Abstract
As the main iron storage site in the body and the main source of the iron-regulatory hormone, hepcidin, the liver plays a pivotal role in iron homeostasis. A variable degree of hepatic iron accumulation has long been recognized in a number of chronic liver diseases. Both alcoholic and non-alcoholic steatohepatitis display increased iron deposits in the liver, with an hepatocellular, mesenchymal, or mixed pattern, and recent reports have documented a concomitant aberrant hepcidin expression that could be linked to different coincidental pathogenic events (e.g. the etiological agent itself, necroinflammation, metabolic derangements, genetic predisposition). The present study reviews the pathogenic mechanisms of iron accumulation in steatohepatitis during alcoholic and non-alcoholic liver disease and the role of excess iron in chronic disease progression.
Highlights
In spite of the diverse etiology, alcoholic liver disease (ALD) and non-alcoholic fatty liver disease (NAFLD) share many epidemiological, clinical, and pathogenetic features
Additional factors that might contribute to hepatic iron excess in NAFLD are necrosis,[42] which might lead to iron leaking from dying hepatocytes and subsequent phagocytosis by liver macrophages, or the induction of hepcidin by inflammatory cytokines,[7] causing iron accumulation in Kupffer cells (KC) (Fig. 1)
Hepcidin was positively correlated with hepatic lobular inflammation in NASH, non-NASH patients, and in the whole metabolic syndrome (MS) group, while in the NASH group, it was positively correlated with the NAFLD Activity Score (NAS) score
Summary
In spite of the diverse etiology, alcoholic liver disease (ALD) and non-alcoholic fatty liver disease (NAFLD) share many epidemiological, clinical, and pathogenetic features They both represent major causes of chronic liver disease worldwide,[1,2] and both encompass a spectrum of disorders ranging from simple fatty liver (steatosis) to hepatocyte injury and inflammation (alcoholic steatohepatitis [ASH] and non-alcoholic steatohepatitis [NASH]), cirrhosis, and superimposed hepatocellular carcinoma (HCC). Hepatocellular and/or mesenchymal iron deposition, usually slight or mild, might be found in chronic non-cirrhotic liver disease, regardless of its cause.[3] Various non-specific factors (mainly inflammation and cell necrosis), together with polymorphisms in iron-related genes or pathogenic interactions between iron itself and the etiological agent (hepatotropic virus, alcohol, increased supply of free FA to the liver or insulin resistance), might be responsible. The central regulator of iron homeostasis is hepcidin, a small peptide hormone
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