静脉用蔗糖铁治疗维持性血液透析肾性贫血患者效果分析

目的观察静脉用蔗糖铁治疗维持性血液透析(MHD)患者肾性贫血的临床效果和安全性。方法将42例接受维持性血液透析的肾性贫血患者随机分为两组,在给予促红细胞生成素(EPO)治疗的基础上,观察组患者静脉注射蔗糖铁治疗,对照组患者口服琥珀酸亚铁片治疗,观察比较两组患者治疗前和治疗4周、8周后血红蛋白(Hb)、红细胞压积(Hct)、铁蛋白(SF)、转铁蛋白饱和度(TSAT)以及EPO的用量。结果两组患者治疗后Hb、Hct、SF、TSAT均明显增高(P0.05),EPO用量均明显下降(P0.05);观察组患者治疗后Hb、Hct、SF、TSAT改善程度均明显优于对照组(P0.05),治疗8周后EPO用量也明显小于对照组(P0.05)。治疗期间两组患者均未出现明显的不良反应。结论静脉补充蔗糖铁治疗MHD肾性贫血患者能取得较好的临床效果,能改善患者对EPO的反应性、减少EPO用量,降低不良反应发生率。     

蔗糖铁注射液治疗维持性血液透析患者肾性贫血疗效分析

目的比较静脉注射蔗糖铁（森铁能）与口服多糖铁复合物（力蜚能）治疗维持性血液透析患者肾性贫血的疗效与安全性。方法 60例病情稳定的血液透析患者,规律透析2～3次/周。将上述患者随机分为口服组和静脉组,每组各30例,观察期24周。口服组予多糖铁复合物150 mg/d;静脉组每次透析时静脉滴注蔗糖铁100mg,累计1 000 mg后每2周给予维持量100 mg。若患者的血红蛋白（Hb）达到110 g/L或红细胞压积（Hct）达到33%以上,则将重组人促红细胞生成素（rHuEPO）减量以维持Hb及Hct水平。检测补铁前及补铁48、1、2、24周时患者Hb、Hct、血清铁蛋白（SF）以及转铁蛋白饱和度（TSAT）水平。结果治疗后两组Hb、Hct、SF、TSAT均较治疗前明显升高（P〈0.05）,静脉组Hb、Hct、SF、TSAT上升幅度均高于口服组（P〈0.05）。治疗后静脉组rHuEPO用量较治疗前及口服组明显减少（P〈0.05）。两组治疗前后肝功能无显著性差异。治疗后静脉组血清C反应蛋白高于治疗前及口服组,但仍在正常范围内。静脉组不良反应2例,口服组8例。结论静脉用蔗糖铁治疗肾性贫血安全有效,不良反应少,且可减少rHuEPO用量。     

蔗糖铁治疗维持性血液透析患者肾性贫血疗效观察

目的比较静脉用铁剂蔗糖铁（森铁能）和口服铁剂琥珀酸亚铁（速力菲）与基因重组人红细胞生成素（EPO）联合应用治疗尿毒症肾性贫血患者的有效性和安全性。方法选取我院收治40例血液透析患者,随机分为治疗组和对照组各20例,根据公式计算总补铁量,治疗组将蔗糖铁100mg溶于0．9％氯化钠溶液200ml于血液透析后静脉滴注,30-60滴／min,2次／周,直至完成补铁总量。对照组口服琥珀酸亚铁100mg,3;A／d。两组均联合EPO,3000U／次,2次／周皮下注射,治疗6周。观察两组患者治疗前后血红蛋白（Hb）、红细胞比容（HCT）、红细胞计数（RBC）、血清铁蛋白（SF）和转铁蛋白饱和度（TSAT）。结果两组患者治疗前Hb、HCT、RBC、SF、TSAT间差异均无统计学意义（P〉0．05）;治疗后Hb、HCT、RBC、SF、TSAT间差异均有统计学意义（P〈0．05）结论静脉用蔗糖铁联合EPO治疗尿毒症肾性贫血,疗效优于口服补铁,不良反应少。     

蔗糖铁注射液治疗老年维持性血液透析患者肾性贫血的疗效

目的 探讨蔗糖铁注射液对老年维持性血液透析患者肾性贫血治疗的疗效及安全性.方法 选择同期在我院接受维持性血液透析患者(透析龄＞2个月)56例,随机分为口服组和静脉组各28例,分别给予口服铁剂和蔗糖铁静脉推注,比较两组患者纠正肾性贫血的疗效及安全性.结果静脉组治疗4 w时血红蛋白(Hb)、红细胞比容(HCT)、血清铁蛋白(SF)、血清转铁蛋白饱和度(TSAT)升高,较治疗前差异有统计学意义(P＜0.05),口服组治疗8 w时较治疗前比较差异有统计学意义(P＜0.05);在治疗8 w时静脉组Hb、HCT、SF、TSAT的升高程度与口服组比较差异有统计学意义(P＜0.01);静脉组的不良反应少于口服组.结论 静脉注射蔗糖铁与口服铁剂比较可在更短时间内纠正肾性贫血,且不良反应发生率更低,可提高老年维持性血液透析患者的生存质量.     

静脉注射蔗糖铁治疗血液透析患者肾性贫血的临床研究

目的探讨对血液透析患者静脉注射蔗糖铁治疗铁缺乏的有效性和安全性。方法2006年1月～2007年11月在北京市第六医院肾内科进行维持性血液透析治疗的35例患者均应用促红细胞生成素（EPO）及琥珀酸亚铁治疗2个月，血红蛋白（Hb）60—90g／L，红细胞压积（Hct）0．18％～0．3％，血清铁蛋白（SF）〈200μg／L，转铁蛋白饱和度（TSAT）〈30％。停用琥珀酸亚铁后给予蔗糖铁静脉注射治疗，每次100mg，共10次。结果共28例患者完成本次临床观察治疗后，SF、TSAT均有明显升高（P〈0．01）。治疗后较治疗前Hb及Hct升高（P〈0．01）。有7例患者退出观察，1例治疗无效，无明显不良反应发生。结论静脉注射蔗糖铁可有效地纠正维持性血液透析患者的铁缺乏，提高EPO的疗效，不良反应发生率低，安全性好。     

静脉注射蔗糖铁与口服铁剂治疗肾性贫血疗效观察

目的比较静脉注射蔗糖铁与口服铁剂治疗肾性贫血的疗效和安全性。方法选取2009年11月—2011年11月我院收治的慢性肾功能不全(CRF)行持续性血液透析并伴有肾性贫血患者44例。将患者随机分为治疗组和对照组,各22例。治疗组给予蔗糖铁治疗,对照组给予右旋糖酐铁片治疗。观察两组患者血红蛋白(Hb)、血细胞比容(HCT)、血清铁蛋白(SF)、血清转铁蛋白饱和度(TAST),记录促红细胞生成素(Epo)用量及不良反应发生情况。结果治疗前两组Hb、HCT、SF、TAST和Epo用量比较,差异无统计学意义(P0.05);治疗4周、8周、12周,治疗组Hb、HCT、SF和TAST均高于对照组,Epo用量少于对照组(P0.05)。治疗前后两组ALT、AST、碱性磷酸酶(ALP)及清蛋白(ALB)等肝功能指标无明显变化。结论治疗血液透析患者肾性贫血时,首选蔗糖铁,可有效改善贫血症状,提高临床疗效。     

蔗糖铁注射液治疗老年血液透析患者肾性贫血的临床疗效与安全性

目的 比较静脉用蔗糖铁和口服铁剂富马酸亚铁分别与红细胞生成素( EPO)联合应用治疗老年维持性血液透析(MHD)患者肾性贫血的临床疗效和安全性.方法 随机选取30例老年MHD患者分为老年静脉组和老年口服组各15例,老年静脉组将蔗糖铁100 mg稀释于100ml生理盐水于透析结束前30 min静滴,2次/w,直至完成总补铁量.老年口服组患者口服富马酸亚铁颗粒200 mg,3次/d(含铁量200 mg).另外取15例成人MHD患者为成年静脉组,使用蔗糖铁方法同老年静脉组.三组均联合EPO,用法:每周100～ 180 U/kg于血液透析结束时皮下注射,并根据血红蛋白上升情况调整用量.结果 治疗后三组血红蛋白(Hb)、红细胞比容(Hct)、血清铁蛋白(SF)、转铁蛋白饱和度(Ts)均较治疗前明显提高(P＜0.01);老年静脉组Hb上升幅度明显高于老年口服组(P＜0.05),与成年静脉组比较无差异(P＞0.05);总有效率比较老年静脉组高于老年口服组(P＜0.05),与成年静脉组比较无差异(P＞0.05);不良反应发生率老年静脉组低于老年口服组(P＜0.05).老年组C反应蛋白(CRP)、血肌酐(scr)、谷丙转氨酶(ALT)、谷草转氨酶(AST)、血白蛋白(ALB)、总胆红素(Tbi1)治疗前后无明显变化(P＞0.05).结论 静脉用蔗糖铁治疗老年MHD患者肾性贫血,其疗效优于口服富马酸亚铁,与成年MHD患者一致,安全性好,可作为老年MHD肾性贫血患者长期补铁的方法之一.     

蔗糖铁对透析前慢性肾功能不全肾性贫血的影响

目的观察蔗糖铁静脉注射治疗透析前慢性肾功能不全患者肾性贫血的疗效。方法慢性肾功能不全透析前患者26例,血色素（Hb）均〈11g／dl,静脉予以蔗糖铁200mg／月,共12个月。治疗前及治疗过程中每3个月对比观察纠正贫血效果、铁代谢指标变化及不良反应发生情况。结果治疗后Hb、血清铁（SI）、铁蛋白（SF）、转铁蛋白饱和度（TSAT）等均较治疗前显著升高（P均〈0．05）。结论慢性肾功能不全肾性贫血患者透析前静脉给予蔗糖铁纠正贫血疗效明显。     

口服与静脉铁剂治疗血液透析患者贫血的疗效观察

目的比较维持性血液透析患者口服和静脉补铁治疗肾性贫血的疗效,以及对促红细胞生成素(EPO)作用的影响。方法将30例病情稳定的血液透析患者随机分成静脉组和口服组2组各15例,观察期6个月。口服组口服福乃得(含硫酸亚铁525mg)1片/天,静脉组静脉补充铁剂。先按公式在2周内给予负荷剂量,以后每2周给予维持量100mg。若患者的血红蛋白(Hb)达到目标值120g/l,则将EPO的剂量减少25%。结果治疗后两组患者的Hb、红细胞压积(Hct)、铁蛋白(SF)和转铁蛋白饱和度(TSAT)进行性升高,治疗后3个月时口服组和静脉组患者的Hb、Hct、SF和TSAT均较治疗前显著升高,而静脉组升高的幅度明显高于口服组(P<0.01)。透析患者的贫血得到纠正,EPO用量开始减少,同时SF和TSAT保持在较高水平。6个月时EPO用量开始明显减少,减少的幅度明显高于口服组(P<0.01),明显高于治疗前静脉组(P<0.01)。结论长期静脉补铁不仅能及时有效地补充慢性肾衰竭血透患者贫血所需的铁剂,使贫血状况改善,而且能减少EPO用量。     

总剂量注射静脉铁剂对老年腹透患者贫血及微炎症的影响

目的探讨总剂量注射静脉铁剂对老年腹膜透析患者的贫血及微炎症状态的影响。方法选择第二军医人学附属长海医院。肾内科46例长期不卧床腹膜透析（CAPD）患者进行总剂量注射静脉铁剂临床观察。根据年龄分为A组（≥60岁）和B组（〈60岁）,观察用药前后血红蛋白浓度（Hb）、红细胞压积（Hct）、血清铁（SI）、血清铁蛋白（SF）、转铁蛋白饱和度（TSAT）等指标以及血清C-反应蛋白（CRP）、白介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）等炎症指标并监测不良反应。结果（1）用药后的3个月、6个月,两组的Hb、Hct、SF、TSAT较用药前上升,有统计学意义（P〈0．05）。用药6个月后,两组的Hb、Hct、SF、TSAT增加百分数差异无统计学意义（P〉0．05）。（2）用药6个月后,两组患者的血清CRP、IL-6、TNF-α较治疗前有所下降,但无统计学意义（P〉0．05）。（3）A组有1例发生轻度胃肠道反应,B组有1例发生轻微心悸。A组总不良反应发生率（1／26,3．85％）和B组（1／20,5．00％）无统计学意义（P〉0．05）。结论总剂量注射静脉铁剂可有效纠正老年腹膜透析患者的铁缺乏,提高铁利用率,不良反应发生率低,安全性良好,且未加重其微炎症状态。     

LPI-labile plasma iron in iron overload

Labile plasma iron (LPI) represents a component of non-transferrin-bound iron (NTBI) that is both redox-active and chelatable, capable of permeating into organs and inducing tissue iron overload. It appears in various types of hemosiderosis (transfusional and non-transfusional) and in other iron-overload conditions. Sustained levels of LPI could over time compromise organ (e.g. heart) function and patient survival. With the advent of methods for measuring LPI in the clinical setting, it has become possible to assess the implications of LPI in the management of iron overload based on regimens of iron chelation. As LPI is detected primarily in patients with transfusional iron overload and other forms of hemosiderosis, we review here regimens of iron chelation with deferrioxamine and deferiprone (separately or combined) in terms of their efficacy in minimizing daily exposure to LPI in thalassemia major and thalassemia intermedia patients.     

Liver iron concentration, stainable iron, and total body storage iron

Liver iron concentration has been determined chemically in 154 liver biopsies and the findings compared with the routine histological assessment of stainable parenchymal iron, performed by an independent observer. There was a significant correlation between liver iron concentration and histochemical grading but the relationship did not have a normal linear form. Absence of stainable iron corresponded to liver iron concentrations below the mean value for control male subjects (77 μg/100 mg dry liver). In general grade 1 siderosis corresponded to liver iron concentrations in the upper part of the control range and grade 2 siderosis to marginally elevated values. The transition from grade 2 to grade 3 (submaximal) siderosis represented a sharp increase in liver iron concentration and as grade 3 siderosis corresponded to a wide range of chemical values it is also the most difficult histochemical grade to interpret in quantitative terms. Grade 4 siderosis invariably indicated heavy iron excess.

There was a close correlation between liver iron concentration and measurements of total body storage iron obtained by quantitative phlebotomy in patients with idiopathic haemochromatosis and by determination of DTPA-chelatable body iron in a variety of iron-loading disorders.

     

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.     

Nutritional iron requirements and food iron absorption

To prevent nutritional iron deficiency, sufficient iron must be absorbed from the diet to meet the normal physiological requirements. Daily iron losses in males are about 1 mg (14 micrograms kg-1), while the average additional requirements incurred in women include menstruation (0.6 mg), pregnancy (2.7 mg) and lactation (less than 0.3 mg). Requirements during pregnancy are not evenly distributed and increase to between 5-6 mg in the last trimester of pregnancy, which is more than can be absorbed from even an optimal diet. While the amounts absorbed are affected by the iron content of the diet, the composition of the latter is even more relevant. About one-quarter of the iron in haem proteins is absorbed regardless of the other components in the diet, while non-haem iron absorption is subject to the interplay of promoting and inhibiting substances in the diet. Thus diets rich in enhancers of non-haem iron absorption, chiefly meat and/or ascorbic acid, have high iron bioavailability (about 3 mg d-1) while diets in which inhibitors, such as polyphenols and phytates, predominate are poor sources of iron (less than 1 mg d-1). Examination of the relative proportions of promoters and inhibitors of iron absorption in individual foodstuffs and the measured iron absorption from them may be useful in predicting the overall iron bioavailability from mixed diets.     

Relationship among plasma iron, plasma iron turnover, and reticuloendothelial iron release

A circadian rhythm was demonstrated in 10 males and 10 females with respective mean decreases in plasma iron concentration at 18 hr of 62% and 47% of morning values. Ferrokinetic studies performed on 5 normal males and 5 normal females showed a more rapid disappearance rate and lower plasma iron turnover in the evening. Parallel studies were done on 6 normal males in the morning and 4 normal males in the evening of the release of reticuloendothelial iron at 8 and 18 hr after intravenous injection of 59Fe chondroitin ferrous sulfate. The 6-hr release in the morning was 54.1% and in the evening 25.9%. Composite data from morning and evening showed a correlation between plasma iron level and plasma iron turnover (r = 0.76, p less than 0.001). A similar correlation existed between the plasma iron level and the percent of radioiron released from the reticuloendothelial system (r = 0.67, 0.02 less than p less than 0.05). These data are consistent with a fluctuating iron release from the reticuloendothelial cell in normal subjects, which would account for the diurnal variation in plasma iron.     

Body iron metabolism and pathophysiology of iron overload

Iron is an essential metal for the body, while excess iron accumulation causes organ dysfunction through the production of reactive oxygen species. There is a sophisticated balance of body iron metabolism of storage and transport, which is regulated by several factors including the newly identified peptide hepcidin. As there is no passive excretory mechanism of iron, iron is easily accumulated when exogenous iron is loaded by hereditary factors, repeated transfusions, and other diseased conditions. The free irons, non-transferrin-bound iron, and labile plasma iron in the circulation, and the labile iron pool within the cells, are responsible for iron toxicity. The characteristic features of advanced iron overload are failure of vital organs such as liver and heart in addition to endocrine dysfunctions. For the estimation of body iron, there are direct and indirect methods available. Serum ferritin is the most convenient and widely available modality, even though its specificity is sometimes problematic. Recently, new physical detection methods using magnetic resonance imaging and superconducting quantum interference devices have become available to estimate iron concentration in liver and myocardium. The widely used application of iron chelators with high compliance will resolve the problems of organ dysfunction by excess iron and improve patient outcomes.     

铁过载检测与祛铁治疗

临床上对于低危骨髓增生异常综合征(myelodysplastic syndromes,MDS)、再生障碍性贫血(aplastic anemia,AA)以及β珠蛋白生成障碍性贫血等疾病的患者来说,输血治疗是挽救其生命和     

Regulation of iron absorption and storage iron turnover

The regulation of iron supply to plasma was studied in male rate. Repeated exchange transfusions were first carried out with plasma from iron-deficient or iron-loaded animals. There was no recognizable effect on the amount of iron entering the plasma as evidenced by plasma iron concentration or iron absorption by recipient animals. In other studies, iron compounds having different tissue distribution were injected. Subsequent iron release was greater from reticuloendothelial cells than from other iron-loaded tissues. When requirements for transferrin iron were increased by exchange transfusion with high reticulocyte blood, within minutes there was a doubling of the rate of tissue iron donation. It was concluded from these studies that (1) iron turnover in the plasma is primarily determined by the number of tissue receptors for iron, particularly those of the erythron, (2) that the amount of iron supplied by each donor tissue is dependent on the output of other donor tissues, and (3) that a humoral mechanism regulating iron exchange is unlikely in view of the speed of response and magnitude of changes in plasma iron turnover. It is proposed that there is some direct mechanism that determines the movement of iron from donor tissues to unsaturated transferrin binding sites.