Red cell superoxide dismutase is increased in iron deficiency anemia

Red blood cells (RBC) from iron-deficient rats were found to generate more malonyldialdehyde after in vitro incubation with H2O2 than RBC from control rats (p less than 0.001). The iron-deficient RBC, however, had a higher content of superoxide dismutase (SOD) than control RBC (p less than 0.02). This finding suggests an increased formation of SOD compensatory to an increased oxidant stress.     

Severe thrombocytopenia in iron deficiency anemia

Mild-to-moderate thrombocytopenia has been reported as an occasional finding in patients with iron deficiency. The present case describes a multiparous woman who presented with increased menorrhagia, severe anemia (3.0 g/dl) and thrombocytopenia (9,000 platelets/mm3). Her bone marrow examination showed iron deficiency, megakaryocytopenia, and erythroid hypoplasia but no other evidence of a primary marrow disorder. Her symptoms, the thrombocytopenia and the megakaryocytopenia, resolved with iron replacement. This case demonstrates the profound degree to which thrombopoiesis can be affected in iron deficiency.     

Carbonyl iron therapy for iron deficiency anemia

To determine if elemental carbonyl iron powder is safe and effective therapy for iron deficiency anemia, 20 nonanemic and 32 anemic volunteers were studied. Single doses of 1,000 to 10,000 mg of carbonyl iron (15 to 150 times the 65 mg of iron in the usual dose of ferrous sulfate) were tolerated by nonanemic volunteers with no evidence of toxicity and only minor gastrointestinal side effects. Anemic volunteers (menstruating women who had previously donated blood) were treated with several regimens providing 1,000 to 3,000 mg of carbonyl iron daily in one to three doses for 8 to 28 days. After 12 weeks anemia was corrected in 29 of 32 patients, and serum ferritin was greater than 12 micrograms/L in 14. Hemoglobin regeneration proceeded at a rate similar to that described for therapy with oral iron salts and parenteral iron dextran. There was no evidence of hematologic, hepatic, or renal toxicity, but mild gastrointestinal side effects occurred in a majority of anemic volunteers. Carbonyl iron is an effective, inexpensive treatment for iron deficiency anemia, is accompanied by tolerable side effects and may have an advantage over therapy with iron salts by substantially reducing or eliminating the risk of iron poisoning in children.     

网织红细胞血红蛋白含量结合铁代谢参数在诊断成人缺铁性贫血中的临床价值

目的 探讨网织红细胞血红蛋白含量(Ret-He)结合铁代谢参数诊断成人缺铁性贫血(IDA)的临床价值。方法 选取该院血液科2018-11～2019-10收治的165例患者,检测各自红细胞参数[血红蛋白(Hb)、红细胞平均体积(MCV)、红细胞平均血红蛋白含量(MCH)]、网织红细胞参数(Ret-He)、铁代谢参数[血清铁(SI)、血清铁蛋白(SF)]及炎症标志物[C反应蛋白(CRP)]。根据Hb水平和骨髓铁染色结果将受试者分为缺铁性贫血组(IDA组) 53例、非缺铁性贫血组(NIDA组) 34例、缺铁非贫血组35例和对照组43例,比较各组间上述指标的差异,并考虑炎症的影响。绘制各血液分析指标单独诊断IDA和Ret-He+SI+SF结合诊断IDA的受试者工作特征(ROC)曲线,计算各自的灵敏度和特异度。结果 IDA组各参数水平明显低于NIDA组、缺铁非贫血组和对照组,差异均有统计学意义(P 0. 05); NIDA组SI、SF水平明显高于缺铁非贫血组和对照组,差异均有统计学意义(P 0. 05);缺铁非贫血组Ret-He、Hb、MCV、MCH、SI、SF水平明显低于对照组,差异均有统计学意义(P 0. 05)。炎症组与无炎症组患者血液SI、SF水平差异有统计学意义(P 0. 05),Ret-He、Hb、MCV、MCH水平差异无统计学意义(P 0. 05)。ROC曲线分析结果表明,Ret-He诊断IDA的cut-off值为28. 8 pg,灵敏度为91. 1%,特异度为90. 9%,曲线下面积(AUC)为0. 947(95%CI:0. 875～0. 984)。Ret-He+SI+SF结合诊断IDA的灵敏度为92. 7%,特异度为93. 5%,AUC为0. 959(95%CI:0. 900～0. 988)。结论 Ret-He结合SI、SF诊断IDA具有较高的临床价值,其综合诊断效能优于Ret-He、Hb、MCV、MCH、SI、SF等指标的单独诊断。     

Relationship between glycosylated hemoglobin and iron deficiency anemia: A common but overlooked problem

IntroductionBoth diabetes mellitus (DM) and iron deficiency anemia (IDA) are prevalent in every area of the world, and so, the possibility of these two diseases co-existing is also very high. It is our belief that clinical results of any correlation between iron status of the body and glycosylated haemoglobin (HbA1c) would be beneficial to many patients, therefore in this study, the effect of IDA on HbA1c was investigated.Materials – methodsA total of 146 patients with DM and IDA were evaluated prospectively. While the patients were administered 270 mg/day of ferrous sulphate (80 mg elemental iron) orally for three months for the treatment of IDA, no interventions were made for the treatment of DM. Patient levels of hemoglobin (Hb), hematocrit, red blood cells (RBC), mean corpuscular volume (MCV), platelet, white blood cells (WBC), serum iron, serum iron binding capacity (SIBC), ferritin, fasting plasma glucose (FPG), HbA1c, body mass index (BMI), C-reactive protein (CRP) values were measured at baseline and at the third month of treatment with iron, and were compared.ResultsThe median age of our patients was 45 (40–50) and median duration of diabetes was 3 years (1,75–5). While the baseline median Hb was 10.4 (mg/dL) (9.5–11.1), MCV was 74 (fL) (70.8–77), ferritin was 4 (ug/L) (3–6) at three months, Hb was measured at 12.6 (mg/dL) (12.1–13.2), MCV was measured at 82 (fL) (80–86), ferritin was measured at 15 (ug/L) (9–21.2) and was significantly higher compared to baseline values (p < 0.001). The baseline median HBA1c of patients was 7.09 ± 0.51 (%) and three month HBA1c was 6.69 ± 0.53 (%), which was significantly lower than when comparing baseline values with values at third month (p < 0.001). Baseline and three month values for FPG were 118 (mg/dL) (108–132) and 116 (mg/dL) (106–125) respectively, and there was no significant difference (p:0.07). A 2.2 mg/dL (1.5–3.5) increase in median Hb level accompanied a 0.4 % (0.2–0.6) decrease in median HbA1c levels (Spearman rho = ?0.362; p < 0.001).ConclusionOur study has shown conclusivly that IDA is related to increased HbA1c concentrations and HbA1c decreases significantly following treatment with iron. IDA should be considered before making any decisions regarding diagnosis or treatment according to HbA1c.     

Iron refractory iron deficiency anemia

Iron refractory iron deficiency anemia is a hereditary recessive anemia due to a defect in the TMPRSS6 gene encoding Matriptase-2. This protein is a transmembrane serine protease that plays an essential role in down-regulating hepcidin, the key regulator of iron homeostasis. Hallmarks of this disease are microcytic hypochromic anemia, low transferrin saturation and normal/high serum hepcidin values. The anemia appears in the post-natal period, although in some cases it is only diagnosed in adulthood. The disease is refractory to oral iron treatment but shows a slow response to intravenous iron injections and partial correction of the anemia. To date, 40 different Matriptase-2 mutations have been reported, affecting all the functional domains of the large ectodomain of the protein. In vitro experiments on transfected cells suggest that Matriptase-2 cleaves Hemojuvelin, a major regulator of hepcidin expression and that this function is altered in this genetic form of anemia. In contrast to the low/undetectable hepcidin levels observed in acquired iron deficiency, in patients with Matriptase-2 deficiency, serum hepcidin is inappropriately high for the low iron status and accounts for the absent/delayed response to oral iron treatment. A challenge for the clinicians and pediatricians is the recognition of the disorder among iron deficiency and other microcytic anemias commonly found in pediatric patients. The current treatment of iron refractory iron deficiency anemia is based on parenteral iron administration; in the future, manipulation of the hepcidin pathway with the aim of suppressing it might become an alternative therapeutic approach.     

Frequency of hypoferritinemia, iron deficiency and iron deficiency anemia in outpatients

The prevalence rates of hypoferritinemia (IDec/one abnormal indicator), iron deficiency (IDef/two abnormal indicators) and iron deficiency anemia (IDA) in children who were referred to the outpatient clinics of the Department of Pediatrics for the first time within 1 month were investigated. Exclusion criteria were iron therapy before and during the study period and a history of chronic illness. Acute-phase reactants, such as erythrocyte sedimentation rate and C-reactive protein levels, were measured in all cases indicative of infectious diseases. Blood samples were obtained from each study patient admitted to the outpatient clinics during the study period. The hospital charts were later further evaluated, and samples of patients with any current illness known to interact with the iron status of the patient were discarded, and patients were contacted to supply new samples about 1 month after treatment of the infection. Thus, in patients with indications of an infection, samples obtained 1 month after treatment were assessed.The children (n = 557) were divided into four age groups: those aged 4 months to 2 years (group I), 2-6 years (group II), 7-12 years (group III) and 12-18 years (group IV). Children with a decrease in serum ferritin levels without anemia (IDec), and those with lower ferritin, transferrin saturation (TS) and serum iron (SI) concentration (IDef) were evaluated. IDA was diagnosed if hemoglobin (Hb) concentrations were lower than those adjusted for age, ferritin <12 ng/ml and TS 相似文献   

Effect of iron deficiency anemia on the levels of hemoglobin A1c in nondiabetic patients

The major form of glycohemoglobin is hemoglobin A1c (HbA1c). The HbA1c fraction is abnormally elevated in chronic hyperglycemic diabetic patients and correlates positively with glycemic control. Previous studies suggest that iron deficiency anemia (IDA) affects the levels of HbA1c. The aim of this study was to determine the effect of IDA on HbA1c levels in nondiabetic patients. The population studied consisted of 50 patients (30 women, 20 men, mean age 35.7 +/- 11.9 years) with IDA and 50 healthy subjects that were matched for age and sex. Patients who had glucose tolerance abnormalities (impaired glucose tolerance or diabetes mellitus), hemoglobinopathies, hemolytic anemia, chronic alcohol ingestion and chronic renal failure were excluded from the study. Hematologic investigations, fasting and postprandial glucose and HbA1c levels were measured in all subjects before iron therapy. All patients with IDA were treated with iron 100 mg/day for 3 months. We repeated the laboratory investigation after iron therapy. Before iron treatment, the mean HbA1c (7.4 +/- 0.8%) level in patients with IDA was higher than in a healthy group (5.9% +/- 0.5) (p < 0.001). In patients with IDA, HbA1c decreased significantly after iron treatment from a mean of 7.4% +/- 0.8 to 6.2% +/- 0.6 (p < 0.001). Iron deficiency must be corrected before any diagnostic or therapeutic decision is made based on HbA1c.     

Deformability of erythrocytes in iron deficiency anemia

Summary The rheological properties of erythrocytes of 14 patients with iron deficiency anemia were studied by filtration of cells through polycarbonate filters with a nominal pore diameter of 5 m and by viscosity measurements of erythrocyte suspensions with a hematocrit of 80%. Erythrocytes of the patients passed through the filter pores more slowly than the cells from controls. The diminished deformability of the erythrocytes of the patients was solely due to an unfavorable ratio of cell surface area to microcytic cell volume. The viscosity of the ghost suspensions of the patients showed a normal flexibility. The hemoglobin content of the isolated ghosts was diminished, indicating an in-increased hemoglobin fluidity in the interior of the intact cells. The viscosity of erythrocytes of the patients was slightly increased at low shear rates but was normal at intermediate and high shear rates. We suggest that the decreased erythrocyte flexibility of microcytosis at low shear rates is no longer present at higher shear rates because of an increased fluidity of the intracellular hemoglobin. We discuss whether or not this mechanism also operates in vivo. The in vitro diminished deformability of erythrocytes explains the shortened survival of the patients' erythrocytes in vivo.This work was supported by the Deutsche Forschungsgemeinschaft