Case Report
Hemosiderosis due to Chronic Alcoholism
Pinar Tosun Tasar1*, Ozlem Ozdemir1, Omer Binicier2 and Omer Selahattin Topalak2
1 Department of Internal Medicine, Dokuz Eylul University Faculty of Medicine, Izmir/Turkey
2 Department of Internal Medicine, Division of Gastroenterology, DokuzEylul University Faculty of Medicine, Izmir/Turkey
- *Corresponding Author:
- Pinar TosunTasar
Department of Internal Medicine
DokuzEylül University Faculty of Medicine, Izmir, Turkey
Tel: +9005053988985
E-mail: pinar.tosun@gmail.com
Received date: March 11, 2014; Accepted date: March 28, 2014; Published date: April 01, 2014
Citation: Tasar PT, Ozdemir O, Binicier O, Topalak OS (2014) Hemosiderosis due to Chronic Alcoholism. J Gastroint Dig Syst 4:182. doi:10.4172/2161-069X.1000182
Copyright: © 2014 Tasar PT, 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
Alcoholic liver disease is characterized with excess consumption of alcohol for long term and variable hepatic injury. Chronic alcohol consumption often leads to a disease called alcoholic liver disease [ALD]. It is generally with an accompaning iron accumulation. Increased plasma iron levels and tissue iron overload stimulate synthesis of hepcidin, resulting with release of iron from macrophages and duodenal enterocytes to the plasma. This homeostasis ensures that plasma iron level is maintained within a constant range and excess absorption and accumulation of iron in tissues are prevented. Alcohol-induced oxidative stress in hepatocytes is one of the main mechanisms by which hepcidin expression in the liver is down-regulated by alcohol. The decrease in liver hepcidin synthesis leads to an increase in intestinal iron transport and liver iron content. We report a case hemosiderosis secondary to chronic alcoholism.