Inflammatory bowel disease type influences development of elevated liver enzymes

Background and Aim Up to a third of patients with inflammatory bowel disease (IBD) have elevated liver enzymes (ELE). We evaluated the incidence, predictors, and outcomes associated with ELE in a diverse and vulnerable IBD cohort. Methods We retrospectively evaluated 336 IBD patients receiving care...

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Published in:JGH open Vol. 6; no. 12; pp. 846 - 853
Main Authors: Cheng, Yao‐Wen, McLean, Richard, Sewell, Justin L, Huang, Chiung‐Yu, Khalili, Mandana
Format: Journal Article
Language:English
Published: Melbourne Wiley Publishing Asia Pty Ltd 01-12-2022
John Wiley & Sons, Inc
Wiley
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Summary:Background and Aim Up to a third of patients with inflammatory bowel disease (IBD) have elevated liver enzymes (ELE). We evaluated the incidence, predictors, and outcomes associated with ELE in a diverse and vulnerable IBD cohort. Methods We retrospectively evaluated 336 IBD patients receiving care at the San Francisco safety net gastroenterology clinics between June 1996 and December 2019. Baseline characteristics were captured at first visit, then patients were followed until last clinic activity or death. Testing and etiology, pattern of ELE defined as transient (<1 month) or persistent (≥1 month), were assessed. Multivariate modeling evaluated predictors of ELE at baseline, new ELE at follow‐up, and pattern of ELE. Results Baseline median age was 40.3 years, 62% male, 46% White (13% Black, 19% Asian, and 18% Latino), and 59% had ulcerative colitis (UC). Among those without known liver disease (n = 14), 51.6% (166 of 322; 52 at baseline, 114 during follow‐up) had ELE. In multivariate logistic regression, 5‐aminosalicylic acid use (odds ratio [OR] 2.2, 95% confidence interval [CI]: 1.07–4.4, P = 0.03) and higher body mass index (OR 1.08, 95% CI: 1.02–1.14, P = 0.01) were associated with baseline ELE. In multivariate Cox regression, UC (vs. Crohn's disease [CD]) had a 34% lower risk of developing new ELE during follow‐up (hazard ratio [HR] 0.66, 95% CI: 0.46–0.95, P = 0.02). Mortality rate was higher for patients with ELE (0% normal vs 2.3% transient ELE vs 6.5% persistent ELE, P < 0.001). Conclusion ELE is prevalent in IBD, especially in CD, and associated with higher rates of mortality. Identification and management of ELE particularly when persistent are important to IBD outcomes. We evaluated the incidence, predictors, and outcomes associated with elevated liver enzymes (ELE) in a diverse and vulnerable inflammatory bowel disease cohort. In multivariate Cox regression, ulcerative colitis (vs Crohn's disease) had a 34% lower risk of developing new ELE during follow‐up (hazard ratio 0.66, 95% confidence interval: 0.46–0.95, P = 0.02). Mortality rate was higher for patients with ELE (0% normal vs 2.3% transient ELE vs 6.5% persistent ELE, P < 0.001).
Bibliography:Author contribution
This work was in part supported by the National Institutes of Health, Grant Number K24AA022523 (M.K.) and P30 DK026743.
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Declaration of conflict of interest
Yao‐Wen Cheng and Richard McLean contributed to the acquisition of data. Yao‐Wen Cheng, Justin L. Sewell, Chiung‐Yu Huang, and Mandana Khalili contributed to analysis and interpretation of data. All authors contributed to study concept, design, manuscript drafting, and manuscript revision. All authors approved the final version of the manuscript.
Financial support
Mandana Khalili is a recipient of research grant (to her institution) from Gilead Sciences Inc, and Intercept Pharmaceuticals and she has served as consultant for Gilead Sciences Inc.
Mandana Khalili, M.D.
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Guarantor of the article: Mandana Khalili, M.D.
Author contribution: Yao‐Wen Cheng and Richard McLean contributed to the acquisition of data. Yao‐Wen Cheng, Justin L. Sewell, Chiung‐Yu Huang, and Mandana Khalili contributed to analysis and interpretation of data. All authors contributed to study concept, design, manuscript drafting, and manuscript revision. All authors approved the final version of the manuscript.
Financial support: This work was in part supported by the National Institutes of Health, Grant Number K24AA022523 (M.K.) and P30 DK026743.
Declaration of conflict of interest: Mandana Khalili is a recipient of research grant (to her institution) from Gilead Sciences Inc, and Intercept Pharmaceuticals and she has served as consultant for Gilead Sciences Inc.
ISSN:2397-9070
2397-9070
DOI:10.1002/jgh3.12831