Severe alcoholic hepatitis-current concepts, diagnosis and treatment options
Alcoholic hepatitis(AH) is an acute hepatic manifesta-tion occurring from heavy alcohol ingestion. Alcoholic steatohepatitis(ASH) is histologically characterized by steatosis, inflammation, and fibrosis in the liver. Despite the wide range of severity at presentation, those with severe ASH(Maddrey’s...
Saved in:
Published in | World journal of hepatology Vol. 6; no. 10; pp. 688 - 695 |
---|---|
Main Authors | , |
Format | Journal Article |
Language | English |
Published |
United States
Baishideng Publishing Group Inc
27.10.2014
|
Subjects | |
Online Access | Get full text |
Cover
Loading…
Summary: | Alcoholic hepatitis(AH) is an acute hepatic manifesta-tion occurring from heavy alcohol ingestion. Alcoholic steatohepatitis(ASH) is histologically characterized by steatosis, inflammation, and fibrosis in the liver. Despite the wide range of severity at presentation, those with severe ASH(Maddrey’s discriminant function ≥ 32) typically present with fever, jaundice, and abdominal tenderness. Alcohol abstinence is the cornerstone of therapy for AH and, in the milder forms, is sufficient for clinical recovery. Severe ASH may progress to multi-or-gan failure including acute kidney injury and infection. Thus, infection and renal failure have a major impact on survival and should be closely monitored in patients with severe ASH. Patients with severe ASH have a re-ported short-term mortality of up to 40%-50%. Severe ASH at risk of early death should be identified by one of the available prognostic scoring systems before consid-ering specific therapies. Corticosteroids are the main-stay of treatment for severe ASH. When corticosteroids are contraindicated, pentoxifylline may be alternatively used. Responsiveness to steroids should be assessed at day 7 and stopping rules based on Lille score should come into action. Strategically, future studies for pa-tients with severe ASH should focus on suppressing inflammation based on cytokine profiles, balancing he-patocellular death and regeneration, limiting activation of the innate immune response, and maintaining gut mucosal integrity. |
---|---|
Bibliography: | Won Kim;Dong Joon Kim;Department of Internal Medicine,Seoul MetropolitanGovernment Seoul National University Boramae Medical Center;Department of Internal Medicine,Hallym Uni-versity College of Medicine ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 Correspondence to: Dong Joon Kim, MD, PhD, Professor, Department of Internal Medicine, Hallym University College of Medicine, #153 Gyo-dong, Chuncheon-si, Gangwon-do, Chuncheon 200-704, South Korea. djkim@hallym.ac.kr Author contributions: Kim W collected data, reviewed literatures, and wrote the manuscript; Kim DJ designed this review, appraised critically and revised the manuscript. Telephone: +82-33-2405646 Fax: +82-33-2418064 |
ISSN: | 1948-5182 1948-5182 |
DOI: | 10.4254/wjh.v6.i10.688 |