreted in the context of hepatic steatosis.

Indexed as

Corrected T1hepatic steatosisLiver-related outcomesMagnetic resonance imagingMortality

Identifiers

PMID42309239
PMCPMC13452995

What Socratic holds

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Registered trials

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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 Socratic graph.