摘要
目的 探讨严重急性呼吸综合征 (SARS)并发肝脏损害的临床特征、变化趋势及其机制。方法 选择 2 0 0 3年 3月至 6月在北京佑安医院住院的SARS患者 15 4例 ,观察临床症状、体征、肝功能和血气分析等实验室指标。其中46例患者系统检测了血清IL 1β、IL 2、IL 4、IL 6、IL 8、IL 10和TNFα。有 3例死亡患者行尸检病理学检查。 结果 3 7.66%的SARS患者入院时ALT升高 ,随病程的延长逐渐下降 ,至第 3周时降至 5 .2 %。入院时白蛋白及胆红素的异常率分别为 5 .19%和 8.44 %。乳酸脱氢酶 (LDH)和磷酸肌酸同工酶 (CK MB)与ALT的相关性分别为 0 .63 8和 0 .60 1。肝脏病理学检查提示急性炎症改变。ALT异常组在未吸氧状态下有 84.48%的患者PaO2 低于 10 .64kPa ,而ALT正常组有 45 .83 %的患者PaO2 低于 10 .64kPa ,两者之间差异有显著性 (P <0 .0 1)。IL 1β、IL 2、IL 6、IL 8和IL 10水平在ALT正常组与异常组均高于正常对照组 (P <0 .0 5~ 0 .0 1)。ALT异常组IL 1β、IL 6和IL 10显著高于ALT正常组 (P <0 .0 5 )。结论 SARS患者容易并发以转氨酶短暂升高为特点的肝脏损害 ,表现为急性非特异性炎症改变。系统性炎性反应综合征 (SIRS)和缺氧是导致肝损害的重要原因。
Objective To summarize the clinical features, changing trend and mechanism of liver injury in patients with severe acute respiratory syndrome (SARS).Methods We collected and analyzed the clinical and some laboratory data of 154 patients with SARS admitted to the isolation wards of Beijing Youan Hospital from March 11 to June 3, 2003. Serum IL-1β,IL-2,IL-4,IL-6,IL-8,IL-10,TNF-α were detected in 46 cases. Autopsy and pathological observations were performed in 3 deseased cases.Results Serum ALT level was elevated in 37.66% SARS patients during admission but turned to normal gradually within 3 weeks in most cases, serum albumin and bilirubin were elevated in 5.19% and 8.44% of SARS patients, respetively. The correlations between lactate dehydrogenase, creatine phosphate isoenzyme and ALT were 0.638 and 0.601, respectively. PaO 2 was lower than 10.64kPa in 84.48% of elevated ALT patients. but in 45.83% of patients with normal ALT. There was siginficant difference between these two groups (P<0.01). The levels of IL-1β、IL-2、IL-6、IL-8、IL-10 in SARS patients were higher than those in the normal control group (P<0.05~0.01). The levels of IL-1β,IL-6 and IL-10 in patients with elevated ALT were higher than those with normal ALT(P<0.05).Conclusion Liver damage occurs frequently in SARS patients having elevated serum ALT and non-specific hepatic inflammatory changes. Systemic inflammatory response syndrome and anoxia are the major mechanisms involved in liver injury.
出处
《肝脏》
2003年第3期1-3,共3页
Chinese Hepatology
基金
北京市科技计划重大项目资助 (H0 2 0 92 0 0 2 0 0 91 )