Why Do Children in Slums Suffer from Anemia, Iron, Zinc, and Vitamin A Deficiency? Results from a Birth Cohort Study in Dhaka.
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ABSTRACT:
SUBMITTER: Mahfuz M
PROVIDER: S-EPMC6949995 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Iron refractory iron deficiency anemia is a hereditary recessive anemia due to a defect in the TMPRSS6 gene encoding Matriptase-2. This protein is a transmembrane serine protease that plays an essential role in down-regulating hepcidin, the key regulator of iron homeostasis. Hallmarks of this disease are microcytic hypochromic anemia, low transferrin saturation and normal/high serum hepcidin values. The anemia appears in the post-natal period, although in some cases it is only diagnosed in adulthood. The disease is refractory to oral iron treatment but shows a slow response to intravenous iron injections and partial correction of the anemia. To date, 40 different Matriptase-2 mutations have been reported, affecting all the functional domains of the large ectodomain of the protein. In vitro experiments on transfected cells suggest that Matriptase-2 cleaves Hemojuvelin, a major regulator of hepcidin expression and that this function is altered in this genetic form of anemia. In contrast to the low/undetectable hepcidin levels observed in acquired iron deficiency, in patients with Matriptase-2 deficiency, serum hepcidin is inappropriately high for the low iron status and accounts for the absent/delayed response to oral iron treatment. A challenge for the clinicians and pediatricians is the recognition of the disorder among iron deficiency and other microcytic anemias commonly found in pediatric patients. The current treatment of iron refractory iron deficiency anemia is based on parenteral iron administration; in the future, manipulation of the hepcidin pathway with the aim of suppressing it might become an alternative therapeutic approach.
| S-EPMC3669438 | biostudies-literature
Project description:Iron is essential for life because it is indispensable for several biological reactions, such as oxygen transport, DNA synthesis, and cell proliferation. Over the past few years, our understanding of iron metabolism and its regulation has changed dramatically. New disorders of iron metabolism have emerged, and the role of iron as a cofactor in other disorders has begun to be recognized. The study of genetic conditions such as hemochromatosis and iron-refractory iron deficiency anemia (IRIDA) has provided crucial insights into the molecular mechanisms controlling iron homeostasis. In the future, these advances may be exploited to improve treatment of both genetic and acquired iron disorders. IRIDA is caused by mutations in TMPRSS6, the gene encoding matriptase-2, which downregulates hepcidin expression under conditions of iron deficiency. The typical features of this disorder are hypochromic, microcytic anemia with a very low mean corpuscular volume of erythrocytes, low transferrin saturation, no (or inadequate) response to oral iron, and only a partial response to parenteral iron. In contrast to classic iron deficiency anemia, serum ferritin levels are usually low-normal, and serum or urinary hepcidin levels are inappropriately high for the degree of anemia. Although the number of cases reported thus far in the literature does not exceed 100, this disorder is considered the most common of the "atypical" microcytic anemias. The aim of this review is to share the current knowledge on IRIDA and increase awareness in this field.
| S-EPMC4439901 | biostudies-literature
Project description:Purpose: The goal of this study was to probe for the effects of iron-deficiency anemia on the cardiac transciprtome using RNA-seq Methods: C57B6 mice were weaned onto a control or iron-deficient diet for 6 weeks. Hearts were removed and total mRNA was submitted for RNA-seq. Sequencing data was aligned using STAR and differetial gene expression analysis conducted in R using EdgeR and DESeq2. qRT–PCR validation for genes of interest was performed using TaqMan and SYBR Green assays. Results: We mapped about 24 million sequence reads per sample to the mouse genome (build mm10) and identified 13,590 transcripts in the hearts of control and iron-deficient mice after removing lowly expressed genes and PCR duplicates. Differential gene expression analysis showed approximately 78% downregulated and 22% upregulated genes in iron-deficiency anemia compared to controls. PCA plot showed control and iron-deficient hearts clustering in two distinct and separate clusters. Conclusions: Our study represents the first whole-transcriptomic study on cardiac samples obtained from iron-deficient and anemic mice, with biologic replicates, generated by RNA-seq technology. The RNA-seq data presented here can be used by others to explore which pathways are affected by iron-deficiency anemia
2020-12-03 | GSE162493 | GEO
Project description:Postpartum depression (PPD) is a serious pubic health concern and known to have the adverse effects on mother's perinatal wellbeing; and child's physical and cognitive development. There were limited literatures on PPD in Bangladesh, especially in urban slum context. The aim of this study was to assess the burden and risk factors of PPD among the urban slum women. A cross-sectional study was conducted between November-December 2017 in three urban slums on 376 women within first 12 months of postpartum. A validated Bangla version of Edinburgh Postnatal Depression Scale was used to measure the depression status. Respondent's socio-economic characteristics and other risk factors were collected with structured validated questionaire by trained interviewers. Unadjusted Prevalence Ratio (PR) and Adjusted Prevalence Ratio (APR) were estimated with Generalized Linear Model (GLM) and Generalized Estimating Equation (GEE) respectively to identify the risk factors of PPD. The prevalence of PPD was 39.4% within first 12 months following the child birth. Job involvement after child delivery (APR = 1.9, 95% CI = 1.1, 3.3), job loss due to pregnancy (APR = 1.5, 95% CI = 1.0, 2.1), history of miscarriage or still birth or child death (APR = 1.4, 95% CI = 1.0, 2.0), unintended pregnancy (APR = 1.8, 95% CI = 1.3, 2.5), management of delivery cost by borrowing, selling or mortgaging assets (APR = 1.3, 95% CI = 0.9, 1.9), depressive symptom during pregnancy (APR = 2.5, 95% CI = 1.7, 3.8) and intimate partner violence (APR = 2.0, 95% CI = 1.2, 3.3), were identified as risk factors. PPD was not associated with poverty, mother in law and any child related factors. The burden of postpartum depression was high in the urban slum of Bangladesh. Maternal mental health services should be integrated with existing maternal health services. Research is required for the innovation of effective, low cost and culturally appropriate PPD case management and preventive intervention in urban slum of Bangladesh.
| S-EPMC6497249 | biostudies-literature
Project description:Iron deficiency contributes to anemia after transplantation. The magnitude of iron loss from blood loss in the peri-transplantation period has not been quantified. We prospectively estimated phlebotomy and surgical losses over the first 12-weeks following transplantation in 39 consecutive renal transplant recipients on hemodialysis (HD), peritoneal dialysis (PD), or chronic kidney disease (CKD). At transplant, ferritin levels were <200 ng/ml in 51% of the patients, and iron saturation was </=20% in 44%. CKD patients more commonly had ferritin levels <200 ng/ml than either HD or PD patients (100% vs. 21% vs. 67%, P < 0.0002, respectively). Blood loss was similar among HD, PD and CKD patients (833 +/- 194 vs. 861 +/- 324 vs. 755 +/- 79 ml respectively, P = NS), and no difference between deceased and living donor transplant recipients (881 +/- 291 vs. 788 +/- 162 ml, P = 0.33). Based on baseline hemoglobin (Hgb) of 11.8 g/dl, we estimated that an additional 330 mg of iron was needed to normalize hemoglobin to 13 g/dl, and 605 mg to increase hemoglobin to 14 g/dl. Blood and iron losses over the first 12 weeks post-transplant are substantial and may warrant early administration of intravenous iron.
| S-EPMC2754723 | biostudies-literature
Project description:BackgroundVaccine-preventable infectious diseases are often responsible for childhood morbidity and high rates of mortality. Immune response to the vaccine is associated with multiple factors in early childhood and measured by antibody titers. Among them, micronutrient deficiencies such as vitamin D and zinc deficiencies are the most important in resource-limited settings like Bangladesh.ObjectiveWe aimed to evaluate the association of vaccine response to low serum zinc and vitamin D levels in children.MethodsWe evaluated vaccine response for measles and poliovirus, tetanus and pertussis toxoid, and Ig A antibody levels to rotavirus by ELISA and serum vitamin D and zinc at 7 and 15 months in the MAL-ED birth cohort of the Bangladesh site. By using population-specific generalized estimating equations (GEE), the association between each explanatory variable and the binary outcome variable was examined longitudinally where the dependent variable was vaccine titers and the independent variables were low serum vitamin D and zinc levels.ResultsThe GEE multivariable model identified a positive association between serum zinc level and tetanus vaccine titer (OR: 1.84; 95% CI: 1.07-3.17 and p value = 0.028) after adjusting for age, gender, birth weight, WAMI score, diarrhea, ALRI, exclusive breastfeeding, serum ferritin, serum retinol and undernutrition (stunting, wasting, underweight). No association was found between the rest of the vaccine titers with serum vitamin D and zinc level (p > 0.05).ConclusionIn the MAL-ED birth cohort, where children were followed for five years, serum zinc level had a positive impact on tetanus vaccine titers.
| S-EPMC7735373 | biostudies-literature
Project description:In humans, poor nutrition, malabsorption and variation in cobalamin (vitamin B12) metabolic genes are associated with hematological, neurological and developmental pathologies. Cobalamin is transported from blood into tissues via the transcobalamin (TC) receptor encoded by the CD320 gene. We created mice carrying a targeted deletion of the mouse ortholog, Cd320. Knockout (KO) mice lacking this TC receptor have elevated levels of plasma methylmalonic acid and homocysteine but are otherwise healthy, viable, fertile and not anemic. To challenge the Cd320 KO mice we maintained them on a vitamin B12-deficient diet. After 5 weeks on this diet, reproductive failure develops in Cd320 KO females but not males. In vitro, homozygous Cd320 KO embryos from cobalamin-deficient Cd320 KO dams develop normally to embryonic day (E) 3.5, while in vivo, few uterine decidual implantation sites are observed at E7.5, suggesting that embryos perish around the time of implantation. Dietary restriction of vitamin B12 induces a severe macrocytic anemia in Cd320 KO mice after 10-12 months while control mice on this diet are anemia-free up to 2 years. Despite the severe anemia, cobalamin-deficient KO mice do not exhibit obvious neurological symptoms. Our results with Cd320 KO mice suggest that an alternative mechanism exists for mice to transport cobalamin independent of the Cd320 encoded receptor. Our findings with deficient diet are consistent with historical and epidemiological data suggesting that low vitamin B12 levels in humans are associated with infertility and developmental abnormalities. Our Cd320 KO mouse model is an ideal model system for studying vitamin B12 deficiency.
| S-EPMC6168973 | biostudies-literature
Project description:Previous trials of prenatal iron supplementation had limited measures of maternal or neonatal iron status.The purpose was to assess effects of prenatal iron-folate supplementation on maternal and neonatal iron status.Enrollment occurred June 2009 through December 2011 in Hebei, China. Women with uncomplicated singleton pregnancies at ?20 wk gestation, aged ?18 y, and with hemoglobin ?100 g/L were randomly assigned 1:1 to receive daily iron (300 mg ferrous sulfate) or placebo + 0.40 mg folate from enrollment to birth. Iron status was assessed in maternal venous blood (at enrollment and at or near term) and cord blood. Primary outcomes were as follows: 1) maternal iron deficiency (ID) defined in 2 ways as serum ferritin (SF) <15 ?g/L and body iron (BI) <0 mg/kg; 2) maternal ID anemia [ID + anemia (IDA); hemoglobin <110 g/L]; and 3) neonatal ID (cord blood ferritin <75 ?g/L or zinc protoporphyrin/heme >118 ?mol/mol).A total of 2371 women were randomly assigned, with outcomes for 1632 women or neonates (809 placebo/folate, 823 iron/folate; 1579 mother-newborn pairs, 37 mothers, 16 neonates). Most infants (97%) were born at term. At or near term, maternal hemoglobin was significantly higher (+5.56 g/L) for iron vs. placebo groups. Anemia risk was reduced (RR: 0.53; 95% CI: 0.43, 0.66), as were risks of ID (RR: 0.74; 95% CI: 0.69, 0.79 by SF; RR: 0.65; 95% CI: 0.59, 0.71 by BI) and IDA (RR: 0.49; 95% CI: 0.38, 0.62 by SF; RR: 0.51; 95% CI: 0.40, 0.65 by BI). Most women still had ID (66.8% by SF, 54.7% by BI). Adverse effects, all minor, were similar by group. There were no differences in cord blood iron measures; >45% of neonates in each group had ID. However, dose-response analyses showed higher cord SF with more maternal iron capsules reported being consumed (? per 10 capsules = 2.60, P < 0.05).Prenatal iron supplementation reduced anemia, ID, and IDA in pregnant women in rural China, but most women and >45% of neonates had ID, regardless of supplementation. This trial was registered at clinicaltrials.gov as NCT02221752.
| S-EPMC4516762 | biostudies-literature
Project description:Iron deficiency is usually attributed to chronic blood loss or inadequate dietary intake. Here, we show that iron deficiency anemia refractory to oral iron therapy can be caused by germline mutations in TMPRSS6, which encodes a type II transmembrane serine protease produced by the liver that regulates the expression of the systemic iron regulatory hormone hepcidin. These findings demonstrate that TMPRSS6 is essential for normal systemic iron homeostasis in humans.
| S-EPMC3104019 | biostudies-literature
Project description:Importance:It remains uncertain whether vitamin C routinely used with oral iron supplements is essential for patients with iron deficiency anemia (IDA). Objective:To compare the equivalence and assess the safety of oral iron supplements plus vitamin C or oral iron supplements alone in patients with IDA. Design, Setting, and Participants:This single-center, open-label, equivalence randomized clinical trial was conducted from January 1, 2016, to December 30, 2017, in Huashan Hospital, Fudan University. Adult patients with newly diagnosed IDA were enrolled. Participants were randomly assigned (1:1) to the oral iron supplements plus vitamin C group or the oral iron supplements-only group. Data analysis was performed from March to December 2018. Interventions:Patients were randomized to receive a 100-mg oral iron tablet plus 200 mg of vitamin C or a 100-mg iron tablet alone every 8 hours daily for 3 months. Main Outcomes and Measures:The primary outcome was the change in hemoglobin level from baseline to 2 weeks of treatment, and an equivalence margin of 1 g/dL in hemoglobin was chosen for the demonstration of comparable efficacy. Secondary outcomes included the change in the reticulocyte percentage after 2 weeks of treatment, the increase in hemoglobin level after 4 weeks of treatment, the increase in serum ferritin level after 8 weeks of treatment, and adverse events. Results:Among the 440 randomized patients (220 each in the oral iron supplements plus vitamin C group and iron-only group; 426 women [96.8%]; mean [SD] age, 38.3 [11.7] years), all were assessed for the primary outcome, and 432 (98.2%) completed the trial. From baseline to the 2-week follow-up, the mean (SD) change in hemoglobin level was 2.00 (1.08) g/dL in the oral iron supplements plus vitamin C group and 1.84 (0.97) g/dL in the oral iron supplements-only group (between-group difference, 0.16 g/dL; 95% CI, -0.03 to 0.35 g/dL), thus meeting the criteria for equivalence. The mean (SD) change in serum ferritin level from baseline to 8-week follow-up was 35.75 (11.52) ng/mL in the vitamin C plus iron group and 34.48 (9.50) ng/mL in the iron-only group (between-group difference, 1.27 ng/mL; 95% CI, -0.70 to 3.24 ng/mL; P?=?.21). There were no significant differences between the 2 groups regarding the rates of adverse events (46 [20.9%] vs 45 [20.5%]; difference, 0.4%; 95% CI, -6.7% to 8.5%; P?=?.82). No patient withdrew because of adverse events. Conclusions and Relevance:Among patients with IDA, oral iron supplements alone were equivalent to oral iron supplements plus vitamin C in improving hemoglobin recovery and iron absorption. These findings suggest that on-demand vitamin C supplements are not essential to take along with oral iron supplements for patients with IDA. Trial Registration:ClinicalTrials.gov Identifier: NCT02631668.
| S-EPMC7607440 | biostudies-literature