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接受直接作用抗病毒药物治疗的血小板减少的慢性丙型肝炎患者血小板计数显著改善的相关因素

Factors Associated with Significant Platelet Count Improvement in Thrombocytopenic Chronic Hepatitis C Patients Receiving Direct-Acting Antivirals.

作者信息

Chen Yen-Chun, Chang Te-Sheng, Chen Chien-Hung, Cheng Pin-Nan, Lo Ching-Chu, Mo Lein-Ray, Chen Chun-Ting, Huang Chung-Feng, Kuo Hsing-Tao, Huang Yi-Hsiang, Tai Chi-Ming, Peng Cheng-Yuan, Bair Ming-Jong, Yeh Ming-Lun, Lin Chih-Lang, Lin Chun-Yen, Lee Pei-Lun, Chong Lee-Won, Hung Chao-Hung, Huang Jee-Fu, Yang Chi-Chieh, Hu Jui-Ting, Lin Chih-Wen, Wang Chia-Chi, Su Wei-Wen, Hsieh Tsai-Yuan, Lin Chih-Lin, Tsai Wei-Lun, Lee Tzong-Hsi, Chen Guei-Ying, Wang Szu-Jen, Chang Chun-Chao, Yang Sheng-Shun, Wu Wen-Chih, Huang Chia-Sheng, Hsiung Chou-Kwok, Kao Chien-Neng, Tsai Pei-Chien, Liu Chen-Hua, Lee Mei-Hsuan, Dai Chia-Yen, Kao Jia-Horng, Chuang Wan-Long, Lin Han-Chieh, Chen Chi-Yi, Tseng Kuo-Chih, Yu Ming-Lung

机构信息

Department of Internal Medicine, Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Chiayi School of Medicine, Tzuchi University, Hualien 970, Taiwan.

Division of Hepatogastroenterology, Department of Internal Medicine, Chiayi Chang Gung Memorial Hospital and College of Medicine, Chang Gung University, Taoyuan 333, Taiwan.

出版信息

Viruses. 2022 Feb 7;14(2):333. doi: 10.3390/v14020333.

DOI:10.3390/v14020333
PMID:35215926
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8879038/
Abstract

To clarify the predictive factors of significant platelet count improvement in thrombocytopenic chronic hepatitis C (CHC) patients. CHC patients with baseline platelet counts of <150 × 10/μL receiving direct-acting antiviral (DAA) therapy with at least 12-weeks post-treatment follow-up (PTW12) were enrolled. Significant platelet count improvement was defined as a ≥10% increase in platelet counts at PTW12 from baseline. Platelet count evolution at treatment week 4, end-of-treatment, PTW12, and PTW48 was evaluated. This study included 4922 patients. Sustained virologic response after 12 weeks post-treatment was achieved in 98.7% of patients. Platelet counts from baseline, treatment week 4, and end-of-treatment to PTW12 were 108.8 ± 30.2, 121.9 ± 41.1, 123.1 ± 43.0, and 121.1 ± 40.8 × 10/μL, respectively. Overall, 2230 patients (45.3%) showed significant platelet count improvement. Multivariable analysis revealed that age (odds ratio (OR) = 0.99, 95% confidence interval (CI): 0.99-1.00, = 0.01), diabetes mellitus (DM) (OR = 1.20, 95% CI: 1.06-1.38, = 0.007), cirrhosis (OR = 0.66, 95% CI: 0.58-0.75, < 0.0001), baseline platelet counts (OR = 0.99, 95% CI: 0.98-0.99, < 0.0001), and baseline total bilirubin level (OR = 0.80, 95% CI: 0.71-0.91, = 0.0003) were independent predictive factors of significant platelet count improvement. Subgroup analyses showed that patients with significant platelet count improvement and sustained virologic responses, regardless of advanced fibrosis, had a significant increase in platelet counts from baseline to treatment week 4, end-of-treatment, PTW12, and PTW48. Young age, presence of DM, absence of cirrhosis, reduced baseline platelet counts, and reduced baseline total bilirubin levels were associated with significant platelet count improvement after DAA therapy in thrombocytopenic CHC patients.

摘要

为明确血小板减少的慢性丙型肝炎(CHC)患者血小板计数显著改善的预测因素。纳入基线血小板计数<150×10⁹/μL且接受直接抗病毒药物(DAA)治疗并至少有12周治疗后随访(PTW12)的CHC患者。血小板计数显著改善定义为PTW12时血小板计数较基线增加≥10%。评估治疗第4周、治疗结束时、PTW12和PTW48时的血小板计数变化情况。本研究共纳入4922例患者。98.7%的患者在治疗后12周实现了持续病毒学应答。从基线、治疗第4周、治疗结束时到PTW12的血小板计数分别为108.8±30.2、121.9±41.1、123.1±43.0和121.1±40.8×10⁹/μL。总体而言,2230例患者(45.3%)血小板计数有显著改善。多变量分析显示,年龄(比值比(OR)=0.99,95%置信区间(CI):0.99 - 1.00,P = 0.01)、糖尿病(DM)(OR = 1.20,95%CI:1.06 - 1.38,P = 0.007)、肝硬化(OR = 0.66,95%CI:0.58 - 0.75,P < 0.0001)、基线血小板计数(OR = 0.99,95%CI:0.98 - 0.99,P < 0.0001)以及基线总胆红素水平(OR = 0.80,95%CI:0.71 - 0.91,P = 0.0003)是血小板计数显著改善的独立预测因素。亚组分析表明,无论是否存在重度肝纤维化,血小板计数有显著改善且实现持续病毒学应答的患者,从基线到治疗第4周、治疗结束时、PTW12和PTW48血小板计数均显著增加。年轻、患有DM、无肝硬化、基线血小板计数降低以及基线总胆红素水平降低与血小板减少的CHC患者接受DAA治疗后血小板计数显著改善相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89ac/8879038/6e64ce5a924d/viruses-14-00333-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89ac/8879038/5d1a1d8dc7b0/viruses-14-00333-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89ac/8879038/f405ca08fe9d/viruses-14-00333-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89ac/8879038/95eb6b5eec1e/viruses-14-00333-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89ac/8879038/6e64ce5a924d/viruses-14-00333-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89ac/8879038/5d1a1d8dc7b0/viruses-14-00333-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89ac/8879038/f405ca08fe9d/viruses-14-00333-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89ac/8879038/95eb6b5eec1e/viruses-14-00333-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89ac/8879038/6e64ce5a924d/viruses-14-00333-g004.jpg

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