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Vitamin E Improves Transplant‐Free Survival and Hepatic Decompensation Among Patients With Nonalcoholic Steatohepatitis and Advanced Fibrosis
Author(s) -
VilarGomez Eduardo,
Vuppalanchi Raj,
Gawrieh Samer,
Ghabril Marwan,
Saxena Romil,
Cummings Oscar W.,
Chalasani Naga
Publication year - 2020
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.30368
Subject(s) - medicine , interquartile range , hazard ratio , gastroenterology , decompensation , body mass index , fibrosis , cirrhosis , vitamin d and neurology , steatohepatitis , confidence interval , surgery , fatty liver , disease
Vitamin E improves liver histology in adults with nonalcoholic steatohepatitis (NASH) but not diabetes, but its impact on long‐term patient outcomes is unknown. We evaluated whether vitamin E treatment improves clinical outcomes of NASH patients with bridging fibrosis or cirrhosis. Two hundred and thirty‐six patients with biopsy‐proven NASH and bridging fibrosis or cirrhosis seen at Indiana University Medical Center between October 2004 and January 2016 were included. Ninety of them took 800 international units/day of vitamin E for ≥2 years (vitamin E users) and were propensity‐matched to 90 adults who did not take vitamin E (controls) after adjusting for fibrosis severity, age, gender, body mass index, comorbidities and their treatment, low‐density lipoprotein cholesterol, liver biochemistries, and length of follow‐up on vitamin E. Covariate‐adjusted Cox and competing risk regression models were assessed to evaluate the association between vitamin E treatment and patient outcomes. The median follow‐up was 5.62 (interquartile range [IQR], 4.3‐7.5) and 5.6 (IQR, 4‐6.9) years for vitamin E users and controls, respectively. Vitamin E users had higher adjusted transplant‐free survival (78% versus 49%, P < 0.01) and lower rates of hepatic decompensation (37% versus 62%, P = 0.04) than controls. After controlling for severity of fibrosis, calendar year of patient enrollment, and other potential confounders, vitamin E treatment decreased the risk of death or transplant (adjusted hazard ratio, 0.30; 95% confidence interval [CI], 0.12‐0.74; P < 0.01) and hepatic decompensation (adjusted sub‐HR, 0.52; 95% CI, 0.28‐0.96; P = 0.036). These benefits were evident in both those with diabetes and those without diabetes. Adjusted 10‐year cumulative probabilities of hepatocellular carcinoma, vascular events, and nonhepatic cancers were not different between vitamin E–exposed patients and controls. Conclusion: Vitamin E use was associated with improved clinical outcomes in patients with NASH and bridging fibrosis or cirrhosis.