alexa Non-Alcoholic Fatty Liver Disease as a Risk Factor for Acute Pancreatitis: A Case Control Study | OMICS International | Abstract
ISSN: 2165-7548

Emergency Medicine: Open Access
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Research Article

Non-Alcoholic Fatty Liver Disease as a Risk Factor for Acute Pancreatitis: A Case Control Study

Abhinav Agrawal, Manan Parikh and Sarfaraz Jasdanwala*

Department of medicine, Monmouth Medical Center, USA

*Corresponding Author:
Sarfaraz Jasdanwala
MD, Doctor internist to the University
hospital Souro Sanou, Department of internal medicine
immunology and hematology Mail box 676 Teaching
Higher institute of the health sciences of the
Polytechnic University of Bobo - Dioulasso, USA
Tel: 732-923-5000
E-mail: [email protected]

Received Date: May 08, 2015; Accepted Date: May 20, 2015; Published Date: May 27, 2015

Citation: Agrawal A, Parikh M, Jasdanwala S (2015) Non-Alcoholic Fatty Liver Disease as a Risk Factor for Acute Pancreatitis: A Case Control Study. Emerg Med (Los Angel) 5:261. doi:10.4172/2165-7548.1000261

Copyright: © 2015 Agrawal A, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Objective: Visceral obesity is an etiological factor and a marker of poor prognosis in acute pancreatitis (AP). Non-Alcoholic Fatty Liver Disease (NAFLD), a marker for visceral obesity, has also been recognized to have a stronger correlation to poor outcomes. With this study, we aim to assess the role of NAFLD as an etiologic factor in patients with AP.
Materials and Methods: In this retrospective electronic medical record (EMR) based case control study of 530 non-alcoholic adults were classified into cases with acute pancreatitis and controls without pancreatitis. Further subgroup was classified based on gallstone formation as an etiology of pancreatitis. Data was evaluated with McNemar’s Test.
Results: Results showed that patients with AP due to Gallstones had a higher incidence of NAFLD as seen on abdominal imaging [OR=1.688, p=0.0235 (CI: 1.070-2.701)], but Patients with AP due to unclear etiology did not have statistically significant higher rates of NAFLD [OR: 1.400, CI: 0.688 – 2.919]. Patients with AP due to all etiologies combined had higher incidence of NAFLD [(OR: 1.596, CI: 1.094-2.349, P-value 0.0145)].
Conclusion: We conclude from this study shows that NAFLD may be an independent risk factor for development of acute pancreatitis. It is also possible that NAFLD may have pathophysiologic interplay with formation of gallstones that is a known risk factor for acute pancreatitis.

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