比较依地酸钙钠依地酸(钠钙)和succimer (DMSA)无机铅中毒的治疗。

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比较依地酸钙钠依地酸(钠钙)和succimer (DMSA)无机铅中毒的治疗。

中国Toxicol(费拉)。2009年11月,47 (9):841 - 58。doi: 10.3109 / 15563650903321064。

PubMed ID
19852620 (在PubMed
]
文摘

简介:本文综述了实验和临床研究相比效果(影响尿液排泄,血液和组织铅浓度,解决功能和生存)的依地酸钙钠依地酸(钠钙)和succimer (DMSA)无机铅中毒的治疗。它还总结了药代动力学和药效学方面和治疗的副作用。Toxline,方法:Medline和Embase搜索所有可用年到2009年6月。必威国际app药物动力学和药效学:口服DMSA的吸收比依地酸钙钠更完整;后者必须管理非肠道。两种解毒剂分布主要细胞外地。依地酸钙钠代谢,而DMSA广泛代谢半胱氨酸的二硫混合。两解毒剂消除半衰期小于60分钟。没有证据表明任何主要程度上要么是通过血脑屏障的解药。依地酸钠钙螯合物引起的位移与Pb2 +中央Ca2 +离子。的性质DMSA-lead螯合不太明确。 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.

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