Ruha Anne-Michelle, Curry Steven C, Gerkin Richard D, Caldwell Kathleen L, Osterloh John D, Wax Paul M
Department of Medical Toxicology, Banner Good Samaritan Medical Center, Phoenix, AZ 85006, USA.
Arch Pathol Lab Med. 2009 Jan;133(1):87-92. doi: 10.5858/133.1.87.
Public awareness of methylmercury in fish has caused patients to seek testing for mercury poisoning. In some patients, the diagnosis of mercury poisoning has been made based on urine mercury excretions following oral dosing of meso-dimercaptosuccinic acid (DMSA), a metal chelator. However, studies comparing urine mercury excretion following DMSA in healthy non-fish eaters with healthy fish eaters could not be located.
To describe urinary mercury excretion before and after DMSA in healthy fish eaters and non-fish eaters, and to determine whether urine mercury excretion after DMSA would rise above baseline levels to a greater extent in fish eaters.
A total of 24 healthy physicians were assigned to 1 of 3 groups based on fish consumption: non-fish eaters; 1 to 2 fish servings per week; and 3 or more servings per week. Blood mercury concentrations and 12-hour urine mercury and creatinine excretions were measured before and after oral ingestion of 30 mg of DMSA per kilogram of body weight.
A total of 24 subjects completed the study, and 2 subsequently were excluded. No difference in baseline urinary mercury excretion was detected between groups. All groups demonstrated an increase in urinary mercury excretion following DMSA, which was higher in fish eaters (P = .04). Multiple linear regression found that the best predictor of a rise in urine mercury excretion following DMSA challenge was the prechelation blood mercury concentration.
In this study of healthy physicians, oral DMSA produced a rise in urine mercury excretion both in non-fish eaters and fish eaters. The increase in chelated mercury excretion was higher in fish eaters. A simple rise in chelated mercury excretion over baseline excretion is not a reliable diagnostic indicator of mercury poisoning.
公众对鱼类中甲基汞的认知促使患者寻求汞中毒检测。在一些患者中，汞中毒的诊断是基于口服金属螯合剂内消旋二巯基丁二酸（DMSA）后的尿汞排泄情况。然而，未能找到比较健康的非食鱼者与健康的食鱼者在服用DMSA后尿汞排泄情况的研究。
描述健康食鱼者和非食鱼者在服用DMSA前后的尿汞排泄情况，并确定食鱼者在服用DMSA后尿汞排泄量是否会比基线水平升高得更多。
根据鱼类摄入量，将24名健康医生分为3组中的1组：非食鱼者；每周食用1至2份鱼；每周食用3份或更多份鱼。在口服每千克体重30毫克DMSA前后，测量血汞浓度以及12小时尿汞和肌酐排泄量。
共有24名受试者完成了研究，随后排除了2名。各组之间未检测到基线尿汞排泄的差异。所有组在服用DMSA后尿汞排泄量均增加，食鱼者增加得更高（P = 0.04）。多元线性回归发现，DMSA激发后尿汞排泄量增加的最佳预测指标是螯合前血汞浓度。
在这项针对健康医生的研究中，口服DMSA使非食鱼者和食鱼者的尿汞排泄量均增加。食鱼者螯合汞排泄量的增加更高。螯合汞排泄量相对于基线排泄量的简单增加并非汞中毒的可靠诊断指标。
