Serum Hepcidin Levels Research Articles

Correlation between serum hepcidin level and stages of chronic kidney disease: A cross sectional study

Introduction: Chronic Kidney Disease (CKD) has been associated with significant mortality and morbidity. Despite significant numbers of cases, biomarkers related to iron status and development of anaemia in these patients has not been looked upon extensively. Few biomarkers have been studied, one of which is serum hepcidin levels. We aimed to estimate the serum hepcidin levels in patients with CKD and its correlation with its successive stages. Materials and Methods: The study design was cross-sectional observational study. 51 patients of CKD KDIGO stage II to V were included and patients of obstructive uropathy or malignancy or transplant recipient were excluded from the study. The aim of the study was to evaluate the association between serum hepcidin levels and Stages of CKD in terms of eGFR. Results: The mean serum hepcidin levels which were found in Stage II, III, IV and V of CKD patients was 65.48, 116.03, 136.61 and 160.37 ng/ml respectively. There was a strong negative correlation between eGFR and serum hepcidin level, and this correlation was statistically significant (r = -1.0, p = <0.001). The Krushkal-Wallis Test also provided p value of <0.001 when stages of CKD and serum hepcidin levels were correlated. Conclusion: There was significant positive correlation of serum hepcidin with the stages of CKD (P < 0.001) and the levels of serum hepcidin were found to be significantly higher as the stage increased. Thus, serum hepcidin may be used as a marker of iron metabolism, prognosis and progress of disease in the CKD patients.

Serum Hepcidin and C Reactive Proteins as Predictive Markers for Post Acne Scarring

Abstract Background Acne vulgaris is a common inflammatory skin condition affecting a large section of population. Hepcidin, a small peptide produced by the liver, is a recently discovered key regulator of iron homeostasis that was classified as a typeII acute phase protein. The synthesis of hepcidin is greatly stimulated by inflammation or by iron overload. C‑reactive protein (CRP) is one of the best indicators of systemic inflammation, considering that its serum levels show no circadian change across the 24 hrs. IL‑1, IL‑6 and TNF‑α that are found in the acne lesions are also major inducers of CRP production by the liver. Thus, CRP levels could be elevated in acne if the amount of local inflammation is high enough. Aim of the Work To measure serum Hepcidin and C reactive proteins in acne vulgaris patients & assess their ability as predictive serum markers for postacne scarring. Patients and Methods This Observational Cross sectional study, was carried out on 60 moderate, severe & very severe acne patients aged from 16 to 40 years old (with and without postacne scarring), recruited from the outpatient clinics of Dermatology, Venereology & Andrology departments of Ain-Shams University and MUST university Hospitals, from February 2019 toFebruary 2020. Results Levels of serum hepcidin protein of studied acne pateints were higher than normal range, while CRP serum levels were almost within normal range. Besides, Pateints with post acne scars had significantly lower serum hepcidin levels and higher CRP levels than pateints without. Furthermore, there was highly significant negative correlation between Hepcidin protein serum levels and duration and grade of acne, as well as post acne scarring grade. However, there was highly significant positive correlation between CRP serum levels and duration and grade of acne, as well as post acne scarring grade. Conclusion Serum hepcidin and CRP levels may provide an objective tool to predict the clinical outcome of acne vulgaris lesions and might help in determining the susceptible patients for scarring thus, configuring the therapeutic plan to start an aggressive treatment in patients prone to scar formation regardless of the clinical severity of acne vulgaris itself.

Elevated first-trimester hepcidin level is associated with reduced risk of iron deficiency anemia in late pregnancy: a prospective cohort study.

Iron deficiency (ID) and iron deficiency anemia (IDA) during pregnancy are highly prevalent worldwide. Hepcidin is considered an important biomarker of iron status. Currently, few longitudinal cohort studies have assessed the potential causal relationship between hepcidin and ID/IDA. Therefore, we aimed to investigate the association of first-trimester maternal serum hepcidin with third-trimester ID/IDA risk in a prospective cohort. Total of 353 non-ID/IDA pregnant women at 11-13 weeks' gestation were enrolled in Southern China and followed up to 38 weeks of gestation. Data on demography and anthropometry were obtained from a structured questionnaire at enrollment. Iron biomarkers including hepcidin were measured at enrollment and follow-up. Regression models were used to evaluate the association of first-trimester hepcidin with third-trimester ID/IDA risk. Serum hepcidin levels substantially decreased from 19.39 ng/mL in the first trimester to 1.32 ng/mL in the third trimester. Incidences of third-trimester ID and IDA were 46.2 and 11.4%, respectively. Moreover, moderate and high levels of first-trimester hepcidin were positively related to third-trimester hepcidin (log-transformed β = 0.51; 95% CI = 0.01, 1.00 and log-transformed β = 0.66; 95% CI = 0.15, 1.17). Importantly, elevated first-trimester hepcidin was significantly associated with reduced risk of third-trimester IDA (OR = 0.38; 95% CI = 0.15, 0.99), but not with ID after adjustment with potential confounders. First-trimester hepcidin was negatively associated with IDA risk in late pregnancy, indicating higher first-trimester hepcidin level may predict reduced risk for developing IDA. Nonetheless, given the limited sample size, larger studies are still needed.

Serum hepcidin levels in chronic liver disease: a systematic review and meta-analysis.

Dysregulation of hepcidin-iron axis is presumed to account for abnormal iron status in patients with chronic liver disease (CLD). Our aim is to determine the effect of specific etiologies of CLD and of cirrhosis on serum hepcidin levels. PubMed, Embase, Web of Science were searched for studies comparing serum hepcidin levels in patients with CLD to that in controls using enzyme-linked immunosorbent assay. The study was conducted in accordance with the Preferred Reporting Items for Systematic Review and Meta-Analysis Guidelines. Statistical analysis was carried out with STATA using random effects model to calculate the mean difference (MD) between two groups. Hepcidin levels were significantly lower in subjects with hepatitis C virus (16 studies) [MD-1.6 (95 % CI:-2.66 to-0.54), p<0.01] and alcoholic liver disease (3 studies) [MD-0.84 (95 % CI:-1.6 to-0.07), p=0.03] than controls. Serum hepcidin was significantly higher in subjects with non-alcoholic fatty liver disease (12 studies) [MD 0.62 (95 % CI: 0.21 to 1.03), p<0.01], but did not differ in subjects with hepatitis B and controls (eight studies) [MD-0.65 (95 % CI:-1.47 to 0.16), p=0.12]. Hepcidin levels were significantly lower in patients with cirrhosis of any etiology (four studies) [MD-1.02 (CI:-1.59 to-0.45), p<0.01] vs. controls (CI: confidence interval). Serum hepcidin levels are altered in common forms of CLD albeit not in a consistent direction. Additional study is needed to determine how changes in hepcidin levels are related to dysregulation of iron metabolism in CLD.

The effect of blood transfusion on serum hepcidin levels in chronically transfused patients of β-thalassemia major: An observational study in a tertiary care centre in Western Maharashtra.

Hepcidin is the key regulator of systemic iron homeostasis. In iron-loading anemias, hepcidin levels are regulated by opposite forces of erythropoiesis and iron overload. In β-thalassemia major patients, transfusions are the predominant cause of iron overload; in such chronically transfused patients, hepcidin concentrations are significantly higher than nontransfused patients, due to both increased iron load of transfusions and the suppression of ineffective erythropoiesis. This study aims to evaluate the effect of blood transfusions on serum hepcidin levels in chronically transfused patients of β-thalassemia major and correlate with hemoglobin and serum ferritin levels of pre- and posttransfusion. Thirty-three β-thalassemia major patients requiring monthly transfusions were included in the study. Blood samples, collected pretransfusion and 7 days posttransfusion, were evaluated for hemoglobin, serum ferritin, and serum hepcidin using enzyme immunoassay. Data were statistically analyzed through SPSS software and P < 0.05 is considered statically significant. Posttransfusion levels of hemoglobin, serum ferritin, and serum hepcidin increased. Posttransfusion levels of hepcidin were near normal levels. Pre- and posttransfusion hepcidin concentrations were significantly associated with hemoglobin levels. Serum hepcidin concentrations vary depending on the degree of erythropoiesis drive and level of anemia. We found that the serum hepcidin levels decrease over the inter-transfusion interval and transfusions cause suppression of ineffective erythropoiesis by the increase in hemoglobin. Posttransfusion values of hepcidin in our study were closer to normal levels which may be due to lower erythropoietic drive posttransfusion. We suggest that the measurement of serum hepcidin in chronically transfused β-thalassemia patients can be used as a follow-up investigation for better management of these patients.

Reduced levels of hepcidin associated with lower ferritin concentration and increased number of previous donations in periodic blood donors: a pilot study.

Hepcidin is one of the major negative regulators of iron balance. Periodic blood donors are highly susceptible to have iron deficiency. Our goal was to evaluate the possible association between serum hepcidin levels and iron homeostasis parameters in periodic blood donors. We enrolled a total of n=39 periodic healthy blood donors (n=24 M and n=15 F). A solid phase enzyme-linked immunosorbent assay (ELISA) was used to measure endogenous hepcidin-25 levels in serum biospecimens collected from each study participant. Statistical analysis was performed to evaluate possible associations between hepcidin levels and ferritin, transferrin, total iron binding capacity (TIBC), unsaturated iron binding capacity (UIBC), transferrin saturation (TSAT), and number of previous donations. Reduced serum hepcidin levels significantly correlated with reduced serum ferritin concentration (r = 0.56, IC95%: 0.51-0.60, p < 0.01). A multiple linear regression analysis showed that hepcidin levels were independently and negatively correlated with ferritin (p < 0.01). In addition, the number of previous blood donations was significantly associated with reduced hepcidin levels, independently of the other covariates (p < 0.01). Reduced serum hepcidin levels were significantly associated with reduced levels of ferritin and with increased number of previous donations suggesting its possible clinical role as non-invasive "point-of-care" in predicting iron deficiency among periodic blood donors.

Low Serum Hepcidin Levels in Patients with Ulcerative Colitis - Implications for Treatment of Co-existent Iron-Deficiency Anemia.

Ulcerative colitis (UC) is often associated with anemia. Hepcidin, the central regulator of iron homeostasis, is known to be induced by inflammation and suppressed by anemia. It is not clear how hepcidin is affected in those with UC, when both inflammation and anemia may co-exist.Such knowledge may hold implications for treatment. Hematological and iron-related parameters, C-reactive protein (CRP), growth differentiation factor 15 (GDF-15) and erythroferrone (ERFE) (erythroid regulators of hepcidin) levels were estimated in blood from those with UC and in control subjects. Values for hematological and iron-related parameters showed evidence of iron-deficiency and resultant anemia, in patients with UC. The presence of UC was significantly associated with inflammation. Serum levels of ERFE, but not of GDF-15, were significantly higher in patients with UC than in control patients, while hepcidin levels were significantly lower. Serum hepcidin concentrations in patients with UC correlated positively with serum iron, ferritin and GDF-15, and negatively with serum ERFE. The iron status and serum hepcidin levels in UC patients with co-existent anemia were significantly lower and serum ERFE values significantly higher than in those with UC without anemia. The effect of anemia on hepcidin predominated over that of inflammation in patients with UC, resulting in suppressed hepcidin levels. This effect is possibly mediated through erythroferrone. We suggest that a serum hepcidin-guided approach may be useful to guide use of oral iron supplements to treat co-existent iron-deficiency anemia in patients with UC and other chronic inflammatory diseases.

The association between growth differentiation factor-15, erythroferrone, and iron status in thalassemic patients

BackgroundIron overload can result in grave consequences in thalassemic patients, despite the availability of iron chelators. Therefore, alternative pathways aiming to reduce iron toxicity are currently investigated. Among which, reduction of iron absorption through control of hepcidin production appears to be promising. In this study, we investigated growth differentiation factor-15 (GDF15) and erythroferrone (ERFE) as potential suppressors of hepcidin.MethodsThis cross-sectional study was conducted on 61 thalassemic patients and 60 healthy controls. The frequency of GDF15 gene polymorphism (rs4808793) (-3148C/G), serum level of GDF15 and erythroferrone were measured and correlated with those of hepcidin and serum ferritin.ResultsThe presence of GDF15 gene mutations were significantly higher in the patients’ group compared to controls (P value 0.035). Also, thalassemia patients had significantly higher levels of GDF15 and ERFE and lower hepcidin levels than controls (P value < 0.001). Serum hepcidin level showed significantly negative correlations with GDF15, ERFE, reticulocyte count, LDH level, and serum ferritin. Contrarily, it had highly significant positive correlation with hemoglobin.ConclusionsHigh level of GDF15 and/or ERFE may inhibit hepcidin production and increase iron load in patients with thalassemia; therefore, medications that suppress their actions may provide new therapeutic potentials for iron toxicity.ImpactIron overload continues to be a major contributor to high morbidity and mortality in patients with thalassemia.New strategies together with proper chelation, need to be developed to minimize the effect of iron toxicity.Growth differentiation factor-15 (GDF15) and erythroferrone (ERFE) inhibit hepcidin production and increase iron levels in conditions with ineffective erythropoiesis.Medications that suppress the production or interfere with the action of GDF15 or ERFE may represent new therapeutic potentials for iron toxicity.Prevention of iron toxicity will significantly reduce morbidity and mortality and improve the quality of life of thalassemia patients.

Chronic intermittent hypobaric hypoxia improves iron metabolism disorders via the IL-6/JAK2/STAT3 and Epo/STAT5/ERFE signaling pathways in metabolic syndrome rats

AimOur previous study demonstrated that chronic intermittent hypobaric hypoxia (CIHH) improved iron metabolism disorder in obese rats through the downregulation of hepcidin. This study aimed to observe the molecular mechanism of CIHH in improving iron metabolism disorders, especially by Janus kinase/signal transducer and activation of the transcription (JAK/STAT) signaling pathway in metabolic syndrome (MS) rats. MethodsSix-week-old male Sprague-Dawley rats were randomly divided into four groups: CON, CIHH (subjected to hypobaric hypoxia simulating 5000-m altitude for 28 days, 6 h daily), MS (induced by high fat diet and fructose water), and MS+CIHH. The serum levels of glucose, lipid metabolism, iron metabolism, interleukin-6 (IL-6), erythropoietin (Epo) and hepcidin were measured. The protein expressions of JAK2, STAT3, STAT5, bone morphogenetic protein 6 (BMP6), small mothers against decapentaplegic 1 (SMAD1) and hepcidin were examined. The mRNA expressions of erythroferrone (ERFE) and hepcidin were analyzed. ResultsThe MS rats displayed obesity, hyperglycemia, hyperlipidemia, iron metabolism disorder, increased IL-6 and hepcidin serum levels, upregulation of JAK2/STAT3 signaling pathway, decreased Epo serum levels, downregulation of STAT5/ERFE signaling pathway in spleen, upregulation of BMP/SMAD signaling pathway in liver, and increased hepcidin mRNA and protein expression compared to CON rats. All the aforementioned abnormalities in MS rats were ameliorated in MS + CIHH rats. ConclusionsCIHH improved iron metabolism disorders, possibly by inhibiting IL-6/JAK2/STAT3 and activating Epo/STAT5/ERFE signaling pathway, thus downregulating hepcidin in MS rats.

Induction of Hepcidin Expression in the Renal Cortex of Sickle Cell Disease Mice.

In patients with sickle cell disease (SCD), chronic hemolysis and frequent blood transfusions cause iron overload and accumulation in the kidneys. The iron deposition is found in the renal cortex and correlates with the severity of hemolysis. In this study, we observed a significant accumulation of iron in the renal cortex of a mouse model of SCD, and assessed the expression of the proteins involved in maintaining renal iron homeostasis. Despite the intracellular iron accumulation, the levels of the transferrin receptor in the kidneys were increased, but the levels of the iron exporter ferroportin were not altered in SCD mice. Ferroportin is regulated by hepcidin, which binds to it and promotes its degradation. We found reduced serum hepcidin levels but increased renal hepcidin production in SCD mice. Furthermore, we observed significant macrophage infiltration and increased expression of intercellular adhesion molecule 1 in the endothelial cells of the kidneys in SCD mice. These observations correlated with elevated levels of proinflammatory cytokines IL-1β and IL-6, which can potentially stimulate hepcidin expression. Taken together, our results demonstrate that in individuals with SCD, a renal inflammation state induces renal hepcidin production that blocks the upregulation of ferroportin levels, resulting in dysregulation of iron homeostasis in the kidney and iron deposition in the renal cortex.

Clinical Significance of Serum Iron Metabolism-Related Markers in Patients with Nasopharyngeal Carcinoma

Introduction: It is known that iron metabolism is dysregulated in nasopharyngeal carcinoma (NPC). However, a meaningful assessment of the iron metabolic status in cancer patient is still under debate. This study aims to evaluate the status of iron metabolism, as well as to explore the correlation between those related serum markers and clinicopathological features of patients with NPC. Methods: Peripheral blood was collected from 191 pretreatment NPC patients and 191 healthy controls. The red blood cell parameters, plasma Epstein-Barr virus (EBV) DNA load, serum iron (SI), total iron-binding capacity (TIBC), transferrin, soluble transferrin receptor (sTFR), ferritin, and hepcidin were quantitatively detected. Results: The mean levels of hemoglobin and red blood cell count in the NPC group were significantly lower than those in the control group, while no statistical differences in mean MCV were found between the two groups. Median levels of SI, TIBC, transferrin, and hepcidin were significantly lower in the NPC group than in the control group. Compared to patients with the T1-T2 classification, patients with the T3-T4 classification exhibited significantly lower expression levels of SI and TIBC. Serum levels of ferritin and sTFR were significantly higher in patients with M1 classification than those with M0 classification. The EBV DNA load was associated with serum levels of sTFR and hepcidin. Conclusion: NPC patients had functional iron deficiency. The degree of iron deficiency was related to the tumor burden and metastasis of NPC. EBV might be involved in the regulation of iron metabolism in the host.

Effect of diet-induced weight loss on iron status and its markers among young women with overweight/obesity and iron deficiency anemia: a randomized controlled trial.

Obesity and iron deficiency are prevalent health problems that affect billions of people all over the world. Obesity is postulated to relate to iron deficiency via reduced intestinal iron absorption due to increased serum hepcidin level, which is mediated by chronic inflammation. Weight loss in individuals with overweight or obesity and iron deficiency anemia is believed to be associated with an improvement in iron status however the evidence from clinical trials is scarce. This study was conducted to evaluate the effect of diet-induced weight loss on iron status and its markers among young women with overweight/obesity and iron deficiency anemia. The study design was a single-blinded, randomized controlled trial with two parallel arms (weight loss intervention vs control). Study participants were recruited using the convenience sampling method through public advertisements posted and disseminated through social media. Interested and potential participants were asked to visit the Diet Clinic for eligibility screening. A total of 62 women were recruited and randomized into weight loss intervention and control group. The intervention duration was three months. The intervention group received individual consultation sessions with the dietitian and tailored energy-restricted diets. Physical activity levels, dietary intake, anthropometric measurements and clinical markers were measured at baseline and end of the trial. There was a significant decrease (p < 0.001) in body weight of the intervention group (-7.4 ± 2.7 kg) that was associated with significant improvements in iron status and its markers (p < 0.01). The intervention group experienced a significant increase in hemoglobin (0.5 ± 0.6 g/dL), serum ferritin (5.6 ± 5.8 ng/mL), and serum iron (13.0 ± 16.2 µg/dL), and a significant decrease in high-sensitivity C-reactive protein (-5.2 ± 5.6 mg/L), and serum hepcidin level (-1.9 ± 2.2 ng/mL) at the end of the trial. Our findings indicate that diet-induced weight loss among participants was associated with an improvement in iron status and its related clinical markers. [https://www.thaiclinicaltrials.org/show/TCTR20221009001], identifier [TCTR20221009001].

Evaluation of Some Serological Indicators in Women with Polycystic Ovary Syndrome in Baquba , Iraq

Polycystic ovary syndrome (PCOS) is receiving increasing attention, due to its association with many health troubles such as infertility and diabetes. The purpose of our study is to estimate the serum level of some indicators in women patients with PCOS. This study was conducted prospectively on 70 participating women who attended Al-Batool Teaching Hospital in Baquba (Iraq), with ages between (18-35) years, from February 2020 to November 2022. All the participating women were separative into two groups: )Control( group included 30 healthy women,and (PCOS) group included 40 women suffer from polycystic ovary syndrome. Ultrasound and analyzes of the sex hormones of the participants were used to confirm the detection of PCOS. Serological biomarkers were measured for both groups, including histidine, ferritin, follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin, and estrogen (E2). Results proven a notable reduction in the serum levels of hepcidin and FSH in PCOS group compared to healthy control group. In contrast, a considerable increases in levels of LH, prolactin, ferritin, and estrogen E2 hormone were observed in patients with PCOS. It was founded that these biochemical indicators may be a reliable diagnostic measure for polycystic ovary syndrome cases. Bangladesh Journal of Medical Science Vol.22 (Special Issue) 2023 p.4-9

Elevated Urinary Hepcidin Level and Hypoferremia in Infants with Febrile Urinary Tract Infection: A Prospective Cohort Study.

To evaluate the kinetics of serum and urinary hepcidin levels along with anemia-related parameters during the infection course of infants with febrile urinary tract infection (UTI), we enrolled febrile infants aged one to four months in this prospective study. Febrile patients with UTI were allocated into Escherichia coli (E. coli) or non-E. coli groups according to urine culture results. Septic workup, blood hepcidin, iron profile, urinalysis, and urinary hepcidin-creatinine ratio were collected upon admission and 3 days after antibiotic treatment. In total, 118 infants were included. On admission, the febrile UTI group showed a significant reduction in serum iron level and a significant elevation of urinary hepcidin-creatinine ratio compared to the febrile control counterpart. Moreover, urinary hepcidin-creatinine ratio had the highest odds ratio, 2.01, in logistics regression analysis. After 3 days of antibiotic treatment, hemoglobin and the urinary hepcidin-creatinine ratio were significantly decreased. Patients with an E. coli UTI had a significantly decreased urinary hepcidin-creatinine ratio after 3 days of antibiotics treatment, whereas the non-E. coli group showed insignificant changes. Our study suggested that the urinary hepcidin-creatinine ratio elevated during acute febrile urinary tract infection and significantly decreased after 3 days of antibiotics treatment, especially in E. coli UTI.

Effect of Eculizumab on Iron Metabolism in Transfusion-independent Patients With Paroxysmal Nocturnal Hemoglobinuria

Effect of Eculizumab on Iron Metabolism in Transfusion-independent Patients With Paroxysmal Nocturnal Hemoglobinuria

Is iron deficiency caused by BMPR2 mutations or dysfunction in pulmonary arterial hypertension patients?

Iron deficiency is common in idiopathic and heritable pulmonary arterial hypertension patients (I/HPAH). A previous report suggested a dysregulation of the iron hormone hepcidin, which is controlled by BMP/SMAD signaling involving the bone morphogenetic protein receptor 2 (BMPR-II). Pathogenic variants in the BMPR2 gene are the most common cause of HPAH. Their effect on patients'hepcidin levels has not been investigated. The aim of this study was to assess whether iron metabolism and regulation of the iron regulatory hormone hepcidin was disturbed in I/HPAH patients with and without a pathogenic variant in the gene BMPR2 compared to healthy controls. In this explorative, cross-sectional study hepcidin serum levels were quantified by enzyme-linked immunosorbent assay. We measured iron status, inflammatory parameters and hepcidin modifying proteins such as IL6, erythropoietin, and BMP2, BMP6 in addition to BMPR-II protein and mRNA levels. Clinical routine parameters were correlated with hepcidin levels. In total 109 I/HPAH patients and controls, separated into three groups, 23 BMPR2 variant-carriers, 56 BMPR2 noncarriers and 30 healthy controls were enrolled. Of these, 84% had iron deficiency requiring iron supplementation. Hepcidin levels were not different between groups and corresponded to the degree of iron deficiency. The levels of IL6, erythropoietin, BMP2, or BMP6 showed no correlation with hepcidin expression. Hence, iron homeostasis and hepcidin regulation was largely independent from these parameters. I/HPAH patients had a physiologically normal iron regulation and no false elevation of hepcidin levels. Iron deficiency was prevalent albeit independent of pathogenic variants in the BMPR2 gene.

HBB Gene Mutations and Their Pathological Impacts on HbE/β-Thalassaemia in Kuala Terengganu, Malaysia.

β-thalassaemia is a disorder caused by mutations in the β-globin gene, leading to defective production of haemoglobins (Hb) and red blood cells (RBCs). It is characterised by anaemia, ineffective erythropoiesis, and iron overload. Patients with severe β-thalassaemia require lifelong blood transfusions. Haemoglobin E beta-thalassaemia (HbE/β-thalassaemia) is a severe form of β-thalassaemia in Asian countries. More than 200 alleles have been recognised in the β-globin region. Different geographical regions show different frequencies of allelic characteristics. In this study, the spectrum of β-thalassaemia (β-thal) alleles and their correlation with iron overload, in HbE/β-thalassaemia patients, β-thalassaemia trait, and HbE trait were studied. Blood samples (n = 260) were collected from 65 β-thalassaemia patients, 65 parents (fathers and/or mothers) and 130 healthy control individuals. Haematological analyses, iron profiles, and serum hepcidin levels were examined for all participants. DNA was extracted from patients' and their parents' blood samples, then subjected to PCR amplification. Multiplex amplification refractory mutation system PCR (MARMS-PCR) was conducted for eighteen primers to detect the mutations. There was severe anaemia present in HbE/β-thalassaemia patients compared to their parents and healthy controls. The ferritin and iron levels were significantly increased in patients compared to their parents and healthy controls (p = 0.001). Two common mutations were detected among the patient group and three mutations were detected among their parents, in addition to seven novel mutations in HbE/β-thalassaemia patients (explained in results). Some mutations were associated with severe anaemia in β-thalassaemia patients. The detection of mutations is a prognostic marker, and could enhance the appropriate management protocols and improve the haematological and biochemical statuses of β-thalassaemia patients.

Maternal serum iron status, hepcidin and interleukin-6 levels in women with preeclampsia.

Introduction: Preeclampsia can lead to a number of adverse maternal and perinatal effects. The association between iron status [serum iron, ferritin and total iron-binding capacity (TIBC)], unsaturated iron-binding capacity, hepcidin, interleukin-6 (IL-6) levels and preeclampsia is not fully understood. Objective: To assess the levels of iron status, hepcidin and interleukin-6 in women with preeclampsia compared with healthy pregnant women. Method: A case-control study (60 women were recruited in each group) was conducted at Saad Abuelela Maternity Hospital in Khartoum, Sudan. Sociodemographic and clinical data were gathered through a questionnaire. The levels of iron status, hepcidin and IL-6 were measured using applicable methods. Results: There was no significant difference in the median [interquartile range (IQR)] of age, parity or body mass index between the two groups. Moreover, the median (IQR) of the iron status, hepcidin and interleukin-6 did not differ between women with preeclampsia and healthy controls. There were no significant correlations between haemoglobin, hepcidin and IL-6. There were also no significant correlations between serum iron, serum ferritin, hepcidin and IL-6. However, there was a significant positive correlation between hepcidin and IL-6 (r = 0.393, p = 0.002). Conclusion: In this study, women with preeclampsia had levels of iron status, hepcidin and IL-6 similar to those observed in healthy pregnant women. There was no significant correlation between iron status, hepcidin and IL-6.

Effect of Hydromethanolic Extract of Stem Bark of Lannea kerstingii on Anemia and Hepcidin Production

Introduction: Stem bark of Lannea kerstingii is used in Togo for its anti-anemic effect. The aim of this study was to verify the efficacy of extracts of L. kerstingii’s bark in the treatment of anemia and to explore its mechanism of action. Materials and Method: L. kerstingii stem bark was collected in the city of Kpalimé, located at 120 km northwest of Lomé. Hydromethanolic extract was obtained by evaporation. Two protocols were carried out and 20 twelve-week-old rats that had an average weight of 175.17±16.8 grams were used. The first protocol consisted of inducing anemia in rats by intraperitoneal injection of phenylhydrazine, then force-feeding them with L. kerstingii extract and measuring the effect of this extract on their hemoglobin levels. The second protocol investigated the effect of the extract on the serum hepcidin level, after oral administration of carbon tetrachloride to rats. Hepcidin levels were measured by the ELISA technique. Results: L. kerstingii stem bark extract significantly corrected the anemia induced by phenylhydrazine use: in fact, the anemia of rats that received L. kerstingii extracts was corrected. Control rats that received folic acid had a correction of their anemia too. But, rats that received only saline remained anemic. However, no correlation between the level of extract consumption and the level of hepcidin was established. Conclusion: L. kerstingii bark hydroethanolic extracts increase hemoglobin levels in anemic rats. The main challenge that needs to be solved is determining the minimum dose to be consumed to ensure its effectiveness.&#x0D; Keywords: Lannea kerstingii, anemia, hepcidin, wistar rat.

The tendency of anemia of inflammation in periodontal diseases.

Anemia of inflammation (AI) is associated with inflammatory diseases, and inflammation-induced iron metabolism disorder is the major pathogenic factor. Earlier studies have reported a tendency of AI in periodontitis patients, but the explicit relationship and possible pathological mechanisms remain unclear. Here, the analyses of both periodontitis patients and a mouse model of ligature-induced experimental periodontitis showed that periodontitis was associated with lower levels of hemoglobin and hematocrit with evidence of systemic inflammation (increased white blood cell levels) and evidence of iron restriction (low serum iron along with a high serum hepcidin and ferritin levels), in accordance with the current diagnosis criteria for AI. Moreover, periodontal therapy improved the anemia status and iron metabolism disorders. Furthermore, the increased level of hepcidin and significant correlation between hepcidin and key indicators of iron metabolism emphasized the pivotal role of hepcidin in the pathogenesis of periodontitis-related AI. Administration of the signal transducer and activator of transcription 3 (STAT3) inhibitors Stattic suggested that the IL-6-STAT3-hepcidin signaling pathway participated in this regulatory process. Together, these findings demonstrated that periodontitis should be considered an inflammatory disease that contributes to the development of AI; furthermore, IL-6-STAT3-hepcidin signaling pathway plays a key regulatory role in the pathogenesis of periodontitis-related AI. Our study will provide new insights into the systemic effects of periodontitis, while meaningfully expanding the spectrum of inflammatory diseases that contribute to AI.