Djordjević Jelena, Svorcan Petar, Vrinić Dusica, Dapcević Branka
KBC Zvezdara, Centar za gastroenterologiju i hepatologiju, Beograd, Serbia.
Vojnosanit Pregl. 2010 Feb;67(2):166-9. doi: 10.2298/vsp1002166d.
BACKGROUND/AIM: Splenomegaly is a frequent finding in patients with liver cirrhosis and portal hypertension and may cause hypersplenism. The occurrence of thrombocytopenia in those patients can be considered as an event with multiple etiologies. Two mechanisms may act alone or synergistically with splenic sequestration. One is central which involves either myelosuppression because of hepatitis viruses or the toxic effects of alcohol abuse on the bone marrow. The second one involves the presence of antibodies against platelets. It also depends upon the stage and etiology of liver disease. The aim of the study was to investigate a correlation between the platelet count and spleen size and the risk factors for thrombocytopenia in patients with liver cirrhosis.
We studied 40 patients with decompensated liver cirrhosis who were hospitalized in the Department of Gastroenterohepatology. The liver function was graded according to Child Pugh score. Spleen size was defined ultrasonografically on the basis of craniocaudal length. Suspicion of portal hypertension was present when longitudinal spleen length was more than 11 cm. Thrombocytopenia was determined by platelet count under 150,000/mL.
We did not find any significant correlation between hepatic dysfunction and spleen size (p = 0.9), and between hepatic dysfunction and thrombocytopenia (p = 0.17). Our study did not find any significant correlation between spleen size and peripheral platelet count (p = 0.5), but we found a significant correlation between thrombocytopenia and etiology of cirrhosis - decreased platelet count was more common among patients with cirrhosis of alcoholic etiology than in other etiologies of cirrhosis (p = 0.001).
According to our study, liver cirrhosis, portal hypertension and thrombocytopenia could be present even in the absence of enlarged spleen suggesting the involvement of other mechanisms of decreasing platelet account.
背景/目的：脾肿大在肝硬化和门静脉高压患者中很常见，可能导致脾功能亢进。这些患者血小板减少的发生可被视为多种病因导致的结果。两种机制可能单独起作用或与脾扣押协同作用。一种是中枢性的，涉及肝炎病毒引起的骨髓抑制或酒精滥用对骨髓的毒性作用。另一种涉及抗血小板抗体的存在。它还取决于肝病的阶段和病因。本研究的目的是调查肝硬化患者血小板计数与脾脏大小之间的相关性以及血小板减少的危险因素。
我们研究了40例在胃肠肝病科住院的失代偿期肝硬化患者。肝功能根据Child Pugh评分进行分级。脾脏大小通过超声根据头尾长度确定。当脾脏纵向长度超过11 cm时，怀疑存在门静脉高压。血小板减少通过血小板计数低于150,000/mL来确定。
我们未发现肝功能障碍与脾脏大小之间存在任何显著相关性（p = 0.9），也未发现肝功能障碍与血小板减少之间存在显著相关性（p = 0.17）。我们的研究未发现脾脏大小与外周血小板计数之间存在任何显著相关性（p = 0.5），但我们发现血小板减少与肝硬化病因之间存在显著相关性——酒精性肝硬化患者的血小板计数下降比其他病因的肝硬化患者更常见（p = 0.001）。
根据我们的研究，即使没有脾脏肿大，也可能存在肝硬化、门静脉高压和血小板减少，这表明其他降低血小板计数的机制也参与其中。
