Liver iron concentration in chronic viral hepatitis: a study of 98 patients

Piperno, Alberto; D'Alba, Roberta; Fargion, Silvia; Roffi, Luigi; Sampietro, Maurizio; Parma, Stefania; Arosio, Valeria; Faré, Maristella; Fiorelli, G.

doi:10.1097/00042737-199512000-00014

Cited by 63 publications

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“…Hepatic iron concentration (HIC) was determined in 97 patients (71 men, 26 women) by atomic absorption spectrophotometry (Perkin-Elmer S2380, Norwalk, CT) on samples of at least 0.5 mg dry weight (normal values Յ30 µmol/g in men and Յ17 µmol/g in women 3 ). The hepatic iron index (ratio of HIC [µmol/g] to age [years]) was calculated.…”

Section: Methodsmentioning

confidence: 99%

“…7,9 These aspects have recently been extensively reviewed by Bonkowsky et al 10,11 The hemochromatosis gene, which is very frequent in whites, could have a role in the development of hepatic iron overload in CH in these populations. 3,12 Based on the association between the hemochromatosis gene and HLA-A3 antigen, this hypothesis was tested by HLA typing in patients and families, 3,13 but, at that time, no direct confirmation could be achieved, because the gene had not yet been identified. The recent isolation of the hemochromatosis gene, 14 a major histocompatibility complex class I-like gene now designated HFE, provides the opportunity of analyzing the role of HFE gene mutations on the development of iron overload in patients with CH directly.…”

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Hepatic iron overload in patients with chronic viral hepatitis: Role of HFE gene mutations

et al. 1998

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Mild to moderate hepatic iron overload is frequent in patients with chronic viral hepatitis (CH). We evaluated the role of hemochromatosis (HFE) gene mutations and other acquired factors in the development of iron overload in these patients. We studied 110 patients with chronic B or C viral hepatitis (31 women, 79 men), including 20 with cirrhosis, and 139 controls. Hepatic iron was evaluated by semiquantitative analysis in all the patients, and hepatic iron concentration (HIC) was determined in 97 of them (26 women, 71 men). C282Y and H63D mutations were sought in all the subjects by a polymerase chain reactionrestriction assay. The frequency of HFE genotypes and alleles did not differ in patients and controls. No relation was detected between hepatic iron stores and HFE gene mutations in women. In men, all C282Y heterozygotes had iron overload, and the H63D mutation was significantly more frequent in patients with more marked hepatic siderosis than in those with mild or no siderosis (P ‫؍‬ .0039) and in controls (P ‫؍‬ .0008). Heavy alcohol intake and hepatic cirrhosis were also associated with increased hepatic iron stores in the men. In the 71 men in whom HIC was measured, multiple regression analysis showed that this variable was related independently only to alcohol intake and HFE gene mutations. We suggest that in patients with CH, iron accumulates in the liver as the result of an interplay between genetic and acquired factors, and that increased liver iron stores may influence progression toward liver fibrosis. (HEPATOLOGY 1998;28:1105-1109

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Hepatic iron overload in patients with chronic viral hepatitis: Role of HFE gene mutations

et al. 1998

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“…This is the case of chronic hepatitis C, insulin resistance-associated hepatic iron overload syndrome, and end-stage liver disease [7][8][9][10][11][12] (see below). In fact, investigations into the effects of low iron-overload in various hepatic diseases have suggested that iron may play a role as a cofactor in lipid peroxidation and fibrogenesis [7,13,14].…”

Section: Regional Iron Accumulation: Viral Hepatitis and Fatty Liver mentioning

confidence: 99%

Iron chelation beyond transfusion iron overload

Pietrangelo

2007

Am. J. Hematol.

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The effects of systemic iron overload in hereditary (e.g., classic HFE hemochromatosis) or acquired disorders (e.g., transfusion-dependent iron overload) are well known. Several other iron overload diseases, with an observed mild-to-moderate increase in iron in selected organs (e.g., the liver or the brain), or with ``misdistribution{''} of iron within cells (e.g., reticuloendothelial cells) or subcellular organelles (e.g., mitochondria), have been recognized more recently. The deleterious impact of any excess iron may be high as active redox iron may directly contribute to cell damage or affect signaling pathways involved in cell necrosis-apoptosis or organ fibrosis and cancer. This article discusses the potential use of iron chelation therapy to treat iron overload from causes other than transfusion overload.

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“…Serum markers of iron overload are frequently elevated in HCV, more often in HCV than other causes of chronic liver disease excluding hereditary hemochromatosis (HH). [4][5][6] Elevated hepatic iron concentration (HIC) has been associated with a poor response to interferon alfa, 7,8 but with an improved response after phlebotomy. Phlebotomy alone has also been shown to result in significant reduction in transaminase levels in patients with chronic HCV.…”

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Heterozygosity for hereditary hemochromatosis is associated with more fibrosis in chronic hepatitis C

et al. 1998

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Hepatic iron has been associated with more aggressive liver disease in chronic viral hepatitis. We evaluated whether the recently described C282Y mutation of the hemochromatosis gene, designated HFE (responsible for at least 83% of hereditary hemochromatosis), was associated with more advanced liver disease in chronic hepatitis C. One hundred thirty-seven patients with biopsy-proven chronic hepatitis C were studied and liver biopsies scored for necroinflammation (grade 0-18) and fibrosis (stage 0-6). Genomic DNA was amplified by polymerase chain reaction and the C282Y mutation identified by restriction with RsaI and electrophoretic separation of restriction fragments. Ten (7.3%) patients had the C282Y mutation. No C282Y homozygous patients were identified. Age, sex distribution, and estimated weekly alcohol consumption were not significantly different between those with and without the mutation. Serum ferritin was higher in the heterozygotes (mean, 339 g/L) compared with homozygous wild types (153 g/L; P ‫؍‬ .0005). In the majority of patients, liver iron was graded 0 out of 4, but hepatocyte iron staining was more commonly present in heterozygotes compared with homozygous normals (30% compared with 4% [P ‫؍‬ .02]). Liver disease was more advanced in those with the mutant allele (mean fibrosis stage: 3.6, compared with wild type: 1.5 [P ‫؍‬ .01]). Cirrhosis was found more often in those with the mutation (40%) compared with those without (8.7%) (P ‫؍‬ .01; odds ratio: 7.6 [1.9-31.2]). There was no significant difference in inflammation scores between heterozygotes and wild type (mean, 5.4 compared with 4

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Liver iron concentration in chronic viral hepatitis: a study of 98 patients

Cited by 63 publications

References 0 publications

Hepatic iron overload in patients with chronic viral hepatitis: Role of HFE gene mutations

Hepatic iron overload in patients with chronic viral hepatitis: Role of HFE gene mutations

Iron chelation beyond transfusion iron overload

Heterozygosity for hereditary hemochromatosis is associated with more fibrosis in chronic hepatitis C

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