Chronic liver diseases and iron: a concise review with emphasis on hypotransferrinemia and hypohepcidinemia

Abstract

Iron studies in chronic liver diseases (CLDs) have a long history. Currently we can mention certainties, uncertainties, and hopes related to this topic. It is certain that iron metabolism problems and hepatic siderosis are frequent in CLDs and they get more frequent as CLD progresses, but true iron overload is rare. There are conflicting literature data on the mechanism of siderosis, the role of iron in CLD pathogenesis, and the potential benefits of iron removal. We may hope that pharmacological approaches targeting iron metabolism disorders of CLD will be actively evaluated in the future. In this review, we aimed to present a general outlook of this extensively studied topic.

Characterization of Oxidative Stress and Ammonia According to the Different Grades of Hepatic Encephalopathy

“…Environmental and endogenous stressors that contributed to the generation of OxS in patients with CLD were alcohol, cigarette smoking, nonalcoholic fatty liver disease, infection virus Hepatitis Type C, anti-inflammatory drugs, hypoxia-ischemic due to chronic anemia, inflammation, and iron overload. The latter is generated by an exogenous route, caused by ferrous sulfate-fumarate or dextran iron, and an endogenous route through increase in intestinal absorption of iron, with decrease pro-duction of the iron regulatory hormone (hepcidin) [51], and the release of the heme group from hemoglobin through iron uncoupling by lysis of the erythrocytes in liver or spleen secondary to portal hypertension or variceal hemorrhage. This free iron in blood in Fe2+ form (ferrous ion) is oxidized to Fe3+ (ferric ion), which is catalyzed by H 2 O 2 through the "Fenton reaction" producing more reactive free radical as the hydroxyl [52], capable of damaging lipids and proteins in patients with CLD.…”