缺铁性贫血中肠道菌群作用的研究进展

缺铁性贫血是临床最常见的贫血类型之一,已知缺铁性贫血会导致机体免疫力下降,影响心血管系统,对儿童和青少年的智力发育造成损害。然而越来越多的学者发现缺铁还会引起肠道菌群结构发生改变,影响肠道菌群的代谢。短链脂肪酸作为肠道菌群代谢的主要产物,受铁的制约最大。短链脂肪酸对机体肠道健康起着至关重要的作用,因此缺铁是有害的。另外临床工作中发现益生菌联合铁剂治疗缺铁性贫血,疗效更显著；铁剂联合抗菌药物对细菌相关疾病的治疗效果大大提高,说明铁与肠道菌群关系密切。本文就缺铁性贫血与肠道菌群关系的研究进展作一综述。     

^59Fe在幼年和成年大鼠整体及器官中的滞留动态

缺铁性贫血是世界各国包括我国最常见的一种贫血。在儿童,其发病率很高,不容忽视。儿童易发生缺铁性贫血的原因,一般认为是由于婴幼儿生长发育快,对铁的需要量较多,而摄入量不足。除此之外,是否还有其他原因,     

MCH、MCV、RDW-CV、HbA_2和红细胞脆性试验在地中海贫血和缺铁性贫血鉴别诊断中的应用

目的:探讨平均红细胞血红蛋白量(MCH)、平均红细胞体积(MCV)、红细胞分布宽度变异系数(RDW-CV)、血红蛋白A_2(Hb A_2)和红细胞脆性试验在地中海贫血和缺铁性贫血鉴别中的价值。方法:以地中海贫血基因诊断和血清铁蛋白测定作为确诊地中海贫血和缺铁性贫血的分组依据,选择2012年1月1日至2014年12月31日广州军区总医院经分子生物学和血清铁蛋白检测的156例患者为研究对象,将其分为地中海贫血组115例(其中α地中海贫血77例,β地中海贫血37例,α地中海贫血复合β地中海贫血1例)和缺铁性贫血组41例;比较患者的MCH、MCV、RDW-CV、Hb A_2和红细胞脆性等血液学指标,采用ROC曲线评价鉴别地中海贫血和缺铁性贫血的血液学指标,试找出最适合鉴别这2种贫血的截断值(cut-off值),以截断值计算上述血液学指标鉴别这2种贫血的灵敏度、特异性、预测值与准确率。结果:地中海贫血患者与缺铁性贫血患者的MCH、MCV和红细胞脆性差异有统计学意义(P0.05),RDW-CV差异无统计学意义(P0.05)。MCH、MCV和红细胞脆性的ROC曲线下面积依次为0.641、0.654、0.778,其最佳截断值分别为23.65 pg、72.8 f L、43.5%;MCH、MCV和红细胞脆性试验在鉴别地中海贫血和缺铁性贫血中的灵敏度分别为89.84%、83.94%、80.42%。Hb A_2在α地中海贫血患者与缺铁性贫血患者间差异无统计学意义(P0.05);Hb A_2在β地中海贫血患者与缺铁性贫血患者间差异有统计学意义(P0.001),Hb A_2在ROC曲线下面积为0.925,最佳截断值为2.93%,鉴别β地中海贫血和缺铁性贫血的灵敏度为92.50%。结论:用MCH、MCV、Hb A_2、红细胞脆性试验最佳截断值对鉴别地中海贫血和缺铁性贫血有一定的价值;Hb A_2在鉴别α地中海贫血和缺铁性贫血中无意义;Hb A2鉴别β地中海贫血和缺铁性贫血的灵敏度高。     

基于儿童缺铁性贫血预防办法的研究

缺铁性贫血在临床上作在比较常见世界性一种儿童营养类疾病,影响了儿童的身心健康发展。如果儿童发生缺铁性贫血,常常会导致其身体发迟缓、智力变弱等,给患病儿童和家长带来了身心上的痛苦和经济负担。本文内容从儿童缺铁性贫血产生的原因来分析,同时结合儿童缺铁性贫血的现状,关于如何通过补充乳铁蛋白来预防儿童缺铁性贫血提出了相关措施与办法。     

跨膜丝氨酸蛋白酶6与贫血

跨膜丝氨酸蛋白酶6基因（transmembrane serine protease 6 gene,TMPRSS6）是一种主要在肝脏中表达,编码II型跨膜丝氨酸蛋白酶的基因,它的突变可导致严重贫血的发生。TMPRSS6突变后可造成铁调节激素肝杀菌肽在机体缺铁状态下也表达增加,这造成小肠对食物铁的吸收减少而出现缺铁性贫血。TMPRSS6突变与贫血关系的发现一方面有利于对铁代谢调节机制的深入理解,另一方面也为铁代谢紊乱相关疾病如贫血等的治疗带来了希望。     

纳米铁制剂仿制药的研发探讨

缺铁性贫血已经成为影响人类健康的重要疾病之一,补铁是临床上治疗铁缺乏症的主要手段。自1949年第一个纳米铁制剂——蔗糖铁注射液(Venofer~?)被用于治疗铁缺乏症上市以来,世界范围内已批准上市多个纳米铁制剂及其仿制药。纳米铁制剂一般由铁核和不同的碳水化合物外壳组成,铁核、不同的碳水化合物外壳及其相互作用共同决定了纳米铁的体内行为。由于纳米铁制剂属于一种非生物复杂药物(NBCD),活性成分的结构和特征不能被完全表征,其生产、储存和临床应用都可能影响其有效性和安全性,这对纳米铁制剂仿制药的研发、生产、质量控制及上市后的监管等都提出了巨大挑战。通过介绍纳米铁制剂的结构、理化性质、作用机制和临床应用情况,分析了从生产到临床使用过程中可能影响纳米铁制剂的安全性和有效性的潜在因素,以期为纳米铁制剂仿制药的研发提出建议。     

妊娠期营养干预对孕妇缺铁性贫血治疗效果评价及妊娠结局的影响

目的：探讨妊娠期个性化膳食营养干预对孕妇缺铁性贫血的治疗效果及其对妊娠结局的影响。方法：选取2018年1月—2020年1月来我院就诊的妊娠期缺铁性贫血孕妇180例，依据治疗原则并参照孕妇意愿随机分成个性化膳食营养干预组（57例）、铁剂治疗组（55例）、铁剂治疗联合个性化膳食营养干预组（68例）。另取同期间来我院产检的正常孕妇作为空白对照组（60例），分别给予相应的干预手段。8 w后检测孕妇血常规和铁代谢等相关指标，并统计分析妊娠结局。结果：干预前，个性化膳食营养干预组、铁剂治疗组、铁剂治疗联合个性化膳食营养干预组3组间血红蛋白（Hb）、红细胞数（RBC）、血细胞比容（Hct）、血清铁（SI）、血清铁蛋白（SF）、可溶性血清铁蛋白受体（sTfR）水平不存在显著差异（P>0.05），与空白对照组相比，存在显著差异（P<0.01）。干预后，3组血红蛋白（Hb）分别是（106.35±16.64）、（108.37±14.41）、（107.8±12.18）g/L，红细胞数（RBC）分别是（4.24±0.72）×1012/L、（4.31±0.66）×1012/L、（4.38±0.59）×1012/L，血细胞比容（Hct）分别是（0.41%±0.35%）、（0.42%±0.25%）、（0.43%±0.19%），血清铁蛋白（SF）分别是（57.83±10.41）、（58.33±11.03）、（59.28±12.18）μg/L，血清铁（SI）分别是（11.57±3.76）、（11.60±3.46）、（11.58±2.90）μmol/L，可溶性血清铁蛋白受体（sTfR）分别是（2.13±1.12）、（2.10±0.62）、（2.11±0.73）mg/L，与干预前相比存在显著差异（P<0.01）。治疗过程中不良反应的发生率，个性化膳食营养干预组为1.75%，铁剂治疗组为7.27%，铁剂治疗联合个性化膳食营养干预组为5.88%，各组间不良反应的发生率存在显著差异（P<0.05）。采用不同治疗方法，3组缺铁性贫血的治愈率分别为89.47%、94.55%、98.53%，3组间缺铁性贫血的治愈率存在显著差异（P<0.05）。不良妊娠结局的发生率，4组间妊娠期高血压疾病、早产和低体重出生儿发生率存在显著差异（P<0.05），妊娠期糖尿病、胎膜早破和产后出血发生率不存在显著差异（P>0.05）。结论：妊娠期单纯性营养干预对缺铁性贫血的治疗效果次于铁剂治疗效果，但不良反应的发生率较低，两种干预方法联合应用效果更佳，且有利于降低不良妊娠结局发生的风险。     

作物铁生物强化

铁是植物必需的微量元素。缺铁不仅影响植物的生长,更影响作物的营养品质。铁营养摄入不足是导致人体缺铁性贫血的主要原因。在膳食结构中,以谷物为主食,特别是发展中国家的人群,缺铁性贫血更为严重。因此,以提高作物食用部分铁含量为目标的"铁生物强化"意义重大。首先,介绍了植物铁吸收、转运和储存的分子机制;其次,总结了提高作物铁含量和生物有效性的方法 ;最后,对未来作物铁生物强化的研究方向提出了展望。     

提高铁的吸收,利用与防止缺铁性贫血

缺铁性贫血是常见的营养缺乏症之一。导致缺铁的原因,往往不是因为摄入的铁不足,而是因为对食物中铁的吸收,利用率不高,一航来说,植物性食物中铁的吸收率从１％－７％,动物性食物最高为２０％,平均约为１０％。本文介绍了缺铁性贫血的原因和症状,并着重介绍了提高铁吸收,利用的方法。     

高铁酵母的研究初报

铁是人体必需的微量元素之一。铁离子是红细胞中血红蛋白的组成成分,缺铁会引致缺铁性贫血。据世界卫生组织(WHO)报导,缺铁性贫血是遍及全球的营养缺乏症,特别是发展中国家更为严重。我国儿童缺铁性贫血患病率约占50％以上。如果用硫酸亚铁和乳酸亚铁等制剂作     

The influence of lactoferrin, orally administered, on systemic iron homeostasis in pregnant women suffering of iron deficiency and iron deficiency anaemia

Iron is a fundamental element for humans as it represents an essential component of many proteins and enzymes. However, this element can also be toxic when present in excess because of its ability to generate reactive oxygen species. This dual nature imposes a tight regulation of iron concentration in the body. In humans, systemic iron homeostasis is mainly regulated at the level of intestinal absorption and, until now, no regulated pathways for the excretion of iron have been found. The regulation and maintenance of systemic iron homeostasis is critical to human health. Excessive iron absorption leads to iron-overload in parenchyma, while low iron absorption leads to plasma iron deficiency, which manifests as hypoferremia (iron deficiency, ID) and ID anaemia (IDA). ID and IDA are still a major health problem in pregnant women. To cure ID and IDA, iron supplements are routinely prescribed. The preferred treatment of ID/IDA, consisting in oral administration of iron as ferrous sulphate, often fails to exert significant effects on hypoferremia and may also cause adverse effects. Lactoferrin (Lf), an iron-binding glycoprotein abundantly found in exocrine secretions of mammals, is emerging as an important regulator of systemic iron homeostasis. Recent data suggest that this natural compound, capable of interacting with the most important components of iron homeostasis, may represent a valuable alternative to iron supplements in the prevention and cure of pregnancy-associated ID and IDA. In this review, recent advances in the molecular circuits involved in the complex cellular and systemic iron homeostasis will be summarised. The role of Lf in curing ID and IDA in pregnancy and in the maintenance of iron homeostasis will also be discussed. Understanding these mechanisms will provide the rationale for the development of novel therapeutic alternatives to ferrous sulphate oral administration in the prevention and cure of ID and IDA.     

植物铁代谢及植物铁蛋白结构与功能研究进展

铁在生命过程中起着很重要的作用,植物缺铁后叶绿素合成受阻而导致的黄化症状已成为世界性植物营养失调问题。与之相随,人类铁营养的缺乏也极为严重,因此研究植物铁代谢并且开发安全、天然、高效的补铁因子具有重要的意义。到目前为止,在已经发现的植物中,只有豆科类植物是将其种子中～90％的铁储藏在铁蛋白中,所以来源于豆科类植物的铁蛋白是一个理想的补铁资源。与动物铁蛋白相比,植物铁蛋白具有两个显著的特点：首先,植物铁蛋白在其N端具有一个独特的EP肽段;其次,植物铁蛋白只含有H型亚基,且有两种不同的H型亚基组成。主要阐述有关植物铁代谢及铁蛋白的结构、功能的最新研究进展。     

Iron status and the female athlete

Iron deficiency (ID) is the most prevalent micronutrient deficiency disorder in the world. In the developed world, the greatest prevalence of ID and iron deficiency anemia (IDA) occurs in premenopausal women. Premenopausal women experience ID and IDA due to inadequate consumption of dietary iron coupled with iron losses through physiologic processes such as menstruation. Further, female athletes may experience an elevated risk of ID and IDA, as hepcidin, a peptide hormone that inhibits iron absorption and sequesters iron in the macrophage, may rise in response to physical activity. Declines in physical and cognitive performance have been demonstrated in female athletes with ID and IDA. Performance decrements are attenuated as iron status improves. This review will focus on iron status in female athletes, and will include a review of nutritional countermeasures to prevent ID and IDA.     

Plasma selenium status in children with iron deficiency anemia

Iron and selenium are trace elements necessary for the maintenance of life and health. Iron deficiency is the most common nutritional deficiency among children in the world. The purpose of this study was to evaluate plasma selenium concentrations in children with iron deficiency anemia (IDA). Plasma selenium levels were investigated in 56 children with IDA and in 48 control subjects aged 1-8 years. A spectrofluorometric method was used for the determination. Plasma selenium concentrations in children with IDA (33.6+/-8.2 microg/l) were significantly lower than in the control group (56.0+/-17.0 microg/l) (p<0.001). However, there was no relation between plasma selenium, iron and hemoglobin concentrations.     

Erythrocyte CuZn superoxide dismutase activity is decreased in iron-deficiency anemia

Iron and copper and essential microminerals that are intimately related. The present study was performed to determine the effect of iron-deficiency anemia (IDA) and treatment with iron on laboratory indicators of copper status. Hemoglobin, mean corpuscular volume erythrocyte Zn protoporphyrin, serum ferritin, serum copper, serum ceruloplasmin, and erythrocyte CuZn-superoxide dismutase (SOD) activity were studied in 12 adult women with IDA before and after iron treatment for 60–90 d (100 mg/d Fe, as ferric polymaltose) and in 27 women with normal iron status. Prior to treatment with iron, serum copper and ceruloplasmin were not different between the groups and treatment with iron did not affect these measures. IDA women, before and after treatment with iron, presented a 2.9- and 2-fold decrease in erythrocyte CuZn-SOD activity compared to women with normal iron status (p <0.001). Treatment with iron increased erythrocyte CuZn-SOD activity of the IDA group; however, this change was not statistically significant. in conclusion, CuZn-SOD activity is decreased in IDA. Measurement of this enzyme activity is not useful for evaluating copper nutrition in iron-deficient subjects.     

Integrated strategies needed to prevent iron deficiency and to promote early child development

Iron deficiency (ID) and iron deficiency anemia (IDA) are global public health problems that differentially impact pregnant women and infants in low and middle income countries. IDA during the first 1000 days of life (prenatally through 24 months) has been associated with long term deficits in children's socio-emotional, motor, cognitive, and physiological functioning. Mechanisms linking iron deficiency to children's development may include alterations to dopamine metabolism, myelination, and hippocampal structure and function, as well as maternal depression and unresponsive caregiving, potentially associated with maternal ID. Iron supplementation trials have had mixed success in promoting children's development. Evidence suggests that the most effective interventions to prevent iron deficiency and to promote early child development begin early in life and integrate strategies to ensure adequate iron and nutritional status, along with strategies to promote responsive mother-child interactions and early learning opportunities.     

Lactoferrin efficacy versus ferrous sulfate in curing iron deficiency and iron deficiency anemia in pregnant women

Iron deficiency (ID) and iron deficiency anemia (IDA) are the most common iron disorders throughout the world. ID and IDA, particularly caused by increased iron requirements during pregnancy, represent a high risk for preterm delivery, fetal growth retardation, low birth weight, and inferior neonatal health. Oral administration of ferrous sulfate to cure ID and IDA in pregnancy often fails to increase hematological parameters, causes adverse effects and increases inflammation. Recently, we have demonstrated safety and efficacy of oral administration of 30% iron saturated bovine lactoferrin (bLf) in pregnant women suffering from ID and IDA. Oral administration of bLf significantly increases the number of red blood cells, hemoglobin, total serum iron and serum ferritin already after 30 days of the treatment. The increasing of hematological values by bLf is related to the decrease of serum IL-6 and the increase of serum hepcidin, detected as prohepcidin, whereas ferrous sulfate increases IL-6 and fails to increase hematological parameters and prohepcidin. bLf is a more effective and safer alternative than ferrous sulfate for treating ID and IDA in pregnant women.     

The effects of iron deficiency on neutrophil/monocyte apoptosis in children

OBJECTIVES: Iron is essential for DNA synthesis; its deficiency may lead to impaired DNA synthesis and subsequent alterations in levels of apoptosis. Here, we have aimed to investigate effects of iron deficiency anaemia (IDA) on apoptotic response of phagocytic cells and to understand whether the effect is reversible after iron supplementation. MATERIALS AND METHODS: Forty-nine IDA patients and 26 healthy controls, aged between 6 months and 12 years with similar demographic status, were considered. Neutrophil- and monocyte-apoptotic responses of IDA patients and the control group were compared by flow cytometry. Then, IDA patients were provided with oral iron supplementation. On day 15 of iron therapy, neutrophil- and monocyte-apoptotic responses of IDA patients were rechecked and were compared to those of control group. RESULTS: Neutrophil- and monocyte-apoptotic responses in terms of early and late percentages of apoptosis, and percentages of necrotic cells, were significantly less in IDA patients compared to the control group. The significantly low apoptotic responses of IDA patients rose to levels of the control group by day 15 of iron therapy. Besides, the effect of IDA on apoptotic responses was found to be more enhanced in severe IDA patients that those of mild IDA patients. CONCLUSION: Correction of differences after iron supplementation therapy implies that IDA might be a cause for changes in neutophil- and monocyte-apoptotic responses. The impact of this diminution of apoptotic cellular function in IDA should be further investigated, with longitudinal studies, in order to document the impact of any severe and/or long-lasting IDA on autoimmunity and malignancy.     

Supplementation with Sucrosomial® iron leads to favourable changes in the intestinal microbiome when compared to ferrous sulfate in mice

BioMetals - Iron deficiency is one of the most common nutritional deficiencies worldwide and is often treated with oral iron supplements. However, commonly used supplements, including those based...     

Biliary excretion of excess iron in mice requires hepatocyte iron import by Slc39a14

Iron is essential for erythropoiesis and other biological processes, but is toxic in excess. Dietary absorption of iron is a highly regulated process and is a major determinant of body iron levels. Iron excretion, however, is considered a passive, unregulated process, and the underlying pathways are unknown. Here we investigated the role of metal transporters SLC39A14 and SLC30A10 in biliary iron excretion. While SLC39A14 imports manganese into the liver and other organs under physiological conditions, it imports iron under conditions of iron excess. SLC30A10 exports manganese from hepatocytes into the bile. We hypothesized that biliary excretion of excess iron would be impaired by SLC39A14 and SLC30A10 deficiency. We therefore analyzed biliary iron excretion in Slc39a14-and Slc30a10-deficient mice raised on iron-sufficient and -rich diets. Bile was collected surgically from the mice, then analyzed with nonheme iron assays, mass spectrometry, ELISAs, and an electrophoretic assay for iron-loaded ferritin. Our results support a model in which biliary excretion of excess iron requires iron import into hepatocytes by SLC39A14, followed by iron export into the bile predominantly as ferritin, with iron export occurring independently of SLC30A10. To our knowledge, this is the first report of a molecular determinant of mammalian iron excretion and can serve as basis for future investigations into mechanisms of iron excretion and relevance to iron homeostasis.