Iron Deficiency Research Articles

The association between body mass index, exercise capacity, and health-related quality of life in heart transplant recipients

IntroductionPre-transplant obesity and weight gain after heart transplantation are both associated with increased risk of poor clinical outcomes. We aimed to assess the association between overweight or obesity, exercise capacity, and health-related quality of life in heart transplant recipients.MethodsThis study is based on baseline data from the IronIC trial, in which we randomized 102 heart transplant recipients with iron deficiency to ferric derisomaltose or placebo. We performed cardio pulmonary exercise testing in all participants. To assess quality of life, we used the SF-36v2 questionnaire, using two sum scores: the physical component summary and the mental component summary. A minimal clinically important difference was defined as ≥2 and ≥3 for the physical and the mental component summary, respectively.Results24/102 heart transplant recipients (24%) had a body mass index (BMI) ≥30 kg/m2. Peak oxygen consumption was 17.3 ± 4.6 ml/kg/min in the obese group vs. 24.7 ± 6.4 ml/kg/min in the group with a BMI <30 for a between-group difference of 7.4 (95% confidence interval 4.7–10.2) ml/kg/min: p < 0.001. The physical component summary score was on average 5.2 points lower in the patients with a body mass index ≥30 than in the lower weight group (p = 0.04).ConclusionAlmost a quarter of our heart transplant recipients in long-term follow-up had a BMI ≥30 kg/m2. These patients had substantially lower exercise capacity and lower quality of life in the physical domain.

The problem of excessive hair loss as a signal for the diagnosis of coeliac disease – A family case

Celiac disease is an autoimmune disorder in which the small intestine is damaged after ingesting gluten. Baldness often co-occurs with various systemic diseases including autoimmune diseases. In addition, alopecia can result from nutritional deficiencies. In the case of celiac disease, we are mainly talking about deficiencies of iron, fat-soluble vitamins (A,D,E,K), vitamin B12 and folic acid. Telogenetic alopecia (TE) is diffuse and reversible alopecia, and the causes of this condition can be nutritional deficiencies and impaired absorption. Celiac disease has been linked to alopecia areata (AA). We describe the case of a mother and daughter with a history of hair loss, which represented the only incipient (mother’s case) and subsequent (daughter’s case) extraintestinal manifestation of celiac disease.

Comparative evaluation of different oral iron salts in the management of iron deficiency anemia.

Anemia affects one-fourth of the world's population and is caused mostly by iron deficiency. Iron supplementation is the most essential strategy for preventing iron deficiency anemia. Conventional oral iron salts have many drawbacks such as poor absorption & bioavailability, and poor tolerability resulting in poor clinical outcomes. To compare the effectiveness and safety of ferrous ascorbate, ferrous fumarate, ferrous bis-glycinate, and Sucrosomial iron in the management of iron deficiency anemia. The study is a retrospective observational clinical study comprising 260 subjects with hemoglobin between 7-10g/dl. The patients were divided into four groups I, II, III, and IV, and received ferrous fumarate, ferrous ascorbate, ferrous bis-glycinate, and Sucrosomial iron respectively. Hematological profile and iron store indices were measured at baseline and month 3. One-way ANOVA followed by Tukey multiple comparison test was used to assess statistical significance (P < 0.05) using GraphPad Prism V.9.3.1 software. The observational study showed that hemoglobin levels were significantly increased in the ferrous ascorbate group (11.86 ± 0.09; P < 0.0001), ferrous fumarate group (11.72 ± 0.08; P < 0.0001), ferrous bis-glycinate group (11.69 ± 0.11; P = 0.0003) and Sucrosomial iron group (12.20 ± 0.1; P < 0.0001) compared to the baseline. The Sucrosomial iron-supplemented group showed significantly higher improvement in hemoglobin levels and serum ferritin levels compared to conventional oral iron salts (P < 0.05) with a better safety profile. The Sucrosomial iron showed significantly higher improvement in hemoglobin levels and higher improvement in iron store indices parameters along with a good tolerability profile compared to other conventional oral iron salts.

Randomized Controlled Trial of Intravenous Ferric Carboxymaltose vs Oral Iron to Treat Iron Deficiency Anemia After Variceal Bleed in Patients With Cirrhosis.

Limited evidence exists on the optimal strategy to correct iron deficiency anemia after variceal bleeding (VB) in cirrhosis. This trial compared the efficacy and safety of intravenous ferric carboxymaltose (IV-FCM) with those of oral iron therapy in this cohort. In this open-label, single-center, randomized controlled trial, eligible patients with hemoglobin <10 g/dL and iron deficiency (ferritin <100 ng/mL) after VB received either IV-FCM (1,500-2,000 mg) divided into 2 doses (n = 48) or oral carbonyl iron (100 mg elemental iron/day) (n = 44) for 3 months. The primary outcome was change in hemoglobin at 3 months. Secondary outcomes included improvement in anemia (last hemoglobin >12 g/dL), normalization of iron stores (ferritin >100 ng/mL), liver-related adverse events, adverse drug reactions, and changes in quality of life (CLDQOL questionnaire). Baseline characteristics, including median Child-Turcotte-Pugh score 7 (interquartile range [IQR] 6-9), Model for End-Stage Liver Disease score 12 (IQR 10-17), blood hemoglobin (8.25 ± 1.06 g/dL), and ferritin (30.00 ng/mL [15.00-66.50]), were comparable in both arms. The median increase in hemoglobin at 3 months in the IV and oral arms was 3.65 g/dL (IQR 2.55-5.25) and 1.10 g/dL (IQR 0.05-2.90 g/dL) ( P < 0.001), respectively. Iron stores normalized in 84.6% and 21% of the IV and oral arms, respectively ( P < 0.001). Anemia improved in 50% and 21.9% in the IV and oral arms, respectively ( P < 0.009). Patients in the IV arm showed a significant improvement in all domains of CLDQOL. Liver-related adverse events were comparable in both arms. Transient mild/moderate hypophosphatemia developed in 43% of patients receiving IV-FCM. Intravenous iron replacement is efficacious and safe to treat iron deficiency anemia after VB in patients with cirrhosis.

Beta-Thalassemia in Adulthood Previously Suspected as Treatment-Resistant Iron Deficiency Anemia: A Case Report

Beta-Thalassemia in Adulthood Previously Suspected as Treatment-Resistant Iron Deficiency Anemia: A Case Report

Evaluation of Brainstem Auditory-Evoked Potentials in Infants with Iron Deficiency Anemia

Purpose: To evaluate and compare the brain functions of infants with and without Iron Deficiency anaemia (IDA) electrophysiologically with brainstem auditory potentials (BAEPs). Materials and Methods: BAEP tests were performed on 26 healthy infants and 26 infants with iron deficiency anaemia, aged 6-24 months, who were followed through the Paediatric Haematology Department at SDU Faculty of Medicine. Children were classified as anaemic if their haemoglobin (Hb) level fell below -2 standard deviations for their age. All patients diagnosed with iron deficiency anaemia received 5 mg/kg/day of divalent iron glycine sulphate complex in three doses daily for a duration of 12 weeks, to be taken on an empty stomach. Both group were orally administered Chloral hydrate at a dosage of 50mg/kg prior to the BAEP test to induce sedation. The BAEP was recorded at a sound intensity level of 90 decibels, with a frequency of 10 Hertz, and with click stimuli ranging from 1000 to 2000. The BAEP test was administered to the IDA group before and after treatment, as well as to the control group, with a 3-month interval between tests. Results: 14 (53.8%) of the IDA patients were males, and 16 (61.5%) of the control group were females. Patients with IDA had an average age of 14.4±3.09 months, while the control group patients have an average age of 11.2±4.04 months. Patients with iron deficiency anaemia had lower pre-treatment levels of Hb, Hct, MCV, MCH, MCHC, transferrin saturation percentage, and ferritin compared to the control group, whereas platelet and RDW values were greater (p˂0.001). The study compared the Brainstem Auditory Evoked Potential (BAEP) values of patients with Iron Deficiency Anaemia (IDA) before treatment with those of control patients. The results indicated that the III-V interval, showing nerve conduction time, was significantly prolonged in the pre-treatment BAEPs (p˂0.05). There was no significant difference in interpeak latencies between the control group and patients with iron deficiency anaemia (IDA) following therapy (p˂0.05). Significant differences were found in the I-III, III-V, and I-V interpeak latencies of individuals with iron deficiency anaemia before and after treatment (p

Effect of Low-Dose Iron Supplementation on Early Development in Breastfed Infants

Breastfed infants are at risk of iron deficiency, which is associated with suboptimal development. There is a paucity of evidence on the effects of iron supplementation on child development, and current guidelines are divergent. To assess whether daily iron supplementation, 1 mg/kg, between 4 and 9 months in exclusively or predominantly breastfed infants improves psychomotor development at 12 months. This was a randomized, double-blind, placebo-controlled trial conducted between December 2015 and May 2020 with follow-up through May 2023 in an outpatient setting in Poland and Sweden. Participants were healthy singleton infants born at term with birth weight greater than 2500 g who were exclusively or predominantly breastfed (>50%) and did not have anemia (hemoglobin >10.5 g/dL) at age 4 months. Exclusion criteria included major illness, congenital anomaly, food allergy, and difficulty communicating with caregivers. Iron (micronized microencapsulated ferric pyrophosphate), 1 mg/kg, or placebo (maltodextrin) once daily from age 4 to 9 months. The primary outcome was psychomotor development assessed by motor score of Bayley Scales of Infant and Toddler Development III at 12 months, adjusted for gestational age, sex, and maternal education. Secondary outcomes included cognitive and language scores at 12 months; motor, cognitive, and language scores at 24 and 36 months; iron deficiency (serum ferritin <12 ng/mL), and iron deficiency anemia (iron deficiency and hemoglobin <10.5 g/dL) at 12 months. Of 221 randomized infants (111 female), 200 (90%) were included in the intention-to-treat analysis (mean [SD] age, 12.4 [0.8] months). Iron supplementation (n = 104) compared to placebo (n = 96) had no effect on psychomotor development (mean difference [MD] for motor score, -1.07 points; 95% CI, -4.69 to 2.55), cognitive score (MD, -1.14; 95% CI, -4.26 to 1.99), or language score (MD, 0.75; 95% CI, -2.31 to 3.82) at 12 months. There were no significant differences at 24 and 36 months. The intervention did not reduce the risk for iron deficiency (relative risk [RR], 0.46; 95% CI, 0.16 to 1.30) or iron deficiency anemia (RR, 0.78; 95% CI, 0.05 to 12.46) at 12 months. No benefit was found with daily low-dose iron supplementation between 4 and 9 months with respect to psychomotor development, risk of iron deficiency, or iron deficiency anemia among breastfed infants in a setting of low risk of anemia. ClinicalTrials.gov Identifier: NCT02242188.

Efficacy of Intravenous Iron Infusion in Gestational Iron Deficiency Anemia in Dubai, United Arab Emirates, During 2018–2019: A Retrospective Study

Efficacy of Intravenous Iron Infusion in Gestational Iron Deficiency Anemia in Dubai, United Arab Emirates, During 2018–2019: A Retrospective Study

Severe Unexplained Iron Deficiency Anemia in Children: High Yield of Upper Gastrointestinal Endoscopy Regardless of Gastrointestinal Symptoms.

In this retrospective study spanning 2016 to 2022, we aimed to evaluate the diagnostic utility of upper gastrointestinal endoscopy (UGE) in children under 18 years presenting with severe unexplained iron deficiency anemia (IDA), defined as microcytic anemia of hemoglobin ≤7g/dL with low ferritin levels. Out of 106 children hospitalized for severe anemia, 29 had unexplained IDA (mean hemoglobin level of 6.2 [3.2 to 6.9] gr/dL), and 25 of them underwent UGE. The mean age was 10.7 ± 3.9 years, with 76% being female. Ten children (40%) had gastrointestinal (GI) symptoms at presentation. The cause of IDA was found in 18 (72%) of 25 children who underwent UGE, of whom 12 were without GI symptoms. Gastric nodularity, erosions, or polyps were observed in 68%, and gastritis was evident in 72% based on histopathology. Helicobacter pylori was found in 50% of those with gastritis. Follow-up showed normalized hemoglobin levels in 92% of cases, with only 2 children requiring repeat iron therapy. Our findings underscore the importance of incorporating UGE into the diagnostic investigation of severe unexplained IDA in children, irrespective of the presence of GI symptoms.

A commentary on studies of brain iron accumulation during ageing.

Brain iron content is widely reported to increase during "ageing", across multiple species from nematodes, rodents (mice and rats) and humans. Given the redox-active properties of iron, there has been a large research focus on iron-mediated oxidative stress as a contributor to tissue damage during natural ageing, and also as a risk factor for neurodegenerative disease. Surprisingly, however, the majority of published studies have not investigated brain iron homeostasis during the biological time period of senescence, and thus knowledge of how brain homeostasis changes during this critical stage of life largely remains unknown. This commentary examines the literature published on the topic of brain iron homeostasis during ageing, providing a critique on limitations of currently used experimental designs. The commentary also aims to highlight that although much research attention has been given to iron accumulation or iron overload as a pathological feature of ageing, there is evidence to support functional iron deficiency may exist, and this should not be overlooked in studies of ageing or neurodegenerative disease.

A Case of Rickets and Pediatric Iron Deficiency Anemia in Alabama

A Case of Rickets and Pediatric Iron Deficiency Anemia in Alabama

Preparation of Rehmanniae Radix Praeparata polysaccharide iron(III) complex and evaluation of its biological activity.

This study extracted and purified a polysaccharide from Rehmanniae radix praeparata (RGP) with an average molecular weight. The structural characteristicsof RGP and its iron(III) complex, RGP-Fe(III),were examinedfor their antioxidant properties and potential in treating iron deficiency anemia (IDA). Analysis revealedthatRGP comprised Man, Rha, Gal,and Xyl, with a sugar residue skeleton featuring1→3; 1→2, 3; and 1→2,3, 4 linkages, among others. RGP-Fe(III) had amolecular weight of 4.39×104 Da.Notably, RGP-Fe(III) exhibited superiorantioxidant activity compared toRGPalone. InIDA rat models,treatmentwithRGP-Fe(III)led to increasedweight gain, restorationof keyblood parameters including hemoglobin, red blood cells,and mean hemoglobin content, elevatedserum ironlevels,and decreasedtotal iron-binding capacity.Histologicalexamination revealedno observabletoxic effects of RGP-Fe(III) on the liver and spleen.These findings suggest the potential of RGP-Fe(III) as a therapeutic agent for managing IDA and highlight its promising antioxidant properties.

Identification of three mechanistic pathways for iron-deficient heart failure.

Current understanding of iron-deficient heart failure is based on blood tests that are thought to reflect systemic iron stores, but the available evidence suggests greater complexity. The entry and egress of circulating iron is controlled by erythroblasts, which (in severe iron deficiency) will sacrifice erythropoiesis to supply iron to other organs, e.g. the heart. Marked hypoferraemia (typically with anaemia) can drive the depletion of cardiomyocyte iron, impairing contractile performance and explaining why a transferrin saturation < ≈15%-16% predicts the ability of intravenous iron to reduce the risk of major heart failure events in long-term trials (Type 1 iron-deficient heart failure). However, heart failure may be accompanied by intracellular iron depletion within skeletal muscle and cardiomyocytes, which is disproportionate to the findings of systemic iron biomarkers. Inflammation- and deconditioning-mediated skeletal muscle dysfunction-a primary cause of dyspnoea and exercise intolerance in patients with heart failure-is accompanied by intracellular skeletal myocyte iron depletion, which can be exacerbated by even mild hypoferraemia, explaining why symptoms and functional capacity improve following intravenous iron, regardless of baseline haemoglobin or changes in haemoglobin (Type 2 iron-deficient heart failure). Additionally, patients with advanced heart failure show myocardial iron depletion due to both diminished entry into and enhanced egress of iron from the myocardium; the changes in iron proteins in the cardiomyocytes of these patients are opposite to those expected from systemic iron deficiency. Nevertheless, iron supplementation can prevent ventricular remodelling and cardiomyopathy produced by experimental injury in the absence of systemic iron deficiency (Type 3 iron-deficient heart failure). These observations, taken collectively, support the possibility of three different mechanistic pathways for the development of iron-deficient heart failure: one that is driven through systemic iron depletion and impaired erythropoiesis and two that are characterized by disproportionate depletion of intracellular iron in skeletal and cardiac muscle. These mechanisms are not mutually exclusive, and all pathways may be operative at the same time or may occur sequentially in the same patients.

Gene expression of iron transporters, markers of vascularization and structural integrity in placenta of mothers with and without anemia.

To compare the mRNA expression of placental iron transporters (TfR-1 and FPN), markers of placental vascularization (VEGF and sFLT1) and marker of structural integrity (LMN-A) in term women with and without iron deficiency anemia. A total of 30 pregnant women were enrolled; 15 cases of iron deficiency anemia (Hb 7-10.9 gm/dL) and 15 gestational age matched healthy controls (Hb ≥ 11 gm/dL). Peripheral venous blood was collected for assessment of hemoglobin levels and serum iron profile. Placental tissue was used for assessing the mRNA expression of TfR-1, FPN, VEGF, sFLT-1 and LMN-A via real time PCR. Placental expression of TfR-1, VEGF and LMN-A was increased in pregnant women with anemia compared to healthy pregnant controls. Placental expression of sFLT-1 was decreased in pregnant women with anemia compared to healthy pregnant controls. There was no change in the placental expression of FPN. The increased expression of TfR-1, VEGF and LMN-A in cases of iron deficiency anemia are most likely to be compensatory in nature to help maintain adequate fetal iron delivery. Compensatory changes in the placenta aimed at buffering transport of iron to the fetus are seen in pregnant women with anemia compared to healthy pregnant controls.

Low Vitamin A Status: A Potential Limiting Factor for Hemoglobin Improvement to Iron–Folic Acid Supplementation in Adolescent Girls with Iron Deficiency Anemia

Low Vitamin A Status: A Potential Limiting Factor for Hemoglobin Improvement to Iron–Folic Acid Supplementation in Adolescent Girls with Iron Deficiency Anemia

Critical re-evaluation of the identification of iron deficiency states and effective iron repletion strategies in patients with chronic heart failure.

According to current guidelines, iron deficiency is defined by a serum ferritin level <100 ng/ml or a transferrin saturation (TSAT) <20% if the serum ferritin level is 100-299 μg/L. These criteria were developed to encourage the use of intravenous iron as an adjunct to erythropoiesis-stimulating agents in the treatment of renal anaemia. However, in patients with heart failure, these criteria are not supported by any pathophysiological or clinical evidence that they identify an absolute or functional iron deficiency state. A low baseline TSAT-but not serum ferritin level-appears to be a reliable indicator of the effect of intravenous iron to reduce major heart failure events. In randomized controlled trials, intravenous iron decreased the risk of cardiovascular death or total heart failure hospitalization in patients with a TSAT <20% (risk ratio 0.67 [0.49-0.92]) but not in patients with a TSAT ≥20% (risk ratio 0.99 [0.74-1.30]), with the magnitude of the risk reduction being proportional to the severity of hypoferraemia. Patients who were enrolled in clinical trials solely because they had a serum ferritin level <100 μg/L showed no significant benefit on heart failure outcomes, and it is noteworthy that serum ferritin levels of 20-300 μg/L lie entirely within the range of normal values for healthy adults. Current guidelines reflect the eligibility criteria of clinical trials, which inadvertently adopted unvalidated criteria to define iron deficiency. Reliance on these guidelines would lead to the treatment of many patients who are not iron deficient (serum ferritin level <100 μg/L but normal TSAT) and ignores the possibility of iron deficiency in patients with a low TSAT but with serum ferritin level of >300 μg/L. Importantly, analyses of benefit based on trial eligibility-driven guidelines substantially underestimate the magnitude of heart-failure-event risk reduction with intravenous iron in patients who are truly iron deficient. Based on all available data, we recommend a new mechanism-based and trial-tested approach that reflects the totality of evidence more faithfully than the historical process adopted by clinical investigators and by the guidelines. Until additional evidence is forthcoming, an iron deficiency state in patients with heart failure should be defined by a TSAT <20% (as long as the serum ferritin level is <400 μg/L), and furthermore, the use of a serum ferritin level <100 μg/L alone as a diagnostic criterion should be discarded.

Deworming and micronutrient status by community open defecation prevalence: An observational study using nationally representative data from India, 2016-2018.

Micronutrient deficiencies are widespread in India. Soil-transmitted helminth (STH) infections are acquired by interaction with soil and water contaminated by human feces and lead to blood loss and poor micronutrient absorption. The current recommendation for control of STH-related morbidity is targeted deworming, yet little is known about the effectiveness of deworming on micronutrient status in varying sanitation contexts. Ranging between 1% and 40% prevalence across Indian states, open defecation (OD) remains high despite India's investments at elimination by promoting community-wide sanitation. This variation provides an opportunity to study the relationship between deworming, micronutrient status, and OD at-scale. Cross-sectional datasets that were representative for India were obtained the Comprehensive National Nutrition Survey in 2016 to 2018 (n = 105,060 individuals aged 1 to 19 years). Consumption of deworming medication was described by age and community OD level. Logistic regression models were used to examine the relationship between deworming, cluster OD, and their interactions, with anemia and micronutrient deficiencies (iron, zinc, vitamin A, folate, and vitamin B12), controlling for age, sex, wealth, diet, and seasonality. These regression models further allowed us to identify a minimum OD rate after which deworming becomes ineffective. In sensitivity analyses, the association between deworming and deficiencies were tested in subsamples of communities classified into 3 OD levels based on statistical tertiles: OD free (0% of households in the community practicing OD), moderate OD (>0% and <30%), or high OD (at least 30%). Average deworming coverage and OD prevalence in the sample were 43.4% [IQR 26.0, 59.0] and 19.1% [IQR 0, 28.5], respectively. Controlling for other determinants of nutritional status, adolescents living in communities with higher OD levels had lower coverage of deworming and higher prevalence of anemia, zinc, vitamin A, and B12 deficiencies. Compared to those who were not dewormed, dewormed children and adolescents had lower odds of anemia (adjusted odds ratio 0.72, (95% CI [0.67, 0.78], p < 0.001) and deficiencies of iron 0.78, (95% CI [0.74, 0.82], p < 0.001) and folate 0.69, (95% CI [0.64,0.74], p<0.001)) in OD free communities. These protective effects remained significant for anemia but diminished for other micronutrient deficiencies in communities with moderate or high OD. Analysis of community OD indicated a threshold range of 30% to 60%, above which targeted deworming was no longer significantly associated with lower anemia, iron, and folate deficiency. The primary limitations of the study included potential for omitted variables bias and inability to capture longitudinal effects. Moderate to high rates of OD significantly modify the association between deworming and micronutrient status in India. Public health policy could involve sequencing interventions, with focus on improving deworming coverage in communities that have achieved minimum thresholds of OD and re- triggering sanitation interventions in high OD communities prior to deworming days, ensuring high coverage for both. The efficacy of micronutrient supplementation as a complementary strategy to improve nutritional outcomes alongside deworming and OD elimination in this age group needs further study.

Iron homeostasis, recycling and vulnerability in the stressed kidney: A neglected dimension of iron-deficient heart failure.

The available evidence suggests that the kidney may contribute importantly to the development of an iron deficiency state in patients with heart failure and may be injured by therapeutic efforts to achieve iron repletion. The exceptional workload of the proximal renal tubule requires substantial quantities of iron for ATP synthesis, which it derives from Fe3+ bound to transferrin in the bloodstream. Following ferrireduction, Fe2+ is conveyed by divalent transporters (e.g. DMT1) out of the endosome of the proximal renal tubule, and highly reactive Fe2+ can be directed to the mitochondria, sequestered safely in a ferritin nanocage or exported through the actions of hepcidin-inhibitable ferroportin. The actions of ferroportin, together with transferrin endocytosis and DMT1-mediated transport, play a key role in the recycling of iron from the tubular fluid into the bloodstream and preventing the loss of filtered iron in the urine. Activation of endogenous neurohormonal systems and proinflammatory signalling in heart failure decrease megalin-mediated uptake and DMT1 expression, and increase hepcidin-mediated suppression of ferroportin, promoting the loss of iron in the urine and contributing to the development of an iron deficiency state. Furthermore, the failure of ferroportin-mediated efflux at the basolateral membrane heightens the susceptibility of the renal tubules to cytosolic excesses of Fe2+, causing lipid peroxidation and synchronized cell death (ferroptosis) through the iron-dependent free radical theft of electrons from lipids in the cell membrane. Ferroptosis is a central mechanism to most disorders that can cause acute and chronic kidney disease. Short-term bolus administration of intravenous iron can cause oxidative stress and is accompanied by markers of renal injury. Experimentally, long-term maintenance of an iron-replete state is accompanied by accelerated loss of nephrons, oxidative stress, inflammation and fibrosis. Intravenous iron therapy increases glomerular filtration rate rapidly in patients with heart failure (perhaps because of a haemodynamic effect) but not in patients with chronic kidney disease, and the effects of intravenous iron on the progression of renal dysfunction in the long-term trials - AFFIRM-AHF, IRONMAN and HEART-FID - have not yet been reported. Given the potential role of dysregulated renal iron homeostasis in the pathogenesis of iron deficiency and the known vulnerability of the kidney to intravenous iron, the appropriate level of iron repletion with respect to the risk of acute and chronic kidney injury in patients with heart failure requires further study.

Evaluation of erythrocyte and reticulocyte indices in a newborn with severe hemolytic disease

Currently, significant progress has been made in the prevention, diagnosis and treatment of hemolytic disease of the fetus and newborn. However, the development of anemia in a newborn child due to this disease remains an urgent problem for both neonatologists and pediatricians. In such children, a comprehensive assessment of the hemogram is of particular importance. The study of erythrocyte and reticulocyte parameters of a general blood test is necessary to determine prognostic criteria for the restoration of hematopoiesis and determine the status of iron deficiency. A clinical observation of a newborn child with the development of anemia due to hemolytic disease of the fetus and newborn is presented (clinical case). A dynamic analysis of reticulocyte parameters (absolute and relative numbers) and reticulocyte fractions was carried out. An increase in reticulocytes (absolute and relative numbers) was established, mainly due to the fraction of immature reticulocytes during the development of anemia in a newborn child. Such indicators as the hemoglobin content in reticulocytes, the average hemoglobin content in an erythrocyte, the average hemoglobin concentration in an erythrocyte in a general blood test in an infant during the neonatal period remained within the reference values. The data obtained made it possible to determine a personalized approach to the treatment of anemia and avoid blood transfusion in this child.

Prevention of Anaemia in Pregnancy: A Five-Year Scoping Review

Abstract: Approximately 50% of pregnant women globally suffer from pregnancy-related anaemia, which is a serious issue for reproductive health and can lead to a number of complications, including low birth weights, premature deliveries, foetal deformities, and feto-maternal mortality. Aim: This study aimed to evaluate the suggested strategies to prevent anaemia in pregnancy through a 5-year scoping review (November, 2017 to November, 2022). Methods: A comprehensive list of keyword combinations linked to anemia prevention in pregnancy and pertinent approaches to inform the search strategy were evaluated. Significant events, including pregnancy and anemia, were cross-referenced with the frequency and variability of terms across time. Literature from Pubmed (MEDLINE), Google Scholar, PLOS One, and Cochrane database were reviewed. Results: Evidence-based preventative therapy options for iron deficiency anaemia in pregnancy include prophylactic iron supplementation, food fortification with iron and folate, and health education. There is a wealth of research on the effects of these therapies on the occurrence of anaemia during pregnancy. However, these prospects are endangered by several variables, such as inadequate health facilities, low maternal health literacy, low utilisation of maternal health care in developing countries, a dearth of resources for health education, and lack of a government policy that prevents anaemia during pregnancy. Conclusion: If the highlighted challenges are appropriately addressed through the provision of health education material, the effectiveness of anaemia prevention in pregnancy could be sustained.