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丙型肝炎病毒感染患者抗病毒治疗期间血小板计数迅速增加。

Rapid increase of platelet counts during antiviral therapy in patients with hepatitis C virus infection.

作者信息

Ishizu Yoji, Ishigami Masatoshi, Hayashi Kazuhiko, Honda Takashi, Kuzuya Teiji, Ito Takanori, Fujishiro Mitsuhiro

机构信息

Department of Gastroenterology and Hepatology, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Department of Gastroenterology and Hepatology, Meijo Hospital, Nagoya, Japan.

出版信息

Hepatol Res. 2020 Jan;50(1):47-56. doi: 10.1111/hepr.13426. Epub 2019 Oct 25.

DOI:10.1111/hepr.13426
PMID:31496023
Abstract

AIM

The cause of thrombocytopenia in patients with chronic hepatitis C virus (HCV) infection is multifactorial: hypersplenism, decreased thrombopoietin levels, and myelosuppression induced by HCV. Platelet counts increase after eradication of HCV; however, this mechanism is not fully understood. Therefore, the aim of this study was to determine the influence of these three factors on platelet counts.

METHODS

We retrospectively analyzed data from 109 HCV-infected patients with platelet counts ≤150 × 10 /μL who achieved viral eradication using interferon-free anti-HCV therapy. Changes in hematological parameters, thrombopoietin levels, HCV titers, and spleen volumes, and the correlations among them were evaluated.

RESULTS

HCV RNA levels significantly decreased at 4 weeks after initiating antiviral therapy. Platelet counts rapidly increased at 4 weeks from baseline (120 ± 35 vs. 106 ± 28 × 10 /μL, P < 0.001), and remained at a plateau until 48 weeks after initiating antiviral therapy. Neutrophil counts showed the same pattern. Spleen volume was evaluated in 32 patients and, among them, it decreased in 21 patients, but remained unchanged in seven and increased in four. In addition to patients with decreased spleen volume, patients with unchanged spleen volume showed marginally increased platelet counts. Thrombopoietin levels did not correlate with platelet counts.

CONCLUSIONS

Platelet counts increased at 4 weeks after starting anti-HCV treatment. Our results suggest that this rapid change was possibly caused by improvement of hypersplenism and HCV-induced myelosuppression resulting from anti-HCV therapy.

摘要

目的

慢性丙型肝炎病毒(HCV)感染患者血小板减少的原因是多因素的:脾功能亢进、血小板生成素水平降低以及HCV诱导的骨髓抑制。HCV根除后血小板计数会增加;然而,这一机制尚未完全明确。因此,本研究的目的是确定这三个因素对血小板计数的影响。

方法

我们回顾性分析了109例血小板计数≤150×10⁹/μL且使用无干扰素抗HCV疗法实现病毒根除的HCV感染患者的数据。评估血液学参数、血小板生成素水平、HCV滴度和脾脏体积的变化以及它们之间的相关性。

结果

开始抗病毒治疗4周后HCV RNA水平显著下降。血小板计数从基线开始在4周时迅速增加(120±35对106±28×10⁹/μL,P<0.001),并在开始抗病毒治疗后48周一直保持在平台期。中性粒细胞计数呈现相同模式。对32例患者评估了脾脏体积,其中21例脾脏体积减小,7例保持不变,4例增大。除脾脏体积减小的患者外,脾脏体积不变的患者血小板计数也略有增加。血小板生成素水平与血小板计数无相关性。

结论

开始抗HCV治疗4周后血小板计数增加。我们的结果表明,这种快速变化可能是由于抗HCV治疗导致脾功能亢进和HCV诱导的骨髓抑制得到改善所致。

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