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Iron Stores (iron + store)

Distribution by Scientific Domains
Medical Sciences96%
Distribution within Medical Sciences
Gastroenterology & Hepatology22%
Hematology16%
Dermatology6%
12 Other Subdomains56%

Kinds of Iron Stores

  • body iron store
    		•

    Selected Abstracts

    Helicobacter pylori Infection and Iron Stores: A Systematic Review and Meta-analysis

    HELICOBACTER, Issue 5 2008
    Khitam Muhsen
    Abstract Background and Aims:, We carried out a systematic literature review and meta-analysis to evaluate the existing evidence on the association between Helicobacter pylori infection and iron stores. Methods:, Twelve case reports and case series, 19 observational epidemiologic studies and six intervention trials were included in the review. Results:, Although only few studies controlled for multiple potential confounders, most studies reported a positive association, linking between H. pylori and decreased body iron stores in symptomatic and asymptomatic H. pylori -infected subjects. H. pylori infection may be regarded as a risk factor for reduction in body iron stores and also for iron deficiency or iron deficiency anemia, especially in high-risk groups. The results of the meta-analysis of thoroughly designed and analyzed studies revealed an increased risk for iron deficiency anemia; pooled odds ratio (OR) 2.8 (95% confidence interval (CI) 1.9, 4.2) and also for iron deficiency; pooled OR 1.38 (95%CI 1.16,1.65) among H. pylori -infected subjects. The biologic mechanism by which H. pylori induces the alteration in the iron stores is not fully understood, but it seems to involve several pathways, including gastrointestinal blood loss, decrease in the absorption of dietary iron, and enhanced uptake of the iron by the bacterium. Conclusions:,H. pylori is associated with reduced iron stores. Future research is needed to determine whether this relationship is a causal association and to better understand its biologic mechanism. The impact of anti- H. pylori therapy on improvement of iron stores needs to be further evaluated in large and well-controlled trials. [source]

    Preferential patterns of myocardial iron overload by multislice multiecho T*2 CMR in thalassemia major patients

    MAGNETIC RESONANCE IN MEDICINE, Issue 1 2010
    Antonella Meloni
    Abstract T*2 multislice multiecho cardiac MR allows quantification of the segmental distribution of myocardial iron overload. This study aimed to determine if there were preferential patterns of myocardial iron overload in thalassemia major. Five hundred twenty-three thalassemia major patients underwent cardiac MR. Three short-axis views of the left ventricle were acquired and analyzed using a 16-segment standardized model. The T*2 value on each segment was calculated, as well as the global value. Four main circumferential regions (anterior, septal, inferior, and lateral) were defined. Significant segmental variability was found in the 229 patients with significant myocardial iron overload (global T*2 <26 ms), subsequently divided into two groups: severe (global T*2 <10 ms) and mild to moderate (global T*2 between 10 and 26 ms) myocardial iron overload. A preferential pattern of iron store in anterior and inferior regions was detected in both groups. This pattern was preserved among the slices. The pattern could not be explained by additive susceptibility artifacts, negligible in heavily iron-loaded patients. A significantly higher T*2 value in the basal slice was found in patients with severe iron overload. In conclusion, a segmental T*2 cardiac MR approach could identify early iron deposit, useful for tailoring chelation therapy and preventing myocardial dysfunction in the clinical setting. Magn Reson Med, 2010. © 2010 Wiley-Liss, Inc. [source]

    Functional studies of frataxin

    ACTA PAEDIATRICA, Issue 2004
    G Isaya
    Mitochondria generate adenosine triphosphate (ATP) but also dangerous reactive oxygen species (ROS). One-electron reduction of dioxygen in the early stages of the electron transport chain yields a superoxide radical that is detoxified by mitochondrial superoxide dismutase to give hydrogen peroxide. The hydroxyl radical is derived from decomposition of hydrogen peroxide via the Fenton reaction, catalyzed by Fe2+ ions. Mitochondria require a constant supply of Fe2+ for heme and iron-sulfur cluster biosyntheses and therefore are particularly susceptible to ROS attack. Two main antioxidant defenses are known in mitochondria: enzymes that catalytically remove ROS, e.g. superoxide dismutase and glutathione peroxidase, and low molecular weight agents that scavenge ROS, including coenzyme Q, glutathione, and vitamins E and C. An effective defensive system, however, should also involve means to control the availability of pro-oxidants such as Fe2+ ions. There is increasing evidence that this function may be carried out by the mitochondrial protein frataxin. Frataxin deficiency is the primary cause of Friedreich's ataxia (FRDA), an autosomal recessive degenerative disease. Frataxin is a highly conserved mitochondrial protein that plays a critical role in iron homeostasis. Respiratory deficits, abnormal cellular iron distribution and increased oxidative damage are associated with frataxin defects in yeast and mouse models of FRDA. The mechanism by which frataxin regulates iron metabolism is unknown. The yeast frataxin homologue (mYfhlp) is activated by Fe(II) in the presence of oxygen and assembles stepwise into a 48-subunit multimer (,48) that sequesters <2000 atoms of iron in a ferrihydrite mineral core. Assembly of mYfhlp is driven by two sequential iron oxidation reactions: a fast ferroxidase reaction catalyzed by mYfh1p induces the first assembly step (,,3), followed by a slower autoxidation reaction that promotes the assembly of higher order oligomers yielding ,48. Depending on the ionic environment, stepwise assembly is associated with the sequestration of 50,75 Fe(II)/subunit. This Fe(II) is initially loosely bound to mYfh1p and can be readily mobilized by chelators or made available to the mitochondrial enzyme ferrochelatase to synthesize heme. However, as iron oxidation and mineralization proceed, Fe(III) becomes progressively inaccessible and a stable iron-protein complex is produced. In conclusion, by coupling iron oxidation with stepwise assembly, frataxin can successively function as an iron chaperon or an iron store. Reduced iron availability and solubility and increased oxidative damage may therefore explain the pathogenesis of FRDA. [source]

    Anaemia after renal transplantation

    EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 2005
    M. Lorenz
    Abstract Anaemia is a frequent complication among long-term renal transplant recipients. A prevalence of approximately 40% has been reported in several studies. If renal function declines to stage 5 kidney disease, the prevalence of anaemia in kidney transplants is even higher. A positive correlation between haemoglobin concentration and creatinine clearance has been reported, which is a function of endogenous erythropoietin production by the functioning graft. Inflammation related to a retained kidney graft may cause hypo-responsiveness to erythropoietic agents once kidney transplant recipients return to dialysis. Furthermore, the use of azathioprine, mycophenolate mofetil and sirolimus may be associated with post-transplant anaemia. Along with erythropoietin deficiency, depletion of iron stores is one of the major reasons for anaemia in the kidney transplant population. The proportion of hypochromic red blood cells appears to be a useful parameter to measure iron supply and utilization as well as to estimate mortality risks in kidney transplant recipients. While anaemia is an important cardiovascular risk-factor after transplantation, our data suggest that anaemia is not associated with mortality and graft loss. Nevertheless, inadequate attention is paid so far to the management of anaemia after renal transplantation. A promising future aspect for risk reduction of cardiovascular disease includes the effect of erythropoietic agents on endothelial progenitor cells. [source]

    Impact of parturition on iron status in nonanaemic iron deficiency

    EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 10 2003
    A. Krafft
    Abstract Background, Iron-deficient nonanaemic parturients risk underdiagnosis as a result of the reliance on postpartum ferritin and haemoglobin as markers of iron status. Ferritin is an acute-phase protein whose levels increase during the inflammatory response, as occurs after delivery. Our aims were to evaluate the impact of parturition on iron status, erythropoiesis and the inflammatory response, and identify the optimal parameters and timing for diagnosing iron deficiency in the presence of postpartum inflammation. Materials and methods, Conventional parameters of iron status, erythropoiesis and the inflammatory response (serum ferritin, serum iron, transferrin saturation, C-reactive protein) were compared with more recent parameters [soluble transferrin receptors (sTfR), hypochromic red cells, reticulocyte indices] within 48 h either side of delivery in 64 iron-deficient nonanaemic women (defined by a prepartum serum ferritin , 15 µg L,1, and a pre- and postpartum haemoglobin of , 11·0 g dL,1 and , 10·0 g dL,1, respectively). Results, Mean sTfR decreased pre to postpartum from 7·3 to 5·8 µg mL,1 (P < 0·01), while mean serum ferritin increased from 9·7 to 16·9 µg L,1 (P < 0·01). Serum ferritin did not correlate with haemoglobin pre or postpartum (r = 0·04, P = 0·7; r = 0·2, P = 0·09), but a correlation persisted postpartum between hypochromic red blood cells and haemoglobin (r = ,0·26; P < 0·05). The percentage of hypochromic red cells remained virtually unchanged pre- and postpartum (4·0% vs. 3·8%; NS). Postpartum mean reticulocyte haemoglobin content (CHr) was 27·1 ± 1·6 pg. Conclusion, Iron status should be tested prepartum, in the absence of an inflammatory response, rather than in the early postpartum. A valuable additional parameter, where available, might be the hypochromic red cell percentage, which is virtually uninfluenced by the inflammatory response. Furthermore, hypochromic red cell percentage, CHr and sTfR can be helpful to differentiate between functional iron deficiency and depleted iron stores. [source]

    Iron status in Danish men 1984,94: a cohort comparison of changes in iron stores and the prevalence of iron deficiency and iron overload

    EUROPEAN JOURNAL OF HAEMATOLOGY, Issue 6 2002
    Nils Milman
    Abstract:,Background and objectives : From 1954 to 1987, flour in Denmark was fortified with 30 mg carbonyl iron per kg. This mandatory fortification was abolished in 1987. The aim of this study was to compare iron status in Danish men before and after abolition of iron fortification. Methods : Iron status (serum ferritin, haemoglobin), was assessed in population surveys in Copenhagen County during 1983,84 comprising 1324 Caucasian men (1024 non-blood-donors, 300 blood donors) and in 1993,94 comprising 1288 Caucasian men (1103 non-blood-donors, 185 donors), equally distributed in age cohorts of 40, 50, 60 and 70 yr. Results : In the 1984 survey median serum ferritin values in the four age cohorts in non-blood-donors were 136, 141, 133 and 111 µg/L, and in the 1994 survey 177, 173, 186 and 148 µg L ,1 , respectively. The difference was significant in all age groups ( P <0.001). There was no significant difference between the two surveys concerning the prevalence of small iron stores (ferritin 16,32 µg L ,1 ), depleted iron stores (ferritin <16 µg L ,1 ) or iron-deficiency anaemia (ferritin <13 µg L ,1 and Hb <5th percentile for iron-replete men). However, from 1984 to 1994, the prevalence of iron overload (ferritin >300 µg L ,1 ) increased from 11.3% to 18.9% ( P <0.0001). During the study period there was an increase in body mass index ( P <0.0001), alcohol consumption ( P <0.03) and use of non-steroid anti-inflammatory drugs (NSAID) ( P <0.0001), and a decrease in the use of vitamin,mineral supplements ( P <0.04) and in the prevalence of tobacco smoking ( P <0.0001). In contrast, median ferritin in blood donors showed a significant fall from 1984 to 1994 (103 vs. 74 µg L ,1 , P <0.02). Conclusion : Abolition of iron fortification reduced the iron content of the Danish diet by an average of 0.24 mg MJ ,1 , and the median dietary iron intake in men from 17 to 12 mg d ,1 . From 1984 to 1994, body iron stores and the prevalence of iron overload in Danish men increased significantly, despite the abolition of food iron fortification. The reason appears to be changes in dietary habits, with a lower consumption of dairy products and eggs, which inhibit iron absorption, and a higher consumption of alcohol, meat, and poultry, containing haem iron and enhancing iron absorption. The high prevalence of iron overload in men may constitute a health risk. [source]

    ORIGINAL ARTICLE Clinical haemophilia: Remission of paroxysmal atrial fibrillation with iron reduction in haemophilia A

    HAEMOPHILIA, Issue 5 2010
    L. R. ZACHARSKI
    Summary., Two male first cousins with mild haemophilia A had baseline factor VIII levels of 12,15% and experienced bleeding requiring coagulation factor infusion therapy with trauma and surgical procedures. Both the patients with haemophilia A also had electrocardiographically documented symptomatic paroxysmal atrial fibrillation (PAF) for several years that had become resistant to pharmacological suppression. Radiofrequency ablation was considered in both the cases but deferred considering refusal of consent by the patients to undergo the procedure. Remission of arrhythmias has been reported in patients with iron-overload syndromes. Body iron stores assessed by serum ferritin levels were elevated in both men but neither had the C282Y or H63D genes for haemochromatosis. Calibrated reduction of iron stores by serial phlebotomy, avoiding iron deficiency, was followed by remission of symptomatic PAF in both cases. Iron reduction may be an effective treatment for arrhythmias apart from the classic iron-overload syndromes and deserves further study particularly in patients with bleeding disorders who might be at risk for arrhythmias and other diseases of ageing. [source]

    Helicobacter pylori Infection and Iron Stores: A Systematic Review and Meta-analysis

    HELICOBACTER, Issue 5 2008
    Khitam Muhsen
    Abstract Background and Aims:, We carried out a systematic literature review and meta-analysis to evaluate the existing evidence on the association between Helicobacter pylori infection and iron stores. Methods:, Twelve case reports and case series, 19 observational epidemiologic studies and six intervention trials were included in the review. Results:, Although only few studies controlled for multiple potential confounders, most studies reported a positive association, linking between H. pylori and decreased body iron stores in symptomatic and asymptomatic H. pylori -infected subjects. H. pylori infection may be regarded as a risk factor for reduction in body iron stores and also for iron deficiency or iron deficiency anemia, especially in high-risk groups. The results of the meta-analysis of thoroughly designed and analyzed studies revealed an increased risk for iron deficiency anemia; pooled odds ratio (OR) 2.8 (95% confidence interval (CI) 1.9, 4.2) and also for iron deficiency; pooled OR 1.38 (95%CI 1.16,1.65) among H. pylori -infected subjects. The biologic mechanism by which H. pylori induces the alteration in the iron stores is not fully understood, but it seems to involve several pathways, including gastrointestinal blood loss, decrease in the absorption of dietary iron, and enhanced uptake of the iron by the bacterium. Conclusions:,H. pylori is associated with reduced iron stores. Future research is needed to determine whether this relationship is a causal association and to better understand its biologic mechanism. The impact of anti- H. pylori therapy on improvement of iron stores needs to be further evaluated in large and well-controlled trials. [source]

    Chronic telogen effluvium or early androgenetic alopecia?

    INTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 11 2004
    Rodney Sinclair MBBS
    A 16-year-old girl presented with a 12-month history of generalized hair shedding from the scalp. The onset of shedding coincided with the development of Hashimoto's thyroiditis and iron deficiency. At the time of initial presentation, the Hashimoto's thyroiditis had been treated with Neo-Mercazole and she was euthyroid. Her iron stores were low, with a ferritin level of 13 µg/L. As she was vegetarian, oral iron replacement therapy was commenced without further investigation. On follow-up 6 months later, her iron stores were normal (ferritin, 36 µg/L), but the hair shedding had continued. On examination, there was a positive hair pull test from both the vertex of the scalp and the occipital scalp. There was mild bitemporal recession, but no widening of the central part, and she appeared to have a full, thick head of hair (Fig. 1). Additional investigations at that time revealed normal thyroid function and negative antinuclear antibody (ANA) and syphilis serology. She was on no medication other than Neo-Mercazole. Serum testosterone, dihydroepiandosterone sulphate (DHEAS) and sex hormone binding globulin (SHBG) were normal. Two 4-mm punch biopsies were taken from the vertex of the scalp; one was sectioned horizontally and the other vertically. The vertical section was unremarkable. On the horizontal section, there were 32 hair follicles in total, 30 of which were terminal hairs and two of which were vellus hairs. One hair was in telogen. The ratio of terminal to vellus hairs was 15 : 1. Figure 1. Initial presentation A diagnosis of chronic telogen effluvium was made. The condition was explained to the patient and she was reassured that chronic telogen effluvium is not a progressive condition and does not lead to baldness. No treatment was recommended. At follow-up 12 months later, the hair loss had obviously progressed and the patient was assessed as having Ludwig Stage 1 androgenetic alopecia with widening of the central part (Fig. 2). Repeat blood tests showed normal iron studies, thyroid function, and hormone parameters. Three 4-mm punch biopsies were taken from the vertex of the scalp and all were sectioned horizontally. The terminal to vellus hair ratios were 1 : 1, 2.6 : 1, and 1.9 : 1. A diagnosis of androgenetic alopecia was made and she was commenced on oral spironolactone, 200 mg/day. Figure 2. Presentation after 12 months [source]

    Single value of serum transferrin receptor is not diagnostic for the absence of iron stores in anaemic patients with rheumatoid arthritis

    INTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY, Issue 3 2003
    S. Siebert
    Summary Serum transferrin receptor (sTfR) concentrations were measured in anaemic patients with rheumatoid arthritis (RA). Serum transferrin receptor concentrations were positively correlated with the percentage of hypochromic cells and negatively correlated with MCH. There was a weak correlation with serum ferritin (sFn) concentration but not with reticulocyte count. Thus, high concentrations of sTfR indicate iron-deficient erythropoiesis rather than levels of storage iron in the tissues. Patients were divided into three groups on the basis of sFn concentration: those with probable tissue iron deficiency, those with adequate iron stores and those with intermediate values of sFn which did not allow classification. The median sTfR concentration was significantly higher in the iron-deficient group than in the other two groups but because of overlap between the three groups, a single sTfR value was of limited value in determining the level of storage iron in an individual with RA. [source]

    Comparison of manual and automated ELISA methods for serum ferritin analysis

    JOURNAL OF CLINICAL LABORATORY ANALYSIS, Issue 5 2005
    Fabian Rohner
    Abstract Serum ferritin concentration is a sensitive measure of body iron stores. The aim of this study was to compare the performance of two commercially available enzyme-linked immunoassays (ELISAs) for serum ferritin: a widely used manual assay kit (Spectro Ferritin MT®), and a new fully automated assay (Immulite®). We analyzed serum samples from Moroccan school-aged children (n=51) from a rural area with a high prevalence of iron deficiency anemia (IDA). Four replicates of each sample were analyzed using both assays. For the manual method, the interassay repeatability was 24%, 22%, and 11%, and intraassay precision was 18.3%, 9.2%, and 9.1% at increasing serum ferritin concentrations. Using the automated assay, the interassay repeatability was 7%, 6%, and 6%, and intraassay precision was 1.5%, 5.4%, and 5.5% at increasing serum ferritin concentrations. The two assays were well correlated (y=1.16x+1.83; r=0.98). However, the limits of agreement (LOAs) were wide, particularly at low concentrations. A comparison of the assay results with recommended cutoffs for serum ferritin generated sharply different estimates of the prevalence of iron deficiency (ID) in the sample. We conclude that the automated assay has several potential advantages compared to the manual method, including better precision, less operator dependence, and faster sample through-put. J. Clin. Lab. Anal. 19:196,198, 2005. © 2005 Wiley-Liss, Inc. [source]

    Population-based study of the relationship between mutations in the hemochromatosis (HFE) gene and arthritis

    JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 3 2006
    Colin A Sherrington
    Abstract Background and Aim:, Mutations in the hemochromatosis (HFE) gene are carried by one in three individuals of British Isles descent and may result in increased iron stores. These increased iron stores could potentially induce or exacerbate diseases, such as arthritis, in which iron has a role in pathogenesis. Although arthritis is a well-known association of clinically overt hereditary hemochromatosis, controversy surrounds the role of mutations in the HFE gene as risk factors for arthritis. The aim of the present study was to determine whether mutations in the HFE gene are associated with an increased prevalence of arthritis. Methods:, A population-based study was conducted in Busselton, Western Australia, of the prevalence of arthritis in 1372 individuals of British Isles descent. Participants completed a questionnaire and general physical examination. Analysis for C282Y and H63D HFE mutations was undertaken. Unadjusted and adjusted odds ratios (OR) were calculated for the relationship between HFE mutations and the prevalence of self-reported, doctor-diagnosed arthritis. Results:, There was no association between the presence of HFE mutations and the prevalence of self-reported, doctor-diagnosed arthritis (C282Y/wild type (WT) adjusted OR = 1.041 (95% confidence interval (CI) 0.68,1.61), H63D/WT OR = 0.76 (95% CI 0.53,1.08), C282Y/C282Y OR = 0.39 (95% CI 0.04,3.63), C282Y/H 63D OR = 0.808 (95% CI 0.27,2.42), H63D/H63D OR = 0.419 (95% CI 0.13,1.36)). Overall adjusted OR for arthritis in participants with one or more HFE mutations was 0.81 (95% CI 0.61,1.09). Conclusions:, Mutations of the HFE gene are not risk factors for arthritis in populations of British Isles descent. [source]

    Genetic testing for HFE hemochromatosis in Australia: The value of testing relatives of simple heterozygotes

    JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 7 2002
    JULEEN A CAVANAUGH
    AbstractBackground : It is unclear whether screening of relatives of C282Y and H63D heterozygotes (other than compound heterozygotes) for hemochromatosis will detect sufficient numbers of cases to justify introduction of this screening strategy. Methods : Conditional probabilities were determined using published Australian allele frequencies and penetrance data to determine the detection rate of hemochromatosis by testing the siblings and offspring of heterozygotes (subjects with only one HFE mutation). Results : The number of individuals who are at risk of developing increased body iron stores because of HFE mutations is substantially higher (1 in 80) than previously estimated. In addition, 33% of the Australian population are heterozygous for either C282Y or H63D. Based on population estimates, the relative risk to the offspring of C282Y and H63D heterozygotes of developing increased iron stores is 4.1 and 1.5, respectively, while the relative risk to each sibling is 2.3 and 1, respectively. The risk of developing clinical features of hemochromatosis or hepatic fibrosis is likely to be substantially lower. Conclusions : Although the detection rate from testing the families of unaffected heterozygotes is low, this can be justified as a clinically useful screening strategy. At the present time this strategy should be restricted to first-degree relatives of heterozygotes. Further studies are recommended to determine if cascade genetic screening is a cost-effective alternative to general population screening. © 2002 Blackwell Publishing Asia Pty Ltd [source]

    Predictors of the efficacy of interferon therapy for patients with chronic hepatitis C before and during therapy: how does this modify the treatment course?

    JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 2000
    Yasushi Shiratori
    Antiviral therapy for hepatitis C virus (HCV) infection should be based on the natural history of HCV infection; there is a sequential, but slow, progression from chronic hepatitis to cirrhosis, leading to death from either liver failure or hepatocellular carcinoma (HCC). The risk of HCC development increases in association with the advance of fibrosis, and antiviral therapy can reduce this risk. More than 30 indices have been proposed as ,predictors' of favourable response to IFN therapy: host factors (age, gender, duration of HCV-infection, alcohol intake, hepatic iron stores, platelet count, histological staging of the liver disease), viral factors (HCV RNA levels in serum, HCV subtype, diversity of the hypervariable region, mutation of non-structure 5A gene), and IFN factors (dose, duration of treatment, type, treatment regimens i.e. every day vs three times a week, escalating dose regimen). Before starting IFN therapy, HCV subtype and pretreatment HCV RNA load, as well as the fibrotic stage of the liver, should be determined. The response to IFN therapy should be monitored by the HCV RNA status in serum during therapy, and the treatment regimen modified, or discontinued as required. A sustained virological response should be checked at more than 3 months after the completion of therapy. Even though the risk of HCC is markedly reduced in sustained responders, it is possible to develop HCC several years after completion of IFN therapy. [source]

    Ferroportin q248h, Dietary Iron, and Serum Ferritin in Community African-Americans With Low to High Alcohol Consumption

    ALCOHOLISM, Issue 11 2008
    Victor R. Gordeuk
    Background:, Alcohol consumption is associated with increased iron stores. In sub-Saharan Africa, high dietary ionic iron and the ferroportin Q248H allele have also been implicated in iron accumulation. We examined the associations of ferroportin Q248H, alcohol and dietary iron with serum ferritin, aspartate aminotransaminase (AST) and alanine aminotransaminase (ALT) concentrations in African-Americans. Methods:, Inner-city African-Americans (103 men, 40 women) were recruited from the community according to reported ingestion of >4 alcoholic drinks/d or <2/wk. Typical daily heme iron, nonheme iron and alcohol were estimated using University of Hawaii's multiethnic dietary questionnaire. Based on dietary questionnaire estimates we established categories of < versus ,56 g alcohol/d, equivalent to 4 alcoholic drinks/d assuming 14 g alcohol per drink. Results:, Among 143 participants, 77% drank <56 g alcohol/d and 23%,56 g/d as estimated by the questionnaire. The prevalence of ferroportin Q248H was 23.3% with alcohol >56 g/d versus 7.5% with lower amounts (p = 0.014). Among subjects with no history of HIV disease, serum ferritin concentration had positive relationships with male gender (p = 0.041), alcohol consumption (p = 0.021) and ALT concentration (p = 0.0001) but not with dietary iron intake or ferroportin Q248H. Serum AST and ALT concentrations had significant positive associations with male gender and hepatitis C seropositivity but not with alcohol or dietary iron intake or ferroportin Q248H. Conclusions:, Our findings suggest a higher prevalence of ferroportin Q248H with greater alcohol consumption, and this higher prevalence raises the possibility that the allele might ameliorate the toxicity of alcohol. Our results suggest that alcohol but not dietary iron contributes to higher body iron stores in African-Americans. Studies with larger numbers of participants are needed to further clarify the relationship of ferroportin Q248H with the toxicity of alcohol consumption. [source]

    COMPARISON OF INTRAVENOUS IRON SUCROSE VERSUS LOW-MOLECULAR-WEIGHT IRON DEXTRAN IN CHRONIC KIDNEY DISEASE

    JOURNAL OF RENAL CARE, Issue 2 2009
    Smeeta Sinha
    SUMMARY Background: Low-molecular-weight iron dextran (CosmoFer®) is the only form of parenteral iron that can be administered as a total dose infusion (TDI) in the United Kingdom (UK). This study aimed to evaluate the safety and efficacy of TDI CosmoFer in comparison to intravenous iron sucrose infusion (Venofer®) in patients with chronic kidney disease (CKD). Methods and Results: A retrospective study of outpatients with CKD undergoing intravenous TDI CosmoFer or Venofer infusion was conducted at Salford Royal Hospital and Sunderland Royal Hospital. A total of 979 doses of CosmoFer and 504 doses of Venofer were administered. There were three minor adverse events in patients receiving CosmoFer compared with one minor event in a Venofer treated patient. There were no anaphylactoid-type reactions in either group. Serum haemoglobin, ferritin and transferrin saturation (TSAT) improved significantly 4,6 months postinfusion in both treatment groups. Conclusion: TDI CosmoFer is an efficacious method of replenishing iron stores in CKD patients in an outpatient setting. Furthermore, TDI CosmoFer is safe and not associated with an increase in adverse events compared to Venofer. [source]

    Raised serum ferritin predicts non-response to interferon and ribavirin treatment in patients with chronic hepatitis C infection

    LIVER INTERNATIONAL, Issue 3 2002
    S Distante
    Abstract: Background/Aim: Previous studies have indicated that response to interferon therapy is inversely proportional to the amount of body iron stores. We have studied the relationship between serum ferritin, transferrin saturation, liver iron, presence of HFE-C282Y gene mutation and response to treatment in patients with chronic hepatitis C infection. Methods: Two hundred and fifty-six naive, HCV-RNA positive patients (60% males, median age 38 years, range 21,70) were treated with interferon and ribavirin for 6 months. Iron indices and the presence of the C282Y mutation were measured. In 242 (94%) patients iron deposition were determined by Perls staining method. Patients with negative HCV-RNA at 6 months after the end of treatment were defined as sustained viral responders. Results: Non-responders (n = 127) had significantly higher median s-ferritin values compared with sustained viral responders (130 µg/L vs. 75 µg/L P < 0.001). There was no difference in transferrin saturation among the two response groups. Only 23% (4/7) of patients with Perls grade 1 in liver biopsies responded to treatment vs. 54% (122/225) patients without iron deposition (P = 0.02), however, 10/13-non-responders had HCV genotype one. Two patients (0.8%) were homozygous for the C282Y mutation, 36 patients were heterozygous (14%). Among mutation carriers 26/38 achieved sustained response compared with 102/216 non-carriers (68% vs. 48%, P = 0.02). In a multivariate analysis s-ferritin (P = 0.030) and C282Y carrier status (P = 0.012) remained independent predict of sustained response. Conclusions: Raised s-ferritin values predicate non-response to interferon-ribavirin therapy in hepatitis C patients. Response rate in C282Y mutation carriers seems greater than in non-carriers. [source]

    Liver transplantation for hereditary hemochromatosis

    LIVER TRANSPLANTATION, Issue 8 2001
    David J. Brandhagen MD
    Although hereditary hemochromatosis (HHC) is relatively common, it is an uncommon indication for orthotopic liver transplantation (OLT). The diagnosis of HHC in patients with end-stage liver disease is difficult because many of these patients have elevated serum and tissue iron levels. Of patients undergoing OLT with iron stores in the range typical for HHC, approximately 10% are homozygous for the C282Y mutation. Most studies published to date noted decreased survival in patients who underwent OLT for HHC compared with those who underwent OLT for other indications. Death in patients with HHC was caused by increased infectious and cardiac complications. Decreased post-OLT survival in patients with iron overload appears to be independent of HFE gene status. This suggests that regardless of the cause, iron overload may be detrimental in patients undergoing OLT. Follow-up of patients undergoing OLT for HHC and case reports of the inadvertent transplantation of a liver from a donor with HHC has furthered our understanding of the pathophysiological state of iron overload in HHC. [source]

    Vegetarian and vegan diets in type 2 diabetes management

    NUTRITION REVIEWS, Issue 5 2009
    Neal D Barnard
    Vegetarian and vegan diets offer significant benefits for diabetes management. In observational studies, individuals following vegetarian diets are about half as likely to develop diabetes, compared with non-vegetarians. In clinical trials in individuals with type 2 diabetes, low-fat vegan diets improve glycemic control to a greater extent than conventional diabetes diets. Although this effect is primarily attributable to greater weight loss, evidence also suggests that reduced intake of saturated fats and high-glycemic-index foods, increased intake of dietary fiber and vegetable protein, reduced intramyocellular lipid concentrations, and decreased iron stores mediate the influence of plant-based diets on glycemia. Vegetarian and vegan diets also improve plasma lipid concentrations and have been shown to reverse atherosclerosis progression. In clinical studies, the reported acceptability of vegetarian and vegan diets is comparable to other therapeutic regimens. The presently available literature indicates that vegetarian and vegan diets present potential advantages for the management of type 2 diabetes. [source]

    Moving Toward a Plant-based Diet: Are Iron and Zinc at Risk?

    NUTRITION REVIEWS, Issue 5 2002
    Janet R. Hunt Ph.D.
    With reduced intake of meat and increased intake of phytate-containing legumes and whole grains, movement toward plant-based diets reduces dietary iron and zinc absorption. Although vegetarians have lower iron stores, adverse health effects of lower iron and zinc absorption have not been demonstrated with varied, plant-based diets consumed in developed countries. Improved assessment methods and monitoring are needed to detect and prevent possible iron and zinc deficiency with plant-based diets. [source]

    Iron and Colorectal Cancer Risk: Human Studies

    NUTRITION REVIEWS, Issue 5 2001
    F.A.C.S., Richard L. Nelson M.D
    Some reports have associated iron with cancer risk, particularly of the colorectum. This review will focus on the human studies that have investigated this association. Comparative studies were sought in which people with and without colorectal neoplastic lesions, either cancers or adenomatous polyps, were assessed for iron exposure. Iron exposure variables included dietary iron intake, iron vitamin supplementation, body iron stores as measured by ferritin or transferrin saturation, and gene status for hereditary hemochromatosis. Medline was searched for published reports using the key words iron, cancer, colon, rectum, ferritin, transferrin, and hemochromatosis. In addition, the Cochrane Library was searched for relevant studies and several authors were contacted to investigate their awareness of unpublished studies. Studies were categorized by study design and ranked for quality of innovation in design, sample size, and thoroughness of iron status ascertainment. Thirty-three studies were reviewed in 26 publications. Of the larger studies, approximately three-quarters supported the association of iron, in all three strata of exposure, with colorectal neoplasia risk. Because iron is broadly supplemented in the American diet, the benefits of iron supplementation need to be measured against the long-term risks of increased iron exposure, one of which may be increased risk of colorectal cancer. [source]

    Prevalence of anaemia and the contribution of functional iron deficiency in diabetes related chronic kidney disease

    PRACTICAL DIABETES INTERNATIONAL (INCORPORATING CARDIABETES), Issue 3 2010
    MRCP Specialist Registrar in Diabetes & Endocrinology, MS Rathi MBBS
    Abstract Anaemia is often an unrecognised complication of diabetes that has an adverse effect on the progression of diabetes related complications. Anaemia predicts mortality in diabetes related chronic kidney disease (CKD). Contributors to its development include absolute and/or functional iron deficiency and erythropoietin insufficiency. This study aimed to look at the prevalence of anaemia and markers of iron deficiency in patients with diabetes related CKD. An analysis was done of the results from all patients (225 men, 93 women; mean age 70 years) attending joint diabetes,renal clinics over a 12-month period. Haemoglobin (Hb) was measured in 88%. The mean Hb was 12.6g/dl in men and 11.7g/dl in women. A total of 21.5% (11.5% men, 10% women) had Hb <11g/dl who should have anaemia management as per National Institute for Health and Clinical Excellence guidelines. Among the anaemic population, CKD stage 3 was present in 25% of men and in 8% of women, with CKD stage 4 present in 20% of men and in 32% of women. Fifty-three percent had absolute iron deficiency (serum ferritin <100,g/L) and 41% had inadequate iron stores (serum ferritin between 100 and 500,g/L). Functional iron deficiency defined by serum ferritin >100,g/L and red cell hypochromasia ,6% was noted in 21.6% of anaemic patients. Anaemia is a frequent finding in patients with diabetes related CKD. A significant proportion of patients had functional iron deficiency that required iron therapy for optimisation of their iron stores before starting erythropoiesis-stimulating agents. Measurement of red cell hypochromasia is a valuable tool to detect this group of patients. Copyright © 2010 John Wiley & Sons. [source]

    Regulatory mechanisms of intestinal iron absorption,Uncovering of a fast-response mechanism based on DMT1 and ferroportin endocytosis

    BIOFACTORS, Issue 2 2010
    Marco T. Núñez
    Abstract Knowledge on the intestinal iron transport process and the regulation of body iron stores has greatly increased during the last decade. The liver, through the sensing of circulating iron, is now recognized as the central organ in this regulation. High iron levels induce the synthesis of hepcidin, which in turn decreases circulating iron by inhibiting its recycling from macrophages and its absorption at the intestine. Another mechanism for the control of iron absorption by the enterocyte is an active Iron Responsive Element (IRE)/Iron Regulatory Protein (IRP) system. The IRE/IRP system regulates the expression of iron uptake and storage proteins thus regulating iron absorption. Similarly, increasing evidence points to the transcriptional regulation of both divalent metal transporter 1 (DMT1) and ferroportin expression. A new mechanism of regulation related to a phenomenon called the mucosal block is starting to be unveiled. The mucosal block describes the ability of an initial dose of ingested iron to block absorption of a second dose given 2,4 h later. Here, we review the mechanisms involved in the expression of DMT1 and ferroportin, and present recent evidence on the molecular components and cellular processes involved in the mucosal block response. Our studies indicate that mucosal block is a fast-response endocytic mechanism destined to decrease intestinal iron absorption during a high ingest of iron. [source]

    There is no clear association between low serum ferritin and chronic diffuse telogen hair loss

    BRITISH JOURNAL OF DERMATOLOGY, Issue 5 2002
    R. Sinclair
    SummaryBackground Low iron stores are considered a possible cause of chronic diffuse telogen hair loss in women. Estimation of serum ferritin is recommended as part of the initial assessment when women present with chronic diffuse telogen hair loss, and iron supplementation therapy is commonly recommended for those found to have low iron stores. Objectives To evaluate the relationship between low serum ferritin (,20 µg L,1) and chronic diffuse telogen hair loss in women. Methods Between 1997 and 1999, 194 consecutive women who presented to a specialist hair clinic were assessed for diffuse telogen hair loss of greater than 6 months duration. All underwent biochemical investigations that included serum ferritin and had two 4-mm punch biopsies taken from the vertex of the scalp. One biopsy was sectioned horizontally and the other vertically. Results Twelve women were found to have a serum ferritin of 20 µg L,1 or less (6·2%). Androgenetic alopecia was found on scalp biopsy in seven of these 12 women, while the other five women had normal histology. The five women with low iron stores and normal histology were treated with iron supplementation alone. This was continued until the serum ferritin was > 20 µg L,1. Cessation or reversal of hair loss was not seen in any of these women. Conclusions No direct relationship between low serum ferritin and hair loss can be established. The usefulness of serum ferritin in the routine investigation of women with chronic diffuse telogen hair loss is unclear, as is the role of iron supplementation therapy in the management of hair loss. [source]

    Role of iron in carcinogenesis: Cancer as a ferrotoxic disease

    CANCER SCIENCE, Issue 1 2009
    Shinya Toyokuni
    Iron is abundant universally. During the evolutionary processes, humans have selected iron as a carrier of oxygen inside the body. However, iron works as a double-edged sword, and its excess is a risk for cancer, presumably via generation of reactive oxygen species. Thus far, pathological conditions such as hemochromatosis, chronic viral hepatitis B and C, exposure to asbestos fibers, as well as endometriosis have been recognized as iron overload-associated risks for human cancer. Indeed, iron is carcinogenic in animal experiments. These reports unexpectedly revealed that there are target genes in iron-induced carcinogenesis and that iron-catalyzed oxidative DNA damage is not random in vivo. Several iron transporters and hepcidin, a peptide hormone regulating iron metabolism, were discovered in the past decade. Furthermore, a recent epidemiological study reported that iron reduction by phlebotomy decreased cancer risk in the apparently normal population. These results warrant reconsideration of the role of iron in carcinogenesis and suggest that fine control of body iron stores would be a wise strategy for cancer prevention. (Cancer Sci 2009; 100: 9,16) [source]