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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepcidin is a regulatory peptide hormone acts by limiting intestinal iron absorption and promoting iron retention. Determining the level of hepcidin in anemia of prematurity might be important in preventing iron overload. This study aimed to determine serum levels of prohepcidin in newborns with anemia of prematurity, to assess the effect of a single erythrocyte transfusion on serum prohepcidin levels, and to determine the possible relationships between prohepcidin levels and serum iron and complete blood count parameters. Nineteen premature newborns with anemia of prematurity who had been treated with erythrocyte transfusions were included in this study. Just before, and 48 hours after, each transfusion, venous blood samples were collected from patients. Serum prohepcidin levels before and after erythrocyte transfusion were 206.5+/-27.3 and 205.7+/-47.1 ng/mL, respectively; no statistically significant differences were found. No significant differences existed before or after transfusion regarding serum total iron and ferritin levels, iron-binding capacity, or mean corpuscular hemoglobin concentration. No significant correlations existed between serum prohepcidin levels and other parameters, either before or after transfusions. Our results showed that there were no statistically significant differences between serum prohepcidin levels before and after a single erythrocyte transfusion in premature newborns.
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PMID:Erythrocyte transfusions and serum prohepcidin levels in premature newborns with anemia of prematurity. 1981 9

Hepcidin is a small, defensin-like peptide whose production by hepatocytes is modulated in response to anemia, hypoxia, or inflammation. We studied correlations of hepcidin concentrations with markers of iron status, erythropoietin therapy, and markers of inflammation among 130 kidney allograft recipients. In addition, we assessed the prevalence of anemia and its relation to hepcidin. Soluble receptor of transferrin (sTfR), high-sensitivity C-reactive protein (hsCRP), TNF-alpha, interleukin (IL)-6, prohepcidin, and hepcidin were measured using commercially available kits. According to the WHO definition, the prevalence of anemia was 28%. Among anemic recipients we found a significantly higher values of serum creatinine, serum prohepcidin, hepcidin, (hsCRP), TNF-alpha, IL-6, ferritin, and proteinuria in addition to more frequent use of rapamycin and significantly lower use of CSA with lower CSA concentrations, as well as lower cholesterol, hemoglobin, and estimated glomerular filtration rate (eGFR) (by the Modification of Diet in Renal Disease equation). Serum prohepcidin significantly correlated with creatinine, GFR, time after transplantation, albumin, hsCRP, IL-6, and TNF-alpha, whereas hepcidin-25 correlated with serum iron, ferritin, hsCRP, IL-6, hemoglobin, transferrin saturation (TSAT), creatinine, and GFR. Multiple regression analysis showed that prohepcidin was independently related only to GFR and ferritin. Upon multiple regression analysis, predictors of serum hepcidin were eGFR, ferritin, and hsCRP, explaining 79% of the variation of hepcidin values. In conclusion, the prevalence of anemia was relatively high among a population of kidney allograft recipients. The pathogenesis of anemia is mulitfactorial. Elevated hepcidin levels among kidney transplant recipients may be due to low-grade inflammation, which is frequently encountered in this population, and mainly to impaired renal function, but it did not seem to be a major pathogenetic factor for anemia in this population.
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PMID:A possible role of hepcidin in the pathogenesis of anemia among kidney allograft recipients. 1985 75

Hepcidin is the central regulator of systemic iron homeostasis. Dysregulation of hepcidin production results in a variety of iron disorders. Hepcidin deficiency is the cause of iron overload in hereditary hemochromatosis, iron-loading anemias, and hepatitis C. Hepcidin excess is associated with anemia of inflammation, chronic kidney disease and iron-refractory iron deficiency anemia. Diagnostic and therapeutic applications of this new knowledge are beginning to emerge. Dr. Ernest Beutler played a significant role in advancing our understanding of the function of hepcidin. This review is dedicated to his memory.
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PMID:The role of hepcidin in iron metabolism. 1990 44

Mild-to-moderate anemia often develops in the setting of acute or chronic immune activation and is termed anemia of chronic disease (ACD) or anemia of inflammation. Anemia of chronic disease is the second most common type of anemia (after anemia of iron deficiency) and results in increased morbidity and mortality of the underlying disease. Anemia of chronic disease is mediated by inflammatory cytokines and is characterized by low serum iron (hypoferremia) and often increased reticuloendothelial stores of iron. Hepcidin is the master regulator of iron homeostasis and its synthesis is inhibited by iron deficiency and stimulated by inflammation. The serum hepcidin level is useful in identifying iron deficiency in patients with ACD. Successful treatment of the underlying disease improves ACD. If that is not possible and if anemia is symptomatic, treatment with erythropoietic agents, supplemented with iron if necessary, is helpful in many cases.
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PMID:Anemia of chronic disease (anemia of inflammation). 1990 47

Hepcidin is a peptide produced by hepatocytes and detectable in blood and urine. Urinary hepcidin excretion appeared to be significantly increasing in humans with acute and chronic infections or inflammatory diseases. However, the effects of common tropical parasitic infections on hepcidin have not been sufficiently examined. We carried out a study in school children from Mali living in a neighborhood where Plasmodium falciparum malaria and Schistosoma haematobium infections are prevalent. Anemia (hemoglobin < 120 g/l) prevalence was very high among these children (68%); 24% had iron deficiency anemia. The prevalence of infections was also high (65% had at least one infection and 41% had C-reactive protein (CRP) levels > 10 mg/L). S. haematobium was diagnosed in 64%. We assessed first morning urine hepcidin excretion in a sub-sample of 15 children with either S. haematobium, P. falciparum malaria or none; 14 of these 15 children were included in the analyses. Children with P. falciparum malaria excreted significantly higher levels of hepcidin than those with S. haematobium (chi2 = 3.86; p = 0.05) or without any infection (chi2 = 5.95; p = 0.01). Urinary hepcidin correlated significantly with CRP (Spearman's r = 0.59; p = 0.001) and serum ferritin (Spearman's r = 0.73; p = 0.003). Our study confirms the still limited evidence of an association between human malaria and increased urinary hepcidin and points out the need for further studies to define the contribution of hepcidin to anemia associated with this disease.
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PMID:[Hepcidin and Plasmodium falciparum malaria in anemic school children in Mali]. 1995 May 37

Hepcidin is a small acute phase peptide that regulates iron absorption. It is induced by inflammation and infection, but is repressed by anaemia and hypoxia. Here we further reveal that hepcidin transcription also involves interactions between functional metal response elements (MREs) in its promoter, and the MRE-binding transcription factor-1. Analysis of hepcidin mRNA and protein levels in hepatoma cells suggests that its expression may be regulated by divalent metal ions, with zinc inducing maximal effects on hepcidin levels. These data suggest that this peptide may be a pleiotropic sensor of divalent metals, some of which are xenobiotic environmental toxins.
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PMID:Divalent metal-dependent regulation of hepcidin expression by MTF-1. 2002 31

Anemia of chronic disease is normocytic and normochromic. One of the mechanisms is misbalance of iron metabolism. Hepcidin, a kind of protein secreted by liver is considered to be the hormone regulating iron metabolism. It binds to ferroportin and induces the latter one's internalization. Thus, iron transportation from iron storage cells to serum is reduced. Cytokines are elevated in chronic disease. They stimulate hepcidin expression in liver through JAK2/STAT3 pathway. As a result, iron absorption and reabsorption is blocked, which leads to the misbalance of iron metabolism in anemia of chronic disease. In this article, the hepcidin and its relation to iron metabolism and anemia in chronic disease are reviewed.
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PMID:[New insights on hepcidin in anemia of chronic disease]. 2003 Sep 59

Iron maldistribution has been implicated in multiple diseases, including the anemia of inflammation (AI), atherosclerosis, diabetes, and neurodegenerative disorders. Iron metabolism is controlled by hepcidin, a 25-amino acid peptide. Hepcidin is induced by inflammation, causes iron to be sequestered, and thus, potentially contributes to AI. Human hepcidin (hHepc) overexpression in mice caused an iron-deficient phenotype, including stunted growth, hair loss, and iron-deficient erythropoiesis. It also caused resistance to supraphysiologic levels of erythropoiesis-stimulating agent, supporting the hypothesis that hepcidin may influence response to treatment in AI. To explore the role of hepcidin in inflammatory anemia, a mouse AI model was developed with heat-killed Brucella abortus treatment. Suppression of hepcidin mRNA was a successful anemia treatment in this model. High-affinity antibodies specific for hHepc were generated, and hHepc knock-in mice were produced to enable antibody testing. Antibody treatment neutralized hHepc in vitro and in vivo and facilitated anemia treatment in hHepc knock-in mice with AI. These data indicate that antihepcidin antibodies may be an effective treatment for patients with inflammatory anemia. The ability to manipulate iron metabolism in vivo may also allow investigation of the role of iron in a number of other pathologic conditions.
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PMID:Antihepcidin antibody treatment modulates iron metabolism and is effective in a mouse model of inflammation-induced anemia. 2043 Sep 64

Hepcidin is a recently recognized defensin-like peptide, which is considered to be the central regulator of iron metabolism. Hepcidin decreases the expression of iron transporting molecules. Hepcidin reduces gastrointestinal iron absorption, iron release from the macrophages, and hence it decreases serum iron levels. Clarification of hepcidin role in iron homeostasis could provide an explanation to anemia of inflammation and chronic diseases. At start of our work there was no commercially available method for measuring urine hepcidin levels. The aim of our study was to develop an easily achievable, reliable quantification method for the determination of urine hepcidin levels in human, in addition to examine a possible association of hepcidin with neonatal iron homeostasis. According to the sequence of native, human hepcidin we have synthesized peptide derivatives from which 1-7 peptide derivatives might be suitable representatives of the 25-amino-acid form of hepcidin in immune adsorption method. We presented a novel laser-desorption mass spectrometry based semi-quantitative, reproducible method for measuring hepcidin concentration in human urine first using the synthesized peptide derivative acetyl-1-25 peptide as hepcidin related internal standard. We described an easy and quickly achievable solid-phase extraction method which is suitable for purification of urine and concentration of hepcidin. In our study we have first measured serum prohepcidin and urine hepcidin in healthy human newborns. Serum prohepcidin levels showed no significant changes, however, urine hepcidin levels increased significantly during the first postnatal days. Serum prohepcidin and urine hepcidin levels showed no significant association in healthy human newborns. Associations have been demonstrated between cord blood prohepcidin values and mean corpuscular hemoglobin concentration as well as between urine hepcidin levels and serum iron and total iron binding capacity values. We have demonstrated that neonates with detectable non-protein-bound iron levels in cord blood were presented with lower prohepcidin concentrations. In summary, our results suggest a possible link between hepcidin and early iron adaptation of newborn's, however, further investigations should be done to elucidate this issue.
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PMID:[Role of iron metabolism-regulator hepcidin in perinatal iron homeostasis]. 2006 Dec 65

The hepatic peptide hormone hepcidin regulates dietary iron absorption, plasma iron concentrations, and tissue iron distribution. Hepcidin acts by causing the degradation of its receptor, the cellular iron exporter ferroportin. The loss of ferroportin decreases iron flow into plasma from absorptive enterocytes, from macrophages that recycle the iron of senescent erythrocytes, and from hepatocytes that store iron, thereby lowering plasma iron concentrations. Malfunctions of the hepcidin-ferroportin axis contribute to the pathogenesis of different anemias. Deficient production of hepcidin causes systemic iron overload in iron-loading anemias such as beta-thalassemia; whereas hepcidin excess contributes to the development of anemia in inflammatory disorders and chronic kidney disease, and may cause erythropoietin resistance. The diagnosis of different forms of anemia will be facilitated by improved hepcidin assays, and the treatment will be enhanced by the development of hepcidin agonists and antagonists.
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PMID:Targeting the hepcidin-ferroportin axis in the diagnosis and treatment of anemias. 2006 43


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