慢性汞中毒患者脑脊液汞含量的探讨

目的分析慢性汞中毒患者脑脊液汞含量的变化,探讨汞的神经毒性机制。方法选择9例慢性汞中毒患者作为中毒组,8例非汞接触患者为对照组,用碱性氯化亚锡还原-冷原子吸收光谱法测定24 h尿汞(U-Hg)和脑脊液汞(CSF-Hg)含量,用酸陸氯化亚锡还原-冷原子吸收光谱法测定同一天的血汞(B-Hg)含量；5例慢性汞中毒患者作驱汞前后B-Hg、U-Hg和CSF-Hg含量比较。结果中毒组B-Hg、U-Hg含量[(250．00±48．54)、(160．07±91．15)nmol/L]均明显高于对照组[(81．04±63．01)、(24．73±9．96)nmol/L],差异有统计学意义(P＜0．01)；中毒组CSF-Hg含量为(20．22±10．21) nmol/L,对照组CSF-Hg未检出。5例慢性汞中毒患者用二巯丙磺酸钠作2～3疗程驱汞治疗,B-Hg、U- HC、CSF-Hg含量治疗前分别为(258．00±48．68)、(141．02±63．74)和(22．60±7．14)nmol/L,治疗后明显下降,分别为(172．00±68．34)、(39．22±11．83)和(11．32±4．92)nmol/L,差异有统计学意义(P＜0．05或P＜0．01)。中毒组CSF-Hg含量与B-Hg含量有相关关系(P＜0．05),与U-Hg含量无相关关系(P＞0．05),但驱汞治疗后,CSF-Hg含量的下降与B-Hg、U-Hg含量下降的相关性均无统计。结论慢性汞中毒患者CSF-Hg含量随外周血汞升高而升高,但与U-Hg含量无关；而驱汞治疗后,B-Hg、U-Hg含量已正常,但CSF-Hg含量仍较高,其可能为引起慢性汞中毒患者神经行为功能改变和震颤等临床表现的基础物质。

Mercury concentration in cerebrospinal fluid in patients with chronic mercury poisoning

OBJECTIVE: To investigate the changes of mercury (Hg) levels in cerebrospinal fluid (CSF) in patients with chronic mercury poisoning and elucidate the neurotoxic mechanism of mercury. METHODS: Nine patients with chronic mercury poisoning (poisoning group) as well as eight patients without exposure to mercury were included in this study. Mercury concentrations of 24 hour urine (U-Hg) and CSF (CSF-Hg) were measured with cold-vapor atomic absorption spectrometry-alkali stannous chloride method. The concentration of blood (B-Hg) at the same day was measured with cold-vapor atomic absorption spectrometry-acidic stannous chloride method. In five patients of poisoning group, these concentrations before chelation therapy were compared with those after chelation therapy. RESULTS: The levels of B-Hg, U-Hg, and CSF-Hg in poisoning group (250.00 +/- 48.54, 160.07 +/- 91.15, 20.22 +/- 10.21 nmol/L, respectively) were significantly higher than those in control group (81.04 +/- 63.01, 24.73 +/- 9.96 nmol/L, undetectable, respectively; P < 0.01). In nine patients of poisoning group, CSF-Hg concentrations were correlated with B-Hg (r = 0.675, P < 0.05), but not U-Hg. After chelation therapy with dimercaptopropane sulfonate in five patients of poisoning group, the levels of B-Hg, U-Hg, and CSF-Hg were decreased significantly (P < 0.05). The reduction of CSF-Hg was not related with B-Hg and U-Hg. CONCLUSION: CSF-Hg concentration in chronic mercury poisoning patient is increased with the rise of B-Hg, but not U-Hg. When the levels of B-Hg and U-Hg drop to normal, the CSF-Hg level is still high enough to be detected. It indicates that mercury is combined with protein after entering brain and this complex is difficult to cross through blood-cerebral barrier. The complex may cause neuromuscular disorder and fremitus in chronic mercury poisoning.