Iron Deficiency Research Articles

Behind the veil of anemia: Assessment of iron, folic acid, and vitamin B12 deficiencies and their association with red cell indices in anemic and non-anemic women

During pregnancy anemia is a common health issue with various factors influencing its occurrence. It is a major public health problem in India. It is believed that 2.36 billion individuals are affected globally, and it is also an endemic problem in India. Iron deficiency often leads to iron deficiency anemia (IDA), significantly influencing maternal and fetal health.This study aims to investigate the complete blood count and nutritional parameters including Iron profile, vitamin B12, and Folic acid in anemic and non-anemic participants.The study involved 458 women of which 300 were anemic women and 158 were non-anemic women, predominantly from rural areas. The severity of anemia was classified as per WHO guidelines. The CBC was estimated by a 3-part hematology analyzer Medonic M-series, while the iron profile, vitamin B12, and folic acid were measured by using an automated analyzer Abbott Architect 1000 SR.The severity of anemia among the anemic women, classified according to WHO guidelines, revealed that 38.7% had mild anemia, 32.7% had moderate anemia, and 28.6% had severe anemia. 39.3% women exhibited microcytic hypochromic cells, 38% had normocytic normochromic cells, and 22.7% exhibited macrocytic cells. 56.6% had iron deficiency, 10% had folate deficiency, 16.7% had vitamin B12 deficiency, 6.7% had iron+vitamin B12+folic acid deficiency and 10% had vitamin B12+folic acid deficiency. Based on the severity only vitamin B12 was significantly reduced in severe (145.65±58.43) than moderate (177.06±66.24) and mild group (174.43±68.43), p=0.042. Hemoglobin showed a positive correlation with iron level (r=0.523, p<0.0001), and a negative correlation with ferritin (r=-0.355, p<0.0001).: These findings provide valuable insights into the nutritional status of the anemic women and highlights the need for targeted interventions to address micronutrient deficiencies during pregnancy.

Management of iron deficiency anemia in pregnancy in India: A review of current practices and challenges

Iron deficiency anaemia (IDA) is a major global health concern that can lead to difficulties for both the mother and the foetus, especially in pregnant women. The physiological demand of iron during pregnancy increases threefold to support fetoplacental development and maternal adaptation to pregnancy. This study aimed to identify gaps in current IDA management, limitations of conventional oral iron therapy, and the need for effective and well-tolerated treatments.The objective of this study was to understand the gap of current treatment options in IDA management, its limitations, and possible effective strategies for better management.A questionnaire-based opinion survey involving top gynecologists across India was conducted. The survey aimed to gather data on the challenges faced with conventional oral iron therapy, the desire for a change in oral iron salts, and the preference for novel oral iron prescriptions for their patients.Data obtained from the survey showed that 82% of gynecologists and obstetricians noticed challenges with conventional oral iron therapy. 86% wanted to change the oral iron salts, and 70% would like to prescribe novel oral iron for their patients. Ferric maltol, a novel form of chelated oral iron, was introduced as a potential solution for IDA management. It has been studied in various clinical indications, such as IDA associated with inflammatory bowel disease, chronic kidney disease, and pulmonary hypertension, showing significant improvements in hemoglobin and iron indices with good tolerability throughout treatment duration.The study results demonstrate that ferric maltol is a suitable and convenient treatment option for individuals seeking long-term, convenient, and well-tolerated management of IDA.

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.

Iron and bones: Effects of iron overload, deficiency and anemia treatments on bone

Iron and bones: Effects of iron overload, deficiency and anemia treatments on bone

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

Effect of Low-Dose Iron Supplementation on Early Development in Breastfed Infants: A Randomized Clinical Trial.

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

Hospitalization of patients with nutritional anemia in the United States in 2020

BackgroundNutritional anemia is highly prevalent and has triggered a globally recognized public health concern worldwide.ObjectiveTo better understand the prevalence of anemia and the state of nutritional health in developed countries to inform global nutritional health and better manage the disease.MethodWe employed the Healthcare Cost and Utilization Project (HCUP)-2020 National Inpatient Health Care Data (NIS), administered by The Agency for Healthcare Research and Quality. Nutritional anemia was diagnosed according to the International Classification of Diseases, 10th Revision (ICD-10). Matching analysis and multivariate regression were used to adjust for patient and hospital characteristics. Controls were obtained by stratifying and matching for age and sex.ResultsThe 2020 HCUP-NIS database encompassed a survey over 6.4 million hospitalized patients, among which 1,745,350 patients diagnosed with anemia, representing approximately 26.97% of the hospitalized population, over 310,000 were diagnosed with nutritional anemia, and 13,150 patients were hospitalized for nutritional anemia as primary diagnosis. Hospitalization rate for nutritional anemia exhibited an increased age-dependent increase nationwide, especially among females, who displayed 1.87 times higher than males. Notably, in comparison to the control group, individuals of the Black race exhibit a higher prevalence of nutritional anemia (case group: 21.7%, control group: 13.0%, p &amp;lt; 0.001). In addition, hospitalization rates were higher among low-income populations, with lower rates of private insurance (case group: 18.7%, control group: 23.5%, p &amp;lt; 0.001) and higher rates of Medicaid insurance (case group: 15.4%, control group: 13.9%, p &amp;lt; 0.001). In areas characterized by larger urban centers and advanced economic conditions within the urban–rural distribution, there was an observed increase in the frequency of patient hospitalizations. Iron deficiency anemia emerged as the predominant subtype of nutritional anemia, accounting for 12,214 (92.88%). Secondary diagnosis among patients hospitalized for nutritional anemia revealed that a significant number faced concurrent major conditions like hypertension and renal failure.ConclusionIn economically prosperous areas, greater attention should be given to the health of low-income individuals and the older adult. Our findings hold valuable insights for shaping targeted public health policies to effectively address the prevalence and consequences of nutritional anemia based on a overall population health.

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.

Fluorescence lifetime of plant leaves with sub-nanosecond resolution

Abstract The study aimed to develop a measurement apparatus for in vivo chlorophyll-a (Chl-a) fluorescence decay measurements of plants by means of Time Correlated Single Photon Counting (TCSPC). In this approach, sub-nanosecond laser pulses with a repetition rate of 10 MHz are applied to excite the sample, followed by the analysis of arrival times of the emitted fluorescence photons. Photon statistics are generated by iteratively fitting the sum of 2 exponential functions. The tool was tested on both plastid and in vivo leaf samples of Savoy cabbage (Brassica oleracea var. sabauda) with 3-4 subsequent leaves giving a complete sample coverage starting from the outermost. The Chl-a fluorescence lifetime exhibited a gradual increase in both the isolated plastid suspensions and the in vivo leaf samples towards the innermost leaf layers explained by an increase of natural absence of light (etiolation syndrome). Furthermore, cadmium stress and iron deficiency were investigated on treated sugar beet (Beta vulgaris) samples in vivo using TCSPS measurements. The reduced fluorescence quenching resulted in an increased fluorescence lifetime. Finally, a long-term (10 week) testing of the setup was carried out on Chl-retaining resurrection Haberlea rhodopensis plants protecting themselves by an elevated non-photochemical quenching yielding a decrease of fluorescence lifetime during their desiccation.&amp;#xD;

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.

The Puzzle of Aspirin and Iron Deficiency: The Vital Missing Link of the Iron-Chelating Metabolites

Acetylsalicylic acid or aspirin is the most commonly used drug in the world and is taken daily by millions of people. There is increasing evidence that chronic administration of low-dose aspirin of about 75–100 mg/day can cause iron deficiency anaemia (IDA) in the absence of major gastric bleeding; this is found in a large number of about 20% otherwise healthy elderly (&gt;65 years) individuals. The mechanisms of the cause of IDA in this category of individuals are still largely unknown. Evidence is presented suggesting that a likely cause of IDA in this category of aspirin users is the chelation activity and increased excretion of iron caused by aspirin chelating metabolites (ACMs). It is estimated that 90% of oral aspirin is metabolized into about 70% of the ACMs salicyluric acid, salicylic acid, 2,5-dihydroxybenzoic acid, and 2,3-dihydroxybenzoic acid. All ACMs have a high affinity for binding iron and ability to mobilize iron from different iron pools, causing an overall net increase in iron excretion and altering iron balance. Interestingly, 2,3-dihydroxybenzoic acid has been previously tested in iron-loaded thalassaemia patients, leading to substantial increases in iron excretion. The daily administration of low-dose aspirin for long-term periods is likely to enhance the overall iron excretion in small increments each time due to the combined iron mobilization effect of the ACM. In particular, IDA is likely to occur mainly in populations such as elderly vegetarian adults with meals low in iron content. Furthermore, IDA may be exacerbated by the combinations of ACM with other dietary components, which can prevent iron absorption and enhance iron excretion. Overall, aspirin is acting as a chelating pro-drug similar to dexrazoxane, and the ACM as combination chelation therapy. Iron balance, pharmacological, and other studies on the interaction of iron and aspirin, as well as ACM, are likely to shed more light on the mechanism of IDA. Similar mechanisms of iron chelation through ACM may also be implicated in patient improvements observed in cancer, neurodegenerative, and other disease categories when treated long-term with daily aspirin. In particular, the role of aspirin and ACM in iron metabolism and free radical pathology includes ferroptosis, and may identify other missing links in the therapeutic effects of aspirin in many more diseases. It is suggested that aspirin is the first non-chelating drug described to cause IDA through its ACM metabolites. The therapeutic, pharmacological, toxicological and other implications of aspirin are incomplete without taking into consideration the iron binding and other effects of the ACM.