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. METHODS: 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. RESULTS: 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). CONCLUSION: 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.
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. METHODS: 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. RESULTS: 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). CONCLUSION: 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.
Authors: Yunfu Lv; Wan Yee Lau; Hongfei Wu; XiaoYu Han; Xiaoguang Gong; Ning Liu; Jie Yue; Qingqing Li; YeJuan Li; Jie Deng Journal: Exp Biol Med (Maywood) Date: 2017-01-01