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Interference of hepatitis B virus dual infection in platelet count recovery in chronic hepatitis C patients with curative antiviral therapy

机译:乙型肝炎病毒双重感染在慢性丙型肝炎患者治疗抗病毒治疗患者中的血小板计数回收

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Abstract Background and Aim Hepatitis C virus infection is associated with thrombocytopenia. Thrombocytopenia recovers after viral eradication. The current study explored the rate and factors associated with platelet (PLT) recovery, which may represent the degree of liver fibrosis regression. Methods A total of 466 patients who achieved a sustained virological response were enrolled to compare the PLT change after a mean follow‐up period of 85.5?months (range 12–163?months). Results Platelet counts increased significantly after achieving sustained virological response (from 166?±?55?×?10 3 to 201?±?61?×?10 3 ? u /L, P ??0.001). The median PLT count increment was 5.03?×?10 3 ? u /L per year. Logistic regression analysis revealed that factors associated with slow PLT count recovery were high pretreatment PLT counts (odds ratio [OR]/ 95% confidence intervals [CI]: 0.992/0.989–0.996, P ??0.001) and hepatitis B virus (HBV) co‐infection (OR/CI: 0.416/0.220–0.785, P ?=?0.007). High PLT counts were the only factor associated with slow PLT recovery in patients with mild liver disease (F0–2) (OR/CI: 0.992/0.987–0.996, P ??0.001). On the other hand, HBV co‐infection was the only factor associated with slow PLT recovery in patients with advanced fibrosis (OR/CI: 0.207/0.054–0.789, P ?=?0.02). Linear regression analysis of factors correlated to the delta PLT count change per year in patients with F0–2 included pretreatment white blood cell (β: ?0.001; CI: ?0.002–0.000; P ?=?0.01) and pretreatment PLT counts (β: ?0.037; CI: ?0.061 to ?0.013; P ?=?0.003). HBsAg seropositivity was the only factor correlated to the delta PLT count change per year (β: ?10.193; CI: ?16.752–3.635; P ?=?0.003) among patients with F3–4. Conclusions Platelet counts recovered after hepatitis C virus eradication. HBV dual infection disrupted PLT count recovery, especially in CHC patients with advanced liver disease.
机译:摘要背景和AIM丙型肝炎病毒感染与血小板减少症有关。血小板减少症在病毒根除后恢复。目前的研究探讨了与血小板(PLT)恢复相关的速率和因素,这可能代表肝纤维化回归程度。方法共有466名达到持续病毒学反应的患者,以比较PLT在平均随访期间的改变为85.5?月(范围为12-163个月)。结果血小板计数在实现持续的病毒学响应后显着增加(从166?±55?×10 3到201?±61?×10 3?U / L,P≤103.0.001)。中位数plt计数增量为5.03?×10 3?每年U / L. Logistic回归分析显示,与缓慢PLT计数回收相关的因素是高预处理PLT计数(差距[或] / 95%置信区间[CI]:0.992 / 0.989-0.996,P = 0.001)和乙型肝炎病毒( HBV)共感染(或/ CI:0.416 / 0.220-0.785,P?= 0.007)。高分子计数是轻度肝病(F0-2)(或/ Ci:0.992 / 0.987-0.996,P≤0.001)的患者患者缓慢PLT恢复相关的唯一因素。另一方面,HBV共感染是与晚期纤维化患者(或/ CI:0.207 / 0.054-0.789,P?= 0.02)相关的患者患者缓慢PLT恢复相关的唯一因素。线性回归分析与F0-2患者每年δPLT计数的因素相关的因素包括预处理白细胞(β:β:0.001; CI:?0.002-0.000; p?= 0.01)和预处理PLT计数(β :?0.037; CI:0.061至0.013; p?= 0.003)。 HBsAg血清阳性是F3-4患者中每年与每年ΔClt计数变化相关的唯一因素(β:?10.193; ci; p?= 0.003)。结论缺点后血小板计数消除后恢复。 HBV双重感染扰乱了PLT计数回收,特别是在CHC患有先进的肝病患者中。

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