Mingyue Cai1, Wensou Huang2, Chaoshuang Lin3, Zhengran Li4, Jiesheng Qian5, Mingsheng Huang6, Zhaolin Zeng7, Jingjun Huang8, Hong Shan9, Kangshun Zhu10. 1. Department of Radiology, the Third Affiliated Hospital, and Interventional Radiology Institute, Sun Yat-sen University, 600 Tianhe Road, Guangzhou, Guangdong, 510630, China. cai020@yeah.net. 2. Department of Radiology, the Third Affiliated Hospital, and Interventional Radiology Institute, Sun Yat-sen University, 600 Tianhe Road, Guangzhou, Guangdong, 510630, China. huangwensou@sina.com. 3. Department of Infectious Diseases, the Third Affiliated Hospital, Sun Yat-sen University, 600 Tianhe Road, Guangzhou, Guangdong, 510630, China. linchaoshuang@126.com. 4. Department of Radiology, the Third Affiliated Hospital, and Interventional Radiology Institute, Sun Yat-sen University, 600 Tianhe Road, Guangzhou, Guangdong, 510630, China. andyreede@msn.com. 5. Department of Radiology, the Third Affiliated Hospital, and Interventional Radiology Institute, Sun Yat-sen University, 600 Tianhe Road, Guangzhou, Guangdong, 510630, China. qjsyf@163.com. 6. Department of Radiology, the Third Affiliated Hospital, and Interventional Radiology Institute, Sun Yat-sen University, 600 Tianhe Road, Guangzhou, Guangdong, 510630, China. gzhuangms@163.com. 7. Department of Radiology, the Third Affiliated Hospital, and Interventional Radiology Institute, Sun Yat-sen University, 600 Tianhe Road, Guangzhou, Guangdong, 510630, China. cjhx265@163.com. 8. Department of Radiology, the Third Affiliated Hospital, and Interventional Radiology Institute, Sun Yat-sen University, 600 Tianhe Road, Guangzhou, Guangdong, 510630, China. 263632777@qq.com. 9. Department of Radiology, the Third Affiliated Hospital, and Interventional Radiology Institute, Sun Yat-sen University, 600 Tianhe Road, Guangzhou, Guangdong, 510630, China. shanhong@mail.sysu.edu.cn. 10. Department of Radiology, the Third Affiliated Hospital, and Interventional Radiology Institute, Sun Yat-sen University, 600 Tianhe Road, Guangzhou, Guangdong, 510630, China. zhksh010@163.com.
Abstract
OBJECTIVES: To investigate the predictors of platelet increment and risk factors for major complications after partial splenic embolization (PSE) in cirrhosis. METHODS: Between March 2010 and June 2012, 52 cirrhotic patients with severe thrombocytopenia underwent PSE. Multiple variables were analyzed to identify the correlated factors affecting platelet increment and major complications after PSE. RESULTS: Linear mixed model analysis indicated the splenic infarction ratio (P < 0.001), non-infarcted splenic volume (P = 0.012), and cholinesterase level (P < 0.001) were significantly associated with the platelet increment after PSE. In receiver operating characteristic (ROC) analysis, the cut-off values of the splenic infarction ratio, and non-infarcted splenic volume for achieving an increment of ≥60.0 × 10(9)/L in platelet counts at 1 year after PSE were 64.3% and 245.8 mL, respectively. After PSE, eight patients developed major complications. Multivariate logistic regression analysis indicated major complications were significantly associated with the infarcted splenic volume (P = 0.024) and Child-Pugh score (P = 0.018). In ROC analysis, the cut-off values of these two factors for discriminating the uncomplicated and complicated were 513.1 mL and 9.5, respectively. CONCLUSIONS: The platelet increment after PSE depends on the splenic infarction ratio, non-infarcted splenic volume and cholinesterase level. But a large infarcted splenic volume and a high Child-Pugh score may cause complications. KEY POINTS: • The platelet increment after PSE greatly depends on the splenic infarction ratio. • The non-infarcted splenic volume significantly affects the efficacy of PSE. • A high cholinesterase level contributes to the improvement of thrombocytopenia after PSE. • The non-infarcted splenic volume significantly affects the relapse of hypersplenism. • Complications are significantly associated with the infarcted splenic volume and Child-Pugh score.
OBJECTIVES: To investigate the predictors of platelet increment and risk factors for major complications after partial splenic embolization (PSE) in cirrhosis. METHODS: Between March 2010 and June 2012, 52 cirrhoticpatients with severe thrombocytopenia underwent PSE. Multiple variables were analyzed to identify the correlated factors affecting platelet increment and major complications after PSE. RESULTS: Linear mixed model analysis indicated the splenic infarction ratio (P < 0.001), non-infarcted splenic volume (P = 0.012), and cholinesterase level (P < 0.001) were significantly associated with the platelet increment after PSE. In receiver operating characteristic (ROC) analysis, the cut-off values of the splenic infarction ratio, and non-infarcted splenic volume for achieving an increment of ≥60.0 × 10(9)/L in platelet counts at 1 year after PSE were 64.3% and 245.8 mL, respectively. After PSE, eight patients developed major complications. Multivariate logistic regression analysis indicated major complications were significantly associated with the infarcted splenic volume (P = 0.024) and Child-Pugh score (P = 0.018). In ROC analysis, the cut-off values of these two factors for discriminating the uncomplicated and complicated were 513.1 mL and 9.5, respectively. CONCLUSIONS: The platelet increment after PSE depends on the splenic infarction ratio, non-infarcted splenic volume and cholinesterase level. But a large infarcted splenic volume and a high Child-Pugh score may cause complications. KEY POINTS: • The platelet increment after PSE greatly depends on the splenic infarction ratio. • The non-infarcted splenic volume significantly affects the efficacy of PSE. • A high cholinesterase level contributes to the improvement of thrombocytopenia after PSE. • The non-infarcted splenic volume significantly affects the relapse of hypersplenism. • Complications are significantly associated with the infarcted splenic volume and Child-Pugh score.
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