Serum Hepcidin Levels Research Articles

Iron Deficiency Anemia in Children and Adolescents with Type I Diabetes, Is it a Real Problem?

Abstract Background: Iron deficiency anemia (IDA) in children with type I diabetes (T1D) represents a significant burden. Aim of Study: To asses iron status in children and adoles-cent with T1D of and to correlate it with glycemic control and diabetic vascular complications. Patients and Methods: Two hundred children with T1D recruited from Pediatrics and Adolescent Diabetes Unit (PADU), Ain Shams University in the period from December 2019 to July 2020. They were 123 males (61.5%) and 77 females (38.5%) aged 10.97±3.93 years (Range: 2-18 years). History taking, fundus examination and general examination were done stressing on anthropometric measurements. Labo-ratory evaluation including complete blood count, glycosylated haemoglobin (HbA1c), urinary albumin/creatinine ratio (ACR), lipid profile and patients with microcytic hypochromic anaemia underwent Serum iron, total iron-binding capacity (TIBC), serum ferritin, Hepcidin, Anti-tissue transglutaminase (IgA), Occult blood in stool and H-pylori antigen in stool. Results: Seventy two of diabetic children were anemic (36%) and fifty one had IDA (25.5). IDA was more prevalent in males. Children with T1D and IDA experienced more clinically significant hypoglycemic attacks, more DKA attacks, high fatigue severity scale and history of menorrhagia. Low body weight, low BMI, low mean corpuscular volume (MCV), high TIBC and low hepcidin level were present in diabetic children with IDA. They also had high HbA1c, neuropathy, high triglycerides and high level of low density lipoprotein (LDL cholesterol). Conclusions: IDA is a significant morbidity among chil-dren with T1D and it should be screened. Serum hepcidin levels are significantly associated with iron status in children, and could be useful indicators of ID.

Evidence of dysregulated iron homeostasis in newly diagnosed diabetics, but not in pre-diabetics.

Diabetes mellitus has been reported to be associated with increased serum levels of ferritin. The basis of this association is unclear. It is also not precisely known whether other iron-related parameters, including hepcidin (the central regulator of systemic iron homeostasis), are affected under these circumstances. This study attempted to determine this. Adult men (normoglycemic or newly diagnosed with diabetes or pre-diabetes) were recruited. Anthropometric, metabolic, and hematological and iron-related parameters in blood were measured. Indices of insulin resistance (HOMA-IR) and pancreatic beta cell function (HOMA-β) were calculated. Subjects in the 3 groups were similar in age, and anthropometric and hematological parameters. Serum ferritin and hepcidin levels were higher in diabetics, than in pre-diabetics and in control subjects. These elevations seen were not linked to the presence of inflammation. HOMA-IR was higher in diabetics, and HOMA-β lower in diabetics and pre-diabetics, than in control subjects. HOMA-IR and serum ferritin were positively correlated with one another. Elevated levels of serum ferritin and hepcidin in newly diagnosed diabetics (but not pre-diabetics) indicate dysregulated iron homeostasis, with the former positively associated with insulin resistance in these patients.

Association of vitamin A with anemia and serum hepcidin levels in children aged 6 to 59 mo

ObjectiveThis study evaluates the association of serum retinol, hepcidin levels, and anemia in children. MethodsThis cross-sectional study included 312 children, ages 6 to 59 mo, from Rio de Janeiro, Brazil. The association between hepcidin and retinol levels, hematologic parameters, and body mass index (BMI) was analyzed using a generalized linear model with and without adjustment for C-reactive protein (CRP) level. Logistic regression analysis was used to test anemia as an outcome and serum retinol level as a predictive variable using the odds ratio (OR) function. ResultsAnemia was present in 14.6% of the children, 5.8% presented iron deficiency anemia, and 9.6% had vitamin A deficiency. The increase in serum retinol levels reduced the chances of anemia (OR = 0.13; confidence interval = 0.29–0.59). When CRP level was not adjusted for in the multiple regression analyses, retinol, ferritin levels, and BMI/age were predictors of serum hepcidin levels (β = –3.36, 0.14, 1.02, respectively; P = 0.032). Accordingly, serum retinol levels were inversely associated with CRP levels (β = –0.025 and P < 0.001). ConclusionsThe association between serum retinol and hepcidin levels in children ages 6 to 59 mo seems to be dependent on inflammation. Taken together, the results reinforce the need for the development of further studies to better understand the relationship between vitamin A and anemia of inflammation.

Correlation Between Serum Ferritin and Hepcidin Levels in Chronic Hepatitis C Patients.

BackgroundIn addition to the known role of serum ferritin as an inflammatory mediator, its role in the induction of serum hepcidin is yet to be elucidated. This study aimed to identify a correlation between serum ferritin and hepcidin levels in chronic hepatitis C (CHC) patients and healthy individuals.MethodologyA total of 44 male subjects, selected by convenient sampling technique, were included in this study. The study population was divided into group I including 22 healthy males and group II including age-matched 22 CHC patients. Serum hepcidin and serum ferritin levels of study participants in both groups were assessed. Serum parameters were compared between two groups using the Mann-Whitney U test. Spearman correlation test was applied between serum ferritin and serum hepcidin in each group. P-values of ≤0.05 were considered significant.ResultsThe median values of serum ferritin in group I and group II were in the normal range, though serum ferritin of CHC patients was significantly higher than the healthy population (p = 0.03). The median values of serum hepcidin in both groups were below the normal range. In CHC patients, a negative nonsignificant correlation (rho = -0.34, p = 0.13) was observed between serum ferritin and serum hepcidin. A positive nonsignificant correlation (rho = 0.19, p = 0.4) was observed between serum ferritin and serum hepcidin in the healthy population.ConclusionsOur study could not bring forth any conclusive remarks in favor of serum ferritin as an inflammatory mediator raising serum hepcidin levels among CHC patients. A negative nonsignificant correlation between studied parameters in CHC patients may indicate the involvement of some other factor such as hepatitis C virus in the reduction of serum hepcidin levels.

Erythroferrone and hepcidin as mediators between erythropoiesis and iron metabolism during allogeneic hematopoietic stem cell transplant.

Hematopoietic cell transplantation (HCT) brings important alterations in erythropoiesis and iron metabolism. Hepcidin, which regulates iron metabolism, increases in iron overload or inflammation and decreases with iron deficiency or activated erythropoiesis. Erythroferrone (ERFE) is the erythroid regulator of hepcidin. We investigated erythropoiesis and iron metabolism after allogeneic HCT in 70 patients randomized between erythropoietin (EPO) treatment or no EPO, by serially measuring hepcidin, ERFE, CRP (inflammation), soluble transferrin receptor (sTfR, erythropoiesis), serum iron and transferrin saturation (Tsat; iron for erythropoiesis) and ferritin (iron stores). We identified biological and clinical factors associated with serum hepcidin and ERFE levels. Serum ERFE correlated overall with sTfR and reticulocytes and inversely with hepcidin. Erythroferrone paralleled sTfR levels, dropping during conditioning and recovering with engraftment. Inversely, hepcidin peaked after conditioning and decreased during engraftment. Erythroferrone and hepcidin were not significantly different with or without EPO. Multivariate analyses showed that the major determinant of ERFE was erythropoiesis (sTfR, reticulocytes or serum Epo). Pretransplant hepcidin was associated with previous RBC transfusions and ferritin. After transplantation, the major determinants of hepcidin were iron status (ferritin at all time points and Tsat at day 56) and erythropoiesis (sTfR or reticulocytes or ERFE), while the impact of inflammation was less clear and clinical parameters had no detectable influence. Hepcidin remained significantly higher in patients with high compared to low pretransplant ferritin. After allogeneic HCT with or without EPO therapy, significant alterations of hepcidin occur between pretransplant and day 180, in correlation with iron status and inversely with erythroid ERFE.

Does the TMPRSS6 C > T Polymorphism Modify the Endurance Training Effects on Hematological Parameters?

This study investigated the role of TMPRSS6 C > T polymorphism (TMPRP) on the effects of chronic aerobic training on main hematological parameters in male soccer referees, which is yet unknown. Two groups composed of total of 45 healthy male soccer referees and 42 sedentary were compared for hemogram, serum hepcidin, ferritin, and iron levels. TMPRP was determined from genomic DNA samples. Participants' physical and physiological (Yoyo endurance level-2 test) measurements were carried out. The athletic T carrier (Tc = TT + TC) group RBC count was significantly higher than the control (p < 0.01), whereas the athletic CC homozygous group serum iron and transferrin saturation (TS) were lower than the control depending on the TMPRP. The ferritin and iron values of the athletic Tc group were higher than of the athletic CC group (29.2% and 14.1%, respectively; p > 0.05) although the control Tc group RBC (p < 0.05) and iron (23.8%, p > 0.05) values were lower than the control CC due to genetic tendency. The training did not change hepcidin levels. These results suggest that the TMPRP can modify the endurance training effects on iron and TS levels and RBC count (in the CC and Tc groups) respectively. The CC group may be adversely affected for iron and TS from endurance trainings. It may be recommended that the training programs should be organized according to phenotype characteristics.

Effect of oral vitamin C on serum hepcidin level, iron status and inflammation among hemodialysis patients with functional iron deficiency anaemia

Introduction: Hepcidin is a key regulatory peptide in iron homeostasis, the pathogenesis of functional iron deficiency (FID) anemia and erythropoiesis-stimulating agent (ESA) resistance is contributed to the inflammatory mediated increase in the serum hepcidin levels among prevalent hemodialysis (HD) patients. Objectives: To test the reducing therapeutic effect of oral vitamin C supplements on hepcidin levels and iron status among HD patients with FID anemia. Patients and Methods: This study is an interventional prospective cohort study; 48 prevalent HD patients were enrolled. Group one: 31 patients who received the conventional treatment of erythropoietin stimulating agents together with oral supplementation of vitamin C 500 mg every other day dose for 3 months. Group two: 17 patients who received only the conventional therapy of erythropoietin stimulating agents. Patients with hemoglobin level &lt;11 g/dL, ferritin level &gt;200 ng/mL and transferrin saturation (TSAT) &gt;20 % were included. Laboratory parameters: serum hepcidin, high-sensitivity C-reactive protein (hs-CRP) titre, CBC, and iron indices were measured at baseline and after 3 months. Results: On comparing the two groups, oral vitamin C in group 1 resulted in a statistically significant reduction in hepcidin levels [mean 2506.456 ± 1320.53 pg/mL to 1748.396 ± 1432.28 pg/mL (P = 0.03)], and a significant reduction in hs-CRP level [mean 8603.236 ± 2547.77 ng/mL to 5611.296 ± 2829.27 ng/mL] (P = 0.001) after three months of treatment in comparison to control group. A decrease of EPO requirement and elevation of hemoglobin level were observed in a study group with oral vitamin C. Conclusion: Oral vitamin C may be a promising therapy in decreasing serum hepcidin and inflammatory markers among prevalent HD patients with FID anemia.

Serum hepcidin / ferroportin levels in bipolar disorder and schizophrenia

BackgroundDespite several alternatives for cellular iron influx, the only mechanism for cellular iron efflux is ferroportin mediated active transport. In cases of ferroportin dysfunction, iron accumulates in the cell and causes ferroptosis. Hepcidin suppresses ferroportin levels and inflammatory activation increases hepcidin production. Mild inflammation in schizophrenia and bipolar disorder may alter hepcidin and ferroportin. MethodsThe study included a total of 137 patients aged 18–65 years, 57 diagnosed with schizophrenia and 80 with bipolar disorder, according to the DSM-IV diagnostic criteria, and a control group (HC) of 42 healthy individuals. Biochemical analyses, thyroid function tests, hemogram, serum iron level, iron-binding capacity, and ferritin levels were examined. Serum levels of hepcidin and ferroportin were measured with enzyme-linked immunosorbent assay (ELISA) method. ResultsA statistically significant difference was determined between the groups in terms of the serum ferroportin levels (F = 15.69, p < 0.001). Post-hoc analyses showed that the schizophrenia group had higher ferroportin levels than in the bipolar group (p < 0.001) and HCs (p < 0.001). Hepcidin levels did not differ between the groups. Chlorpromazine equivalent doses of antipsychotics correlated with ferroportin levels (p = 0.024). ConclusionFerroportin levels were increased in the schizophrenia group, although iron and hepcidin levels were within normal ranges. Antipsychotics may alter the mechanisms which control ferroportin levels. Further studies are needed to examine the relationships between antipsychotics and iron metabolism for determination of causal relationship.

Galangin mitigates iron overload-triggered liver injury: Up-regulation of PPARγ and Nrf2 signaling, and abrogation of the inflammatory responses

AimHepatotoxicity is a critical consequence of the iron overload conditions such as hemochromatosis and blood transfusion-requiring anemia. Iron induces hepatotoxicity largely through disruption of cellular redox homeostasis and induction of inflammatory responses. The present work explored the hepatoprotective activity of the bio-active flavone galangin against iron-evoked hepatotoxicity. Main methodsIron overload model was established in male Wistar rats via intraperitoneal injection of 150 mg/kg iron-dextran subdivided over a ten-day experimental period. Galangin was administered in a daily oral dose of 15 mg/kg throughout the experimental period. Blood and liver tissue samples were collected on day eleven and subjected to biochemical and molecular investigations. Key findingsGalangin significantly reduced liver iron content and serum ferritin level, and alleviated the iron-evoked oxidative stress. It enhanced the liver cell integrity as reflected by decreased serum activity of the liver enzymes. Mechanistically, galangin up-regulated the redox-regulating transcription factor Nrf2 and its responsive proteins HO-1 and NQO1. Interestingly, galangin up-regulated the antioxidant and anti-inflammatory protein PPARγ and serum hepcidin levels under the iron overload conditions. Equally important, it diminished the nuclear shift of the inflammatory transcription factor NF-κB p65 and down-regulated the levels of the pro-inflammatory cytokines TNF-α and IL-1β. SignificanceThe results of the present study highlight the mitigating activity of galangin against iron-induced hepatotoxicity. The study accentuated targeting of Nrf2, PPARγ, and NF-κB signaling as potential contributing mechanisms. While clinical studies are still required, the current study supports the possible implementation of galangin in controlling iron overload-associated hepatotoxicity.

Hepcidin and Iron Deficiency in Women One Year after Sleeve Gastrectomy: A Prospective Cohort Study.

Iron deficiency with or without anemia, needing continuous iron supplementation, is very common in obese patients, particularly those requiring bariatric surgery. The aim of this study was to address the impact of weight loss on the rescue of iron balance in patients who underwent sleeve gastrectomy (SG), a procedure that preserves the duodenum, the main site of iron absorption. The cohort included 88 obese women; sampling of blood and duodenal biopsies of 35 patients were performed before and one year after SG. An analysis of the 35 patients consisted in evaluating iron homeostasis including hepcidin, markers of erythroid iron deficiency (soluble transferrin receptor (sTfR) and erythrocyte protoporphyrin (PPIX)), expression of duodenal iron transporters (DMT1 and ferroportin) and inflammatory markers. After surgery, sTfR and PPIX were decreased. Serum hepcidin levels were increased despite the significant reduction in inflammation. DMT1 abundance was negatively correlated with higher level of serum hepcidin. Ferroportin abundance was not modified. This study shed a new light in effective iron recovery pathways after SG involving suppression of inflammation, improvement of iron absorption, iron supply and efficiency of erythropoiesis, and finally beneficial control of iron homeostasis by hepcidin. Thus, recommendations for iron supplementation of patients after SG should take into account these new parameters of iron status assessment.

Serum erythroferrone diagnostic value in patients with beta-thalassemia with iron overload

Introduction Patients with beta-thalassemia experience a major complication besides their anemia, which is the iron overload and its complications up to death. Erythroferrone (ERFE) and hepcidin are the major controlling factors for serum iron level, being inversely related to each other. Patients with iron overload are thought to have low serum hepcidin and high serum ERFE levels. So, serum ERFE is postulated to be involved in the pathogenesis of iron overload in patients with β-thalassemia. A cross-sectional study has been conducted, including 112 participants: 80 patients with β-thalassemia and 32 healthy age-matched and sex-matched controls. Serum ERFE, ferritin, and hepcidin were measured by enzyme-linked immunosorbent assay and compared among patients with β-thalassemia and healthy controls. Patients had significantly higher serum ferritin, ERFE, as well as lower serum hepcidin levels as compared with healthy age-matched and sex-matched controls, with P values less than 0.001, less than 0.001, and 0.045, respectively. Serum ERFE may serve as an important marker for iron overload and may represent a future possible therapeutic target using anti-ERFE to control iron overload.

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

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.

Hepcidin in Kawasaki disease: upregulation by acute inflammation in patients having resistance to intravenous immunoglobulin therapy.

Hepcidin is an iron metabolism inhibitor that increases with chronic inflammation. However, it is unclear whether hepcidin indicates acute inflammatory response in Kawasaki disease (KD), which is an acute systemic vasculitis. In this study, we examined the serum hepcidin levels before and after intravenous immunoglobulin (IVIG) therapy in responders and non-responders to IVIG. This was a pilot prospective observational study at a university hospital. All KD patients were initially administered 2g/kg of IVIG as the first IVIG therapy (IVIG1) on day 4 to day 7 after onset. Non-responders to IVIG1 were additionally treated with the second IVIG therapy (IVIG2) using 1g/kg of IVIG. All KD patients were also treated with aspirin. We measured serum hepcidin levels before IVIG1, after IVIG1, and during the recovery period. Among the 31 KD patients, 21 patients and 5 patients improved after IVIG1 (responders-1) and IVIG2 (responders-2), respectively, but 5 patients did not improve after IVIG2 (non-responders). Serum hepcidin levels before IVIG1 were significantly higher in responders-2 (159.0ng/mL) and non-responders (240.0ng/mL), compared to responders-1 (103.0ng/mL). Serum hepcidin levels after IVIG1 were significantly higher in non-responders (163.0ng/mL), compared to responders-1 (43.4ng/mL) and responders-2 (54.6ng/mL). Serum hepcidin levels of non-responders to IVIG were higher before IVIG and remained high after IVIG. Erythrocyte-related indexes, including hemoglobin, reticulocytes, iron, and ferritin before IVIG1, were not significantly different among the three groups. Serum hepcidin might be excessively upregulated by acute inflammation in KD patients having resistance to IVIG. Key Points • Hepcidin, an iron metabolism inhibitor in chronic inflammation, increases during the acute phase of Kawasaki disease. • Hepcidin levels before IVIG of non-responders were higher than those of responders in Kawasaki disease. • Hepcidin might be excessively upregulated by acute inflammation in KD patients having resistance to IVIG.

Serum Hepcidin-25 and Risk of Mortality in Patients on Peritoneal Dialysis.

Background: Increased serum hepcidin-25 level is associated with excess mortality in hemodialysis patients. However, there is a dearth of published information about its predictive effect for survival in patients on peritoneal dialysis (PD). The purpose of this study is to evaluate the association of serum hepcidin-25 with the risk of mortality in PD patients.Methods: Serum hepcidin-25 level was measured using an enzyme-linked immunosorbent assay in a prospective cohort study of PD patients with stored serum samples at baseline. Multivariate linear regression model was used to determine clinical characteristics associated with serum hepcidin-25 concentration. We evaluated the relationship between serum hepcidin-25 and all-cause mortality using a Cox proportional hazards model and the relationship between hepcidin-25 and cardiovascular (CV) and infection-related deaths using competing-risks regression models.Results: In total, 513 PD patients were included in this study. The median serum hepcidin-25 level was 40.9 (17.9–85.9) ng/mL. Body mass index and serum ferritin were positively correlated with serum hepcidin-25 levels. During a median follow-up period of 64.1 months, 122 (24%) patients died, including 61 (50%) CV deaths and 32 (26%) infection-related deaths. In multivariable analysis, patients with the highest tertile of serum hepcidin-25 had a greater risk of all-cause [adjusted hazard ratio (aHR) 1.85, 95% confidence interval (95%CI), 1.14 to 3.00, P = 0.013] and infection-related mortality (adjusted subdistribution hazard ratio [aSHR], 2.61; 95%CI, 1.01 to 6.76, P = 0.049) when compared with those in the second tertile. However, no significant relationship was observed between serum hepcidin-25 and CV mortality.Conclusions: Higher baseline serum hepcidin-25 level was associated with increased risk for all-cause and infection-related mortality in PD patients.

Prognosis of iron deficiency anemia in pregnant women with different somatotypes

BACKGROUND: Anemia during pregnancy, undiagnosed and untreated promptly, is the cause of various obstetric complications: spontaneous miscarriages, premature birth, placental insufficiency, obstetric bleeding, ante- and intrapartum fetal death.&#x0D; AIM: The aim of this study was to evaluate the incidence of iron deficiency anemia in pregnant women with different somatotypes and to develop a prognostic model for the pathology onset.&#x0D; MATERIALS AND METHODS: We examined 390 pregnant women. Somatometry was performed according to the method of R.N. Dorokhov in terms of pregnancy not exceeding 9-10 weeks. Of the examined pregnant women, 110 were of the macrosomatotype, 173 of the meso- and 107 of the microsomatotype. In a clinical blood test, the levels of hemoglobin and red blood cells were determined using well-known methods. Blood iron levels were evaluated by the colorimetric method with ferrozine using a Parma Iron Reagents Kit (Parma Diagnostics Ltd., Russia). Serum hepcidin levels were determined spectrophotometrically using ELISA methods.&#x0D; RESULTS: Iron deficiency anemia was most commonly detected in pregnant women of the macro- and microsomatotype, when compared to those of the mesosomatotype (p 0.05). There was no severe anemia in the study groups. The levels of hematological parameters (serum iron and serum hepcidin) were significantly higher in the group of pregnant women with latent anemia, compared to the study group without signs of anemia (p 0.05). In the second trimester, iron deficiency anemia occurred in the group of patients with latent anemia. Using multiple regression analysis, a formula was obtained for predicting the onset of iron deficiency anemia in pregnant women of different somatotypes.&#x0D; CONCLUSIONS: Hematological parameters (serum iron and serum hepcidin) should be attributed to markers of iron deficiency anemia and timely predict the onset of pathology. The mathematical formula obtained allows predicting with high accuracy the onset of iron deficiency anemia in pregnant women, taking into account the somatotype in the first trimester of pregnancy, and timely preventing the onset of pathology.

Effect of increased blood flow rate on renal anemia and hepcidin concentration in hemodialysis patients

BackgroundIncreasing the blood flow rate (BFR) is a useful method for increasing Kt/V and the clearance for low molecular solutes. Hemodialysis patients are often anemic due to hypoerythropoiesis and their chronic inflammatory state. Hepcidin, a hormone that regulates iron homeostasis, is considered as an indicator of iron deficiency in patients with end-stage renal disease. This study aimed to investigate the effects of an increased BFR during hemodialysis on serum hepcidin levels and anemia.MethodsBetween April 2014 and March 2016, 22 chronic dialysis patients (11 men [50.0 %]; mean [± standard deviation] age, 72 ± 12 years) undergoing maintenance hemodialysis treatment, thrice weekly, were enrolled and followed prospectively for 24 months. In April 2014, the BFR was 200 mL/min; in April 2015 this was increased to 400 mL/min, which was within acceptable limits. The dialysate flow rate remained stable at; 500mlL/min. Blood samples were collected in March 2015 and 2016. The primary endpoint was the comparison of the amounts of erythropoiesis-stimulating agent (ESA) required.ResultsThe increased BFR increased the Kt/V and contributed to significantly decreased urea nitrogen (UN) (p = 0.015) and creatinine (Cr) (p = 0.005) levels. The dialysis efficiency was improved by increasing the BFR. Ferritin (p = 0.038), hepcidin (p = 0.041) and high-sensitivity interleukin-6 (p = 0.038) levels were also significantly reduced. The ESA administered was significantly reduced (p = 0.004) and the Erythropoietin Resistant Index (ERI) significantly improved (p = 0.031). The reduction rates in UN (p < 0.001), Cr (p < 0.001), and beta-2 microglobulin (p = 0.017) levels were significantly greater post the BFR increase compared to those prior to the BFR increase. However, hepcidin was not affected by the BFR change.ConclusionsIncreasing BFR was associated with hemodialysis efficiency, and led to reduce inflammatory cytokine interleukin-6, but did not contribute to reduce C-reactive protein. This reduced hepcidin levels, ESA dosage and ERI. Hepcidin levels were significantly correlated with ferritin levels, and it remains to be seen whether reducing hepcidin leads to improve ESA and iron availability during anemia management.

Lower Level of Interleukin-6 and Hepcidin Found in Lower Density of Physical Exercise among Athlete During Pandemic of Covid-19

The pandemic of Covid-19 affected entire daily human life worldwide, including sports activities among athletes. An athlete was pushed to suit their routine activities with a new health protocol for Covid-19 prevention. Some of them were programmed to train at home with a moderate density of exercise, but others were still in a high density of exercise. This study compared the serum level of hemoglobin (Hb), interleukin-6 (IL-6), and hepcidin among athletes with a high versus moderate exercise density training program during the pandemic. Thirty-four indoor soccer athletes of a soccer football school in Malang voluntarily registered as a subject. Half of them received moderate exercise density exercise programs, and others received high-density exercise programs during June-July 2020. Interleukin-6 and hepcidin level mean was found significantly lower in the moderate group compared to the high-density group. Hemoglobin level mean was found not different between those groups. The lower density of exercise influenced on IL-6 and hepcidin serum level of athlete, but not on hemoglobin level.

Comparisons Between Serum Levels of Hepcidin and Leptin in Male College-Level Endurance Runners and Sprinters.

Background: Hepcidin-25 is a 25 amino acid hepatokine and a key regulator of iron metabolism related to iron deficiency anemia. Recent studies have suggested that an elevated hepcidin level is correlated with low energy availability. Leptin is an appetite-suppressing adipokine and has been reported to stimulate hepcidin production in animals and cultured cells. While leptin is modulated by exercise, it is known that endurance runners and sprinters practice different types of exercise. This study investigated and compared the relationships between hepcidin and leptin levels, iron status, and body fat to understand better the risk of iron deficiency anemia in endurance runners and sprinters.Methods: Thirty-six male college track and field athletes (15 endurance runners and 21 sprinters) were recruited for this study. Dietary intake, body composition, and blood levels of ferritin, hepcidin-25, leptin, and adiponectin were measured. Correlations between hepcidin levels and ferritin, body fat, leptin, and adiponectin were evaluated using Pearson's correlation coefficient for each group.Results: The endurance runners had lower hepcidin levels and higher leptin and adiponectin levels compared with sprinters. Ferritin was positively correlated with hepcidin-25 levels in both the endurance and sprinter groups. A positive correlation was observed between hepcidin-25 and body fat or leptin levels only in sprinters.Conclusion: This is the first study investigating the relationship between blood levels of hepcidin and leptin in athletes. The positive correlation between hepcidin-25 and leptin was observed in sprinters but not endurance runners.

AB0487 HEPSIDINE LEVEL IN PATIENTS WITH ANKYLOSING SPONDYLITIS, RELATIONSHIP WITH HEMOPOESIS AND FERROKINETICS

Background:Hypoferimia, as a manifestation of systemic inflammation, is quite common in patients with ankylosing spondylitis (AS). Anemic syndrome can be represented by anemia of chronic disease (ACD), iron deficiency anemia (IDA) and their combination. Its frequency of occurrences ranges from 18.5 to 45.8 %. The discovery of the hormone hepcidin in 2001 changed the perception of iron metabolism disorders and demonstrated its association with the inflammatory component. Over the last decade, scientific databases have accumulated a lot of information about hepcidin and its role in the development of anemia and the response to inflammation. However, in the context of the AS, such data are contradictory and therefore need further study.Objectives:To determine the level of hepcidin in patients with ankylosing spondylitis and to assess its relationship with hematopoiesis and ferrokinetics.Methods:The hepcidin levels of 76 patients with ankylosing spondylitis (13 women and 63 men with a mean age of 43.67±0.97 years). The diagnosis of AS was made according to the New York modified criteria of 1984. All patients were divided into three groups: without anemia (n=47), with anemia (n=29) and the control group, representative by age and sex (n=26). According to the percentile analysis, all patients were divided into a group with an optimal &lt;25 ng/ml, extremely high - 25-35 ng/ml and a high level of hepcidin &gt; 35 ng/ml. In addition to hepcidin, hematopoiesis and ferrokinetic parameters were measured in each patient: hemoglobin (Hb), erythrocyte, MCV, serum iron, total serum iron-binding capacity (TIBC), serum ferritin, transferrin saturation (TS). Statistical processing of the obtained results was performed with the use of statistical software package “Microsoft Office Excel 2007”.Results:When conducting a percentile comparison in 95 % of people in the control group, the level of hepcidin was in the range of 17.97-38.8 ng/ml (P5 - P95), and in patients with AS in 95 % - 14.62-87.38 ng/ml. At P95, the level of hepcidin in patients with AS was 2.3 times higher than in P95 control group. Comparing the mean values of hepcidin, a significant difference was found between the group of patients without anemia, where it was 36.08±2.57 ng/ml and the group of patients with anemia, where the level of hepcidin was 51.77±4.62 ng/ml. The lowest level of hepcidin was in patients with IDA (35.8 ±7.50 ng/ml), and the highest (62.78±5.94 ng/ml) - among patients with ACD. The group of patients with ACD and iron deficiency, according to the levels of hepcidin (48.53±9.50 ng/ml) took an intermediate place.In terms of hematopoiesis and ferrokinetics, the level of hemoglobin and erythrocytes did not differ significantly between the groups of optimal, extremely high and high levels of hepcidin. According to the levels of serum iron, TS and ferritin in the group of patients with anemia, a significant association with hepcidin was established (with increasing levels of hepcidin, the values of serum iron, TS and ferritin also increased). In contrast,sTfR levels were the highest in the group with optimal hepcidin levels (6.02±0.71 mg/l) and decreased to 4.88±0.64 mg/l in the group with high hepcidin levels. Such changes in hematopoiesis and ferrokinetics were explained by the accumulation of mostly people with symptoms of ACD in the group with high levels of hepcidin, and the group with optimal levels of hepcidin consisted mainly of patients with IDA.Conclusion:Patients with AS have elevated serum hepcidin levels, it is higher in individuals with anemic syndrome than in patients without anemia and is associated with serum iron, TS and ferritin levels.Disclosure of Interests:None declared.

Evaluation of Serum Hepcidin Level in Iraqi Patients with Chronic Hepatitis C and Relation to Serum Iron Status

Evaluation of Serum Hepcidin Level in Iraqi Patients with Chronic Hepatitis C and Relation to Serum Iron Status