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Serum Ferritin

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5601. Relative contribution of iron burden, HFE mutations, and insulin resistance to fibrosis in nonalcoholic fatty liver. Full Text available with Trip Pro

. Univariate analysis demonstrated that the presence of severe fibrosis was independently associated with older age, female sex, overweight, aspartate/alanine aminotransferase ratio, serum ferritin level, fasting glucose and insulin levels, decreased insulin sensitivity, and with histologic features (degree of necroinflammation and steatosis). After adjustment for body mass index (BMI), age, sex, and degree of steatosis, ferritin levels (odds ratio [OR] = 1.77; 95% CI = 1.21- 2.58; P =.0032) and the oral (...) glucose insulin sensitivity (OR = 0.53; CI = 0.33-0.87; P =.0113) were independent predictors of severe fibrosis. In conclusion, the current study indicates that insulin resistance is a major, independent risk factor for advanced fibrosis in patients with NAFLD. Increased ferritin levels are markers of severe histologic damage, but not of iron overload. Iron burden and HFE mutations do not contribute significantly to hepatic fibrosis in the majority of patients with NAFLD.

2004 Hepatology

5602. Increased duodenal expression of divalent metal transporter 1 and iron-regulated gene 1 in cirrhosis. (Abstract)

]), hephaestin, and duodenal cytochrome b (Dyctb) in 46 patients with cirrhosis and 20 control subjects. Total RNA samples were extracted from duodenal biopsy samples and the expression of the iron transport genes was assessed by ribonuclease protection assays. Expression of DMT1 and Ireg1 was increased 1.5 to 3-fold in subjects with cirrhosis compared with iron-replete control subjects. The presence of cirrhosis per se and serum ferritin (SF) concentration were independent factors that influenced

2004 Hepatology

5603. Patient and graft survival after liver transplantation for hereditary hemochromatosis: Implications for pathogenesis. (Abstract)

. All 22 subjects who received liver transplants for HH were male; 13 had other risk factors for liver disease. HH patients had comparatively poor outcomes following transplantation: survival at 1, 3, and 5 years posttransplantation were 72%, 62%, and 55%, respectively. Recurrent hepatocellular cancer was the most common cause of death. There was no convincing evidence of reaccumulation of iron in the grafted liver in HH; however, 1 subject demonstrated increased serum ferritin concentration

2004 Hepatology

5604. Patient compliance with phlebotomy therapy for iron overload associated with hemochromatosis. (Abstract)

to achieve iron depletion; and 3) participation in therapy to maintain serum ferritin serum ferritin concentration, HFE genotype, units of blood removed to achieve iron depletion, and presence or absence of cirrhosis at diagnosis.A total of 118 patients were evaluable for iron depletion and 142 for maintenance therapy; 96.6% achieved iron (...) Patient compliance with phlebotomy therapy for iron overload associated with hemochromatosis. The aim of this study was to evaluate patient compliance with phlebotomy therapy of hemochromatosis-associated iron overload.We reviewed medical records of white adults with hemochromatosis and iron overload diagnosed during medical care. We defined three elements of compliance: 1) achieving iron depletion (serum ferritin

2003 American Journal of Gastroenterology

5605. Development of an HCV infection risk stratification algorithm for patients on chronic hemodialysis. (Abstract)

Development of an HCV infection risk stratification algorithm for patients on chronic hemodialysis. The prevalence of hepatitis C virus (HCV) in patients on chronic hemodialysis (HD) is near 9%. Transaminases, which are lower in HD patients, are not effective in screening for HCV. Our aim was to design an HCV risk stratification strategy incorporating lowered aminotransferase levels and other clinical parameters.Patient serum from 168 consecutive HD patients was analyzed for AST, ALT, ferritin

2002 American Journal of Gastroenterology

5606. Racial differences in the relationship between hepatitis C infection and iron stores. Full Text available with Trip Pro

determined the risk of having increased iron stores, defined as elevation of both serum ferritin and transferrin-iron saturation (TS), in HCV-RNA-positive blacks (n = 100) and nonblacks (n = 126) relative to HCV-RNA-negative blacks (n = 4,002) and nonblacks (n = 10,943). HCV-positive blacks were 5.4 times (95% CI, 1.2 to 24) more likely to have increased iron stores than HCV-positive nonblacks. The proportion of HCV-positive blacks who had increased iron stores was 16.4% among those with abnormal liver

2003 Hepatology

5607. Hepatic iron concentration does not predict response to standard and pegylated-IFN/ribavirin therapy in patients with chronic hepatitis C. (Abstract)

: 40.8+/-10.7) with CHC. 140 patients were treated with standard IFN/ribavirin, 29 patients with pegylated-IFN/ribavirin. Biopsy specimens were evaluated according to the DiBisceglie scoring system and iron grading. HIC was determined by atomic absorption spectroscopy. Ferritin and transferrin saturation and presence of HFE-C282Y and H63D gene mutations were determined at baseline.Nonresponders to combination therapy had higher serum ferritin levels at baseline (p<0.01). There was no difference (...) of HIC, transferrin saturation levels, and the HFE-mutation status between responders and nonresponders. Logistic regression analysis revealed serum ferritin as an independent predictor of response. HIC correlated with the DiBisceglie score (r=0.352, p<0.001), iron grading (r=0.352, p<0.001) and serum ferritin (r=0.335, P<0.001).Pretreatment liver iron concentration does not predict response to combination therapy in patients with CHC. In contrast, high baseline serum ferritin levels are predictors

2004 Journal of Hepatology

5608. Autosomal dominant iron overload due to a novel mutation of ferroportin1 associated with parenchymal iron loading and cirrhosis. (Abstract)

Autosomal dominant iron overload due to a novel mutation of ferroportin1 associated with parenchymal iron loading and cirrhosis. We report the identification of a novel mutation in ferroportin1 in an Australian family with autosomal dominant iron overload. The phenotype of iron overload in one member of this family is associated with high serum ferritin concentration and elevated transferrin saturation. The pattern of iron overload in the liver shows accumulation predominantly in parenchymal

2004 Journal of Hepatology

5609. Noninvasive prediction of cirrhosis in C282Y-linked hemochromatosis. Full Text available with Trip Pro

. Prediction of cirrhosis was assessed first by univariate regression analysis. Variables significantly related to cirrhosis were then evaluated by stepwise linear multivariate regression. Receiver operating characteristic curve analysis of the most informative variables from multivariate analysis was then used to devise a clinically applicable index for the noninvasive prediction of cirrhosis. This index was then validated in 162 C282Y homozygous patients in France. Ferritin, blood platelets (...) , and aspartate transaminase (AST) level were selected for the clinical index. The combination of ferritin levels of 1,000 microg/L or greater, platelet levels of 200 x 10(9)/L or less, and AST levels above the upper limit of normal led to a correct diagnosis of cirrhosis in 77% of Canadian patients. In the French patients, this led to a correct diagnosis of cirrhosis in 90%. In conclusion, in C282Y homozygous patients, a combination of easily measured laboratory variables (ferritin, platelets, AST) can

2002 Hepatology

5610. Increased DMT1 but not IREG1 or HFE mRNA following iron depletion therapy in hereditary haemochromatosis. Full Text available with Trip Pro

patients (prior to and following phlebotomy), in patients with iron deficiency (ID), and in controls.DMT1, IREG1, and HFE mRNA were measured in duodenal tissue of C282Y homozygous HH patients, in ID patients negative for the C282Y mutation with a serum ferritin concentration less than 20 microg/l, and in controls negative for C282Y and H63D mutations with normal iron indices, using real time polymerase chain reaction.DMT1 and IREG1 mRNA levels were not significantly different in non-phlebotomised

2004 Gut

5611. HFE mutations and chronic hepatitis C: H63D and C282Y heterozygosity are independent risk factors for liver fibrosis and cirrhosis. (Abstract)

patients.Allele frequencies of the C282Y and H63D mutation did not differ between HCV patients and healthy controls (6.95 vs. 6.2%; 14.75 vs. 16.4%; n.s.). HFE heterozygous HCV patients had higher ferritin (349+/-37 vs. 193+/-15 microg/l; P<0.0005), TS (38+/-2 vs. 32+/-1%; P<0.0005), serum iron (144+/-6 vs. 121+/-3 microg/dl; P<0.0005), semiquantitative liver iron staining (0.26+/-0.07 vs. 0.09+/-0.03; P<0.006) and fibrosis scores (1.9+/-0.2 vs. 1.4+/-0.1; P<0.003) compared to HFE wildtypes. By multivariate (...) HFE mutations and chronic hepatitis C: H63D and C282Y heterozygosity are independent risk factors for liver fibrosis and cirrhosis. The impact of heterozygous HFE mutations on the course of chronic hepatitis C and iron indices was studied.Ferritin, transferrin saturation (TS), serum iron, C282Y and H63D mutations were determined in 401 patients with chronic hepatitis C virus (HCV) infection and 295 healthy controls. Liver histologies were available in 217 and HCV genotypes in 339

2003 Journal of Hepatology

5612. Concordance of iron indices in homozygote and heterozygote sibling pairs in hemochromatosis families: implications for family screening. (Abstract)

=0.01) were highly concordant in C282Y homozygotes. Heterozygote siblings were concordant for serum ferritin (r=0.76, P=0.0001) and transferrin saturation (r=0.79, P=0.0001). Homozygote-normal same-sex dizygotic twins were concordant for serum ferritin (r=0.62, P=0.0001) but not for transferrin saturation.Concordance of iron indices exists in C282Y homozygote and heterozygote sibling pairs. Siblings of expressing C282Y heterozygotes require phenotypic assessment. These data provide evidence (...) of disease expression, and guidance for family screening strategies of subjects heterozygous for the C282Y mutation.We compared the iron indices of 35 C282Y homozygous and 35 C282Y heterozygous same-sex sibling pairs. To clarify whether concordance between siblings was due to environmental or genetic factors we compared the iron indices of 164 C282Y homozygous-normal, same-sex dizygotic twins.Serum ferritin (r=0.50, P=0.003), hepatic iron concentration (r=0.61, P=0.025) and hepatic iron index (r=0.67, P

2002 Journal of Hepatology

5613. Novel mutation in ferroportin 1 gene is associated with autosomal dominant iron overload. (Abstract)

overload entity, which corresponds to a particular phenotypic expression (high serum ferritin values contrasting with relatively low transferring saturation, and important Kupffer cell iron deposition as compared to hepatocytic iron excess) with poor tolerance of venesection therapy and a dominant pattern of inheritance. Given this dominant transmission, the mixed Causasian-Asian origin of our Asian proband leaves open the issue of the ethnic origin of the new mutation.

2003 Journal of Hepatology

5614. Duodenal expression of iron transport molecules in untreated haemochromatosis subjects. Full Text available with Trip Pro

in haemochromatosis patients and iron replete subjects but in haemochromatosis patients with elevated serum ferritin concentrations, both DMT1 (IRE) and Ireg1 expression were inappropriately increased relative to serum ferritin concentration. Hephaestin and Dcytb levels were not upregulated in haemochromatosis. DMT1 (IRE) and Ireg1 levels showed significant inverse correlations with serum ferritin concentration in each group of patients.These findings are consistent with DMT1 (IRE) and Ireg1 playing primary roles (...) in the adaptive response to iron deficiency. Untreated haemochromatosis patients showed inappropriate increases in DMT1 (IRE) and Ireg1 expression for a given level of serum ferritin concentration, although the actual level of expression of these iron transport genes was not significantly different from that of normal subjects.

2003 Gut

5615. Mild iron overload in patients carrying the HFE S65C gene mutation: a retrospective study in patients with suspected iron overload and healthy controls. Full Text available with Trip Pro

and HFE mutation analysis (for the C282Y, H63D, and S65C mutations) were analysed in 250 healthy control subjects and collected retrospectively in 296 patients with suspected iron overload (elevated serum ferritin and/or transferrin saturation). The frequency of patients having at least mild iron overload, and mean serum ferritin and transferrin saturation values were calculated for each HFE genotype. For patients carrying the S65C mutation, clinical data, liver biopsy results, and amount of blood (...) removed at phlebotomy were determined.The HFE S65C mutation was found in 14 patients and eight controls. In controls, the S65C allele frequency was 1.6%. The S65C allele frequency was enriched in non-C282Y non-H63D chromosomes from patients (4.9%) compared with controls (1.9%) (p<0.05). Serum ferritin was significantly increased in controls carrying the S65C mutation compared with those without HFE mutations. Fifty per cent of controls and relatives having the S65C mutation had elevated serum ferritin

2002 Gut

5616. Infectious and inflammatory stimuli decrease endothelial nitric oxide synthase activity in vitro. (Abstract)

Infectious and inflammatory stimuli decrease endothelial nitric oxide synthase activity in vitro. Perturbation of iron metabolism, especially the increase of serum ferritin levels, is often associated with both inflammation and hypertension. Changes in iron availability can affect an important regulator of vascular tone, the endothelial nitric oxide synthase (eNOS), activated by a heme-dependent dimerization.To study the regulation of the anti-hypertensive eNOS in human endothelial cells (...) , in correlation with iron metabolism alterations and stimuli triggering them in vivo, such as inflammation or infection.Cells were treated with stimuli mimicking infection or inflammation [lipopolysaccharide (LPS) and/or tumor necrosis factor alpha (TNFalpha)]. and iron shortage (succinylacetone and desferrioxamine). The effect on eNOS expression and activation was evaluated, as well as ferritin content.eNOS protein expression was evaluated by separating the monomeric from the active dimeric form by low

2003 Journal of Hypertension

5617. Hemochromatosis mutations are not linked to dilated cardiomyopathy in Israeli patients. Full Text available with Trip Pro

cardiomyopathy. Details were recorded of clinical and echocardiographic parameters. DNA was extracted from peripheral blood and checked for the presence of the C282Y and H63D mutations by a commercially available single nucleotide primer extension assay. A control group of 98 healthy blood donors was also checked for the presence of these mutations. Of the 157 patients, 42 (26.75%) had at least one mutation. Five (3.65%) were homozygotic for the H63D mutation and 37 (23.6%) were heterozygotic for the H63D (...) mutation. The C282Y mutation was not present. In a control population of 98 healthy blood donors, 27 (27.6%) were heterozygous for the H63D population and none had the C282Y mutation (no significant difference between the patients with cardiomyopathy and the healthy blood donors, chi(2) test 0.754). There was a non-significant trend to a difference in the prevalence of homozygotic H63D between the cardiomyopathy patients and the healthy blood donors (3.18% vs. 0%, P=0.076, chi(2) test

2004 European Journal of Heart Failure

5618. Oxidized low-density lipoprotein, iron stores, and haptoglobin polymorphism. (Abstract)

Oxidized low-density lipoprotein, iron stores, and haptoglobin polymorphism. In vitro experimental studies demonstrated that iron promotes free radical-induced low-density lipoprotein (LDL) oxidation.To test the hypothesis that circulating oxidized LDL (oxLDL) levels might be associated with body iron stores (serum ferritin) and iron-related genetic markers (hemochromatosis gene C282Y mutation, haptoglobin polymorphism).We investigated 381 (176 males, 205 females, age 45 +/- 6 years) healthy (...) Caucasians. Serum oxLDL, assayed by a mAb-4E6-based enzyme-linked immunosorbent assay (ELISA), was expressed as oxLDL/LDL ratio to adjust for serum LDL-cholesterol concentration. Hemochromatosis gene C282Y mutation analysis was performed by a Taqman-based polymerase chain reaction (PCR) assay. Haptoglobin (Hp) phenotypes (Hp 1-1, Hp 2-1, Hp 2-2) were determined by starch gel electrophoresis.In stepwise multivariate regression analysis, gender (P < 0.0001), current smoking (P < 0.0001), HDL-cholesterol (P

2004 Atherosclerosis

5619. Left ventricular remodelling, and systolic and diastolic function in young adults with beta thalassaemia major: a Doppler echocardiographic assessment and correlation with haematological data. Full Text available with Trip Pro

data, only serum ferritin showed a weak negative correlation with left ventricular ejection fraction. The patients with the highest serum ferritin (> 2500 ng/ml) had the lowest ejection fraction.Patients with beta thalassaemia on an adequate transfusion and chelation treatment regimen show abnormal left ventricular remodelling with increased volumes, mass, and mass/volume ratio. Systolic chamber function and contractile state are reduced, with a slightly increased afterload. These findings seem (...) mainly to be related to the increased cardiac output caused by chronic anaemia. Left ventricular performance is better preserved when chelation treatment is adjusted to maintain the serum ferritin concentration at < 1000 ng/ml.

2003 Heart

5620. Iron withdrawal strategies fail to prevent the growth of SiHa-induced tumors in mice. (Abstract)

continued for 5 weeks after injection of the tumor cells. Treatment with the maximum tolerated doses of DFO, L1, or starch-DFO conjugate induced no significant iron deprivation in non-iron-overloaded mice, while an iron-poor diet led to a dramatic decrease in serum iron, transferrin iron saturation, and ferritin levels. However, neither iron chelators nor an iron-poor diet could significantly inhibit tumor growth.Despite a potent antitumor effect in vitro, iron chelators fail to prevent the growth

2003 Gynecologic Oncology

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