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首页> 外文期刊>Clinical toxicology: the official journal of the American Academy of Clinical Toxicology and European Association of Poisons Centres and Clinical Toxicologists >A comparison of sodium calcium edetate (edetate calcium disodium) and succimer (DMSA) in the treatment of inorganic lead poisoning.
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A comparison of sodium calcium edetate (edetate calcium disodium) and succimer (DMSA) in the treatment of inorganic lead poisoning.

机译：乙二胺四乙酸钙钠（乙二胺四乙酸钙钠）和琥珀酸酯（DMSA）在无机铅中毒治疗中的比较。

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INTRODUCTION: This article reviews the experimental and clinical studies that have compared the efficacy (impact on urine lead excretion, blood and tissue lead concentrations, resolution of features and survival) of sodium calcium edetate (edetate calcium disodium) and succimer (DMSA) in the treatment of inorganic lead poisoning. It also summarizes the pharmacokinetic and pharmacodynamic aspects and the adverse effects of treatment. METHODS: Medline, Toxline, and Embase were searched for all available years to June 2009. PHARMACOKINETICS AND PHARMACODYNAMICS: The absorption of oral DMSA is more complete than sodium calcium edetate; the latter has to be administered parenterally. Both antidotes are distributed predominantly extracellularly. Sodium calcium edetate is not metabolized, whereas DMSA is extensively metabolized to mixed disulfides of cysteine. The two antidotes have elimination half-lives of less than 60 min. There is no evidence that either antidote crosses the blood-brain barrier to any major extent. Sodium calcium edetate chelates lead by displacement of the central Ca2+ ion with Pb2+. The nature of the DMSA-lead chelate is less clearly defined. There is evidence that the mixed disulfides of cysteine are the active chelating moiety in humans. If this is the case, this suggests that chelation occurs principally, if not exclusively, in the kidney. The primary source of lead mobilized by sodium calcium edetate is bone with an additional contribution from kidney and liver. EFFICACY: Comparison of the experimental studies is complicated by substantial variations in study design, particularly the antidote dose, the route and duration of treatment, the amount and duration of lead dosing, and lack of direct comparison between antidotes (comparison was usually made with control). In experimental studies that used equimolar and clinically relevant antidote doses and assessed the impact of DMSA and sodium calcium edetate on urine lead excretion and/or blood lead concentrations, similar results were found, though no direct comparison between antidotes was undertaken. DMSA was more effective than sodium calcium edetate in reducing the kidney lead concentration, sodium calcium edetate was more effective than DMSA in reducing bone lead concentrations, and there was no consistently observed effect of chelation therapy on brain lead concentrations in these experimental studies. Only two clinical studies have compared equimolar or similar antidote doses in enhancing urine lead excretion; there was no statistical difference between the antidotes, though both studies had limitations. DMSA and sodium calcium edetate had a comparable impact on lowering blood lead concentrations in a clinical study using similar molar antidote doses. ADVERSE EFFECTS: Sodium calcium edetate causes dose-related nephrotoxicity. Both agents deplete zinc and copper, the effect on zinc being significantly greater with sodium calcium edetate. A transient increase in hepatic transaminase activity has been reported with both antidotes but appears to be more common with DMSA and neither has been associated with clinically significant hepatic toxicity. Skin lesions during treatment with sodium calcium edetate are unusual and have been attributed to zinc deficiency. DMSA has occasionally been associated with a severe mucocutaneous reaction necessitating discontinuation of therapy. CONCLUSIONS: Oral DMSA and parenteral sodium calcium edetate are both effective chelators of lead. There are currently insufficient data, however, to conclude that either antidote is superior in enhancing lead excretion. Both antidotes resolve the symptoms of moderate and severe lead toxicity rapidly. Although there is greater clinical experience with sodium calcium edetate, particularly in the treatment of lead encephalopathy, oral DMSA may now be considered as an alternative in circumstances where oral therapy is preferable.
机译：简介：本文回顾了实验和临床研究，比较了乙二胺四乙酸钙钠（乙二胺四乙酸钙）和丁二酸丁二酯（DMSA）的功效（对尿铅排泄，血液和组织铅浓度，特征和生存的影响）。治疗无机铅中毒。它还总结了药代动力学和药效学方面以及治疗的不利影响。方法：对截至2009年6月的所有可用年份，对Medline，Toxline和Embase进行搜索。药代动力学和药动学：口服DMSA的吸收比乙二胺四乙酸钙钠更完整。后者必须肠胃外给药。两种解毒剂主要分布在细胞外。乙二胺四乙酸钠钠不被代谢，而DMSA被广泛代谢为半胱氨酸的混合二硫化物。这两种解毒剂的消除半衰期少于60分钟。没有证据表明任何一种解毒剂都能在很大程度上跨越血脑屏障。乙二胺四乙酸钠钙螯合物是由中央Ca2 +离子被Pb2 +取代而产生的。 DMSA-铅螯合物的性质尚不清楚。有证据表明，半胱氨酸的混合二硫化物是人类的活性螯合部分。如果是这种情况，则表明螯合主要发生在肾脏中，即使不是排他性的。乙二胺四乙酸钠调集的铅的主要来源是骨骼，而肾脏和肝脏也有其他作用。功效：由于研究设计的实质性变化，尤其是解毒剂的剂量，治疗的途径和持续时间，铅给药的量和持续时间以及解毒剂之间缺乏直接比较（比较通常与对照进行比较），使实验研究的比较变得复杂。 ）。在使用等摩尔和临床相关解毒剂剂量并评估DMSA和乙二胺四乙酸钙钠对尿铅排泄和/或血铅浓度影响的实验研究中，虽然未进行解毒剂之间的直接比较，但发现了相似的结果。在这些实验研究中，DMSA在降低肾脏铅浓度方面比乙二胺四乙酸钙更有效，乙二胺四乙酸钠在降低骨铅浓度方面比DMSA更有效，并且在这些实验研究中未始终观察到螯合疗法对脑铅浓度的影响。只有两项临床研究比较了等摩尔或类似解毒剂剂量在增强尿铅排泄方面的作用。尽管两种研究都有局限性，解毒剂之间没有统计学差异。在使用类似摩尔解毒剂剂量的临床研究中，DMSA和乙二胺四乙酸钙钠对降低血铅浓度具有类似的影响。不良影响：依地酸钠钙引起剂量相关的肾毒性。两种试剂都消耗锌和铜，而乙二胺四乙酸钙钠对锌的作用明显更大。两种解毒剂均已报道肝转氨酶活性瞬时升高，但在DMSA中似乎更为常见，且均未与临床上显着的肝毒性相关。用乙二胺四乙酸钙钠治疗期间的皮肤损害是罕见的，并归因于锌缺乏。 DMSA有时与严重的粘膜皮肤反应有关，因此必须停止治疗。结论：口服DMSA和肠胃外乙二胺四乙酸二钠钠都是有效的铅螯合剂。但是，目前尚无足够的数据得出结论，认为任何一种解毒剂在增强铅排泄方面都具有优势。两种解毒剂都能快速缓解中度和重度铅中毒症状。尽管乙二胺四乙酸钙钠具有更大的临床经验，尤其是在治疗铅性脑病中，但在首选口服治疗的情况下，现在可以考虑口服DMSA。

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