慢性汞中毒对凝血及纤溶系统的影响

Effects of chronic mercury poisoning on blood coagulation and fibrolysis systems

目的探究慢性汞中毒对凝血、纤溶系统的影响及其可能的机制。方法采用病例对照及自身病例对照研究方法,采用酶联免疫吸附双抗体夹心法测定血栓调节蛋白(TM)、组织纤溶酶原激活物(t-PA)、组织纤溶酶原激活物抑制物(PAI)含量,并检测白细胞介素(IL)-13、IL-18、血管内皮细胞黏附因子(SICAM-1),采用酶化学法检测超氧化物歧化酶(SOD)活力和脂质过氧化产物(LPO)含量。结果慢性汞中毒患者治疗前TM[(2.36±0.16)ng/ml]较空白对照组[(4.36±0.24)ng/ml]明显降低,差异有统计学意义(P<0.01),经过治疗后,TM明显增高[(4.82±0.34)ng/ml],与治疗前的差异有统计学意义(P<0.05);慢性汞中毒患者t-PA[(3.44±0.34)ng/ml]较空白对照组[(4.52±0.16)ng/ml]明显降低,经过治疗后明显升高[(5.63±0.58)ng/ml],差异均有统计学意义(P<0.05);而PAI则较空白对照组明显升高,分别为(48.23±3.59)、(31.59±2.13)ng/ml,差异有统计学意义(P<0.05),治疗后与治疗前的差异无统计学意义(P>0.05)。慢性汞中毒患者SOD活力[(953.85±9.56)U/g Hb]较空白对照组[(1308.75±10.21)U/g Hb]明显降低,经过治疗后活力[(1217.95±6.29)U/g Hb]明显升高,差异均有统计学意义(P<0.05、P<0.01)。同时表现为LPO明显增加。慢性汞中毒患者IL-13、IL-18、SICAM-1较空白对照组明显升高,差异均有统计学意义(P<0.05、P<0.01),而治疗后与治疗前的差异无统计学意义(P>0.05)。结论慢性汞中毒可能导致患者TM/PC系统、t-PA/PAI系统失衡(抗凝血功能下降,纤溶系统功能抑制)而使机体处于继发性高凝血状态。

Objective To investigate the effects of chronic mercury poisoning on blood coagulation and fibrolysis systems, and the possible mechanism. Methods Twenty-seven patients with chronic mercury poisoning were studied with 30 healthy people as control. Thrombomodulin （TM）, tissue plasimogen activator（ t-PA ）, plasminogen activactor inhibitor （ PM ）, interleukin- 13 （ IL- 13 ）, interleukin- 18 （ IL- 18 ）, soluble intercellular adhesion molecule-I （SICAM-1 ） were examined with ELISA methods, and superoxide dismutase（SOD） and lipid peroxidation（LPO） was examined with chemical catalysis methods.Two to three weeks after treatment with reduced glutathione, tiopronin and daidzein, blood was used for determinine the above items again. Results （1）The concentration of TM in patients[ （2.36 ± 0.16）ng/ml] was significantly lower than in the control[ （4.36 ± 0.24）ng/ml] （ P 〈 0.01 ）, while TM tended to be higher after treatment [ （ 4.82 ±0.34 ） ng/ml ] （ P 〈 0.05 ）. （2） The concentration of t-PA in patients[ （3.44 ± 0.34）ng/ml] was significantly lower than in the control[ （4.52 ± 0. 16）ng/ml] （ P 〈 0.05） ,and was higher significantly[ （5.63 ± 0.58）ng/ml] after treatment（ P 〈 0.05） ;The concentration of PAI in patients[ （48.23 ± 3.59）ng/ml] was significantly higher than in the control[ （31.59 ± 2.13）ng/ml] （P 〈 0.05）, but after treatment no significant change[ （50.71 ± 4.29）ng/ml] was found（ P 〉 0.05）. （3）The activity of SOD in patients[（953.85 ± 9.56）U/g Hb] was significantly lower than in the control[（ 1 308.75 ±10.21 ） U/g Hb]（P 〈0.01）,and was higher significantly[ （1 217.95 ± 6.29）U/g Hb] after treatment（ P 〈 0.05）;and the concentration of LPO in patients[ （9.53 ± 0.26）nmol/ml] was significantly higher than in the control（ P 〈 0.05）, and significantly lower [ （ 7.29 ±0.35 ） nmol/ml ] after treatment （ P 〈 0.05 ）. （4） The concentrations of IL-13[ （35.93 ± 5.28） pg/ml3 ,IL-I8[ （28.79 ± 2.53）pg/ml] ,SICAM-I [ （603.16 ± 29.12）ng/ml] were significantly higher than those in the controls（P 〈 0.05, P 〈 0.01） ,but no significant difference was found after treatment. Conclusion Dysfunction of the TM/protein C system and t-PA/PAI system （i. e. the decrease of anti-coagulation activity and the inhibition of the function for the fibrolysis system） may play a key role in the secondary hypercoagulable state induced by chronic mercury poisoning.