Cytomorphometric analysis of buccal mucosal cells in iron deficiency anemia: A cross-sectional study.

Background: Worldwide, at any given moment, more individuals have iron deficiency anemia (IDA) than any other health problems. Very few studies have been conducted to evaluate changes in oral mucosa in IDA. The present study is undertaken for cytomorphometric analysis of buccal mucosal cells in IDA. Nuclear diameter (ND), cell diameter (CD), nuclear area (NA), cell area (CA), and nuclear-cytoplasmic ratio (N/C) are measured and compared in buccal mucosal cells of IDA patients and controls. Aims: To evaluate cytomorphometric changes in epithelial cells of oral mucosa in IDA and to compare these changes with the controls. Settings and Design: A cross-sectional study. Methods and Materials: Forty cases of IDA and forty cases of control group were selected for the study. IDA cases were diagnosed with decreased Hb level, MCV, MCH, MCHC and confirmed by decreased serum iron and increased total iron-binding capacity levels. Cytomorphometric analysis of buccal mucosa was performed to study CA, CD, NA, ND, and N/C ratio. Statistical Analysis Used: Statistical analysis was done using t- test in SPSS software version 4. Result: Results of our study showed increased cell area, cell diameter, nuclear area, nuclear diameter, and nuclear-cytoplasmic ratio in anemic group as compared to controls. Conclusion: The study suggests that individuals with IDA regardless of clinically visible oral lesions show cytological changes in oral mucosal epithelium. Knowledge of quantitative alterations in oral epithelial cells of IDA patients is important as these alterations are similar to those seen in precancerous and radiation-induced changes. Cytomorphometry is an efficient tool to understand the extent of cellular changes that occur in oral epithelial cells in IDA.

Influence of Helicobacter Pylori Infection on Hepcidin Expression in the Gastric Mucosa.

BACKGROUND: Hepcidin is an antimicrobial peptide and a key hormone involved in iron homeostasis. Hepcidin level is elevated in the serum during the course of Helicobacter pylori infection and hepcidin is considered to contribute to iron deficiency anemia. However, it is unclear whether H. pylori infection influences hepcidin expression in the gastric mucosa. METHOD: In this study, 15 patients with H. pylori-infected nodular gastritis, 43 patients with H. pylori-infected chronic gastritis, and 33 patients without H. pylori infection were enrolled. Endoscopic biopsy, and histological and immunohistochemical analysis were performed to evaluate the expression of hepcidin and its distribution in the gastric mucosa. RESULT: Hepcidin was strongly expressed in the lymph follicles of patients with nodular gastritis. The detection rates of gastric hepcidin-positive lymphocytes in patients with nodular gastritis and chronic gastritis were significantly higher than that without H. pylori infection. Moreover, regardless of the H. pylori infection status, hepcidin was expressed in the cytoplasm and intracellular canaliculi of gastric parietal cells. CONCLUSION: Hepcidin is expressed at a steady state in gastric parietal cells, and H. pylori infection may induce hepcidin expression in lymphocytes present in the gastric mucosal lymphoid follicles. This phenomenon may be associated with systemic hepcidin overexpression and iron deficiency anemia in patients with H. pylori-infected nodular gastritis.

Effects of chronic Helicobacter pylori strain PMSS1 infection on whole brain and gastric iron homeostasis in male INS-GAS mice.

Iron deficiency, the most common micronutrient deficiency in humans, is associated with long-term deficits in cognition and memory if left untreated. Infection with the gastric pathogen Helicobacter pylori has been linked to iron deficiency anemia (IDA). The H. pylori virulence factor cytotoxin-associated gene A (cagA) is proposed to be especially pertinent in iron deficiency. Male INS-GAS/FVB mice were infected with the CagA+ strain pre-murine Sydney strain 1 (PMSS1) for 12-13 or 27-29 weeks to investigate the role of chronic H. pylori infection in iron deficiency and neurological sequelae. Mice at both timepoints demonstrated significantly elevated gastric histopathology scores and inflammatory cytokines compared to sham-dosed controls. However, only mice at 27-29 weeks post infection had changes in hematological parameters, with significantly decreased erythrocyte count, hematocrit, serum hemoglobin, and increased serum total iron binding capacity. Gastric transcription of iron-regulatory genes Hamp and Bmp4 were significantly downregulated at both timepoints. In the brain, iron-dependent myelingergic and synaptic markers were significantly downregulated at 27-29 weeks. These results indicated that long-term infection of the CagA + PMSS1 strain of H. pylori in this study caused anemia, altered gastric iron homeostasis, and neurological changes similar to those reported in other rodent H. pylori CagA- strain infection models.

[Research progress on the regulation mechanisms of iron metabolism in anemia of chronic disease].

Anemia of chronic disease (ACD), complicated by various chronic inflammatory diseases, is the second most prevalent type of anemia after iron deficiency anemia in the world. ACD significantly reduces the life quality of patients with chronic diseases, and represents an independent poor prognostic factor in certain chronic diseases. A large body of studies has demonstrated that most of anemia is related to abnormal iron metabolism. In the past decade, hepcidin, as a key factor in regulating iron metabolism, has attracted enormous attention due to its important role in the pathogenesis of ACD. This article reviews the research progress on the role and underlying regulatory mechanisms of hepcidin in ACD. We also discuss the potential of hepcidin as an effective therapeutic target for ACD treatment, in order to provide a new maneuver for improving the quality of ACD patients' life.

[Clinical management of autoimmune gastritis]. / Autoimmungastritis.

Autoimmune gastritis (AIG) is a chronic immune-mediated inflammation of the gastric corpus/fundus mucosa leading to progressive atrophy of the oxyntic gastric glands (AOM) and their consecutive loss of function. Possible clinical consequences of AIG include iron deficiency anemia, pernicious anemia, gastric neuroendocrine tumors (gNET), and gastric adenocarcinoma. This article provides a review of interdisciplinary aspects of the diagnosis and treatment of AIG.

Iron from nanostructured ferric phosphate: absorption and biodistribution in mice and bioavailability in iron deficient anemic women.

Food fortification with iron nanoparticles (NPs) could help prevent iron deficiency anemia, but the absorption pathway and biodistribution of iron-NPs and their bioavailability in humans is unclear. Dietary non-heme iron is physiologically absorbed via the divalent metal transporter-1 (DMT1) pathway. Using radio- iron isotope labelling in mice with a partial knockdown of intestine-specific DMT1, we assessed oral absorption and tissue biodistribution of nanostructured ferric phosphate (FePO4-NP; specific surface area [SSA] 98 m2g-1) compared to to ferrous sulfate (FeSO4), the reference compound. We show that absorption of iron from FePO4-NP appears to be largely DMT1 dependent and that its biodistribution after absorption is similar to that from FeSO4, without abnormal deposition of iron in the reticuloendothelial system. Furthermore, we demonstrate high bioavailability from iron NPs in iron deficient anemic women in a randomized, cross-over study using stable-isotope labelling: absorption and subsequent erythrocyte iron utilization from two 57Fe-labeled FePO4-NP with SSAs of 98 m2g-1 and 188 m2g-1 was 2.8-fold and 5.4-fold higher than from bulk FePO4 with an SSA of 25 m2g-1 (P < 0.001) when added to a rice and vegetable meal consumed by iron deficient anemic women. The FePO4-NP 188 m2g-1 achieved 72% relative bioavailability compared to FeSO4. These data suggest FePO4-NPs may be useful for nutritional applications.

Interrelations between Iron and Vitamin A-Studied Using Systems Approach.

A deficiency of vitamin A (VAD) and iron is the most common nutritional problem affecting people worldwide. Given the scale of the problem, the interactions between vitamin A and iron levels are widely studied. However, the exact mechanism of the impact of vitamin A on the regulation of iron metabolism remains unclear. An extremely significant issue becomes a better understanding of the nature of the studied biological phenomenon, which is possible by using a systems approach through developing and analyzing a mathematical model based on a Petri net. To study the considered system, the t-cluster analysis, the significance analysis, and the analysis of the average number of transition firings were performed. The used analyses have allowed distinguishing the most important mechanisms (both subprocesses and elementary processes) positively and negatively regulating an expression of hepcidin and allowed to distinguish elementary processes with a higher frequency of occurrence compared to others. The analysis also allowed to resolve doubts about the discrepancy in literature reports, where VAD leads to positive regulation of hepcidin expression or to negative regulation of hepcidin expression. The more detailed analyses have shown that VAD more frequently positively stimulates hepcidin expression and this mechanism is more significant than the mechanism inhibiting hepcidin expression indirectly by VAD.

Hypoxia-Inducible Factor Stabilizers in End Stage Kidney Disease: "Can the Promise Be Kept?"

Anemia is a common complication of chronic kidney disease (CKD). The prevalence of anemia in CKD strongly increases as the estimated Glomerular Filtration Rate (eGFR) decreases. The pathophysiology of anemia in CKD is complex. The main causes are erythropoietin (EPO) deficiency and functional iron deficiency (FID). The administration of injectable preparations of recombinant erythropoiesis-stimulating agents (ESAs), especially epoetin and darbepoetin, coupled with oral or intravenous(iv) iron supplementation, is the current treatment for anemia in CKD for both dialysis and non-dialysis patients. This approach reduces patients' dependence on transfusion, ensuring the achievement of optimal hemoglobin target levels. However, there is still no evidence that treating anemia with ESAs can significantly reduce the risk of cardiovascular events. Meanwhile, iv iron supplementation causes an increased risk of allergic reactions, gastrointestinal side effects, infection, and cardiovascular events. Currently, there are no studies defining the best strategy for using ESAs to minimize possible risks. One class of agents under evaluation, known as prolyl hydroxylase inhibitors (PHIs), acts to stabilize hypoxia-inducible factor (HIF) by inhibiting prolyl hydroxylase (PH) enzymes. Several randomized controlled trials showed that HIF-PHIs are almost comparable to ESAs. In the era of personalized medicine, it is possible to envisage and investigate specific contexts of the application of HIF stabilizers based on the individual risk profile and mechanism of action.

The misogyny of iron deficiency.

Anaemia is common, particularly in women and the commonest underlying cause, iron deficiency, is often overlooked. Anaemia is associated with increased morbidity and mortality in patients undergoing anaesthesia; however, women are defined as being anaemic at a lower haemoglobin level than men. In this narrative review, we present the history of iron deficiency anaemia and how women's health has often been overlooked. Iron deficiency was first described as 'chlorosis' and a cause of 'hysteria' in women and initial treatment was by iron filings in cold wine. We present data of population screening demonstrating how common iron deficiency is, affecting 12-18% of apparently 'fit and healthy' women, with the most common cause being heavy menstrual bleeding; both conditions being often unrecognised. We describe a range of symptoms reported by women, that vary from fatigue to brain fog, hair loss and eating ice. We also describe experiments exploring the physical impact of iron deficiency, showing that reduced exercise performance is related to iron deficiency independent of haemoglobin concentration, as well as the impact of iron supplementation in women improving oxygen consumption and fitness. Overall, we demonstrate the need to single out women and investigate iron deficiency rather than accept the dogma of normality and differential treatment; this is to say, the need to change the current standard of care for women undergoing anaesthesia.

The effect of iron deficiency and anaemia on women's health.

Iron deficiency and anaemia are global health problems and major causes of morbidity in women. Current definitions of anaemia in women are historic and have been challenged by recent data from observational studies. Menstrual loss, abnormal uterine bleeding and pregnancy put women at risk of developing iron deficiency which can result in severe fatigue, reduced exercise capacity and poor work performance. Iron deficiency and anaemia during pregnancy are associated with adverse maternal and fetal outcomes, including neurocognitive deficits in children born to iron-deficient mothers. Both iron deficiency and anaemia are common in women undergoing surgery but their association with poor outcomes remains uncertain. The enduring burden of iron deficiency and anaemia in women suggests that current strategies for recognition, prevention and treatment are limited in their utility. Improvements in our understanding of iron homeostasis and the development of new iron preparations, which are better absorbed with fewer side-effects, may improve therapeutic effectiveness of oral iron. Intravenous iron is efficacious for correcting anaemia rapidly but high-quality data on patient-centred outcomes and cost-effectiveness are currently lacking. Many recommendations for the treatment of iron deficiency and anaemia in national guidelines are not supported by high-quality evidence. There is a need for robust epidemiological data and well-designed clinical trials. The latter will require collaborative working between researchers and patients to design studies in ways that incorporate patients' perspectives on the research process and target outcomes that matter to them.

Association of Myeloperoxidase Gene Polymorphism With Iron Deficiency Anemia in Turkish Children.

This study was performed to investigate the gene polymorphisms of the myeloperoxidase (MPO) enzyme and to determine whether MPO gene polymorphisms influence the response to iron therapy in pediatric patients with iron deficiency anemia (IDA). In this case-control study, 50 Turkish children with IDA and 50 healthy controls were enrolled. Three MPO gene alleles were selected for genotyping in the study: GG, AG, and AA. The relationships of alleles with IDA were analyzed and compared in patients and controls. Pretreatment and posttreatment laboratory parameters and gene polymorphisms were compared in the patient group. There was a significant difference between patients with IDA and controls regarding genotype frequencies of the AA, GG, and AG alleles (P=0.005). However, the AG allele was found to be associated with variations in hemoglobin, red blood cell, hematocrit, mean corpuscular volumes, and mean corpuscular Hb concentrations levels. The frequency of AA, GG, and AG alleles of the MPO gene was potentially associated with changes in iron metabolism and the AG allele led to variations in various hemogram parameters.

Evaluation of angiogenic signaling molecules associated with reactive thrombocytosis in an iron-deficient rat model.

BACKGROUND: Iron deficiency anemia (IDA)-induced reactive thrombocytosis can occur in children and adults. The underlying mechanism for this phenomenon is indeterminate. Traditional cytokines such as thrombopoietin (TPO), interleukin-6 (IL-6), and IL-11 involved in megakaryopoiesis have not been shown to be the cause. Recent studies suggest that growth factors and signaling molecules involved with angiogenesis influence the proliferation and differentiation of megakaryocytes. METHODS: We investigated the possible association between angiogenic cytokines with reactive thrombocytosis due to IDA in an iron-deficient (ID) rat model. Complete blood count, iron panels, and TPO levels were measured at baseline and 5 weeks later in both control (C) and ID rats. Angiogenic cytokines were evaluated in the bone marrow in all rats. RESULTS: We successfully induced IDA in our rats by phlebotomy and reduced iron diet. We did not find an increase of TPO in ID rats. A review of the bone marrow showed an increase in the number of megakaryocytes, vascular structures, as well as increased intensity of stain for vascular endothelial growth factor (VEGF), and CXC chemokine receptor 4 (CXCR4) in rats with IDA compared to controls. CONCLUSIONS: Our results of histological bone marrow data suggest an important role for angiogenesis in the development of IDA-induced thrombocytosis. IMPACT: Thrombocytosis is common with IDA in both children and adults, but the mechanism is unclear. We confirmed that TPO is not the major driver of iron deficiency-associated thrombocytosis. We confirmed the increase in the number of megakaryocytes in the bone marrow despite stable TPO levels. We provided evidence supporting an important role of angiogenesis in megakaryocytopoiesis/thrombopoiesis with increased vascular structures and angiogenic cytokines in the bone marrow of iron-deficient rats. The demonstration that angiogenesis may play an important role in secondary thrombocytosis could lead to a new approach in treating symptomatic reactive thrombocytosis by targeting angiogenesis.

Physiological and pathophysiological mechanisms of hepcidin regulation: clinical implications for iron disorders.

The discovery of hepcidin has provided a solid foundation for understanding the mechanisms of systemic iron homeostasis and the aetiologies of iron disorders. Hepcidin assures the balance of circulating and stored iron levels for multiple physiological processes including oxygen transport and erythropoiesis, while limiting the toxicity of excess iron. The liver is the major site where regulatory signals from iron, erythropoietic drive and inflammation are integrated to control hepcidin production. Pathologically, hepcidin dysregulation by genetic inactivation, ineffective erythropoiesis, or inflammation leads to diseases of iron deficiency or overload such as iron-refractory iron-deficiency anaemia, anaemia of inflammation, iron-loading anaemias and hereditary haemochromatosis. In the present review, we discuss recent insights into the molecular mechanisms governing hepcidin regulation, how these pathways are disrupted in iron disorders, and how this knowledge is being used to develop novel diagnostic and therapeutic strategies.

Prevalence, correlates and outcomes of absolute and functional iron deficiency anemia in nondialysis-dependent chronic kidney disease.

BACKGROUND: Anemia is associated with adverse outcomes in those with chronic kidney disease (CKD). We examined the association of absolute and functional iron deficiency anemia (IDA) with adverse outcomes (cardiovascular hospitalization, dialysis and mortality) in those with nondialysis-dependent CKD. METHODS: Nondialysis-dependent CKD patients followed in the US Veterans Administration with hemoglobin level measured within 90 days of the date of the second estimated glomerular filtration rate <60 mL/min/1.73 m2 were included. Logistic regression, multivariate Cox proportional hazards and Poisson regression models adjusted for demographics and comorbidities were used to assess the prevalence and correlates of absolute [transferrin saturation (TSAT) ≤20%, ferritin <100 ng/mL] and functional (TSA T≤20%, ferritin >100-500 ng/mL) IDA and the associations of absolute and functional IDA with mortality, dialysis and cardiovascular hospitalization. RESULTS: Of 933 463 patients with CKD, 20.6% had anemia. Among those with anemia, 23.6% of patients had both TSAT and ferritin level measured, of whom 30% had absolute IDA and 19% had functional IDA. Absolute IDA in CKD was not associated with an increased risk of mortality or dialysis but was associated with a higher risk of 1-year {risk ratio [RR] 1.20 [95% confidence interval (CI) 1.12-1.28]} and 2-year cardiovascular hospitalization [RR 1.11 (95% CI 1.05-1.17)]. CKD patients with functional IDA had a higher risk of mortality [hazard ratio (HR) 1.11 (95% CI 1.07-1.14)] along with a higher risk of 1-year [RR 1.21 (95% CI 1.1-1.30)] and 2-year cardiovascular hospitalization [RR 1.13 (95% CI 1.07-1.21)]. Ferritin >500 ng/mL (treated as a separate category) was only associated with an increased risk of mortality [HR 1.38 (95% CI 1.26-1.51)]. CONCLUSIONS: In a large population of CKD patients with anemia, absolute and functional IDA were associated with various clinical covariates. Functional IDA was associated with an increased risk of mortality and cardiovascular hospitalization, but absolute IDA was associated only with a higher risk of hospitalization.

Safety and efficacy of iron isomaltoside 1000/ferric derisomaltose versus iron sucrose in patients with chronic kidney disease: the FERWON-NEPHRO randomized, open-label, comparative trial.

BACKGROUND: The optimal intravenous (IV) iron would allow safe correction of iron deficiency at a single infusion over a short time. The FERWON-NEPHRO trial evaluated the safety and efficacy of iron isomaltoside 1000/ferric derisomaltose (IIM) in patients with non-dialysis-dependent chronic kidney disease and iron deficiency anaemia. METHODS: In this randomized, open-label and multi-centre trial conducted in the USA, patients were randomized 2:1 to a single dose of 1000 mg IIM or iron sucrose (IS) administered as 200 mg IV injections up to five times within a 2-week period. The co-primary endpoints were serious or severe hypersensitivity reactions and change in haemoglobin (Hb) from baseline to Week 8. Secondary endpoints included incidence of composite cardiovascular adverse events (AEs). RESULTS: A total of 1538 patients were enrolled (mean estimated glomerular filtration rate 35.5 mL/min/1.73 m2). The co-primary safety objective was met based on no significant difference in the incidence of serious or severe hypersensitivity reactions in the IIM and IS groups [0.3% versus 0%; risk difference: 0.29% (95% confidence interval: -0.19; 0.77; P > 0.05)]. Incidence of composite cardiovascular AEs was significantly lower in the IIM versus IS group (4.1% versus 6.9%; P = 0.025). Compared with IS, IIM led to a more pronounced increase in Hb during the first 4 weeks (P ≤ 0.021), and change in Hb to Week 8 showed non-inferiority, confirming that the co-primary efficacy objective was met. CONCLUSIONS: Compared with multiple doses of IS, a single dose of IIM induced a non-inferior 8-week haematological response, comparably low rates of hypersensitivity reactions, and a significantly lower incidence of composite cardiovascular AEs.

Anaemia in cardiac surgery - a retrospective review of a centre's experience with a pre-operative intravenous iron clinic.

Pre-operative anaemia is associated with higher rates of transfusion and worse outcomes, including prolonged hospital stay, morbidity and mortality. Iron deficiency is associated with significantly lower haemoglobin levels throughout the peri-operative period and more frequent blood transfusion. Correction of iron stores before surgery forms part of the first pillar of patient blood management. We established a pre-operative anaemia clinic to aid identification and treatment of patients with iron deficiency anaemia scheduled for elective cardiac surgery. We present a retrospective observational review of our experience from January 2017 to December 2019. One-hundred and ninety patients received treatment with intravenous iron, a median of 21 days before cardiac surgery. Of these, 179 had a formal laboratory haemoglobin level measured before surgery, demonstrating a median rise in haemoglobin of 8.0 g.l-1 . Patients treated with i.v. iron demonstrated a significantly higher incidence of transfusion (60%) compared with the non-anaemic cohort (22%) during the same time period, p < 0.001. Significantly higher rates of new requirement for renal replacement therapy (6.7% vs. 0.6%, p < 0.001) and of stroke (3.7% vs. 1.2%, p = 0.010) were also seen in this group compared with those without anaemia, although there was no significant difference in in-hospital mortality (1.6% vs. 0.8%, p = 0.230). In patients where the presenting haemoglobin was less than 130 g.l-1 , but there was no intervention or treatment, there was no difference in rates of transfusion or of complications compared with the anaemic group treated with iron. In patients with proven iron deficiency anaemia, supplementation with intravenous iron showed only a modest effect on haemoglobin and this group still had a significantly higher transfusion requirement than the non-anaemic cohort. Supplementation with intravenous iron did not improve outcomes compared with patients with anaemia who did not receive intravenous iron and did not reduce peri-operative risk to non-anaemic levels. Questions remain regarding identification of patients who will receive most benefit, the use of concomitant treatment with other agents, and the optimum time frames for treatment in order to produce benefit in the real-world setting.

Soluble Transferrin Receptor (sTfR) Identifies Iron Deficiency Anemia (IDA) in Pulmonary Tuberculosis Patients.

BACKGROUND: iron deficiency in pulmonary tuberculosis (TB) patients may weaken their immune system, causing difficulty in overcoming the infection. Accurate diagnosis of iron deficiency anemia (IDA) in pulmonary TB patients is essential. In order to prove the iron deficient state, diagnosis should focus on inflammatory factors, which could highly affect the outcome of iron status, such as measurement of serum ferritin (SF). Soluble Transferrin Receptor (sTfR) is the best parameter to diagnose iron deficiency in the inflammatory condition. This study aimed to understand the role of sTfR to identify IDA in TB patients. METHODS: cross-sectional study were applied to 3 study groups: anemic pulmonary TB (68 subjects), IDA (7 subjects), and non-anemic pulmonary TB (15 subjects). The test averages and correlations between sTfR, SF, and other hematological parameters were measured and analyzed. RESULTS: significant differences of sTfR were found in the anemic TB group compared to the IDA group and also between the IDA and non-anemic TB groups (p<0.0001). However, there was no significant difference (p>0.05) between TB anemic and non-anemic groups. We also found no significant difference between the TB anemic sub-group with normal levels of sTfR compared with the non-anemic group. There was no significant difference of sTfR levels between sub-group of increasing sTfR and group IDA (p>0.05). However, there was strong correlation between sTfR and SF in the IDA group (r=-0.89; p=0.007). CONCLUSION: the findings suggest verifying the sTfR amount in anemic patients with pulmonary TB suffering from inflammation, so that the iron deficiency could be more accurately identified and properly treated.

Anaemia in patients with type 2 diabetes mellitus without nephropathy is related to iron deficiency.

BACKGROUND AND AIMS: Iron deficiency anaemia, although well reported in diabetic nephropathy, has not been well studied in type 2 diabetes patients in the absence of nephropathy. We studied the prevalence of anaemia and iron deficiency in type 2 diabetes patients without nephropathy. MATERIAL AND METHODS: A total of 89 patients were selected for this study. 24 h urine protein less than 500 mg was used as the criteria to rule out diabetic nephropathy. Complete hemogram, iron profile and high sensitivity C reactive protein (hs CRP) levels were performed in each patient.Functional iron deficiency (FID) was defined as serum ferritin more than 100 µg/l with serum transferrin less than 20% and total iron deficiency state was defined as serum ferritin less than 100 µg/l. RESULTS: Fifteen patients (16.8%)had anaemia out of which 13 had total iron deficiency and one each had functional iron deficiency and normal iron status respectively. Assessment of the iron status overall showed that 49 patients had TID (55.05%), 16 had FID (17.9%)and 24 (27.05%) had normal iron status. The hs-CRP was significantly higher in those with iron deficiency. CONCLUSIONS: The present study found a high prevalence of iron deficiency anaemia in type 2 diabetic patients even in the absence of nephropathy. Most of the diabetic subjects also displayed an iron deficiency state the cause of which needs further investigation.

Intravenous ferric carboxymaltose for iron deficiency anemia or iron deficiency without anemia after poor response to oral iron treatment: Benefits and risks in a cohort of 144 children and adolescents.

OBJECTIVE: The objective of this single-center observational study was to determine the clinical and hematologic responses to intravenous ferric carboxymaltose (FCM) in a cohort of pediatric patients with poor response to oral iron therapy. The occurrence of adverse events was systematically recorded for up to 96 hours after infusion. STUDY DESIGN: A retrospective cohort of 144 consecutive patients aged 18 months to < 18 years with iron deficiency anemia (IDA) or iron deficiency (ID) without anemia was investigated. All patients had failed oral iron therapy. The assessments before and after FCM treatment followed a predefined protocol. RESULTS: One hundred of 117 (85 %) of patients with complete data achieved the target ferritin level ≥ 30 µg/L after a single FCM dose. Of 77 patients with IDA and complete data, 38 (49%) showed a complete hematological response within 6-12 weeks; a complete or partial response was achieved by 83%. Clinical symptoms improved in 85% of all patients. In 92% of patients (n = 133 /144), FCM infusion was uneventful. During the 96-hour follow-up, five patients reported potentially related symptoms. No serious adverse events occurred. CONCLUSION: The study confirms the safety and efficacy of FCM in children (aged 18 months and older) and adolescents unresponsive to oral therapy, in real-world experience. Single-dose FCM treatment was followed by clinical improvement with advantages of safety, compliance, and lower cost compared with previous generation parenteral iron preparations that had to be administered in fractionated sessions.

Factors influencing safety and efficacy of intravenous iron-carbohydrate nanomedicines: From production to clinical practice.

Iron deficiency is an important subclinical disease affecting over one billion people worldwide. A growing body of clinical records supports the use of intravenous iron-carbohydrate complexes for patients where iron replenishment is necessary and oral iron supplements are either ineffective or cannot be tolerated by the gastrointestinal tract. A critical characteristic of iron-carbohydrate drugs is the complexity of their core-shell structure, which has led to differences in the efficacy and safety of various iron formulations. This review describes parameters influencing the safety and effectiveness of iron-carbohydrate complexes during production, storage, handling, and clinical application. We summarized the physicochemical and biological assessments of commercially available iron carbohydrate nanomedicines to provide an overview of publicly available data. Further, we reviewed studies that described how subtle differences in the manufacturing process of iron-carbohydrate complexes can impact on the physicochemical, biological, and clinical outcomes of original product versus their intended copies or so-called iron "similar" products.