Camacho-Lobato L, Borges D R
Department of Medicine, Universidade Federal de São Paulo, Brazil.
J Hepatol. 1998 Aug;29(2):233-40. doi: 10.1016/s0168-8278(98)80008-1.
BACKGROUND/AIMS: Liver dysfunction is said to occur only late in the course of schistosomiasis. As albumin levels tend to be normal, the observed prolonged prothrombin time is thought to arise from subclinical consumption coagulopathy. The aim of this study was to further evaluate this matter by studying the role of Schistosoma mansoni and liver function in the genesis of the compromised haemostasis tests in chronic "pure" schistosomiasis patients.
Twenty-five adults with chronic "pure" schistosomiasis were selected: 12 with the hepatointestinal form (group 2) and 13 with the compensated hepatosplenic form (group 3), as well as 10 matched control individuals (group 1). Alcoholism, viral hepatitis B and C, malnutrition (BMI<20 kg/m2), use of anticoagulant or anti-aggregant drugs and chronic diseases apart from schistosomiasis were carefully excluded. All patients were submitted to abdominal ultrasound and upper digestive endoscopy. Blood samples were used for routine hepatic tests and for transthyretin, prothrombin, antithrombin and protein C antigen determinations by immunodiffusion. Laboratory markers of coagulation activation (prothrombin fragment1+2(F1+2), serine esterases-antithrombin complexes (ATM) and plasminogen activator, tissue type activity (t-PA) were also assayed by ELISA and photometric determination, respectively.
Decreased plasma levels of transthyretin (p<0.001), protein C (p:0.006), prothrombin (p:0.022) and antithrombin (p:0.008) contrasted with normal albuminaemia (p:0.094), F1+2 (p:0.061) and ATM (p:0.714) plasma levels in group 3 patients; t-PA activity (p:0.001) on the other hand, were increased in this group.
These results suggest impairment of liver clearance and protein synthesis capacity rather than consumption coagulopathy. They also indicate that changes in liver function are not a late event in the course of schistosomiasis.
背景/目的：据说肝功能障碍仅在血吸虫病病程后期出现。由于白蛋白水平往往正常，观察到的凝血酶原时间延长被认为是由亚临床消耗性凝血病引起的。本研究的目的是通过研究曼氏血吸虫和肝功能在慢性“单纯性”血吸虫病患者止血试验受损发生过程中的作用，进一步评估这一问题。
选取25例慢性“单纯性”血吸虫病成人患者：12例为肝肠型（第2组），13例为代偿性肝脾型（第3组），以及10例匹配的对照个体（第1组）。仔细排除酗酒、乙型和丙型病毒性肝炎、营养不良（体重指数<20kg/m²）、使用抗凝或抗聚集药物以及除血吸虫病外的慢性疾病。所有患者均接受腹部超声和上消化道内镜检查。采集血样用于常规肝功能检查，并通过免疫扩散法测定转甲状腺素蛋白、凝血酶原、抗凝血酶和蛋白C抗原。凝血激活的实验室标志物（凝血酶原片段1+2（F1+2）、丝氨酸酯酶-抗凝血酶复合物（ATM）和组织型纤溶酶原激活物活性（t-PA））也分别通过ELISA和比色法进行检测。
第3组患者血浆中转甲状腺素蛋白（p<0.001）、蛋白C（p:0.006）、凝血酶原（p:0.022）和抗凝血酶（p:0.008）水平降低，而白蛋白血症（p:0.094）、F1+2（p:0.061）和ATM（p:0.714）血浆水平正常；另一方面，该组t-PA活性（p:0.001）升高。
这些结果提示肝脏清除和蛋白质合成能力受损，而非消耗性凝血病。它们还表明肝功能变化并非血吸虫病病程中的晚期事件。
