Iron Profile in Term Small for Gestational Age Infants at 10 Weeks of Age and Correlation With Maternal Iron Profile : A Prospective Cohort Study

Background: Term small for gestational age (SGA) babies are at risk for developing iron deficiency anemia. The association between maternal and infant iron stores is not clear. Objective: To assess proportion of term SGA neonates developing iron deficiency anemia by 10 weeks of age, and measure correlation between iron profile and hepcidin of babies at birth and at 10 weeks of age with maternal iron profile. Design: Prospective cohort study conducted from November, 2018 to April, 2020. Participants: 120 term SGA babies and their mothers. Intervention: Hemogram, iron profile and serum hepcidin (every fourth case) estimated in mother, cord blood and baby at 10 weeks. Babies developing anemia at 6 weeks detected by hemogram and ferritin were started on iron supplementation and excluded from the study. Outcome: Proportion of babies developing iron deficiency anemia at 10 weeks of age. Results: 35 (29.2%) of 120 term SGA babies developed anemia (hemoglobin <9 g/dL) at 6 weeks. Proportion of infants who developed iron deficiency anemia (hemoglobin <9 g/dL and serum ferritin <40 µ/dL) at 6 and 10 weeks of age was 14.2% and 23.3%, respectively. No significant correlation was found bet-ween hemoglobin, iron and hepcidin of the baby in cord blood and at 10 weeks of age with that of mothers. Serum hepcidin in babies at birth (137.5 ng/mL) were higher than maternal values (128 ng/mL). Conclusion: A significant proportion of term SGA infants developed anemia during early infancy, irrespective of maternal iron status.

Study of growth differentiation factor-15 in polytransfused children with ?-thalassemia

Background: Ineffective erythropoiesis is a predominant feature in ?-thalassemia major (?-TM), causing marked erythroid expansion leading to highly raised levels of growth differentiation factor-15 (GDF-15), which, in turn, suppresses hepcidin production in liver resulting in increased iron absorption from gut. We aim to study the serum GDF-15 in polytransfused ?-TM patients and its correlation with serum ferritin and serum hepcidin. Method: Thirty-nine polytransfused ?-TM children aged between 5 and 17 years and 33 age- and gender-matched healthy controls were enrolled in the study. Complete blood count, serum GDF-15, serum ferritin, and serum hepcidin were performed. Results: The mean serum GDF-15, serum hepcidin, and serum ferritin levels were 638.65 ± 306.96 pg/ml, 108.21 ± 191.30 ng/ml, and 2274.60 ± 1216.08 ng/ml, respectively, which were significantly higher than control group (P < 0.001, P = 0.003, P < 0.001, respectively). There was significant positive correlation of GDF-15 with blood transfusions (r = 0.415, P = 0.009), positive correlation with serum ferritin (r = 0.653, P = 0), and significant negative correlation with serum hepcidin (r = ?0.508, P = 0.001). Conclusion: The findings of the present study suggest that GDF-15 is an important regulator of hepcidin in ?-TM patients. GDF-15 and serum hepcidin together can be used to monitor iron overload and its related complications in such patients.

Serum Hepcidin Level among Chronic Kidney Disease Subjects Accessing Healthcare in Braithwaite Memorial Specialist Hospital Port Harcourt

Hepcidin is the major controller of systemic iron homeostasis and the role of the kidney in regulating hepcidin level is vital in the whole process of iron and hepcidin relationship. This study was aimed at evaluating serum Hepcidin level among Chronic Kidney Disease subjects accessing Healthcare in BMSH Port Harcourt Metropolis. The study was conducted in Port Harcourt at Braithwaite Memorial Specialist Hospital among 55 CKD subjects and 33 normal individuals making up the control group. Subjects were selected randomly and 5mls of blood was collected in plain bottle using venipuncture technique for laboratory assessment of hepcidin. Hepcidin was assayed using competitive ELISA method. T-test was used to compare the mean difference oh hepcidin between both groups. Result showed that there was a significant difference in hepcidin level between CKD and control groups; 52.00±36.00ng/ml for CKD group and 16.00±13.00ng/ml for control group, p<0.05. This study has shown that CKD has a significant impact in hepcidin level blood and consequently on iron regulation

Significance of serum hepcidin in assessment of liver inflammation activity among patients with chronic hepatitis B / 预防医学

Objective@#To investigate the value of serum hepcidin in assessment of liver inflammation activity among patients with chronic hepatitis B ( CHB ), so as to provide insights into the assessment of liver inflammation activity among CHB patients.@*Methods@#A total of 79 CHB patients who were admitted to the Affiliated Hospital of Hangzhou Normal University were selected as the experimental group, while 40 healthy volunteers were randomly sampled as controls. Subjects'demographic data, liver function tests and iron metabolism parameters were collected from medical records, and serum hepcidin was measured using enzyme-linked immunosorbent assay ( ELISA ). In addition, ultrasound-guided liver biopsy was performed in CHB patients, and mild and moderate-to-severe CHB were classified according to liver inflammation activity and degree of liver fibrosis. Serum hepcidin levels were compared between the experimental and control groups and between patients with mild and moderate-to-severe CHB. The value of serum hepcidin in assessment of liver inflammation activity was examined among CHB patients using the receiver operating characteristic ( ROC ) curve analysis.@*Results@#Subjects in the experimental group included 54 men ( 68.35% ) and had a mean age of ( 39.06±10.67 ) years, while the controls included 24 men (60.00%) and had a mean age of ( 42.43±11.44 ) years. Lower hepcidin levels were measured in the experimental group than in the control group [( 11.70±5.64 ) vs. ( 17.82±3.63 ) μg/L; P<0.05 ]. There were 54 patients with mild CHB ( 68.35% ) and 25 cases with moderate-to-severe CHB ( 31.65% ), and lower hepcidin levels were detected in patients with moderate-to-severe CHB than in those with mild CHB [ ( 6.92±2.21 ) vs. ( 13.95±5.36 ) μg/L; P<0.05 ]. The area under the ROC curve, optimal cut-off, sensitivity and specificity of serum hepcidin were 0.903 ( P<0.05 ), 10.365 μg/L, 100.0% and 72.2% for assessment of moderate-to-severe CHB, respectively.@*Conclusion@#Serum hepcidin is feasible to evaluate the liver inflammatory activity among patients with CHB.

The expression and clinical significance of peripheral blood interferon-gamma and hepcidin-25 in patients with primary gastric cancer combined with thalassemia minor / 中国医师进修杂志

Objective:To explore the expression and detection significance of peripheral blood interferon-gamma (IFN-γ) and hepcidin-25 (Hepc-25) in primary gastric cancer combined with thalassemia minor.Methods:One hundred and fifty primary gastric cancer combined with thalassemia minor patients admitted to of Jiangsu Province Official Hospital from January 2017 to December 2019 were selected as the research group, and 150 cases of primary gastric cancer without thalassemia minor admitted in the same period were selected as the control group. The levels of peripheral blood IFN-γ and Hepc-25 in the two groups were determined by enzyme-linked immunosorbent assay, and the receiver operating characteristic curve (ROC) was used to evaluate the diagnostic sensitivity and specificity of peripheral blood IFN-γ and Hepc-25 on primary gastric cancer combined with thalassemia minor. The level of hemoglobin (Hb) was measured by the cyanmethemoglobin method, and the Pearson correlation analysis was used to analyzed the relationship among the peripheral blood IFN-γ, Hepc-25 and Hb levels in the research group.Results:The levels of peripheral blood IFN-γ and Hb in the research group were lower than those in the control group: (115.18 ± 27.05) ng/L vs. (137.17 ± 35.66) ng/L, (88.44 ± 10.71) g/L vs. (120.60 ± 29.46) g/L; the level of Hepc-25 in the research group was higher than that in the control group: (49.32 ± 15.05) μg/L vs. (32.66 ± 12.22) μg/L, and the differences were statistically significant ( P<0.05). There were no significant differences in the levels of peripheral blood IFN-γ, Hepc-25 and Hb between the patients with α-thalassemia and β-thalassemia ( P>0.05). The area under the curve (AUC) of thalassemia predicted by of peripheral blood IFN-γ level was 0.709.When the cut-off value was≤138.89 ng/L, its diagnostic sensitivity and specificity were 81.33% and 70.67% respectively, and when the serum AUC of Hepc-25 was 0.811 and cut-off value was ≥ 40.13 μg/L, its diagnostic sensitivity and specificity were 75.33% and 74.00% respectively. Pearson correlation analysis showed that in the research group IFN-γ and Hb had positive correlation ( r = 0.245, P<0.05), Hepc-25 and IFN-γ had negative correlation ( r = - 0.378, P<0.05); Hepc-25 and Hb had negative correlation ( r = - 0.647, P<0.05). Conclusions:The low level of IFN-γ and the high level of Hepc-25 in peripheral blood of patients with primary gastric cancer combined with thalassemia minor are related to Hb and have certain diagnostic value for thalassemia.

Effect of active component compound of Epimedii Folium,Astragali Radix,and Puerariae Lobatae Radix on expression of ADAM17 in HT22 cells by mediating hepcidin / 中国中药杂志

Alzheimer's disease(AD) patients in China have been surging, and the resultant medical burden and care demand have a huge impact on the development of individuals, families, and the society. The active component compound of Epimedii Folium, Astragali Radix, and Puerariae Lobatae Radix(YHG) can regulate the expression of iron metabolism-related proteins to inhibit brain iron overload and relieve hypofunction of central nervous system in AD patients. Hepcidin is an important target regulating iron metabolism. This study investigated the effect of YHG on the expression of a disintegrin and metalloprotease-17(ADAM17), a key enzyme in the hydrolysis of β amyloid precursor protein(APP) in HT22 cells, by mediating hepcidin. To be specific, HT22 cells were cultured in vitro, followed by liposome-mediated siRNA transfection to silence the expression of hepcidin. Real-time PCR and Western blot were performed to examine the silencing result and the effect of YHG on hepcidin in AD cell model. HT22 cells were randomized into 7 groups: control group, Aβ25-35 induction(Aβ) group, hepcidin-siRNA(siRNA) group, Aβ25-35 + hepcidin-siRNA(Aβ + siRNA) group, Aβ25-35+YHG(Aβ+YHG) group, hepcidin-siRNA+YHG(siRNA+YHG) group, Aβ25-35+hepcidin-siRNA+YHG(Aβ+siRNA+YHG) group. The expression of ADAM17 mRNA in cells was detected by real-time PCR, and the expression of ADAM17 protein by immunofluorescence and Western blot. Immunofluorescence showed that the ADAM17 protein expression was lower in the Aβ group, siRNA group, and Aβ+siRNA group than in the control group(P<0.05) and the expression was lower in the Aβ+siRNA group(P<0.05) and higher in the Aβ+YHG group(P<0.05) than in the Aβ group. Moreover, the ADAM17 protein expression was lower in the Aβ+siRNA group(P<0.05) and higher in the siRNA+YHG group(P< 0.05) than in the siRNA group. The expression was higher in the Aβ+siRNA+YHG group than in the Aβ+siRNA group(P<0.05). The results of Western blot and real-time PCR were consistent with those of immunofluorescence. The experiment showed that YHG induced hepcidin to up-regulate the expression of ADAM17 in AD cell model and promote the activation of non-starch metabolic pathways, which might be the internal mechanism of YHG in preventing and treating AD.

Study the role of hepcidin in diagnosis of iron deficiency anemia in young females of northern India

Background: Iron deficiency is one of the most common nutritional disorder. Maintenance of body iron status is an integral part of healthcare in young female of reproductive age group. Thereby early detection could lead to early intervention and reduce its comorbidity.  Indeed, an ideal screening test should be capable of identifying iron deficiency long before developing anemia. Henceforth, the present study was aimed to determine utility of serum hepcidin in iron deficiency and to access the baseline value of hepcidin in young female.Methods: This sectional study was conducted in the Department of biochemistry SGT Medical College Hospital and Research Institute, Budhera, Gurugram. It included non-pregnant female students of age 18-25 years with normal RBC indices and hemoglobin >12 gm%. Estimation of serum hepcidin-25 was by ELISA.Results: The reference range of hepcidin established in this study was 12.14-139.89 ng/ml for females with the mean being 42.4±29.13 ng/ml. It showed higher discriminating power in evaluating iron status in young healthy women (AUC 0.984) with best combination of diagnostic sensitivity (95.7%) and specificity (93.2%) at a cut off of >15.7 ng/ml. Serum hepcidin identified 17% of young healthy females with normal hemoglobin to have functional or storage iron deficiency.Conclusions: The prevention of iron deficiency anemia remains insufficient worldwide especially among underprivileged women and children Therefore, estimation of serum hepcidin may be considered as a valuable tool in assessing iron status in young healthy female population who are the prime target group for iron supplements to reduce comorbidity associated with iron deficiency and anemia.

Evaluation of Some Cytokines, CD4, Hepcidin, Iron, and Some Haematological Parameters of Patients Living with Human Immunodeficiency Virus in Southeastern Part of Nigeria

A study to evaluate the levels of interferon-gamma, interleukins 6 and 10, hepcidin, iron status and some haematological parameters in persons living with human immunodeficiency virus was carried out. A total of 150 subjects aged 18-60 years were enlisted for this study. The subjects were grouped into: Group A (50 control subjects) and Group B (100 HIV subjects, 50 subjects were non ART HIV patients, 50 subjects were on Lamivudine, Tenofavir and Efavirenz). About 7ml of venous blood were collected from each subject;4.5ml of blood were placed into plain tubes for assay of interferon gamma, interleukins (6&10), hepcidin and iron and 2.5ml for FBC, CD4 count and HIV screening. The cytokines and hepcidinwere measured using Melsin ELISA Kits and Teco Diagnostics kits used for iron. Full blood count was determined by automation using Mindray BC-5300, China. The data was analysed with the statistical package for social science (SPSS) version 20 using ANOVA and the level of significance set at P<0.05. The results showed difference that was statistically significant (P<0.05) in IFN-γ (16.25±0.87pg/ml, 29.31±1.44pg/ml,18.49±1.48pg/ml, P=0.000),IL-6(7.98±0.22pg/ml, 11.08±1.21pg/ml,8.79±0.76pg/ml,P=0.000), IL-10(8.52±0.62pg/ml, 16.62±1.53pg/ml,10.39±1.06Pg/ml P=0.000), CD4 (1045.54 ±247.24Cells/L, 195.60 ±35.94Cells/L,10.39±1.06cells/L P=0.000), hepcidin (6.03±1.38ng/ml, 39.59 ±4.50ng/ml, 20.86±3.43ng/ml, P=0.000), Iron (86.29±7.27 μg/dl, 73.43±5.45 μg/dl,85.44±8.45μg/dl, P=0.000), TIBC (345.56±28.40 μg/dl, 287.19 ±8.21μg/dl,305.46±18.82μg/dl, P=0.000),%TSA (25.16±3.18%, 25.61±2.22%,28.08 ±3.42%,P=0.000) WBC (5.87 ±0.88 X 109/L, 4.69±0.72X 109/L,4.80±0.45X 109/L, P=0.000), Neutrophils (60.57±2.83%, 75.16±3.68%,69.04±2.90%, P=0.000), Lymphocytes (30.69 ±2.84%, 17.24±2.50%, 24.46±2.60%,P=0.000), Monocytes (5.59 ±1.2%, 4.18±1.12%,3.97±0.92%, P=0.000), Eosinophils (2.30 ±1.05%, 2.16±0.82%,1.67±0.57%, P=0.000), Basophil 0.86 ±0.39%, 1.31±0.94%, 0.86±0.44%,P=0.018), RBC (4.92±0.30 X 1012/L, 3.34±0.21 X 1012/L,3.60 ±0.18X 1012/L, P=0.000), Haemoglobin (14.75±0.90,g/dl, 10.05±0.65g/dl,10.80±0.53g/dl, P=0.000), PCV (44.25±2.70%, 30.14±1.95,32.56±1.50%, P=0.000), MCV(89.92±2.3fl, 79.49±1.28fl,88.15±2.08fl, P=0.029), MCH (36.12±1.53pg, 26.60±0.48P, P=0.002), Platelets (261.75±22.71 X 109/L, 246.16±9.93 X 109/L,189.32±17.00X 109/L, P=0.000), ESR (7.03 ±1.38mm/hr, 59.52 ±6.46mm/hr,43.34±4.82mm/hr, P=0.000) when compared among Control, Non ART HIV and ART positive subjects.g,28.57±1.78pg, P=0.000), MCHC (368.46±12.28g/l, 318.92±7.33g/l,333.56±22.61g/l. The study shows that interferon gamma, interleukin 6, interleukin 10 and hepcidin are some of the biomarkers in thepathogenesis of HIV. The infection of HIV increases the levels of the cytokines. The cytokines and hepcidin can be used as prognostic and diagnostic markers as their levels decreased with treatment of the patients

Evaluation of Some Cytokines, CD4, Hepcidin, Iron Profile and Some Haematological Parameters of Pulmonary Tuberculosis Patients Coinfected with HIV in Southeast of Nigeria

The study was done to determine the levels of interferon-gamma, interleukin 6, interleukin 10, iron status, hepcidin and haematologicalparameters of patients with pulmonary tuberculosis co-infected with human immunodeficiency virus in Southeast, Nigeria. This study was carried out at the directly observed treatment-short course Tuberculosis (TB DOTS) centre of Federal Medical Centre, Umuahia, located in South-Eastern Nigeria. Therefore, sample size of 240 was used to give room for attrition. A total of two hundred and forty (240) subjects aged 18-60 years were enlisted for this study. Seven milliliters (7ml) of venous blood was collected from each subject and 2.5ml was dispensed into bottles containing di-potassium salt of ethylenediamine tetra-acetic acid (K2-EDTA) and was used for full blood count, CD4 count and HIV screening. Also, 4.5ml was dispensed into plain tubes. Serum was obtained after clotting by spinning at 3000 RPM for 10 minutes and was used for interferon gamma, interleukin-6, and interleukin-10, iron and hepcidin determination. Data was analysed using statistical package for social science (SPSS) version 20. Student t-test, ANOVA (Analysis of Variance), Pearson Product Moment and Chi-Square were the tools employed. Results were expressed as mean ± standard deviation and are presented in table and significance level was set at P<0.05.The results showed difference that was statistically significant (P<0.05) in IFN-γ (P=0.000), IL-6 (P=0.000) IL-10 (P=0.000), CD4 (P=0.000), hepcidin (P=0.000), Iron (P=0.000), TIBC (P=0.000), %TSA (P=0.001) ,WBC (P=0.000), Neutrophils (P=0.000), Lymphocyes (P=0.000), Monocytes (P=0.000), Eosinophils (P=0.000), Basophils (P=0.018), RBC (P=0.000), haemoglobin (P=0.000), PCV (P=0.000), MCV (P=0.000), MCH (P=0.000), MCHC (P=0.000), Platelets (P=0.000), ESR (P=0.000) when compared among control, TB, HIV and TB-HIV subjects respectively. The co infection of HIV on pulmonary TB patients increases the levels of the cytokines. The cytokines and hepcidin can be used as adjunct to prognostic and diagnostic markers as their levels decreased with increased duration of treatment of the patients. The study hasshown wide variations in the haemtological indices studied

Serum Hepcidin as an Inflammatory Marker in Chronic Kidney Disease

Background: Hepcidin is known to be the central regulator of iron homeostasis in the body. It is up-regulated by inflammation and downregulated by anemia. CKD is a state of chronic inflammation seen in kidney.Previous work has shown that serum hepcidin levels were increased in patients with CKD. This was surprising as these patients had a chronic inflammatory state and co-existent anemia. Aim and Objectives: The aim of the study is to estimate the levels of hepcidin in CKD patients and to check the correlation of hepcidin to inflammation in chronic kidney disease. Methods: This cross-sectional study was conducted at the Department of Biochemistry, Central Laboratory, Sree Balaji Medical College and Hospital,Chromepet, Chennai during January 2017 -June 2018 among 50 patients of chronic kidney disease in the age group of 18-60 years. The blood samples were collected using vacutainer system. Samples for serum hepcidin, ferritin and hsCRP were collected in red topped plain vacuum tube. The samples were centrifuged at 3000 rpm for 15 minutes. The samples were then processed, and values were obtained. The data were analysed using SPSS package.Results: The mean values of s. Hepcidin, s. ferritin and hsCRP levels were found to be increased in the study population. The mean value of s. hepcidin was found to have strong positive correlation with the mean values of s. ferritin and hsCRP with r-value > 0.7.Conclusion: Hepcidin levels are elevated in CKD and hepcidin isa predictor of inflammation since it correlated well with the inflammatory markers hsCRP and ferritin levels

Serum iron level in patients with COVID-19: a case report study

Coronavirus disease emerged in Wuhan, China in December 2019 and led to worldwide pandemic in March 2020. Due to early diagnose, treatment and prevent transmission of COVID-19 disease, we need rapid laboratory tests and develop them. This paper focuses on serum Iron level in patients with COVID-19. We assess the serum Iron level due to the following reasons: I. Iron is a key part of hemoglobin structure in which is essential for providing Oxygen to the body organs, particularly for the patients with pulmonary involvement such as COVID-19. II. Iron deficiency can contribute to muscle weakness and reduction of respiratory capacity, at which increases the risk of deterioration of COVID-19 patients. III. Elevation in Hepcidin level (due to the increase in IL-6 level) in COVID-19 patients inhibits Iron absorption from intestinal lumen and blocks the Iron release from macrophages. IV. Iron is an essential element in infectious suppress and inflammatory process. We noticed that most of the patients, especially admitted to hospital due to the respiratory symptoms, have lower serum Iron level.

Can Calprotectin Show Subclinical Inflammation in Familial Mediterranean Fever Patients?

BACKGROUND: Familial Mediterranean fever (FMF) is an autoinflammatory disease that has self-limiting inflammatory attacks during polyserositis. Hepcidin is a protein, and interleukin-6 stimulation increases hepcidin levels. Calprotectin (CLP) is a recently defined cytokine released from monocytes and neutrophils in response to tissue trauma and inflammation. There are studies in the literature showing that it can be used as a biomarker in rheumatic diseases such as ankylosing spondylitis and rheumatoid arthritis. Here, we compared the levels of hepcidin and CLP in healthy individuals and FMF patients during an attack-free period and show its relation to genetic mutations.METHODS: This is a cross-sectional study. Between July 2017 and December 2017, 60 patients diagnosed with FMF an admitted to the Cumhuriyet University Faculty of Medicine Department of Internal Medicine Rheumatology as well as 60 healthy volunteers without any rheumatic, systemic, or metabolic diseases were enrolled in this study. Blood was collected from a peripheral vein to measure serum CLP and hepcidin levels. Blood tests were examined by ELISA; the study protocol was approved by the local ethics committee.RESULTS: Median serum hepcidin level was 468.1 (210.3–807.8) pg/mL in FMF group and 890.0 (495.0–1,716.9) pg/mL in the healthy control (HC) group. There was a statistically significant difference between the two groups (P < 0.001). The median serum levels of CLP in the FMF group were measured as 1,331.4 (969.3–1,584.6 pg/mL and 73.8(45.0–147.9) pg/mL in the HC group. There was a statistically significant difference between the two groups (P < 0.001). Receiver operating characteristic analysis showed that the sensitivity was 66.7% and the specificity was 71.7% at serum hepcidin < 581.25 pg/mL (P < 0.05); the sensitivity was 96.7% and specificity was 100% at CLP > 238 pg/mL (P < 0.05). There was no significant difference between serum hepcidin and CLP levels in FMF patients with M694V homozygous and M694V heterozygous (P > 0.05). There was no significant difference in serum hepcidin levels between FMF patients with and without arthritis, proteinuria, and amyloidosis (P < 0.05). There was no significant correlation between laboratory findings, gender, age, and serum CLP and hepcidin levels (P > 0.05, r < 0.25).CONCLUSION: Serum CLP levels in FMF patients during an attack-free period are significantly higher than in the HC groups. Serum hepcidin levels in FMF patients are significantly lower than in the HC group. Low levels of hepcidin may be explained by including FMF patients during an attack-free period in the study. CLP may be an important biomarker in FMF. A better understanding of the role of these biomarkers in the diagnosis of FMF is needed to evaluate the results in a more comprehensive way.

Relationship between Cardiac Geometry and Serum Hepcidin in Chronic Kidney Disease: Analysis from the KNOW-CKD Study

Hepcidin and Neutrophil Gelatinase-Associated Lipocalin as a Biomarker for Acute Kidney Injury Linked Iron Metabolism

No abstract available.

Urinary Biomarkers may Complement the Cleveland Score for Prediction of Adverse Kidney Events After Cardiac Surgery: A Pilot Study

BACKGROUND: The ability of urinary biomarkers to complement established clinical risk prediction models for postoperative adverse kidney events is unclear. We assessed the effect of urinary biomarkers linked to suspected pathogenesis of cardiac surgery-induced acute kidney injury (AKI) on the performance of the Cleveland Score, a risk assessment model for postoperative adverse kidney events. METHODS: This pilot study included 100 patients who underwent open-heart surgery. We determined improvements to the Cleveland Score when adding urinary biomarkers measured using clinical laboratory platforms (neutrophil gelatinase-associated lipocalin [NGAL], interleukin-6) and those in the preclinical stage (hepcidin-25, midkine, alpha-1 microglobulin), all sampled immediately post-surgery. The primary endpoint was major adverse kidney events (MAKE), and the secondary endpoint was AKI. We performed ROC curve analysis, assessed baseline model performance (odds ratios [OR], 95% CI), and carried out statistical reclassification analyses to assess model improvement. RESULTS: NGAL (OR [95% CI] per 20 concentration-units wherever applicable): (1.07 [1.01–1.14]), Interleukin-6 (1.51 [1.01–2.26]), midkine (1.01 [1.00–1.02]), 1-hepcidin-25 (1.08 [1.00–1.17]), and NGAL/hepcidin-ratio (2.91 [1.30–6.49]) were independent predictors of MAKE and AKI (1.38 [1.03–1.85], 1.08 [1.01–1.15], 1.01 [1.00–1.02], 1.09 [1.01–1.18], and 3.45 [1.54–7.72]). Category-free net reclassification improvement identified interleukin-6 as a model-improving biomarker for MAKE and NGAL for AKI. However, only NGAL/hepcidin-25 improved model performance for event- and event-free patients for MAKE and AKI. CONCLUSIONS: NGAL and interleukin-6 measured immediately post cardiac surgery may complement the Cleveland Score. The combination of biomarkers with hepcidin-25 may further improve diagnostic discrimination.

Predicting hepcidin level using inflammation markers and iron indicators in patients with anemia of chronic disease

ABSTRACT Background: Recently, a small peptide called Hepcidin, was found to have an important role in regulating the iron metabolism in anemia of chronic disease (ACD) patients. Hepcidin is regulated by a variety of conditions at the transcriptional level. Therefore, our study aims to predict the level of hepcidin serum using inflammation markers and iron indicators in patients afflicted with ACD and observe how this severity of inflammation separated the level of interleukin-6 (IL-6), as well the as hepcidin level. Methods: A cross-sectional data analysis was conducted on 80 ACD adult patients treated at the Sanglah Teaching Hospital in Bali, Indonesia. We used hepcidin serum and several markers, such as the hemoglobin level, inflammation markers, renal function tests, IL-6, and iron indicators, to predict the hepcidin level. Results: This study recruited 80 ACD patients, comprising 45 men (56.3%) and 35 women (43.7%). The mean age of the participants was 43 ± 16.5 years. Only IL-6, ferritin and serum creatinine correlate significantly with serum hepcidin from seven variables that were previously eligible to enter the analysis. This study found the model to predict the hepcidin level using IL-6 ferritin and the creatinine level as the hepcidin level (predicted) = −23.76 + 0.396 (IL 6) + 0.448 (ferritin) + 0.310 (creatinine). Conclusion: This study has revealed that the creatinine level, ferritin and IL-6 can be used to predict the hepcidin level in patients with anemia of chronic disease. It is to be hoped that further cohort studies can validate our formula to predict the hepcidin level.

Fisiopatología de la anemia durante el embarazo: ¿anemia o hemodilución?

Iron is essential for health; its deficiency and excess are harmful. Our bodies have a high capacity to store and reuse iron so that its requirement is small (1-2 mg absorbed/day). Hepcidin, a hormone produced in the liver, has an important role in this elements homeostasis by blocking its transport protein, inhibiting its absorption in the duodenum and its release from the iron stores. During pregnancy, there is a new iron requirement for the placenta and fetus. This causes an increase in erythropoiesis; however, hemoglobin concentration decreases due to the greater vascular expansion. This results in hemodilution, which is evident starting the second trimester and returns to pre-gestational values at the end of the third trimester. Maternal iron deficiency anemia becomes a public health problem when it is moderate (7-14,5 g/dL) during pregnancy adversely affect the mother and neonate. For this reason, it is important to confirm if a pregnant woman with low hemoglobin levels is anemic or if it is due to hemodilution, a physiological process during pregnancy that does not require treatment. This review presents evidence to distinguish anemia from physiological hemodilution.

El hierro es un micronutriente fundamental para la salud; su deficiencia o su exceso son dañinos. Por ello, el organismo regula el requerimiento de hierro en base a su alta capacidad para almacenar y reciclar el hierro corporal de tal manera que su requerimiento es mínimo (1 a 2 mg absorbido/día). Esto se regula a través de la hepcidina, una hormona hepática que inhibe a la proteína transportadora de hierro (ferroportina) y con ello disminuye la absorción de hierro, o su liberación en los tejidos donde se almacenan. Durante la gestación hay una mayor necesidad de hierro para la placenta y el feto, y ello se evidencia en un aumento de la eritropoyesis; sin embargo, la concentración de la hemoglobina disminuye por efecto de una mayor expansión vascular. Esto determina una hemodilución que se evidencia a partir del segundo trimestre, y luego se va normalizando al final del tercer trimestre. La anemia materna por deficiencia de hierro se constituye en un problema de salud pública cuando es de magnitud moderada (7 a 14,5 g/dL) en la gestante afecta a la madre y al neonato. Por ello es importante determinar si una gestante con hemoglobina baja es realmente anémica o tiene una hemodilución, que es un proceso fisiológico que no requiere de tratamiento. Esta revisión presenta las evidencias para poder discriminar entre una anemia verdadera gestacional de una hemodilución fisiológica.

Expression and influencing factors of hepcidin in classical paroxysmal nocturnal hemoglobinuria / 中华血液学杂志

Objective@#To investigate the serum expression and influencing factors of hepcidinin patients with classical paroxysmal nocturnal hemoglobinuria (PNH) .@*Methods@#Retrospective analysis of 36 classical PNH patients from 2016.3 to 2017.3. Serum hepcidin concentration was measured by ELISA method. The relationship between serum hepcidin concentration and erythropoiesis and iron homeostasis parameters was evaluated.@*Results@#The median serum hepcidin level of 36 classical PNH patients was 32.03 (23.11, 118.48) μg/L, it was significantly lower than of 181.42 (106.80, 250.53) μg/L in 292 normal control subjects (z=-5.107, P<0.001) . The median serum hepcidin of 56.41 (44.60, 95.06) μg/L in PNH patients with normal ferritin was significantly lower than that in normal controls. The median serum hepcidin concentration 23.75 (21.77, 30.35) μg/L in iron deficiency PNH patients was lower than that in the normal ferritin PNH patients. However, the median serum hepcidin level of classical PNH with elevated ferritin patients 336.19 (304.19, 375.08) μg/L was significantly higher not only than that of normal ferritin and iron deficiency PNH ones, but also than that of normal control subjects. Regression analysis showed that serum ferritin, transferrin saturation and serum albumin level were independent influencing factors of serum hepcidin level in patients with classical PNH.@*Conclusion@#The decreased serum hepcidin level in patients with classical PNH was mainly influenced by iron metabolism factors.

Hepcidin-orchestrated Hemogram and Iron Homeostatic Patterns in Two Models of Subchronic Hepatic injury / 生物医学与环境科学（英文）

OBJECTIVE@#This study was designed to evaluate hematological disorders and the orchestrating roles of hepcidin and IL-6 in rat models of thioacetamide (TAA) and carbon tetrachloride (CCl4) hepatotoxicity.@*METHODS@#Rats were intraperitoneally injected with TAA (10 mg/100 g rat weight dissolved in isosaline) or CCl4 (100 μL/100 g rat weight diluted as 1:4 in corn oil) twice weekly for eight consecutive weeks to induce subchronic liver fibrosis. Blood and tissue samples were collected and analyzed.@*RESULTS@#CCl4 but not TAA significantly decreased the RBCs, Hb, PCV, and MCV values with minimal alterations in other erythrocytic indices. Both hepatotoxins showed leukocytosis, granulocytosis, and thrombocytopenia. By the end of the experiment, the erythropoietin level increased in the CCl4 model. The serum iron, UIBC, TIBC, transferrin saturation%, and serum transferrin concentration values significantly decreased, whereas that of ferritin increased in the CCl4 model. TAA increased the iron parameters toward iron overload. RT-PCR analysis revealed increased expression of hepatic hepcidin and IL-6 mRNAs in the CCl4 model and suppressed hepcidin expression without significant effect on IL-6 in the TAA model.@*CONCLUSION@#These data suggest differences driven by hepcidin and IL-6 expression between CCl4 and TAA liver fibrosis models and are of clinical importance for diagnosis and therapeutics of liver diseases.

Role of redox iron towards an increase in mortality among patients: a systemic review and meta-analysis

An increase in biochemical concentrations of non-transferrin bound iron (NTBI) within the patients with an increase in serum iron concentration was evaluated with the following objectives: (a) Iron overloading diseases/conditions with free radicle form of ‘iron containing’ reactive oxygen species (ROS) and its imbalance mediated mortality, and (b) Intervention with iron containing drugs in context to increased redox iron concentration and treatment induced mortality. Literature search was done within Pubmed and cochrane review articles. The Redox iron levels are increased during dys-erythropoiesis and among transfusion recipient population and are responsive to iron-chelation therapy. Near expiry ‘stored blood units’ show a significant rise in the ROS level. Iron mediated ROS damage may be estimated by the serum antioxidant level, and show reduction in toxicity with high antioxidant, low pro-oxidant levels. Iron drug therapy causes a significant increase in NTBI and labile iron levels. Hospitalized patients on iron therapy however show a lower mortality rate. Serum ferritin is a mortality indicator among the high-dose iron therapy and transfusion dependent population. The cumulative difference of pre-chelation to post chelation ROS iron level was 0.97 (0.62; 1.32; N=261) among the transfusion dependent subjects and 2.89 (1.81–3.98; N=130) in the post iron therapy ‘iron ROS’ group. In conclusion, iron mediated mortality may not be mediated by redox iron among multi-transfused and iron overloaded patients.