Department of Pathology, Kansas University Medical Center, Kansas City, KS, USA.
Int J Lab Hematol. 2012 Oct;34(5):525-32. doi: 10.1111/j.1751-553X.2012.01429.x. Epub 2012 Jun 18.
Thrombocytopenia occurs frequently in chronic hepatitis C. The mechanism of this association was investigated utilizing the immature platelet fraction (IPF%) as an index of platelet production together with assay of thrombopoietin (TPO).
In a cross-sectional study, 47 patients with chronic hepatitis C were studied, 29 with thrombocytopenia and 18 without thrombocytopenia (six patients in each group were on interferon therapy).
IPF% was elevated in the thrombocytopenic compared with the nonthrombocytopenic group (9.0 ± 4.8% vs. 4.7 ± 2.4%, P < 0.001), and an increase in IPF% was significantly associated with thrombocytopenia on multivariable analysis (P < 0.05). Splenomegaly was more common in thrombocytopenic than in nonthrombocytopenic subjects (66% vs. 6%, P < 0.001), and on multivariable analysis, splenomegaly was the factor associated with the highest relative risk of thrombocytopenia (RR = 1.9, P < 0.05). IPF% values were elevated in a similar proportion of thrombocytopenic patients with and without splenomegaly (58% and 60%, respectively). There was no difference in TPO levels between thrombocytopenic and nonthrombocytopenic patients, and TPO levels were not related to the risk of thrombocytopenia on multivariable analysis. Significantly more thrombocytopenic than nonthrombocytopenic subjects had abnormal liver function tests, cirrhosis, and portal hypertension, and a decrease in serum albumin was significantly associated with thrombocytopenia (P < 0.005) on multivariable analysis.
Factors associated with liver disease in general are associated with thrombocytopenia in chronic hepatitis C. Peripheral platelet destruction or sequestration is the major mechanism for thrombocytopenia, with hypersplenism being an important cause. Low TPO levels were not related to the occurrence of thrombocytopenia in this study.
丙型肝炎患者常发生血小板减少症。本研究利用血小板生成指数(不成熟血小板分数[IPF%])和血小板生成素(TPO)检测来探讨这种关联的发生机制。
在一项横断面研究中,共纳入 47 例丙型肝炎患者,其中 29 例伴有血小板减少症,18 例无血小板减少症(每组各有 6 例患者接受干扰素治疗)。
与无血小板减少症组相比,血小板减少症组的 IPF%升高(9.0±4.8%比 4.7±2.4%,P<0.001),且多变量分析显示 IPF%升高与血小板减少症显著相关(P<0.05)。血小板减少症组脾肿大的发生率高于无血小板减少症组(66%比 6%,P<0.001),多变量分析显示脾肿大是血小板减少症发生的相对风险最高的因素(RR=1.9,P<0.05)。脾肿大的血小板减少症患者与无脾肿大的血小板减少症患者的 IPF%升高比例相似(分别为 58%和 60%)。血小板减少症组与无血小板减少症组的 TPO 水平无差异,且 TPO 水平与血小板减少症的发生风险在多变量分析中无相关性。与无血小板减少症组相比,血小板减少症组的肝功能检查异常、肝硬化和门静脉高压的发生率更高,血清白蛋白降低与血小板减少症显著相关(多变量分析,P<0.005)。
与丙型肝炎一般肝脏疾病相关的因素与血小板减少症相关。外周血小板破坏或隔离是血小板减少症的主要发病机制,脾功能亢进是重要的原因。在本研究中,TPO 水平降低与血小板减少症的发生无关。