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Giorgio Maria Saracco, Andrea Evangelista, Sharmila Fagoonee, Giovannino Ciccone, Elisabetta Bugianesi, Gian Paolo Caviglia, Maria Lorena Abate, Mario Rizzetto, Rinaldo Pellicano, Antonina Smedile
AIM: To assess the etiology of chronic liver diseases (CLD) from 1998 to 2014 at the outpatient clinic of Gastroenterology of the main hospital in Northwest of Italy among those dedicated to hepatology. METHODS: A random sample of charts of patients referred to for increased liver enzymes between January 1998 and December 2006, and between January 2012 and December 2014 were reviewed. Etiology search included testing for hepatitis B virus (HBV), hepatitis C virus (HCV), autoimmune hepatitis, primary biliary cirrhosis, Wilson's disease and hereditary hemocromatosis...
September 28, 2016: World Journal of Gastroenterology: WJG
Shinya Akatsuka, Shinya Toyokuni
Though iron is an essential micronutrient for humans, the excess state is acknowledged to be associated with oncogenesis. For example, iron overload in the liver of the patients with hereditary hemocromatosis highly increases the risk of hepatocellular carcinoma. Also, as to asbestos-related mesothelioma, such kinds of asbestos with a higher iron content are considered to be more carcinogenic. Iron is a useful element, which enables fundamental functions for life such as oxygen carrying and electron transport...
July 2016: Nihon Rinsho. Japanese Journal of Clinical Medicine
Herminio López-Escribano, Joana F Ferragut, Maria M Parera, Pilar Guix, José A Castro, M Misericòrdia Ramon, Antònia Picornell
Co-inheritance of mutations in the HFE gene underlying hereditary hemocromatosis (HH) may play a role in the variability of iron status in patients with β-thalassemia (β-thal) minor. Different studies have yielded conflicting results: some suggest iron overload might arise from the interaction of the β-thal trait with homozygosity or even heterozygosity for HFE mutations and others that it was unrelated to the HFE genotype. Because of the high frequency of HFE mutations in the Balearic Islands, where the β-thal trait is also moderately common, it is of interest to evaluate the effect of the co-inheritance of mutations in both genes on the severity of iron loading...
2012: Hemoglobin
Núria Freixenet, Carme Vilardell, Gemma Llauradó, Olga Giménez-Palop, Eugenio Berlanga, Cristina Gutiérrez, Assumpta Caixàs, Joan Vendrell, José Miguel González-Clemente
AIM: To assess the role of iron overload in type 2 diabetic men with hyperferritinemia. METHODS: 150 men were recruited from a genetic screening programme for hereditary hemocromatosis (HH) and were tested for type 2 diabetes, other components of the metabolic syndrome, beta cell function (BCF), insulin sensitivity, high-sensitivity C-reactive protein and iron overload. RESULTS: Fifty-one men had type 2 diabetes. They were older (p=0.017) and 99 had lower BCF (p<0...
February 2011: Diabetes Research and Clinical Practice
Marco Andreani, Francesca Clementina Radio, Manuela Testi, Carmelilia De Bernardo, Maria Troiano, Silvia Majore, Pierfrancesco Bertucci, Paola Polchi, Renata Rosati, Paola Grammatico
Hepcidin is a 25-amino acid peptide, derived from cleavage of an 84 amino acid pro-peptide produced predominantly by hepatocytes. This molecule, encoded by the hepcidin antimicrobial peptide (HAMP) gene shows structural and functional properties consistent with a role in innate immunity. Moreover, as demonstrated in mice and humans, hepcidin is a major regulator of iron metabolism, and acts by binding to ferroportin and controlling its concentration and trafficking. In this study we investigated the influence that mutations in HAMP and/or hemocromatosis (HFE) genes might exert on iron metabolism in a group of poly-transfused thalassemic patients in preparation for bone marrow transplantation...
September 2009: Haematologica
Roberto Miniero, Irene Tardivo, Antonella Roetto, Marco De Gobbi
At age of 3.2 years routine blood analysis showed the presence of a beta-thalassemic trait with unexpected high level of serum iron and high transferrin saturation. Hematological follow-up confirmed the moderate degree of anemia and persisting high levels of iron indices throughout the years with a progressive increase of serum ferritin. At the age of 19 years the patient was diagnosed homozygous for HC63D HFE. The patient referred by us confirm the possibility of precocious alteration of iron indices in patients with heterozygosity for beta-thalassemia inherited together with HFE mutations...
March 2005: Pediatric Hematology and Oncology
Massimo Franchini, Dino Veneri
Hereditary hemochromatosis is a disorder of iron metabolism characterized by a progressive tissue iron overload which leads to an irreversible organ damage if it is not treated timely. The recent developments in the field of molecular medicine have radically changed the physiopathology and the diagnosis of this disease. However, transferrin saturation and serum ferritin are still the most reliable tests for the detection of subjects with hereditary hemochromatosis. Therapeutic phlebotomy is the mainstay of the treatment of hereditary hemochromatosis...
October 2004: Recenti Progressi in Medicina
A Pardo, E Quintero, Y Barrios, M Bruguera, L Rodrigo, C Vila, D Acero, C Guarner, S Pascual, L López, R Moreno, E Fábrega, R Andrade, G Peláez, J Santos, M Buti, M Torres
INTRODUCTION: The prevalence of C282Y homozygosity in patients with hereditary hemochromatosis (HH) has been reported to be markedly lower in the Mediterranean Basin than in northern Europe. In Spain, the available data are contradictory and limited to small series in specific regions. The objective of this study is to determine the prevalence of the 2 main HFE gene mutations in a large series of unrelated Spanish patients with HH from different geographical origins. PATIENTS AND METHOD: The criteria for HH diagnosis were: repeat serum transferrin saturation index (> 45% plus C282Y homozygosity and/or hepatic iron index (> 1...
October 2004: Gastroenterología y Hepatología
Graciela Nardi, Claudia Cadiz, J Lachman, Cecilia Cornelio
Hereditary hemocromatosis (HH) is a genetic disease with a recessive autosomic pattern, in which inadequate iron (Fe) absorption is made by the intestinal cell. As consequence of that process, takes place a progressive accumulation of metal in different organs, predominantly in the liver. This leads to an alteration of liver structure and function: cirrhosis and hepatocarcinoma (1). The gene implied in this pathology was identified (HFE) in 1996. This codes a similar molecule to the mayor histocompatibility complex type 1(MHC-T1 like) that can modulate the transport of PE binding the transferrin receptor...
2003: Acta Gastroenterologica Latinoamericana
No abstract text is available yet for this article.
September 1958: Revue du Rhumatisme et des Maladies Ostéo-articulaires
M Galleano, S Puntarulo
1. Hepatotoxicity is the most common finding in patients with iron overload since the liver is the major recipient of iron excess, even though the kidney could be a target of iron toxicity. The effect of iron overload was studied in the early stages after iron-dextran injection in rats, as a model for secondary hemocromatosis. 2. Total hepatic and kidney iron content was markedly elevated over control values 20 h after the iron administration. Plasma GOT, GPT and LDH activities were not affected, suggesting that liver cell permeability was not affected by necrosis...
October 1994: Brazilian Journal of Medical and Biological Research, Revista Brasileira de Pesquisas Médicas e Biológicas
R Galanello, M A Melis, E Paglietti, G Cornacchia, S de Virgiliis, A Cao
This study shows that hemoglobin H disease patients aged between 0.5 and 44 years, usually (27 out of 30) have normal serum ferritin levels according to age. This reconfirms that in this disease there are usually normal iron stores. However, in a few patients (3 out of 30) increased levels were found. This may be due to inappropriate iron medication, transfusions or associated idiopathic hereditary hemocromatosis gene.
1983: Acta Haematologica
H Schnack, W Waldhäusl
No abstract text is available yet for this article.
April 1, 1966: Wiener Klinische Wochenschrift
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