Systems used to automatically annotate proteins with high accuracy:. Select item s and click on "Add to basket" to create your own collection here entries max. Sampietro M. Mild to moderate iron overload is common in PCT, as iron is one of the factors which trigger the clinical manifestations of the disease through the inactivation of URO-D. A role for genetic hemochromatosis in the development of iron overload in sporadic PCT has been hypothesized in the past. The aim of this work was to investigate whether mutations of HFE, which is a candidate gene for hemochromatosis, play the role of genetic susceptibility factors for PCT in Italian patients, who have a high prevalence of acquired triggering factors, such as hepatitis C virus HCV chronic infection and alcohol.
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Iron in Nonhemochromatotic Liver Disorders
Acetaminophen is considered a safe drug for children, although hepatotoxicity may develop after overdosing. Reports of liver failure after repeated therapeutic doses of the drug have been rare. Intravenous N-acetylcysteine therapy resulted in rapid improvement of the child's clinical condition and laboratory test results. Health care providers should be aware that multiple doses of acetaminophen in infants may lead to acute hepatic failure.
Fulminant Hepatitis After 10 Days of Acetaminophen Treatment at Recommended Dosage in an Infant
Iron is essential for cellular functions, but in excessive amounts it is toxic to cells. The harmful effects are related to increased oxidative stress and production of reactive oxygen species causing oxidative damage to lipids, proteins, and nucleic acids. Heavy iron overload as occurs in primary and secondary hemochromatosis can cause fibrosis of various parenchymal organs such as the liver, heart, and pancreas. Lesser degrees of hepatic iron deposition are also associated with, and seem to be risk factors for, certain nonhemochromatotic liver diseases. Porphyria cutanea tarda is associated with hepatic iron overload and responds to iron-reduction therapy. Other recent evidence indicates that the prevalence of HFE gene mutations is increased in chronic viral hepatitis and that patients with chronic hepatitis C harboring especially the CY mutation are more likely to suffer from advanced hepatic fibrosis or cirrhosis and to do so at younger ages.