病毒性肝炎血小板减少症影响因素的研究

目的探讨病毒性肝炎血小板减少症的发病机制.方法 84例病毒性肝炎患者和20名健康志愿者分为3组,A组(48例病毒性肝炎并血小板减少症患者)、B组(36例病毒性肝炎血小板正常患者)和C组(20名健康志愿者),分别采用酶联免疫吸附法、流式细胞术、腹部彩色B超检测3组血清血小板生成素(TPO)水平、血小板相关免疫球蛋白(PAIg)及其类别PAIgG、PAIgA、PAIgM水平、脾脏大小,采用骨髓穿刺术对其中74例行骨髓细胞学检查.结果血清TPO水平A组低于C组(P<0.01)和B组(P<0.05),严重肝病血清TPO水平与血小板数相关(r=0.374,P<00.01).PAIg、PAIgG水平A组明显高于B组(P<0.001)和C组(P<0.01),血小板数与PAIg水平呈负相关(r=0.446,P<0.01),血小板数与PAIgG水平亦呈负相关(r=-0.462,P<0.01).脾脏肿大发生率A组(77.1%)明显高于B组(47.2%,P<0.01),C组无脾脏肿大发生,血小板数与脾脏大小呈负相关(r=-0.5 81,P<0.01).74例骨髓象显示A组有4例呈骨髓抑制象改变,B组和C组无一例有上述改变.结论严重肝功能受损时血清TPO水平下降,与血小板数减少直接相关.PAIg介导的自身免疫机制在病毒性肝炎血小板减少症中可能起重要作用.脾脏肿大是引起病毒性肝炎血小板减少的因素.初步发现慢性肝病有骨髓抑制现象,可能成为引起病毒性肝炎血小板减少的因素之一.

Study on the influencing factors of thrombocytopenia in viral hepatitis

OBJECTIVE: To explore the pathogenesis of thrombocytopenia in viral hepatitis. METHODS: 84 viral hepatitis patients and 20 healthy controls were divided into three groups: Group A: 48 viral hepatitis patients with thrombocytopenia; Group B: 36 viral hepatitis patients with normal platelet count; and Group C: 20 healthy controls. Serum thrombopoietin (TPO) levels were measured in all subjects by enzyme linked immunosorbent assay. The levels of PAIg, PAIgG, PAIgA, PAIgM were detected in all subjects by flow cytometry. Spleen size was assessed in all subjects by abdominal color ultrasound B Scan. Bone marrow cells were examined in 74 subjects with bone marrow punctures. RESULTS: Serum thrombopoietin level was lower in group A than in group C and in group B. Serum TPO levels were correlated with platelet counts in the patients with advanced liver diseases. PAIg, PAIgG levels were significantly higher in group A than in group B and in group C. An inverse correlation was found between platelet counts and PAIg levels. An inverse correlation was also observed between platelet counts and PAIgG levels. The incidence of splenomegaly was significantly higher in group A (77.1%) than in group B (47.2%), while group C had no splenomegaly. An inverse correlation between spleen size and platelet count was observed (r = -0.581). There were 4 patients in group A with hypoplasia of bone marrow karyocytes, but there were no such cases in groups B and C. CONCLUSIONS: TPO level decreasing in patients with severe liver function impairments correlates with thrombocytopenia in advanced liver diseases. Autoimmune mechanism mediated by PAIg may play an important role in thrombocytopenia associated with viral hepatitis. Splenomegaly is the influencing factor leading to thrombocytopenia in viral hepatitis. Patients with chronic liver diseases had bone marrow depression, which may be a factor inducing thrombocytopenia in patients with viral hepatitis.