Acute liver failure (ALF) caused by hepatitis A is a rare but fatal disease. Here, we developed a model to predict outcome in patients with ALF caused by hepatitis A. The derivation set consisted of 294 patients diagnosed with hepatitis A–related ALF (ALFA) from Korea, and a validation set of 56 patients from Japan, India, and United Kingdom. Using a multivariate proportional hazard model, a risk-prediction model (ALFA score) consisting of age, international normalized ratio, bilirubin, ammonia, creatinine, and hemoglobin levels acquired on the day of ALF diagnosis was developed. The ALFA score showed the highest discrimination in the prediction of liver transplant or death at 1 month (c-statistic, 0.87; 95% confidence interval [CI], 0.84-0.92) versus King’s College criteria (KCC; c-statistic, 0.56; 95% CI, 0.53-0.59), U.S. Acute Liver Failure Study Group index specific for hepatitis A virus (HAV-ALFSG; c-statistic, 0.70; 95% CI, 0.65-0.76), the new ALFSG index (c-statistic, 0.79; 95% CI, 0.74-0.84), Model for End-Stage Liver Disease (MELD; c-statistic, 0.79; 95% CI, 0.74-0.84), and MELD including sodium (MELD-Na; c-statistic, 0.78; 95% CI, 0.73-0.84) in the derivation set (all P < 0.01). In the validation set, the performance of the ALFA score (c-statistic, 0.84; 95% CI, 0.74-0.94) was significantly better than that of KCC (c-statistic, 0.65; 95% CI, 0.52-0.79), MELD (c-statistic, 0.74; 95% CI, 0.61-0.87), and MELD-Na (c-statistic, 0.72; 95% CI, 0.58-0.85) (all P < 0.05), and better, but not statistically significant, than that of the HAV-ALFSG (c-statistic, 0.76; 95% CI, 0.61-0.90; P = 0.28) and new ALFSG indices (c-statistic, 0.79; 95% CI, 0.65-0.93; P = 0.41). The model was well-calibrated in both sets. Conclusion: Our disease-specific score provides refined prediction of outcome in patients with ALF caused by hepatitis A.
Bibliographical noteFunding Information:
Received February 7, 2018; accepted August 20, 2018. Additional Supporting Information may be found at onlinelibrary.wiley.com/doi/10.1002/hep.30262/suppinfo. Supported by a grant from the Korean Association for the Study of the Liver. *These authors contributed equally to this work. © 2018 by the American Association for the Study of Liver Diseases. View this article online at wileyonlinelibrary.com. DOI 10.1002/hep.30262 Potential conflict of interest: Dr. Mochida is on the speakers’ bureau and received grants from AbbVie GK, Bristol-Myers Squibb, Toray, MSD K.K., and Sumitomo Dainippon. He is on the speakers’ bureau for Ajinomoto and Gilead. He received grants from A2 Healthcare, Chugai, and Eisai.
The authors extend their gratitude to the investigators in each center who participated in this study: Dong Hyun Lee, Seung Hyun Ma (Seoul National University); Hee Yeon Kim, Jung Min Bae (Catholic University); Nae-Yun Heo (Inje University); Chang Hyeon Seock, Jihyun An (University of Ulsan); Hana Park, Mi Na Kim (CHA University); Jin Hee Lee, Won Sohn, Ju-Yeon Cho (Sungkyunkwan University); Weiguang Xu (Ajou?University); Chang Hun Lee (Chonbuk National University); Yang Jae Yoo, Chang Ho Jung (Korea?University); Young Oh Kweon, Yu Rim Lee (Kyungpook National University); Soon Koo Baik (Yonsei?University); Jae Young Lee (Yeungnam?University); Oh Sang Kwon, Hyunhwa Yoon (Gachon University); Ki Deok Yoo, Tae?Yeob Kim (Hanyang University); and Hyun Young Woo (Pusan National University).
© 2018 by the American Association for the Study of Liver Diseases.
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