慢性病贫血的铁代谢研究

目的:探讨慢性病贫血(ACD)的铁代谢,有利于临床医师提高对该病的诊治水平。方法:对21例ACD和15例缺铁性贫血(IDA)患者进行Hb、血清铁(SI)、总铁结合力(TIBC)、血清铁蛋白(SF)、可溶性转铁蛋白受体(sTfR)、骨髓涂片铁染色、EPO、白细胞介素(IL)-1、IL-6、IL-8和肿瘤坏死因子-浕(TNF-浕)进行检测,并对结果进行分析。结果:①SI、TIBC、SF和骨髓涂片铁染色对区别ACD和单纯性IDA有很大帮助,2组数据比较差异有统计学意义,P<0.05;②ACD组中存在缺铁(占19.01);③ACD组和IDA组的sTfR水平分别为(2.41±1.20)mg/L和(6.38±3.24)mg/L,2组比较差异有统计学意义,P<0.05;④ACD组EPO水平低于IDA组,而IL-6、IL-8、TNF-浕水平高于IDA组,2组间数据比较除IL-1外,其他细胞因子差异有统计学意义,P<0.05。结论:sTfR是一种新的铁参数,有助于临床医师对ACD与IDA鉴别及合理用药,初步结果显示一些细胞因子在ACD疾病的致病因素中占重要地位。     

消化系统肿瘤性贫血27例铁代谢分析

对27例消化系肿瘤性贫血(TDA)铁代谢观察,显示为三低(SI、TIBC、intra-iron)、一高(FEP)、三正常(TS、SF、extra-iron)。与IDA比较,TIVB、TS等有明显统计学意义。认为造成这种异常除与网状内皮细胞铁释放阻滞及红细胞利用铁能力下降外,尚应注意运铁蛋白质与量的变化。SF对胃溃疡恶变有诊断价值。血清铁代谢变化结合成熟红细胞形态观察,可以发现双向性贫血可能。     

罗沙司他对慢性肾脏病合并地中海贫血患者贫血疗效及铁代谢的影响

目的 观察罗沙司他对慢性肾脏病合并地中海贫血患者贫血疗效及铁代谢的影响。方法 采用前瞻性随机对照研究方法,选取海南医学院第二附属医院2020年8月至2022年8月收治的慢性肾脏病同时合并有地中海贫血患者86例为研究对象,随机分成对照组、观察组。对照组给予重组人促红细胞生成素（rHuEPO）治疗,观察组给予罗沙司他治疗,经过12周治疗,对比两组4周、8周、12周的贫血指标、铁代谢指标、炎症指标情况。结果 两组患者一般基线临床资料、治疗前临床化验指标差异无统计学意义（P>0.05）。两组患者观察4周、8周、12周红细胞计数（RBC）、血红蛋白（Hb）、红细胞压积（HCT）均升高（均P<0.05）,治疗时间延长升高幅度增大;罗沙司他组RBC、Hb、HCT与rHuEPO组相比,升高幅度相差增大（均P<0.05）。rHuEPO组4周、8周、12周血清铁蛋白（SF）、转铁蛋白（Tf）、转铁蛋白饱和度（TSAT）与治疗前数值相比,差异无统计学意义（P>0.05）;r HuEPO组4周、8周总铁结合力（TIBC）、血清铁（SI）水平与治疗前数值相比,差异无统计学意义（P>...     

老年人肾功能、贫血和促红细胞生成素的相关性

目的 通过分析老年人肾小球滤过率（ GFR）和血清促红细胞生成素（EPO）水平对老年贫血患病率的影响,探讨老年贫血发生的相关因素及其与老年人肾功能水平的关系.方法 选取200例年龄≥60岁的老年患者作为观察对象,既往无慢性疾病的健康体检者30人作为正常对照组.采用Cockcroft-Gault方程计算eGFR;根据eGFR分为A组[eGFR＞ 50ml/（ min·1.73m2）,62例]、B组[30ml/（ min· 1.73m2）≤eGFR≤50ml/（ min·1.73m2）,114例]和C组[eGFR＜ 30ml/（ min· 1.73m2）,24例];66例老年贫血患者再根据GFR估算值（eGFR）分为AA组、AB组和AC组（分组标准同上）.测定血红蛋白（Hb）、血肌酐（Scr）、EPO水平.结果 伴随着肾功能水平的降低,老年人贫血患病率呈升高趋势,并且A,B,C3组之间比较均有显著性差异（P＜0.05）;正常对照组Log EPO与Hb呈负相关（r2=0.219,P=0.009）;A组Log EPO与Hb成负相关（r2=0.065,P=0.045）,B组Log EPO与Hb之间无相关关系,C组Log EPO与Hb为正相关（r2=0.294,P=0.006）;老年贫血患者随着肾功能水平的降低,EPO呈现下降趋势,AA组和AC组比较有显著性差异（P=0.042）.结论 老年人肾功能水平中度减退时贫血患病率即显著增加;随着年龄的增长,老年人EPO的分泌代偿性增加,但随着eGFR的不断下降,这种代偿机制逐渐减弱;当肾功能水平严重降低时,EPO分泌的减少是老年贫血发生的主要原因.     

老年人甲状腺激素与钙、磷代谢及骨代谢关系的研究

目的 探讨老年人甲状腺激素(TH)水平与钙、磷代谢及骨代谢关系。方法 选择健康老年治疗组和对照组各60例。治疗组口服甲状腺片10mg·d~(-1),对照组口服VitB_1 30mg·d~(-1),连服6月,所有的受试者治疗前后均检测TH包括促甲状腺激素(TSH)、游离三碘甲状腺原氨酸(FT_3)、游离甲状腺素(FT_4)、总三碘甲状腺原氨酸(TT_3)、总甲状腺素(TT_4)、反三碘甲状腺原氨酸(rT_3)和血钙(Ca)、血磷(P)代谢以及骨代谢生化指标包括骨钙素(BGP)、骨碱性磷酸酶(BALP)、I型前胶原羧基肽(PICP)及尿羟脯氨酸/肌酐(Hop/Cr)、尿胶原吡啶交联/肌酐(Pyd/Cr)的水平并比较它们之间的关系。结果 治疗组TH水平有明显升高,血清Ca、BGP、BALP、PICP的水平也有明显升高,而P的水平、Pyd/Cr、Hop/Cr值则有一定程度的降低,与治疗前比较有显著性差异。对照组服药前后各项指标无显著性差异。结论 给予老年人小剂量的TH补充治疗,可升高血清中TH水平和Ca、BGP、BAL、PICP的水平,降低P的水平、Pyd/Cr、Hop/Cr值,对骨的形成有利。     

老年人贫血诊断标准的探讨

目的：探讨老年人贫血的诊断标准,方法：检测７１７例健康人血红蛋白和平均红细胞血红蛋白含量,分析其与性别、年龄和体重的关系。结果：排除性别和体重对血红蛋白的影响,老年人血红蛋白水平低于中青年。结果：老年人血红蛋白〈１１０ｇ／Ｌ可诊断为贫血。     

铁代谢与心力衰竭关系的研究进展

心力衰竭(心衰)是由各种原因导致的心脏疾病的终末阶段,为当今社会常见的严重疾病,具有发病率高和死亡率高的特点.铁是人体必须的微量元素之一,以离子形式存在于肝、脾、肾、心、骨骼肌和脑等组织中,广泛参与人体的多种生理活动,而铁的代谢平衡是维持人体生命活动的重要部分.多项研究发现铁的代谢与心衰存在一定关系,影响心衰患者的疾病...     

铁代谢研究进展

铁是人体必需的微量元素之一,它除了是构成血红素必不可少的成分外,还参与细胞的增殖和分化,通过催化氧化-还原反应,参与电子传递、细胞呼吸、能量代谢、解毒等许多重要生理过程,同时它也能调节一氧化氮合酶、pkc-β、p21等与细胞生长和功能有关的基因表达[1]。     

Iron and thrombosis

Although essential for cell physiology, an increase or depletion of body iron has harmful effects on health. Apart from iron deficiency anemia and iron overload-related organ tissue damage, there are increasing evidences that body iron status is implicated in atherosclerotic cardiovascular diseases. The hypothesis formulated in 1981 that iron depletion may protect against cardiovascular events is intriguing and has generated a significant debate in the last two decades. Indeed, to study this phenomenon, several investigators have tried to design appropriate experimental and clinical studies and to identify useful biochemical and genetic markers of iron status. The results of the literature on the effect of iron deficiency and overload on vascular health are critically reviewed in this study from a pathogenic and clinical point of view.     

Efficacy for Anemia and Changes in Serum Ferritin Levels by Long‐Term Oral Iron Administration in Hemodialysis Patients

Oral iron preparations are useful for the treatment of anemia in hemodialysis patients; however, long‐term changes in the iron dynamics and effects of anemia are unknown. Serum ferritin levels and erythropoietin‐stimulating agent (ESA)/hemoglobin (Hb) ratios were investigated for 750 days in the following four groups: patients treated with sodium ferrous citrate (SF) (de novo 50 mg/day and 150 mg/day switched from 50 mg/day) and patients treated with 1500 mg/day of ferric citrate (FC) (de novo and switched from 50 mg/day of SF). Compared with the other groups, serum ferritin levels increased less apparently with de novo 50 mg/day SF. ESA/Hb ratios did not change in groups switched from 50 mg/day SF. Conversely, in groups with de novo iron, ESA/Hb ratios decreased and ultimately reached the same levels in all groups. Although more iron results in higher serum ferritin levels, 50 mg/day SF has an equivalent effect for anemia treatment.     

心力衰竭合并贫血和铁缺乏的诊治进展

心力衰竭(心衰)是所有心脏疾病的严重表现或晚期阶段,目前心衰的发病机制和治疗的研究已有显著进展,预后得到改善,但仍不容乐观。贫血和铁缺乏是心衰常见的合并症,无论共存或独立,都与心衰预后不良有关。积极纠正贫血和铁缺乏有助于改善心衰患者症状和提高生活质量。红细胞生成刺激剂常用于心衰患者贫血的纠正,但并未改善预后,且增加不良事件风险。口服补铁方便易得,静脉补铁能改善心衰症状和运动能力,但两者的长期疗效和安全性需进一步研究。     

Erythroblast Iron Metabolism in Sideroblastic and Sideropenic States

Iron appears to exert self-regulatory control over erythroblast iron uptake, iron storage and its incorporation into haem. It does this via iron regulatory proteins (IRPs) which bind reversibly to the iron responsive elements (IREs) on the mRNA of transferrin receptor (TfR), erythroid 5-aminolaevulinic acid synthase (ALA-S2) and ferritin. Iron deficiency leads to the binding of IRP to IRE. This binding inhibits the translation of mRNA for ALA-S2 and ferritin but stabilizes mRNA for TfR expression.

Sideroblastic erythropoiesis is highly ineffective and characterized by mitochondrial iron loading. The study of X-linked sideroblastic anaemia has shown that the entry of iron into the mitochondria is poorly controlled and able to occur when protoporphyrin production is reduced, as is seen with the ALA-S2 mutations, or when it is increased as has been seen with ABC7 transporter mutations.

Sideropenia characterises both iron deficiency anaemia (IDA) and the anaemia of chronic disease (ACD). Erythroblasts in ACD seem doubly equipped to protect their iron supply with their ability to increase the efficiency of transferrin-iron uptake as well as to activate the IRP/IRE system to increase surface TfR production. This increase in efficiency restricts the need to increase surface TfR production and maintains serum soluble TfR (sTfR) values within the normal range in iron replete ACD. The coexistence of iron deficiency with chronic disease, however, is associated with an increase in both the efficiency and number and a highly significant rise in sTfR values.