1.
Lower serum prohepcidin levels associated with lower iron and erythropoietin requirements in hemodialysis patients with chronic hepatitis C.
Caliskan, Y, Yelken, B, Ozkok, A, Gorgulu, N, Yazici, H, Telci, A, Yildiz, A
BMC nephrology. 2012;:56
Abstract
BACKGROUND Patients with chronic HCV infection have increased liver iron. Recently identified protein hepcidin synthesized in the liver, is thought to be a key regulator for iron homeostasis and is induced by infection and inflammation. Lower erythropoietin and iron supplementation requirements were previously reported in HD patients with HCV infection. We investigated the association of prohepcidin with inflammation and iron parameters in HD patients with and without chronic HCV infection. METHODS Sixty patients (27 male, 33 female, mean age 50±15 years) on chronic HD were included. Parameters related to iron metabolism (ferritin, serum iron and total iron binding capacity (TIBC)), inflammation (hs-CRP, TNF-α and IL-6) and prohepcidin levels were measured. The response to treatment (erythropoiesis-stimulating agent (ESA) resistance index) was assessed from the ratio of the weekly erythropoietin (rhuEPO) dose to hemoglobin (Hb) per unit weight. RESULTS Serum prohepcidin levels of HCV positive patients (135±25 ng/mL) were significantly lower than HCV negative patients [148±18 ng/mL, (p=0.025)]. Serum IL-6 levels of HCV positive patients were also significantly lower than HCV negative patients (p=0.016). Serum prohepcidin levels were positively correlated with ferritin (r=0.405, p=0.001) and IL-6 (r=0.271, p=0.050) levels in HD patients. In the HCV positive group, serum prohepcidin levels significantly correlated with ferritin levels (r=0.514 p=0.004). In the HCV negative group, serum prohepcidin levels significantly correlated with serum IL-6 levels (r=0.418, p=0.027). In multiple regression analysis performed to predict prohepcidin in HCV positive patients, serum ferritin was found to be an independent variable (r=0.28, p=0.008). CONCLUSIONS HCV positive HD patients have low levels of serum prohepcidin and IL-6 which might account for iron accumulation together with lower iron and rhuEPO requirements in these patients.
2.
[The effect of tobacco smoking during pregnancy on concentration of pro-hepcidin and some parameters of iron metabolism in matched-maternal cord pairs].
Chełchowska, M, Lewandowski, L, Ambroszkiewicz, J, Swiatek, E, Gajewska, J, Ołtarzewski, M, Laskowska-Klita, T
Przeglad lekarski. 2008;(10):474-8
Abstract
Iron deficiency relatively observed in pregnant women is assumed to be enhanced by cigarette smoking. Hepcidin, a peptide hormone produced by the liver as pro-hepcidin, has recently emerged as a central mediator of iron metabolism. Hepcidin regulates intestinal iron absorption, macrophage iron release, and the placental passage of iron. Maternal smoking is associated with increased fetal iron requirements and stimulates fetal erythropoiesis. This is probably through a hypoxic effect on the fetus, and is dose related to the maternal smoking level. It is known that anemia and hypoxia suppress hepcidine mRNA expression. Therefore the aim of the study was to estimate the effect of tobacco smoking on serum pro-hepcidin levels and some iron parameters in pregnant women and umbilical cord blood. We also studied correlation between pro-hepcidin and others iron markers in mothers and their newborns. Healthy, pregnant women (n = 50), patients of Clinical Department of Obstetrics and Gynecology, Institute of Mother and Child were divided into groups nonsmoking and smoking according to questionnaire declaration. Serum concentrations of pro-hepcidin were determined by immunoenzymathic method using a commercial pro-hepcidin assay (DRG, Germany). Levels of ferritin and transferrin were measured by immunoturbidimetric method and iron by photometric test with ferrozine using HORIBA ABX kits (France) and Cobas Mira analyser (Roche, Switzerland). Levels of hemoglobin and hematocrite were determined using commercially available kits on Pentra 60 analyser (ABX, France). We observed that the mean concentration of pro-hepcidin in serum of smoking pregnant women was statistically lower than in tobacco abstinent (101.9 +/- 28.6 ng/ml vs 88.3 +/- 18.2 ng/ml; p < 0.01). Levels of others studied iron markers were similar in both group except total iron concentration, which was 20% lower in smoking mothers than in nonsmoking ones. In umbilical cord blood of infants born to smoking women level of pro-hepcidin was significantly lower than in tobacco abstinent (54.2 +/- 14.0 ng/ml vs 76.8 +/- 21.4 ng/ml, p < 0.0001). We observed positive correlation between concentrations of that prohormone in serum of mothers and cord blood of their newborns in nonsmoking group (r = 0.54; p < 0.02) as well as in smoking ones (r = 0.68; p < 0.05). In addition, concentrations of ferritin, transferin and total iron were lower by 30%, 13% and 20% respectively in cord blood of smoking than nonsmoking group. The differences were statistically significant (p < 0.05). Our analysis revealed no correlation between serum pro-hepcidin levels and other studied parameters of iron status both in the mothers and children groups. Our results indicate that tobacco smoking during pregnancy affected pro-hepcidine levels in serum of mothers and their newborns. Low concentrations of some iron markers in umbilical cord blood suggest that mother's smoking could lead to subclinical iron deficiency in fetus. No anemia were observed in both studied groups of mothers that could explain no relationships between pro-hepcidin and others parameters of iron status.