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Background: Iron deficiency is prevalent in patients with chronic kidney disease (CKD), even in those without anemia. However, the effects of iron deficiency on CKD progression and all-cause mortality in non-dialysis-dependent CKD (NDD-CKD) patients without anemia remain incompletely understood. Methods: This multicenter retrospective nationwide cohort study included adult patients with non-anemia NDD-CKD from 24 hospitals across China. The study investigated the associations between serum ferritin or transferrin saturation (TSAT) levels and the risks of CKD progression and all-cause mortality. Results: Among 18,878 patients with NDD-CKD, 9,989 patients were included in the kidney outcome analysis, and 18,481 patients in the all-cause mortality analysis. Of the patients with the measurement, 2,450 (27.2%) had ferritin levels ≤ 100ng/mL and 2,440 (13.1%) had a TSAT level ≤ 20%. Compared with patients with TSAT level of > 20%, those with TSAT level of ≤ 20% had significantly higher risks of CKD progression (adjusted hazard ratio [aHR]: 1.66, 95% confidence intervals [CI]: 1.16–2.37; P = 0.005) and all-cause mortality (aHR: 2.21, 95% CI: 1.36–3.57; P = 0.001). The robustness of results was supported by subgroup analyses. However, there was no significant association found between ferritin levels and the risk of CKD progression or all-cause mortality (P > 0.05). Conclusion: Iron deficiency was prevalent in NDD-CKD patients without anemia, and TSAT could be a modifiable risk factor of CKD progression and all-cause mortality. The screening of iron biomarkers, especially TSAT, in the early stage of NDD-CKD is important to assess and improve prognosis. [ABSTRACT FROM AUTHOR]

ABSTRACT: Background: The bone marrow iron study is the gold standard for differentiation of the two most common causes of anemia i.e. iron deficiency anemia (IDA) and anemia of chronic disease (ACD) in the elderly. However, it is often not feasible to do bone marrow examination (BME) in every elderly anemic patient, due to its invasive nature. Hepcidin, a liver-derived peptide, has been identified as the key systemic regulator of iron homeostasis. Our study highlights the potential diagnostic role of serum hepcidin in the evaluation of anemia in elderly. Methodology: Hundred elderly patients (≥60 years of age) having iron deficiency anemia (IDA) or anemia of chronic disease/inflammation (ACD) were the study subjects with 15 age-matched healthy controls. All patients were evaluated with history, clinical examination, routine investigations (complete blood count, liver, and kidney function tests), iron profile, and serum hepcidin. The bone marrow iron study was done in every patient to categorize them as IDA and ACD. Results and Discussion: Serum iron, TIBC, MCV, ferritin, and serum transferrin saturation values were differing significantly between IDA and ACD groups. Serum hepcidin levels can be used confidently to differentiate ACD from IDA (P value <0.001). At serum concentration, 198.82 ng/mL sensitivity of hepcidin to differentiate ACD from IDA was 93.9% and specificity was 92.2%. A subset of patients is misdiagnosed when the serum hepcidin level is used as a sole marker, and this also holds true for serum ferritin. Conclusion: Though serum hepcidin level correlates well with serum iron profile and also serum hepcidin appears to be a useful marker to differentiate ACD from IDA in terms of both sensitivity and specificity, the combined assessment of serum hepcidin and iron profile appears to be a better marker than ferritin and hepcidin alone. This could replace the use of bone marrow iron staining as a diagnostic tool in anemia in elderly. [ABSTRACT FROM AUTHOR]

Rheumatoid arthritis (RA) is an inflammatory autoimmune disease with articular and systemic manifestations, and one of the most common is anemia. This study aims to investigate whether the levels of the soluble receptors sRAGE, sRANKL, and OPG are affected by the distribution of RA patients in subgroups according to soluble transferrin receptor/log ferritin (sTfR-F index) and hemoglobin (Hb) levels and to examine their correlation with indicators of iron metabolism, disease activity, and autoimmune and inflammatory changes. The levels of sRANKL and sRAGE were significantly higher in the subgroup of anemia of chronic disease combined with iron deficiency anemia (ACD/IDA) compared to the ACD group: p < 0.0001 and p < 0.0001. The level of OPG tended to decrease in ACD/IDA (p = 0.053). sRAGE was positively correlated with prohepcidin, RF and anti-CCP antibodies, sRANKL, CRP, and IL-6 only in the ACD group. A negative correlation was found between sRAGE, sRANKL, and serum iron only in the ACD/IDA group. sRANKL was positively correlated with OPG, prohepcidin, CRP, IL-6, RF, anti-CCP antibodies, and DAS28 only in the ACD group. Positive correlations were observed between OPG and ferritin, sTfR, CRP, IL-6, RF, and DAS28, and a negative correlation was observed with serum iron only in the ACD group. Therefore, the investigated soluble receptors may serve as reliable biomarkers involved in the pathogenesis of RA and may contribute to the identification of patients at risk of developing combined anemia. [ABSTRACT FROM AUTHOR]

Iron deficiency (ID) without anemia is common in children with newly diagnosed celiac disease (CD). We aimed to assess the effect of iron supplementation versus no treatment on ferritin levels in newly diagnosed CD patients with ID adhering to a gluten-free diet (GFD). A retrospective review of children < 18 years, with low ferritin (≤ 10 ng/mL) and normal hemoglobin levels diagnosed between 12.2018 and 12.2021. We compared hemoglobin and ferritin levels between patients who received supplemental iron to those who did not. Data, including demographics, laboratory tests, and anthropometrics, were collected at baseline, and at 6 and 12 months following the initiation of the GFD. Adherence to GFD was assessed at each visit. Among 304 children diagnosed during the study period, 43 (14.1%) had iron deficiency anemia and 60 (19.7%) ID without anemia. Among children with ID, 29 (48%) were female, mean age 7.3 ± 3.9 years. Twenty-nine (48%) children received iron supplementation, and 31 (52%) did not. At the 12-month follow-up visit, tissue transglutaminase levels decreased significantly (p < 0.001), from a mean baseline level of 226.6 ± 47.8 to 34.5 ± 46 U/mL in children that received iron supplementation and from 234.2 ± 52.4 to 74.5 ± 88.7 U/mL in non-treated children, with no significant difference between the groups p = 0.22. Ferritin levels increased significantly (p < 0.001), from 9.0 ± 4.7 to 25.2 ± 20.8 ng/mL in patients who received supplementation and from 8.9 ± 3.8 to18.6 ± 9.5 ng/mL in patients who did not, with no significant difference between the groups (p = 0.46). Conclusion: Most children with newly diagnosed celiac disease and iron deficiency, who adhere to GFD, will normalize ferritin levels within 12 months without the need of iron supplementation. What is Known: • Iron deficiency and iron deficiency anemia are common in newly diagnosed celiac disease. • Improved iron absorption may follow mucosal healing process in patients adhering to a strict gluten-free diet. What is New: • This single-center, retrospective cohort study evaluated the effect of iron supplementation versus no treatment on ferritin levels in children with newly diagnosed celiac disease with iron deficiency adhering to a gluten-free diet. • Most children with newly diagnosed celiac disease and iron deficiency, who adhere to gluten-free diet, will normalize ferritin levels within 12 months without the need of iron supplementation. [ABSTRACT FROM AUTHOR]

Chlorosis in azaleas is characterized by an interveinal yellowing of leaves that is typically caused by a deficiency of iron. This condition is usually due to the inability of cells to properly acquire iron as a consequence of unfavorable conditions, such as an elevated pH, rather than insufficient iron levels. The causes and effects of chlorosis were found to have similarities with those pertaining to a recently presented hypothesis that describes a pathogenic process in Alzheimer disease. This hypothesis states that iron becomes sequestered (e.g., by amyloid β and tau), causing a functional deficiency of iron that disrupts biochemical processes leading to neurodegeneration. Additional mechanisms that contribute to iron becoming unavailable include iron-containing structures not undergoing proper recycling (e.g., disrupted mitophagy and altered ferritinophagy) and failure to successfully translocate iron from one compartment to another (e.g., due to impaired lysosomal acidification). Other contributors to a functional deficiency of iron in patients with Alzheimer disease include altered metabolism of heme or altered production of iron-containing proteins and their partners (e.g., subunits, upstream proteins). A review of the evidence supporting this hypothesis is presented. Also, parallels between the mechanisms underlying a functional iron-deficient state in Alzheimer disease and those occurring for chlorosis in plants are discussed. Finally, a model describing the generation of a functional iron deficiency in Alzheimer disease is put forward. [ABSTRACT FROM AUTHOR]

Background: Collagenous gastritis (CG) and Lymphocytic gastritis (LG) are rare types of gastritis. Thick sub-epithelial collagen bands characterize CG. Numerous lymphocytes in the surface and foveolar epithelium characterize LG. We aimed to characterize these disorders in our pediatric unit. Methods: A retrospective review of children diagnosed with CG and LG between 2000 and 2023. Baseline data; demographics, anthropometric, symptoms, laboratory data, macroscopic and histopathologic findings. Follow-up data; treatment, improvement of symptoms and laboratory parameters. Results: We identified 31 children, 11 (35.5%) had CG and 20 (64.5%) LG, mean age 9.07 ± 5.04 years. Seven (22.6%) children were diagnosed between 2000 and 2016 and 24 (77.4%) between 2017 and 2023. Baseline characteristics included gastrointestinal symptoms in 16 (51.6%), iron deficiency anemia in 22 (71%), with a mean hemoglobin level of 8.8 ± 2.5 gr/dl. Gastric endoscopic findings were normal in 12 (38.7%), demonstrated nodularity in 14 (45.2%) and an inflamed mucosa without nodularity in 5 (16.1%). Helicobacter pylori was positive in 3 (9.7%) children, celiac disease was diagnosed in 7 (22.6%). Treatment included iron supplementation in 24 (77.4%), proton pump inhibitors in 16 (51.6%) and a gluten free diet in seven. Mean follow-up was 2.9 ± 2.2 years. Hemoglobin levels normalized in 21/22; however, 9 (29%) patients required repeat iron supplementation. Eight patients had a repeat endoscopy (6 CG and 2 LG) without changes in their gastric histopathology. Conclusions: CG and LG are not rare in pediatric patients. Physicians and pathologist should be aware of these types of gastritis. [ABSTRACT FROM AUTHOR]

Sickle cell disease (SCD) is a prevalent inherited blood disorder arising from a single point mutation that results in substitution of valine with glutamic acid in the Beta hemoglobin chain, making red blood cells assume a banana shape under low oxygen state. It is most prevalent in sub-Saharan Africa, affecting approximately 2% of the population in Mali. This study aimed to evaluate the iron status and associated hematological parameters in SCD patients at steady state in an environment with a high prevalence of iron deficiency. A cross-sectional study was conducted at the Center de Recherche et de Lutte contre la Drépanocytose (CRLD) in Bamako, Mali, involving 757 SCD patients aged 10 to 29 years. Iron deficiency was defined as serum ferritin < 20 ng/mL, while iron overload was associated with serum ferritin > 500 ng/mL. The study population consisted of 171 (22.6%) hemolytic phenotypes (SS and Sβ0) and 586 (77.4%) viscous phenotypes (SC and Sβ+). Iron deficiency was found in 19 SCD patients (2.5%), with a higher prevalence in the SC phenotype (68.4%). All iron-deficient subjects exhibited microcytosis (MCV < 80 fL) and hypochromia (MCH < 26 pg). Hemoglobin levels < 12 g/dL were observed only in homozygous SCD patients. Low reticulocyte counts were noted in iron-deficient subjects with SC and Sβ+ phenotypes, but not in iron-deficient SS subjects. Serum C-reactive protein (CRP) was normal (< 10 mg/L) in all iron-deficient subjects, excluding iron deficiency due to chronic inflammation. Iron deficiency was observed among 2.5% of the study population, with a predominant occurrence among those with SC phenotype. All iron deficient subjects had microcytosis and hypochromia. Hemoglobin levels below 12 g/dL were only found in homozygous SCD patients. Additionally, low reticulocyte counts were noted in iron deficient patients with SC and Sβ+ phenotypes, though not in those with the SS phenotype. These findings contribute to the understanding of iron status in SCD patients in an African context and highlights the importance of monitoring iron levels in these population to prevent complications associated with iron deficiency or overload. [ABSTRACT FROM AUTHOR]

Introduction: Anaemia is the most common Extraintestinal Manifestation (EIM) associated with Ulcerative Colitis (UC) and has been linked to increased mortality in UC patients, with iron deficiency having the most pronounced effect. Moreover, iron deficiency in UC can occur with or without anaemia. Aim: To assess anaemia and iron deficiency, with or without anaemia, in UC patients. Materials and Methods: The present cross-sectional study was conducted in the Department of Medicine, Pt. B.D. Sharma PGIMS, Rohtak, Haryana, India, from August 2020 to December 2021. Study included 75 patients with UC and varying levels of disease activity. A complete haemogram, Red Blood Cell (RBC) indices, and serum iron studies {serum iron levels, Total Iron Binding Capacity (TIBC), Transferrin Saturation (TfS), and serum ferritin} were conducted. Patients were classified as having Iron Deficiency Anaemia (IDA), Anaemia of Chronic Disease (ACD), or mixed anaemia based on the results of the iron studies. Disease activity was assessed using the Mayo score. Patients were divided into group I (mild disease activity) and group II (moderate to severe disease activity). Haemoglobin (Hb), RBC indices and iron levels were compared between the two groups. Independent t-tests and Chi-square tests were employed for statistical analysis. Results: The mean±Standard Deviation (SD) age of the patients was 34.8±14 years, with a male-to-female ratio of 1.7:1. The mean±SD duration of the disease was 28.8±33.8 months (median: 12 months). Fifteen patients had mild disease activity, 52 had moderate activity, and eight had severe activity. The mean±SD Hb level among the patients was 11.1±2.0 g/dL. The mean±SD values for Mean Corpuscular Volume (MCV), Mean Corpuscular Haemoglobin (MCH), and Mean Corpuscular Haemoglobin Concentration (MCHC) were 80.4±7.7 fL, 26.4±4.0 pg, and 32.1±2.5 g/dL, respectively. The mean±SD serum iron level and ferritin levels were 59.3±29.1 mcg/dL and 27.2±27.9 ng/mL, respectively. The mean±SD TfS was 14.3±10.8%, while the mean±SD TIBC was 337.1±80.5 mcg/dL. A total of 45 (60%) patients had anaemia, and 16 (21.3%) patients had iron deficiency without anaemia. Among those with anaemia, 32 (42.7%) had IDA and 13 (17.3%) had mixed anaemia; none of the patients had ACD. In total, 61 (81.3%) patients had iron deficiency, with or without anaemia. Hb, RBC indices and iron studies were comparable between both groups. Conclusion: Iron deficiency anaemia is common in UC patients, affecting 60% of the cohort; however, iron deficiency without anaemia was also observed in 21.3% of patients. Changes in Hb, RBC indices and iron studies were independent of disease activity. [ABSTRACT FROM AUTHOR]

Background: In light of prolonged hypoxia, children with cyanotic heart disase (CHD) are at a high risk of developing iron deficiency iron deficiency (ID) and iron deficiency anemia (IDA). Reticulocyte hemoglobin equivalent (Ret-He) is a novel and dependable indicator for assessing iron status. However, there has been no previous study regarding cut-off value in pediatric CHD group. The purpose of this study is to assess the role of Ret-He and to establish cut-off points in the diagnosis of iron deficiency and IDA in pediatric cyanotic heart disease. Method: This study was conducted in two tertiary hospitals in Jakarta, Indonesia. 59 children with CHD, aged 3 months to 18 years, were enrolled consecutively. To determine iron status, hematological parameters (hemoglobin, hematocrit, mean corpuscular volume, mean corpuscular hemoglobin) and biochemical parameters for iron status (serum ferritin, transferrin saturation) were analysed and compared to Ret-He levels. The receiver operating characteristic (ROC) analysis was performed for the Ret-He cut-off points for ID and IDA. Sensitivity, specificity, positive and negative predictive value were calculated for each cut-off point. Result: Normal iron status was identified in 27 (45.8%) subjects, ID in 8 (13.5%) subjects, and IDA 24 (40.7%) subjects. The ID cut-off value for Ret-He is 28.8 pg (sensitivity 75%, specificity 85.2%, PPV 60%, NPV 92%, and AUC 0.828) and the Ret-He cut-off point for IDA is 28.15 pg (sensitivity 75%, specificity 88.9%, PPV 85.7%, NPV 80%, and AUC 0.824). Hemoglobin should be used in conjunction with Ret-He. ID might be detected in this cohort with Ret-He 28.8 pg and hemoglobin > 16,5 g/dL. While Ret-He 28.15 pg or Ret-He 28.15–28.8 pg with hemoglobin 16.5 g/dL could be used to diagnose IDA. Conclusion: The reticulocyte hemolgobin equivalent could be utilised as an iron status parameter in pediatric CHD, with a cut-off value of 28.8 pg for ID and 28.15 pg for IDA. [ABSTRACT FROM AUTHOR]

Background: Intravenous iron administration is routinely used to treat moderate anemia during pregnancy. Iron sucrose has the disadvantage of repeated doses and increased hospital visits. Ferric carboxymaltose provides rapid replacement of iron storage in a single dose. In this study, we compare the safety and efficacy of the two parenteral iron complexes in the treatment of iron deficiency anemia in pregnancy from gestation age of 14-38 weeks. Methodology: The Obstetrics and Gynecology Department at Rajshree Medical Research Institute in Bareilly conducted this comparative investigation. In order to conduct the study, a total of 100 pregnant women who were diagnosed with moderate anemia between the ages of 14 and 36 weeks of gestation were divided into two groups at random (n = 50) (Group A: Iron sucrose complex (ISC); Group B: Ferric carboxymaltose). Result: In group A of the study, the majority of the patients were women between the ages of 26 and 30 (38%) and between 31 and 35 (44%), respectively. In group A, 8% of patients and 6% in group B had nausea. In group A, 1% of patients reported abdominal pain, whereas in group B, there were no complaints. Conclusion: There aren't many randomized controlled trials comparing ferrous carboxymaltose and ISC in pregnant women between 14 and 28 weeks along with very few prospective studies on FCM. The present study concludes Ferric carboxymaltose to be more efficient with no life-threatening reaction compared with ISC for treatment of moderate iron deficiency anemia in 14-36 weeks of gestation. [ABSTRACT FROM AUTHOR]

Background: Iron deficiency anemia (IDA) increases levels of C-terminal fibroblast growth factor 23 (cFGF23) and platelet count (PLT), each of which is associated with cardiovascular events. Therefore, we hypothesized that iron replacement with ferric citrate hydrate (FC) would decrease cFGF23 levels and PLT in patients with IDA. Methods: In a randomized, open-label, multicenter, 24-week clinical trial, patients with non-dialysis-dependent chronic kidney disease (CKD) and non-CKD complicated by IDA (8.0 ≤ hemoglobin < 11.0 g/dL; and serum ferritin < 50 ng/mL [CKD]; < 12 ng/mL [non-CKD]) were randomized 1:1 to FC-low (500 mg: approximately 120 mg elemental iron/day) or FC-high (1000 mg: approximately 240 mg elemental iron/day). If sufficient iron replacement had been achieved after week 8, further treatment was discontinued. Results: Seventy-three patients were allocated to FC-low (CKD n = 21, non-CKD n = 15) and FC-high (CKD n = 21, non-CKD n = 16). Regardless of CKD status, FC increased serum ferritin and transferrin saturation, did not change intact FGF23 or serum phosphorus, but decreased cFGF23. In FC-low group, median changes in cFGF23 from baseline to week 8 were −58.00 RU/mL in CKD and −725.00 RU/mL in non-CKD; in FC-high group, the median changes were −66.00 RU/mL in CKD and −649.50 RU/mL in non-CKD. By week 8, FC treatment normalized PLT in all patients with high PLT at baseline (>35.2 × 104/µL; FC-low: 1 CKD, 8 non-CKD; FC-high: 3 CKD, 8 non-CKD). Conclusion: Regardless of CKD status, iron replacement with FC decreased elevated cFGF23 levels and normalized elevated PLT in patients with IDA. Clinical trial registration number: jRCT2080223943. [ABSTRACT FROM AUTHOR]

Background: Anemia is common complication in children with chronic kidney disease (CKD) mainly anemia of chronic disease (ACD), but iron deficiency anemia (IDA) is also common. Soluble transferrin receptor (sTfR) is important marker for IDA. This study aims to evaluate the utility of soluble transferrin Receptor-Ferritin Indices as markers of IDA and for differentiation ACD from IDA in childern with chronic kidney disease. Methods: cross-sectional study was conducted at Department of Pediatric Nephrology at Zagazig University Hospital including 45 anemic children (19 ACD, 13 IDA and 13 mixed). The duration of the study ranges from 6 to 12 months, Soluble serum transferrin receptor and Soluble serum transferrin receptor index were measured. Results: There was significant difference regard sTfR and sTfR index IDA group were significantly higher than other two groups then mixed and finally ACD were significantly lower. Conclusion: sTfR value was useful tool for assessment of iron status in patients with CKD, however, they are at best complementary to the existing indices of serum ferritin and TSAT. [ABSTRACT FROM AUTHOR]

Aims: Anemia is the most common extraintestinal complication of inflammatory bowel disease (IBD), with approximately half of cases caused by iron deficiency (ID). Intravenous iron is the preferred ID anemia (IDA) treatment where oral iron is contraindicated, ineffective or not tolerated, or where ID correction is urgent. The objective was to evaluate the cost-utility of ferric derisomaltose (FDI) versus ferric carboxymaltose (FCM) in patients with IBD and IDA in England, in whom IV iron treatment is preferred. Materials and methods: A patient-level simulation model was developed, capturing quality of life (QoL) differences based on SF-36v2 data from the PHOSPHARE-IBD randomized controlled trial, monitoring and incidence of post-infusion hypophosphatemia, and number of iron infusions required. Analyses were conducted over a five-year time horizon from the Department of Health and Social Care (DHSC) perspective, with healthcare provider and societal perspectives adopted in separate analyses. Future costs and effects were discounted at 3.5% per annum and one-way and probabilistic sensitivity analyses were performed. Results: FDI increased quality-adjusted life expectancy by 0.075 QALYs versus FCM from 2.57 QALYs to 2.65 QALYs per patient. Patients receiving FDI required 1.63 fewer iron infusions over the five-year time horizon, driving infusion-related cost savings of GBP 496 per patient (GBP 2,188 versus GBP 1,692) from the DHSC perspective. Costs of monitoring and treating hypophosphatemia after FCM were GBP 226, yielding total savings of GBP 722 per patient (GBP 2,414 versus GBP 1,692) over the five-year time horizon. FDI also led to reduced costs versus FCM in the societal and provider analyses and was therefore the dominant intervention across all three perspectives. Limitations: The analysis did not capture patient adherence, hypophosphatemic osteomalacia, or fractures. Conclusions: Results showed that FDI improved patient QoL and reduced direct healthcare expenditure versus FCM in patients with IBD and IDA in England. PLAIN LANGUAGE SUMMARY: Ferric derisomaltose (FDI) is an intravenous iron approved for the treatment of clinically diagnosed iron deficiency in the United Kingdom (UK), and can be an important therapeutic option for patients with inflammatory bowel disease (IBD), who require regular and rapid iron replenishment. Ferric carboxymaltose (FCM) is the sole alternative intravenous iron formulation available in the UK, but is associated with reduced blood phosphate levels, potentially causing fatigue and weakening of the bones. We conducted an economic analysis to weigh the costs and clinical outcomes associated with FDI and FCM in the UK, for patients with IBD and iron deficiency anemia (IDA). The main clinical difference we investigated was reduced blood phosphate levels, which occurred more often after FCM than FDI. We also incorporated recent quality of life data from a clinical study, and calculated the number of infusions (and associated costs) of each iron formulation, that patients would require over five years. Clinical data were obtained from published medical literature, while cost data came from UK sources including the 2022/2023 National Tariff Payment System and the British National Formulary. Our model showed that FDI was associated with quality of life improvements, fewer overall infusions per treatment course, and reduced costs compared to FCM, from the English Department of Health and Social Care perspective, the societal perspective, and the perspective of individual healthcare providers (namely NHS Trusts) within NHS England. FDI is therefore likely to represent the best value intravenous iron for the treatment of IDA with IBD in the UK. [ABSTRACT FROM AUTHOR]

Copyright of Revista Foco (Interdisciplinary Studies Journal) is the property of Revista Foco and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: In hospitalized patients who are elderly and frequently have multiple comorbidities, anemia is very prevalent. The two types of anemia that are most common are iron deficiency anemia and chronic illness anemia. To assess the frequency and causes of different types of anemia in hospitalized patients using a diagnostic parameter. Materials and Methods: According to the inclusion and exclusion parameters, a total of 111 patients were enrolled. Information was gathered from the patient's medical documents after they were examined. Statistical analysis was done. Results: Anemia was most frequently seen in people between the ages of 31 and 45, with 22.03% of men and 40.38% of women, and a mean age of 37.24. years. Of these, 56.75% had anemia of mild severity. It was also found that patients with chronic kidney disease and iron deficiency are the most common causes of anemia, respectively. Anemia due to chronic disease was more prevalent (30.63%), followed by iron deficiency anemia in 27.92%. Malaise (48.64%) and pallor (36.03%) were the most prevalent symptoms and signs, respectively. Conclusion: In hospitalized patients, anemia played a significant role in deciding mortality, morbidity, and outcomes. Early detection, haemoglobin level restoration, and maintenance in these individuals may have a substantial impact on the clinical improvement of various pathological conditions. [ABSTRACT FROM AUTHOR]

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Iron is an essential element to the well functionning of the organism and requires careful maintenance of its homeostasis. This is mainly due to hepcidin, a hormone secreted by the liver that controls the flow of iron within the body. It has a hyposideremic action by reducing the expression of ferroportin, the only protein known to this day, which can export iron into the extracellular environment. This has the effect of decreasing intestinal absorption and increasing intracellular retention, especially in macrophages. Hepcidin is stimulated by elevation of iron and inflammation while activation of erythropoiesis inhibits it. Understanding its regulation allows a better understanding of the pathophysiological mechanisms of overload diseases and iron deficiency. Therefore, hepcidin analysis is interesting for the exploration of iron homeostasis. In combination with other biological parameters of iron status, it is possible to find better instructions for therapeutic managements of iron metabolism diseases. Thus, an assaying method by coupling liquid chromatography and tandem mass spectrometry has been implemented at Grenoble University Hospital and the analytical performances of this assay met the laboratory requirements in terms of reliability of the analysis. [ABSTRACT FROM AUTHOR]

Background: The prevalence of chronic kidney disease (CKD) has increased in the Indian population during the past three decades. Anaemia is a serious problem in chronic kidney disease due to iron deficiency and low erythropoietin levels. Low haemoglobin levels impact patients' quality of life and raise their risk of cardiovascular disease (CVD) and mortality. Much of the mortality and morbidity in patients with renal failure can be related to the secondary effects of chronic anaemia. Objective: to analyse the effects of normalizing haemoglobin levels with exogenous erythropoietin injection supplement on a patient with anaemia secondary to chronic kidney disease. Methods: 60 patients with chronic kidney disease and anaemiawere observed during this study. As per criteria and after approval from ethical committee study was conducted in our institute. Patients were given erythropoietin alfa on a periodic basis and observed with blood parameters on monthly basis to see the effects of normalization of haemoglobin. Results: Normocytic normochromic anaemia was the predominant type; Diabetes nephropathy was the most encountered form of renal disease followed by chronic glomerular disease and chronic interstitial disease. Improved haemoglobin levels did have statistical end result. Conclusions: Renal anaemia can be corrected with erythropoietin in a chronic kidney disease patient. Regular and consistent dose of exogenous erythropoietin does make significant change in patient's quality of life as well as improved organ vitality. Iron correction is a must along with erythropoietin to reap its entire benefit. [ABSTRACT FROM AUTHOR]

Aims: Iron deficiency is a common finding among patients with heart failure (HF) and is associated with adverse outcomes, including decreased quality of life, increased risk of hospitalization, and decreased survival. Intravenous ferric carboxymaltose (FCM) has been shown to improve outcomes among patients with HF and concomitant iron deficiency, but FCM is associated with an increased risk of hypophosphataemia. We aimed to better characterize this risk among HF populations. Methods and results: This pooled analysis examined data from 41 studies of adults with iron deficiency across disease states and therapeutic areas. Among the 7931 patients treated with FCM available for analysis, 14% made up the HF subgroup. Additional subgroups included women's health (36%), non–dialysis‐dependent chronic kidney disease (NDD‐CKD; 27%), haemodialysis‐dependent chronic kidney disease (HD‐CKD; 1%), gastrointestinal (10%), neurology (3%), and other (10%). The incidence of post‐baseline moderate or severe hypophosphataemia (i.e. serum phosphate [PO43−] level <2.0 mg/dL) varied across the therapeutic areas, with the lowest incidences observed in the HD‐CKD (0%), HF (8.1%), and NDD‐CKD (12.8%) subgroups. The prevalence of moderate or severe hypophosphataemia among the women's health, other, gastrointestinal, and neurology subgroups was 30.1%, 40.6%, 51.0%, and 55.6%, respectively. In the HF subgroup, one patient (<0.1%) had a serum PO43− of <1.0 mg/dL recorded, compared with 4.8% and 4.0% of the subjects in the neurology and gastrointestinal groups, respectively. With the exception of the HD‐CKD subgroup, mean serum PO43− levels decreased through weeks 2 to 4, and then returned toward baseline and plateaued by week 8. The strongest predictor of hypophosphataemia was preserved kidney function (estimated glomerular filtration rate: >60 mL/min/1.73 m2 vs. <30 mL/min/1.73 m2; odds ratio: 12.2). Among patients in the HF subgroup, the incidence of treatment‐emergent adverse events potentially related to hypophosphataemia (e.g. cardiac failure, ventricular tachyarrhythmias, fatigue, muscle weakness, bone pain, neurological symptoms, and muscle pain) was lower among FCM‐treated patients than among those receiving placebo, and lower among patients with a post‐baseline PO43− <2 mg/dL vs. those not meeting such criteria. Conclusions: The risk of laboratory‐assessed hypophosphataemia in HF patients treated with FCM was lower than that seen in patients in other therapeutic areas treated with FCM, and clinical events associated with hypophosphataemia are uncommon with FCM therapy in this population. Appropriate monitoring, particularly soon after administration in the unlikely event of repeated dosing in HF patients, will allow for further refinement of management strategies. [Correction added on 24 February 2023, after first online publication: In the preceding sentence, "...administration, will allow..." has been corrected to "...administration in the unlikely event of repeated dosing in HF patients, will allow..." in this version.] [ABSTRACT FROM AUTHOR]

Mammalian cells require iron to satisfy their metabolic needs and to accomplish specialized functions, such as hematopoiesis, mitochondrial biogenesis, energy metabolism, or oxygen transport. Iron homeostasis is balanced by the interplay of proteins responsible for iron import, storage, and export. A misbalance of iron homeostasis may cause either iron deficiencies or iron overload diseases. The clinical work-up of iron dysregulation is highly important, as severe symptoms and pathologies may arise. Treating iron overload or iron deficiency is important to avoid cellular damage and severe symptoms and improve patient outcomes. The impressive progress made in the past years in understanding mechanisms that maintain iron homeostasis has already changed clinical practice for treating iron-related diseases and is expected to improve patient management even further in the future. [ABSTRACT FROM AUTHOR]

Iron deficiency (ID) is the most common nutritional disorder worldwide. It is often observed in patients with chronic diseases, such as heart failure (HF), chronic kidney disease (CKD), inflammatory bowel disease (IBD) and cancer. ID is associated with poor clinical outcome, including poor performance, reduced quality of life, as well as increased hospitalization and mortality. The aim of this review is to provide an overview about the role of ID in chronic diseases (HF, CKD, IBD, cancer) regarding their current definitions and clinical relevance; diagnostic accuracy of iron parameters in chronic inflammatory conditions and its potential as prognostic markers. Due to different definitions and guideline recommendations of ID, various laboratory parameters for ID diagnostic exist and there is no general consensus about the definition of ID and its treatment. Still, a general trend can be observed across all investigated indications of this review (HF, CKD, IBD, cancer) that serum ferritin and transferrin saturation (TSAT) are the two parameters mentioned most often and emphasized in all guidelines to define ID and guide treatment. The most commonly used threshold values for the diagnosis of ID are TSAT of < 20% and serum ferritin of < 100–300 µg/L. Noteworthy, both TSAT and particularly ferritin are frequently applied, but both may vary due to inflammatory conditions. Studies showed that TSAT is less affected by inflammatory processes and may therefore be more accurate and reliable than serum ferritin, particularly in conditions with elevated inflammatory state. A low iron status and particularly a low TSAT value was associated with a poor outcome in all investigated indications, with the strongest evidence in HF patients. Routine surveillance of iron status in these groups of patients with chronic conditions is advisable to detect ID early. Depending on the inflammatory state, TSAT < 20% may be the more accurate diagnostic marker of ID than ferritin. Moreover, TSAT may also be the more reliable estimate for the prognosis, particularly in HF. [ABSTRACT FROM AUTHOR]

Iron deficiency (ID) is common in patients with cardiovascular disease. Up to 60% of patients with coronary artery disease, and an even higher proportion of those with heart failure (HF) or pulmonary hypertension have ID; the evidence for cerebrovascular disease, aortic stenosis and atrial fibrillation is less robust. The prevalence of ID increases with the severity of cardiac and renal dysfunction and is probably more common amongst women. Insufficient dietary iron, reduced iron absorption due to increases in hepcidin secondary to the low-grade inflammation associated with atherosclerosis and congestion or reduced gastric acidity, and increased blood loss due to anti-thrombotic therapy or gastro-intestinal or renal disease may all cause ID. For older people in the general population and patients with HF with reduced ejection fraction (HFrEF), both anaemia and ID are associated with a poor prognosis; each may confer independent risk. There is growing evidence that ID is an important therapeutic target for patients with HFrEF, even if they do not have anaemia. Whether this is also true for other HF phenotypes or patients with cardiovascular disease in general is currently unknown. Randomized trials showed that intravenous ferric carboxymaltose improved symptoms, health-related quality of life and exercise capacity and reduced hospitalizations for worsening HF in patients with HFrEF and mildly reduced ejection fraction (<50%). Since ID is easy to treat and is effective for patients with HFrEF, such patients should be investigated for possible ID. This recommendation may extend to other populations in the light of evidence from future trials. [ABSTRACT FROM AUTHOR]

Ferritin is an important iron storage protein, which is widely existed in all forms of life. Ferritin can regulate iron homeostasis when iron ions are lacking or enriched in the body, so as to avoid iron deficiency diseases and iron poisoning. Ferritin presents a hollow nanocage, which can store ions or other small molecular substances in the cavity. Therefore, ferritin shows its potential as a functional nanomaterial that can deliver nutrients or drugs in a targeted manner to improve bioavailability. Due to the special structure, the research on ferritin has attracted more and more attention in recent years. In this paper, the structural characteristics of ferritin were introduced, and the natural purification and prokaryotic expression methods of ferritin from different sources were described. At the same time, ferritin can bind to small molecules, so that it has the activity of small molecules, to construct a new type of ferritin. As a result, ferritin plays an important role as a nutrient substance, in targeted transport, and disease monitoring, etc. In conclusion, the yield of ferritin can be improved by means of molecular biology. Meanwhile, molecular modification can be used to make ferritin have unique activity and function, which lays a foundation for subsequent research. The molecular and structural properties of ferritins were clearly described. Isolation and purification technologies of ferritin were compared. Characterization, functions and molecular modifications mechanism of ferritin were reviewed. The applications of ferritin in pharmaceutical and food industry were prospected. [ABSTRACT FROM AUTHOR]

Protoporphyrins are organic compounds with cyclic structure that are synthesised by a wide variety of organisms. In humans, these compounds are detected in blood and urine, with significantly higher levels in blood. Their potential as biomarkers of anemia and other diseases is currently being investigated, as their levels change according to the biochemical processes associated with the disease. The most widely used biomarker of anemia is serum ferritin, but it is unreliable in patients with inflammatory bowel disease (IBD) because its levels can be altered by acute inflammation and/or infections. There is therefore a need to look for new markers to help diagnose anemia in IBD patients. This work develops and validates a method for the determination of three protoporphyrins in human urine: protoporphyrin IX (PPIX), protoporphyrin IX complex with Zn (ZnPPIX) and protoporphyrin IX complex with Fe (II) (FePPIX), the latter also known as heme. The aim is to evaluate their potential as biomarkers of anemic disease in patients diagnosed with IBD. The proposed analytical method is based on high performance liquid chromatography (HPLC) with dual detection based on photodiode array (PDA) and fluorescence (FD). Quantification of the analytes at very low concentrations is possible due to the efficient preconcentration provided by dispersive liquid-liquid microextraction (DLLME) and the sensitivity of the detection systems. The method was validated by evaluating linearity (25–1000 ng mL−1), matrix effect, sensitivity (limits of quantification were between 5 and 11 ng mL−1), selectivity, accuracy, carry-over, dilution integrity, stability and precision (< 12.1 %). Finally, statistical analyses applied to the sample quantification results showed these three markers, together with five clinical markers, were significantly different between anemic and non-anemic IBD patients. [Display omitted] • Heme, PPIX and ZnPPIX are determined in human urine by HPLC with dual detection. • DLLME with chloroform efficiently preconcentrates protoporphyrins. • Anemic and non-anemic IBD patients show different protoporphyrins urinary levels. • Protoporphyrins are promising biomarkers to diagnose anemia in IBD patients. [ABSTRACT FROM AUTHOR]

Ferropenic anemy is the leading iron deficiency disease in the world. The aim was to encapsulate erythrocytes extracted from the blood of Cavia porcellus, in matrices of tara gum and native potato starch. For microencapsulation, solutions were prepared with 20% erythrocytes; and encapsulants at 5, 10, and 20%. The mixtures were spray-dried at 120 and 140 °C. The iron content in the erythrocytes was 3.30 mg/g and between 2.32 and 2.05 mg/g for the encapsulates (p < 0.05). The yield of the treatments varied between 47.84 and 58.73%. The moisture, water activity, and bulk density were influenced by the temperature and proportion of encapsulants. The total organic carbon in the atomized samples was around 14%. The particles had diverse reddish tonalities, which were heterogeneous in their form and size; openings on their surface were also observed by SEM. The particle size was at the nanometer level, and the zeta potential (ζ) indicated a tendency to agglomerate and precipitation the solutions. The presence of iron was observed on the surface of the atomized by SEM-EDX, and FTIR confirmed the encapsulation due to the presence of the chemical groups OH, C-O, C-H, and N-H in the atomized. On the other hand, high percentages of iron release in vitro were obtained between 88.45 and 94.71%. The treatment with the lowest proportion of encapsulants performed at 140 °C obtained the best results and could potentially be used to fortify different functional foods. [ABSTRACT FROM AUTHOR]

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After all, comprehensive HF therapy involves more than the mortality-reducing "pillar" drugs and devices and should include "dotting the i's": optimizing symptoms and quality of life by treating comorbidities such as ID. Iron deficiency impacts diastolic function, aerobic exercise capacity, and patient phenotyping in heart failure with preserved ejection fraction: a subanalysis of the OptimEx-clin study. Effects of ferric carboxymaltose on hospitalisations and mortality rates in iron-deficient heart failure patients: an individual patient data meta-analysis. [Extracted from the article]

Objectives: This study aimed to estimate the serological prevalence of coeliac disease in patients with iron deficiency anaemia (IDA) of unknown cause at a primary healthcare facility in Oman. Methods: This prospective case-finding study was conducted at the primary care clinics in Sultan Qaboos University Hospital, Muscat, Oman from September 2018 to June 2020. Patients aged 18 to 55 years, with a haemoglobin (Hb) level <11.5 g/dL for males and <11.0 g/dL for females and a ferritin level <30 ng/mL for males and <13 ng/mL for females, were included in the study. Blood samples were obtained for initial serological screening using serum immunoglobulin (Ig)A level; those samples with normal levels of IgA, IgA anti-tissue transglutaminase antibody (tTG) and IgA anti-deamidated gliadin peptide (DGP) were determined. Positive IgA-tTG test was confirmed using IgA-endomysial antibodies. Patients with low IgA levels were tested using IgG-tTG and IgG-DGP. Results: A total of 104 patients participated in this study. Eight patients (7.7%) were found to have a positive serological screening result for coeliac disease; of these patients, three (37.5%) had a positive IgA-tTG result. Two of those three (66.7%) had a positive IgA-endomysial antibody. The IgA-DGP result was positive in seven (6.7%) of the 104 patients. Out of those seven patients, two also had a positive IgA tTG. Conclusion: Coeliac disease is not a rare disorder. There is a need to increase awareness among healthcare professionals about coeliac disease and its non-classical manifestations such as IDA. [ABSTRACT FROM AUTHOR]

Leukemia inhibitory factor (LIF), a member of the interleukin 6 family of cytokines, is involved in skeletal metabolism, blastocyst implantation, and stem cell pluripotency maintenance. However, the role of LIF in tooth development needs to be elucidated. The aim of the present study was to investigate the effect of Lif deficiency on tooth development and to elucidate the functions of Lif during tooth development and the underlying mechanisms. First, it was found that the incisors of Lif -knockout mice had a much whiter color than those of wild-type mice. Although there were no structural abnormalities or defective mineralization according to scanning electronic microscopy and computed tomography analysis, 3-dimensional images showed that the length of incisors was shorter in Lif −/− mice. Microhardness and acid resistance assays showed that the hardness and acid resistance of the enamel surface of Lif −/− mice were decreased compared to those of wild-type mice. In Lif −/− mice, whose general iron status was comparable to that of the control mice, the iron content of the incisors was significantly reduced, as confirmed by energy-dispersive X-ray spectroscopy (EDS) and Prussian blue staining. Histological staining showed that the cell length of maturation-stage ameloblasts was shorter in Lif −/− mice. Likewise, decreased expression of Tfrc and Slc40a1, both of which are crucial proteins for iron transportation, was observed in Lif −/− mice and Lif -knockdown ameloblast lineage cell lines, according to quantitative reverse transcription polymerase chain reaction, immunohistochemistry, and Western blot. Moreover, the upregulation of Tfrc and Slc40a1 induced by Lif stimulation was blocked by Stattic, a signal transducer and activator of transcription 3 (Stat3) signaling inhibitor. These results suggest that Lif deficiency inhibits iron transportation in the maturation-stage ameloblasts, and Lif modulates expression of Tfrc and Slc40a1 through the Stat3 signaling pathway during enamel development. [ABSTRACT FROM AUTHOR]