Consensus Statement on the definition and classification of metabolic hyperferritinaemia (original) (raw)
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PLoS ONE, 2008
Objective: During the last 10 years we have experienced an increasing number of referrals due to hyperferritinemia. This is probably due to increased awareness of hereditary hemochromatosis, and the availability of a genetic test for this condition. Most of these referred patients were over-weight middle-aged men with elevated ferritin levels, but without the hemochromatosis-predisposing gene mutations. We evaluated the relationship between hyperferritinemia and the metabolic syndrome in 40 patients.
Liver iron concentration is not raised in patients with dysmetabolic hyperferritinemia
2016
Background & aims. Hyperferritinemia (HF) is frequently present in patients with metabolic syndrome (MS). MS associated with HF is named dysmetabolic hyperferritinemia (DH). There are some publications that propose that DH is associated with a raised liveriron concentration (LIC). We studied the LIC in patients referred for HF to a secondary hospital to determine if there are differences between patients with or without MS. MATERIAL AND METHODS We conducted a prospective study of 132 consecutive patients with HF from January to December 2010. The MS was defined by the International Diabetes Federation criteria (2005). LIC was determined by Magnetic resonance imaging (MRI). RESULTS The number of patients for which there was enough data to determine MS was 97, out of which 54 had MS and 43 had no MS (NMS). In 54/97 patients, MRI for LIC determination was performed. From the MS group, 44 were men (27 underwent MRI) and 10 women (9 MRI). The mean LIC was 27.83 ± 20.90 ?mol/g for the MS ...
Effects of iron overload on chronic metabolic diseases
The lancet. Diabetes & endocrinology, 2014
Iron can affect the clinical course of several chronic metabolic diseases such as type 2 diabetes, obesity, non-alcoholic fatty liver disease, and atherosclerosis. Iron overload can affect major tissues involved in glucose and lipid metabolism (pancreatic β cells, liver, muscle, and adipose tissue) and organs affected by chronic diabetic complications. Because iron is a potent pro-oxidant, fine-tuned control mechanisms have evolved to regulate entry, recycling, and loss of body iron. These mechanisms include the interplay of iron with transferrin, ferritin, insulin, and hepcidin, as well as with adipokines and proinflammatory molecules. An imbalance of these homoeostatic mechanisms results in systemic and parenchymal siderosis that contributes to organ damage (such as β-cell dysfunction, fibrosis in liver diseases, and atherosclerotic plaque growth and instability). Conversely, iron depletion can exert beneficial effects in patients with iron overload and even in healthy frequent bl...
Insulin resistance–associated hepatic iron overload
Gastroenterology, 1999
Hepatic iron overload has been reported in various metabolic conditions, including the insulinresistance syndrome (IRS) and nonalcoholic steatohepatitis (NASH). The aim of this study was to show that such hepatic iron overload is part of a unique and unrecognized entity. Methods: A total of 161 non-C282Y-homozygous patients with unexplained hepatic iron overload were included. We determined the age; sex; presence of IRS (1 or more of the following: body mass index of G25, diabetes, or hyperlipidemia); serum iron tests and liver iron concentration (LIC; reference value, F36 mol/g); liver function test results; C282Y and H63D HFE mutations; and liver histological status. Results: Patients were predominantly male and middle-aged. Most (94%) had IRS. Transferrin saturation was increased in 35% (median, 42%; range, 13%-94%). LIC ranged from 38 to 332 mol/g (median, 90 mol/g), and LIC/age ratio ranged from 0.5 to 4.8 (median, 1.8). Allelic frequencies of both HFE mutations were significantly increased compared with values in normal controls (C282Y, 20% vs. 9%; H63D, 30% vs. 17%), only because of a higher prevalence of compound heterozygotes. Patients with no HFE mutations had similar degrees of iron overload as those with other genotypes, except for compound heterozygotes, who had slightly more iron burden. Steatosis was present in 25% of patients and NASH in 27%. Portal fibrosis (grades 0-3) was present in 62% of patients (grade 2 or 3 in 12%) in association with steatosis, inflammation, and increased age. Sex ratio, IRS, transferrin saturation, and LIC did not vary with liver damage. Serum ferritin concentration, liver function test results, and fibrosis grade were more elevated in patients with steatosis and NASH than in others, but LIC and allelic frequencies of HFE mutations were similar. Conclusions: This study shows that patients with unexplained hepatic iron overload are characterized by a mild to moderate iron burden and the nearly constant association of an IRS irrespective of liver damage.
[Correction of insulin resistance syndrome does not cause normalisation of hyperferritinaemia]
Gastroentérologie clinique et biologique, 2003
The consequences of iron overload from dysmetabolic hyper-ferritinaemia are a strong motivation for an active medical care program. Venesection therapy is known to be effective in controlling iron overload parameters although no study has evaluated the impact of the normalization of metabolic dysfunction on iron overload. To evaluate the impact of normalization of metabolic dysfunction on iron overload. Sixty consecutive patients with dysmetabolic hepatosiderosis were included in a prospective study. Patients with hyper-ferritinaemia above 1000 microg/l were excluded. Multidisciplinary care was offered to all patients to normalize metabolic disorders (body mass index, arterial hypertension, fasting and postprandial hyperglycemia, hyperuricemia, hypercholesterolemia and hypertriglyceridemia) every three months. All patients were followed for one year. At clinical examinations, ferritinaemia concentrations were measured and all dysmetabolic parameters evaluated. MRI was performed at t...