Serum Prohepcidin and Iron Homeostasis in Patients with Breast Cancer

Abstract Abstract 5291 Introduction: Cancer-related anemia (CRA) has multifactorial etiology and complex pathogenesis. It is defined as normochromic, normocytic anemia with reticulocyto-penia and hypoferremia. Hepcidin is recognized as the central factor in causing CRA. Objective: To investigate the changes in the serum levels of prohepcidin (pHp) and markers of iron homeostasis for gathering more data on the pathogenesis of CRA. Patients and Methods: The authors analyzed prospectively 46 newly diagnosed women with breast cancer, aged 29–72 years (average 47.5±9.0 SD), who had the same clinical stage, histology and hormonal status. They were diagnosed and treated in the Clinic of Oncology and Hematology - University Hospital for a 2-year period (2009–2010). Serum pHp levels and common markers of iron status including serum iron (sFe), transferrin saturation, soluble tranferrin receptor (sTfR), Zn-protoporphyrin (ZPP), ferritin as well as vitamin B12 and folate were measured before treatment initiation and two months afterwards. Serum pHp was determined by a competitive immunotest. All statistical data was computed by the methods of variational and correlation analyses. Results and Discussion: For the two-month follow up interval parameters of full blood count remained without statistically significant deviation. Although the analyzed parameters in the first and second blood samples remained within the reference intervals, the decrease of pHp and the changes of iron-containing substances and ZPP in red blood cells cannot be neglected. However the correlation coefficient (R) between decreased pHp, increased sFe (R=0.314), sTfR (R=0.258), ZPP (R=0.118) and decreased ferritin (R=0.099), were low instead of the expected higher relationship. The obtained results do not support the idea that iron increase and other changes of iron homeostasis in these patients is a direct result of regulatory decrease of pHp. The two-month interval is likely short enough to rule out a potential direct suppressive effect of the specific cytotoxic treatment, and therefore we do not discuss such potential influence on iron homeostasis. Conclusion: Iron homeostasis dysregulation is one of CRA components. In its complex pathogenesis several other factors interfere e.g. such related to the disease; therapy related factors; altered erythropoietin production; activation of cytokines (IL-6 is the major promoter of hepcidin production). Disclosures: No relevant conflicts of interest to declare.

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Hepcidin Levels and Their Determinants In Different Types of Myelodysplastic Syndromes

Blood ◽

10.1182/blood.v116.21.4250.4250 ◽

2010 ◽

Vol 116 (21) ◽

pp. 4250-4250

Author(s):

Valeria Santini ◽

Domenico Girelli ◽

Alessandro Sanna ◽

Nicola Martinelli ◽

Lorena Duca ◽

...

Keyword(s):

Iron Overload ◽

Myelodysplastic Syndromes ◽

Iron Homeostasis ◽

Conflicts Of Interest ◽

Iron Status ◽

Transferrin Saturation ◽

Ineffective Erythropoiesis ◽

Transfusion Therapy ◽

Different Types ◽

Serum Hepcidin

Abstract Abstract 4250 Background and Aims. Iron overload is frequently occurring in patients with myelodysplastic syndromes (MDS), with recent data suggesting an impact on both overall and leukemia-free survival1,2. Though prolonged RBC transfusion therapy appears the main contributor, many patients develop iron overload at an early stage of the disease, before the onset of transfusion dependency. It has been postulated that an altered production of hepcidin, the key hormone regulating iron homeostasis, may play a role at this regard. Until recently, studies have been hampered by problems in the development of reliable hepcidin assays, so that only scanty and conflicting data based on semi-quantitative measurement of urinary hepcidin have been reported3,4. This study mainly focused on analyzing serum hepcidin levels in MDS patients by means of a recently validated and improved Mass-Spectrometry based method5. Patients and Methods. One hundred and thirteen consecutive patients (mean age 72.8 ± 9.2 years; 68.1% males) with different types of MDS according to the WHO classification were included in this study. To be enrolled, patients had to be previously untreated or treated only with transfusions. Besides hepcidin, in all subjects we determined serum ferritin, transferrin saturation (TS), non-transferrin-bound-iron (NTBI), along with some putative determinants of hepcidin, like GDF-156 known to be associated with ineffective erythropoiesis, and C-Reactive Protein (CRP) as a surrogate of systemic IL-6 production. Fifty-four healthy individuals (61.1% males) with rigorous definition of normal iron status were used as controls. Main Results. Biochemical markers of iron overload (ferritin and TS), but also CRP and GDF-15 were significantly higher in MDS patients than in controls, even when considering only non-transfused patients. Patients with RARS and the 5q- syndrome appeared as the most iron overloaded, having the highest levels of ferritin, TS, and NTBI. In the whole MDS population, serum hepcidin levels showed a considerable variability, with overall mean values not significantly different from controls [geometric means (gm) with 95% CIs: 5.31 (3.98-7.08) versus 4.2 (3.53-5.0) nM, P=0.28], while the hepcidin/ferritin ratio was significantly lower than in controls [10.1 (7.53-13.53) versus 52.9 (43.6-64.3), P<0.001]. After stratification according to WHO subtypes, hepcidin levels showed significant differences, with the lowest levels in patients with RARS (gm 1.43 nM) and the highest levels in patients with RAEB 1–2 (gm 11.3 nM) and with CMML (gm 10.04 nM) (P=0.003 by ANOVA). The latter groups had substantial elevation of CRP as compared to other MDS subtypes (P=0.008 by ANOVA), while GDF-15 was consistently but uniformly elevated in all MDS subtypes (P=0.97 by ANOVA). Multivariate linear regression models adjusted also for age, sex, and history of RBC transfusions, showed ferritin (β-coefficient 0.45, P=0.002), CRP (β-coefficient 0.21, P=0.02), and different MDS subtypes as the main independent predictors of hepcidin levels. The different degree of correlation between hepcidin and ferritin among the MDS subtypes were analyzed in a general linear model using the F test for slopes. Hepcidin regulation by iron appeared conserved, though relatively blunted in RA, RARS, and 5q- patients, while it was lost in RAEB 1–2 and CMML. Conclusions. Hepcidin levels are consistently heterogeneous in MDS according to different subtypes, likely as the result of the relative strength of competing stimuli. Relative inhibition by ineffective erythropoiesis (but not mediated by GDF-15) seems to prevail particularly in RARS and 5q- syndrome, and is likely to increase the risk of iron overload in these subgroups. On the other hand, patients with RAEB 1–2 and CMML appears to have hepcidin induction that could be driven by cytokines. If confirmed, these results may be relevant not only for a better understanding of iron pathophysiology in MDS, but also for possible future approach with hepcidin modulators7. References: 1) Sanz G, et al. Blood 2008;112: abs 640. 2) Alessandrino EP, et al. Haematologica 2010;95:476-84. 3) Winder A, et al. Br J Haematol 2008;142:669-71. 4) Murphy PT, et al. Br J Haematol 2009;144:451-2. 5) Campostrini N, et al. J Biomed Biotechnol 2010;2010:329646. 6) Tanno T, et al. Nat Med 2007;13:1096-101. 7) Sasu BJ, et al. Blood 2010;115:3616-24. Disclosures: No relevant conflicts of interest to declare.

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Hypercoagulability Linked to Breast Cancer Depends On the Stage and the Duration of the Tumor Evolution

Blood ◽

10.1182/blood.v120.21.3396.3396 ◽

2012 ◽

Vol 120 (21) ◽

pp. 3396-3396

Author(s):

Mourad Chaari ◽

Grigoris T Gerotziafas ◽

Lilia Ghorbal ◽

Vassiliki Galea ◽

Ines Ayadi ◽

...

Keyword(s):

Breast Cancer ◽

Cancer Diagnosis ◽

Thrombin Generation ◽

Conflicts Of Interest ◽

Normal Population ◽

Venous Thromboembolic Event ◽

University Hospital ◽

Hypercoagulable State ◽

Tumor Evolution ◽

Cancer Disease

Abstract Abstract 3396 Introduction The risk of venous thromboembolic event (VTE) in patients with cancer is particularly increased compared to normal population. It seems that this risk depends largely on the characteristics of the tumor, such as its site or its stage of evolution, and the anti-neoplasic treatment. The capacity of thrombin generation and D-dimers levels are two biological markers proposed for the stratification of the risk of VTE. We have analyzed thrombin generation and D-dimers levels in patients with breast cancer as markers of a hypercoagulable state, depending on the stage and the period of the tumor evolution. Materials and methods It is a prospective study carried out at the day hospital of the carcinology department of the University Hospital H. Bourguiba in Sfax-Tunisia, including patients with breast cancer at different stages of evolution and different period elapsed since cancer diagnosis. At the time of inclusion, a venous citrated blood sampling (3.2%) was made. The test of thrombin generation was carried out according to the technique of Calibrated Automated Thrombogram assay (CAT®, Diagnostica Stago, Asnières, France). The parameters of the thrombogram were analyzed: endogenous thrombin potential (ETP), peak of thrombin (peak) and mean rate index (MRI). D-dimers were measured using the STA®- Liatest® D-Di assay (Diagnostica-Stago). Results Sixty one patients were included. Their average age is 51.8 ± 10.9 years old. Depending on the stage of cancer disease, 3 sub-groups of patients were distinguished: early local stage (T1, n=16), advanced local stage (T2-T4; n=25) and metastatic stage (M; n=20). Considering the time passed since diagnosis, we have different periods : inferior to 6 months (n=26), 6 to 12 months (n=7), 12 to 36 months (n=15) and more than 36 months (n=13). The analysis of the different parameters of the thrombogram depending on the cancer stage revealed that patients with an advanced local stage and a period elapsed since cancer diagnosis inferior to 6 months had significantly higher values of ETP and thrombin peak (1708±247 nM.min and 379±80 nM) compared to those with an older cancer (1404±308 nM.min, p<0.05 and 321±52, p<0.05 respectively). The study of D-dimers levels depending on the stage of cancer revealed an increase of this marker according to the severity of the cancer. Patients with metastatic stages have the highest levels (1937 ± 2468 μg/l) compared to patients with an early local stage (615±456 μg/l, p<0.05 ). In addition, the period of time since cancer diagnosis does not have any influence on D-dimers levels. Conclusion The evaluation of the capacity of thrombin generation and D-dimers levels showed that these biological parameters are indeed linked to the stage of evolution and the severity of breast cancer. Therefore, these biological tests underlying an hypercoagulable state have a potential and complementary importance to stratify the risk of VTE in this context. This should be confirmed by the prospective follow-up of the thromboembolic risk existing in the patients with breast cancer. Disclosures: No relevant conflicts of interest to declare.

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Justification of Universal Iron Supplementation for Infants 6-12 months in Regions with a High Prevalence of Thalassemia

10.21203/rs.3.rs-624967/v1 ◽

2021 ◽

Author(s):

Phakatip Sinlapamongkolkul ◽

Pacharapan Surapolchai ◽

Vip Viprakasit

Keyword(s):

Iron Deficiency ◽

Iron Supplementation ◽

Complete Blood Count ◽

Iron Status ◽

Transferrin Saturation ◽

University Hospital ◽

Deficiency Anemia ◽

Increased Risk ◽

Thalassemia Minor ◽

Hb E

Abstract Background Many clinicians hesitate adopting a universal infant iron supplementation program due to the risk of increased iron absorption for those with thalassemia. We aimed to determine thalassemia prevalence in 6- to 12-month old infants, along with the iron status of those with and without thalassemia. Procedures: We performed a cross-sectional descriptive study of infants attending the Well Baby Clinic at Thammasat University Hospital for routine checkups. Complete blood count, hemoglobin electrophoresis, iron parameters, and molecular genetics for common α- and β-thalassemia were evaluated. Results Overall, 97 of 206 (47%) participants had thalassemia minor, the majority having Hb E traits. None had thalassemia intermedia or major. Familial history of anemia or thalassemia presented an increased risk of detecting thalassemia minor in offspring (OR 5.18; 95% CI 2.60-10.33, p = 0.001). There were no statistical differences in transferrin saturation, serum ferritin and hepcidin between iron-replete infants with thalassemia minor and those without. However, one-third of infants with thalassemia minor (31/97) also had iron deficiency anemia (IDA), with a similar risk of having iron deficiency to infants without thalassemia. There was no hepcidin suppression in our infants with thalassemia minor as compared to controls. Conclusions Both thalassemia and IDA are endemic to Southeast Asia. Infants with thalassemia minor, particularly with Hb E and α-thalassemia traits, are at risk of IDA. Our short-term universal iron supplementation program for 6 to 12-month old infants does not appear to increase the risk of those with thalassemia minor developing iron overload in the future.

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Regulatory Mechanisms for Iron Homeostasis Are Present in Small Preterm Newborns

Blood ◽

10.1182/blood.v128.22.2460.2460 ◽

2016 ◽

Vol 128 (22) ◽

pp. 2460-2460

Author(s):

Carina Levin ◽

Marina Marina Peniakov ◽

Dan Reich ◽

Scott Weiner ◽

Jamal Hasnein ◽

...

Keyword(s):

Birth Weight ◽

Blood Transfusion ◽

Preterm Infants ◽

Iron Supplementation ◽

Iron Homeostasis ◽

Reticulocyte Count ◽

Iron Status ◽

Transferrin Saturation ◽

Regulatory Mechanisms ◽

Vlbw Infants

Abstract Iron, an essential micronutrient, plays an important role in cellular functions. To prevent deficiency, iron supplementation is universally recommended for preterm infants; nevertheless, assessment of newborn iron stores is not currently recommended. Both iron deficiency and iron excess early in life can have adverse effects on neurodevelopment and outcomes, and therefore sensitive and specific methods for evaluating iron status and determining optimal iron supplementation are essential. The current study aimed to evaluate iron status and iron-supplementation efficacy/toxicity in preterm infants using new laboratory methods, and to correlate iron status with clinical, nutritional, laboratory and therapeutic factors, and the amount of blood extracted and transfused. We evaluated 50 very low birth weight (VLBW) preterm infants treated under standard protocols at the Emek Medical Center NICU, 26 (54%) male. Iron supplementation was administered enterally from 4 wk of age (4 mg elemental iron/kg body weight daily). Laboratory studies included CBC, reticulocyte count, reticulocyte hemoglobin (Hb) content, iron, transferrin, transferrin saturation, ferritin, erythropoietin, hepcidin, CRP and non-transferrin-bound iron (NTBI) (Aferrix, Israel). Samples were obtained at 3 different times during hospitalization: (-0) before starting oral iron supplementation, (-1) on d 4-7 of supplementation, and (-2) after at least 2 wk of supplementation. To better understand iron metabolism, the analyzed preterm population was divided into subgroups for comparison: infants who did not require blood transfusion (No-BT) vs. those who received one or more transfusions (BT); infants who did not show abnormal NTBI levels (≤0.19 μmol/L; No-NTBI) vs. those with abnormal NTBI levels (≥ 0.2 μmol/L in one or more samples; NTBI). Mean birth weight of the studied infants was 1264.5 ± 342 g, gestational age 29.1 ± 2.5 wk, age at hospital discharge 57.6 ± 20 d and weight at discharge, 2412 ± 421 g. The BT group included 35 (70%) infants. The mean birth weight was lower in the BT vs. No-BT group (1199 ± 351 g vs. 1416±273 g, P = 0.04). Mean red blood cell, Hb, and hematocrit were higher in the BT vs. No-BT group. Conversely, mean platelet count, reticulocyte count, and erythropoietin were higher in the No-BT vs. BT group, suggesting an erythropoietic response to lower Hb levels and utilization of iron through effective erythropoiesis. In the BT group, mean serum iron, ferritin, transferrin saturation and hepcidin were higher, whereas transferrin was lower than in the No-BT group. This reflects increased iron burden induced by the transfusions, making NTBI more likely to develop with potential toxicity. Regarding NTBI, 34 (68%) of the infants were in the No-NTBI group, and 16 (32%) showed increased NTBI levels. The Δiron (sum of iron from diet, supplementation and transfusion minus iron output via blood extractions) before starting supplementation was significantly higher in the NTBI vs. No-NTBI group. Mean transferrin saturation at -0 was higher, whereas transferrin at -2 was lower in the NTBI vs. No-NTBI group, demonstrating a higher iron burden in NTBI infants. The odds of developing NTBI rose 7.2% for each percent increment in transferrin saturation at -0 (O.R. 1.072, 95% CI, 1.005-1.143, P = 0.036), and a cutoff of 26% at -0 gave 80% sensitivity and 41% specificity for the presence of NTBI (AUC 0.68). Thus VLBW infants show evidence of regulatory mechanisms for iron homeostasis and iron utilization for erythropoiesis; however, the protective responses are not developed enough to limit the appearance of circulating free iron with potential toxic effects. Neither adverse effects nor presence of NTBI were associated with enteral iron supplementation. Premature infants who received blood transfusions had a positive iron balance, higher Hb and ferritin levels, and reduced erythropoiesis. Consequently, these babies are more likely to develop free iron. Conventional biomarkers are effective for evaluating iron status in VLBW infants. Transferrin saturation seems to be the most reliable and "physiological" biomarker, and a potential predictor of abnormal NTBI levels. These findings support an individualized approach to iron supplementation based on the characteristics of the specific preterm infant while taking into consideration past need for blood transfusion and the infant's iron status. Disclosures No relevant conflicts of interest to declare.

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Expression of hepcidin in hereditary hemochromatosis: evidence for a regulation in response to the serum transferrin saturation and to non-transferrin-bound iron

Blood ◽

10.1182/blood-2002-11-3610 ◽

2003 ◽

Vol 102 (1) ◽

pp. 371-376 ◽

Cited By ~ 167

Author(s):

Sven G. Gehrke ◽

Hasan Kulaksiz ◽

Thomas Herrmann ◽

Hans-Dieter Riedel ◽

Karin Bents ◽

...

Keyword(s):

Iron Overload ◽

Serum Ferritin ◽

Iron Homeostasis ◽

Iron Status ◽

Hereditary Hemochromatosis ◽

Transferrin Saturation ◽

Serum Transferrin ◽

Transcript Levels ◽

Hepcidin Expression

Abstract Experimental data suggest the antimicrobial peptide hepcidin as a central regulator in iron homeostasis. In this study, we characterized the expression of human hepcidin in experimental and clinical iron overload conditions, including hereditary hemochromatosis. Using quantitative reverse transcriptase-polymerase chain reaction (RT-PCR), we determined expression of hepcidin and the most relevant iron-related genes in liver biopsies from patients with hemochromatosis and iron-stain-negative control subjects. Regulation of hepcidin mRNA expression in response to transferrin-bound iron, non-transferrin-bound iron, and deferoxamine was analyzed in HepG2 cells. Hepcidin expression correlated significantly with serum ferritin levels in controls, whereas no significant up-regulation was observed in patients with hemochromatosis despite iron-overload conditions and high serum ferritin levels. However, patients with hemochromatosis showed an inverse correlation between hepcidin transcript levels and the serum transferrin saturation. Moreover, we found a significant correlation between hepatic transcript levels of hepcidin and transferrin receptor-2 irrespective of the iron status. In vitro data indicated that hepcidin expression is down-regulated in response to non-transferrin-bound iron. In conclusion, the presented data suggest a close relationship between the transferrin saturation and hepatic hepcidin expression in hereditary hemochromatosis. Although the causality is not yet clear, this interaction might result from a down-regulation of hepcidin expression in response to significant levels of non-transferrin-bound iron. (Blood. 2003;102:371-376)

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Iron Status in Mice Carrying a Targeted Disruption of Lactoferrin

Molecular and Cellular Biology ◽

10.1128/mcb.23.1.178-185.2003 ◽

2003 ◽

Vol 23 (1) ◽

pp. 178-185 ◽

Cited By ~ 69

Author(s):

Pauline P. Ward ◽

Marisela Mendoza-Meneses ◽

Grainne A. Cunningham ◽

Orla M. Conneely

Keyword(s):

Iron Homeostasis ◽

Iron Status ◽

Transferrin Saturation ◽

Basal Diet ◽

Postnatal Period ◽

Homologous Gene ◽

Physiological Functions ◽

Adult Mice ◽

Exact Function

ABSTRACT Lactoferrin is a member of the transferrin family of iron-binding glycoproteins present in milk, mucosal secretions, and the secondary granules of neutrophils. While several physiological functions have been proposed for lactoferrin, including the regulation of intestinal iron uptake, the exact function of this protein in vivo remains to be established. To directly assess the physiological functions of lactoferrin, we have generated lactoferrin knockout (LFKO−/−) mice by homologous gene targeting. LFKO−/− mice are viable and fertile, develop normally, and display no overt abnormalities. A comparison of the iron status of suckling offspring from LFKO−/− intercrosses and from wild-type (WT) intercrosses showed that lactoferrin is not essential for iron delivery during the postnatal period. Further, analysis of adult mice on a basal or a high-iron diet revealed no differences in transferrin saturation or tissue iron stores between WT and LFKO−/− mice on either diet, although the serum iron levels were slightly elevated in LFKO-/- mice on the basal diet. Consistent with the relatively normal iron status, in situ hybridization analysis demonstrated that lactoferrin is not expressed in the postnatal or adult intestine. Collectively, these results support the conclusion that lactoferrin does not play a major role in the regulation of iron homeostasis.

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Interrelationships between circulating gastrin and iron status in mice and humans

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.90359.2008 ◽

2008 ◽

Vol 295 (4) ◽

pp. G855-G861 ◽

Cited By ~ 9

Author(s):

Suzana Kovac ◽

Kelly Smith ◽

Gregory J. Anderson ◽

John R. Burgess ◽

Arthur Shulkes ◽

...

Keyword(s):

Iron Homeostasis ◽

Iron Absorption ◽

Iron Status ◽

Transferrin Saturation ◽

Wild Type ◽

Liver Iron ◽

Divalent Metal Transporter 1 ◽

Divalent Metal Transporter ◽

Mrna Concentration

The observations that the peptide hormone gastrin interacts with transferrin in vitro and that circulating gastrin concentrations are increased in the iron-loading disorder hemochromatosis suggest a possible link between gastrin and iron homeostasis. This study tested the hypothesis that gastrin and iron status are interrelated by measurement of iron homeostasis in mice and humans with abnormal circulating gastrin concentrations. Intestinal iron absorption was determined by59Fe uptake following oral gavage, and concentrations of duodenal divalent metal transporter-1 (DMT-1) and hepatic hepcidin mRNAs were determined by quantitative real-time PCR in agastrinemic (GasKO), hypergastrinemic cholecystokinin 2 receptor-deficient (CCK2RKO), or wild-type mice. Iron status was measured by standard methods in the same mice and in hypergastrinemic humans with multiple endocrine neoplasia type 1 (MEN-1). Iron absorption was increased sixfold and DMT-1 mRNA concentration fourfold, and transferrin saturation was reduced 0.8-fold and hepcidin mRNA expression 0.5-fold in juvenile GasKO mice compared with age-matched wild-type mice. In mature mice, few differences were observed between the strains. Juvenile CCK2RKO mice were hypergastrinemic and had a 5.4-fold higher DMT-1 mRNA concentration than wild-type mice without any increase in iron absorption. In contrast to juvenile GasKO mice, juvenile CCK2RKO mice had a 1.5-fold greater transferrin saturation, which was reflected in a twofold increase in liver iron deposition at maturity compared with wild-type mice. The correlation between transferrin saturation and circulating gastrin concentration observed in mutant mice was also observed in human patients with MEN, in whom hypergastrinemia correlated positively ( P = 0.004) with an increased transferrin saturation. Our data indicate that, in juvenile animals when iron demand is high, circulating gastrin concentrations may alter iron status by a CCK2R-independent mechanism.

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ANALYSIS OF RET-HE IN CHRONIC KIDNEY DISEASE PATIENTS AT DR.WAHIDIN SUDIROHUSODO HOSPITAL, MAKASSAR

INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY ◽

10.24293/ijcpml.v25i1.1481 ◽

2019 ◽

Vol 25 (1) ◽

pp. 7

Author(s):

Febrina Rovani ◽

Asvin Nurulita ◽

Mansyur Arif

Keyword(s):

Chronic Kidney Disease ◽

Kidney Disease ◽

Iron Homeostasis ◽

Complete Blood Count ◽

Binding Capacity ◽

Iron Status ◽

Transferrin Saturation ◽

Test Method ◽

Pathology Laboratory ◽

Significant Difference

Anemia, the common feature of Chronic Kidney Disease (CKD), is a multifactorial process due to disordered erythropoiesis and iron homeostasis. Determining the cause of anemia is important for adequate management. A bone marrow biopsy using Prussian Blue as the gold standard for diagnosis is invasive and more complicated to perform. Reticulocytes-Hemoglobin (Ret-He) a new parameter that indicates the hemoglobin content in reticulocytes is faster, easier, and less expensive. This study aimed to analyze the Ret-He in determining the iron status in patients with CKD. A cross-sectional study was held in the Clinical Pathology Laboratory of Dr. Wahidin Sudirohusodo Hospital Makassar during April-August 2016. Forty-five (45) samples were tested for iron serum (Fe), Total Iron Binding Capacity (TIBC), and Complete Blood Count (CBC) ordered by the physician. Reticulocytes-Hemoglobin was tested using the whole blood. Subjects were around the age of 19-71 years, no significant difference was found between numbers of males and females (46.6% and 53.3%). Hemoglobin median was 8 (5.0-15) g/dL, Fe 50 (6-177) U/mL, TIBC 183 (73-379), Transferrin Saturation (Tsat) 25 (5-95)%. Spearman correlation test method showed significant correlations between Ret-He and iron serum r=0.533, p <0.001, Ret-He and TIBC r=0.321 p=0.031 Ret-He and transferrin saturation r=0.416 p=0.019. The Mann-Whitney method showed no significant difference of Ret-He in both groups (Tsat <20% and >20%). There were significant correlations between Ret-He and iron, Ret-He and TIBC, Ret-He and transferrin saturation. A further study using larger samples is suggested to consider factors affecting the result of Ret-He.

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The Association between Hepcidin and Iron Status in Children and Adolescents with Obesity

Journal of Nutrition and Metabolism ◽

10.1155/2021/9944035 ◽

2021 ◽

Vol 2021 ◽

pp. 1-7

Author(s):

Ekkarit Panichsillaphakit ◽

Orapa Suteerojntrakool ◽

Chitsanu Pancharoen ◽

Issarang Nuchprayoon ◽

Sirinuch Chomtho

Keyword(s):

Iron Deficiency ◽

Iron Homeostasis ◽

Complete Blood Count ◽

Iron Status ◽

Standard Deviation Score ◽

Transferrin Saturation ◽

Obese Group ◽

Control Group ◽

Low Grade ◽

Serum Hepcidin

Introduction. Iron deficiency (ID) is the most common nutritional deficiency found in pediatric practice. A higher prevalence of ID may be found in children with obesity. Obesity is a chronic low-grade inflammatory condition. It is postulated that inflammation increases hepcidin, a regulator of iron homeostasis. The aim of this study was to investigate the associations between iron status, hepcidin, and BMI-standard deviation score (BMI-SDS) in children with and without obesity. Methods. A cross-sectional study of Thai children with obesity (5 to 15 years old) versus age- and sex-matched, nonobese controls was conducted. A total of 63 children with obesity and 27 controls were enrolled. Complete blood count, serum iron, ferritin, transferrin saturation, and total iron binding capacity were analyzed. Serum hepcidin-25 was assayed using a hepcidin ELISA Kit (Human Hepc25). Results. There were 63 children with obesity, the median age (IQR) being 10 (9–13) years, and 27 controls. The median (IQR) BMI-SDS of the obese group was 2.3 (2.0–2.6) vs. −0.5 ((−1.3)−0.4) of the control group. ID was diagnosed in 27 children in the obese group (42.9%); 4 of the children with obesity and ID had anemia. Serum hepcidin-25 levels of the children with ID vs. without ID in the obese group were not significantly different (median (IQR) 25 (12.9–49.2) and 26.4 (12.6–43.6), respectively) but both of them were significantly higher than controls (19.7 (8.3–25.5) ng/ml, p = 0.04). BMI-SDS was positively correlated with hepcidin-25 (r = 0.28, p = 0.001). Conclusion. Prevalence of iron deficiency in Thai children with obesity and serum hepcidin-25 was higher than controls. Further study in a larger population, preferably with interventions such as weight loss program, is warranted to clarify this association.

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Role of Hepcidin as a biomarker for iron status in patients on regular hemodialysis after treatment of hepatitis C virus

QJM ◽

10.1093/qjmed/hcab100.117 ◽

2021 ◽

Vol 114 (Supplement_1) ◽

Author(s):

Magdy M El Sharkawy ◽

Haitham E Abdelaziz ◽

Lina E Khedr ◽

Mohamed A Sharaf

Keyword(s):

Hepatitis C ◽

Iron Homeostasis ◽

Complete Blood Count ◽

Iron Status ◽

Transferrin Saturation ◽

Renal Elimination ◽

Serum Hepcidin ◽

The Mean ◽

Esrd Patients ◽

Regular Hemodialysis

Abstract Background Hepcidin, an acute phase reactant protein produced in the liver, is a key regulator of iron homeostasis. Because of its renal elimination and regulation by inflammation, it is possible that progressive renal insufficiency leads to altered hepcidin metabolism. Aim of the work to assess effect of HCV treatment on hepcidin levels in regular heamodialysis patients and its relation to iron status. Patients and Methods This cross sectional study was conducted on 45 ESRD patients on regular hemodialysis. All candidates included in this study subjected to careful history taking, full clinical examination and investigations (including complete blood count, HCVAb, HBVsAg and HIVAb). All patients had positive antibodies for hepatitis C; however, all of them had negative PCR and negative HIV, HBV antibodies. Results In our study, dry weight ranged from 46 to 117 kg with mean 77.36. Weight gain ranged from 2 to 5 kg with mean 3.09.About 87% of patients had LTAVF access. About 12 patients (27%) received blood transfusion once. Timing of transfusion ranged from 4 to 60 month with median of 24 months. Regarding frequency of epoetin dose, 11 patients (24.4%) did not receive epoetin, 16 patients (35.6%) received it twice/week. Only 3 patients (6.7%) received iron therapy for time ranging from 3 to 5 months with mean of 4 months. Mean Hb concentration in our study population was 10.11 ±1.64 gm/dl. The mean of iron was 64.22 ±19.52, TIBC was 409.96 ± 67.85, ferritin was 394.56 ± 239.22 and TSAT% was 22.6 ±7.36. The mean serum hepcidin was 218.51 ±127. Our study demonstrated that increase in serum hepcidin is associated with lower serum Hb and iron levels. On the other hand, there is statistically significant positive correlation between serum hepcidin and both serum ferritin and transferrin saturation. Conclusion Median hepcidin value is elevated in dialysis ESRD patients due to increased inflammation and decreased clearance of hepcidin. Also serum hepcidin levels were lowered in HCV patients. Therefore ESRD patients on maintenance HD after treatment of HCV infection showed elevated levels of serum hepcidin.

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