CASE REPORT: Histological Resolution of Steatohepatitis After Iron Depletion

Abstract

After its description in the early eighties (1), nonalcoholic steatohepatitis (NASH) has become a well-defined clinical entity with potentially dangerous consequences including progression to cirrhosis (2). The pathogenesis of NASH considers the occurrence of fat accumulation in the liver cell followed by a sequential series of events including an inflammatory response leading to hepatocellular injury which may lead to a fibrogenic response (3). While fat accumulation has been mainly related to insulin resistance, factors that trigger inflammation and fibrosis progression are less clear. Iron overload has been regarded as an important factor related to both insulin resistance and oxidative stress (4, 5). In fact, it has been reported that patients with hepatic steatosis have increased ferritin and transferrin saturation reflecting iron overload (6) and that iron depletion may have an insulin-sparing effect (7), which suggests a significant role of iron in the pathogenesis of fatty liver and NASH. Albeit it has been suggested that phlebotomy might be a useful treatment for NASH with concomitant iron overload, published data on the effects of iron depletion on both biochemical and histological alterations in these patients are limited.