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血小板减少症在肝硬度和脾肿大相同等级的晚期慢性丙型肝炎患者中比乙型肝炎患者更为严重。

Thrombocytopenia is more severe in patients with advanced chronic hepatitis C than B with the same grade of liver stiffness and splenomegaly.

机构信息

Department of Clinical Laboratory Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan.

出版信息

J Gastroenterol. 2010 Aug;45(8):876-84. doi: 10.1007/s00535-010-0233-5. Epub 2010 Mar 26.

Abstract

BACKGROUND AND AIM

The mechanism responsible for thrombocytopenia in chronic liver diseases (CLD) is not yet fully understood. The prevalence of thrombocytopenia has been reported to be higher in patients with hepatitis C virus-related hepatocellular carcinoma (CLD-C) than in those with hepatitis B virus-related hepatocellular carcinoma (CDC-B). We have examined the potential difference in thrombocytopenia between patients with CLD-B and those with CLD-C in terms of liver fibrosis adjustment and splenomegaly.

METHODS

The study cohort consisted of 102 patients with CLD-B and 143 patients with CLD-C were enrolled. Liver stiffness, which is reported to be well correlated with the degree of liver fibrosis, was measured by transient elastography.

RESULTS

The analysis of covariance with liver stiffness as a covariate revealed that the platelet count was lower in CLD-C patients than in CLD-B patients. Following stratification for liver stiffness, thrombocytopenia was found to be more severe in CLD-C patients than CLD-B patients with advanced liver stiffness, whereas the degree of splenomegaly was not significantly different. The plasma thrombopoietin level was not different between CLD-B and CLD-C patients with advanced liver stiffness, and the immature platelet number was lower in CLD-C patients despite thrombocytopenia being more severe in these patients.

CONCLUSIONS

CLD-C patients with advanced liver stiffness presented with more severe levels of thrombocytopenia than CLD-B patients even with the same grade of splenomegaly. Impaired platelet production rather than enhanced platelet destruction may underlie the mechanism responsible for thrombocytopenia in patients with CLD.

摘要

背景与目的

慢性肝脏疾病(CLD)导致血小板减少的机制尚未完全明确。已有研究报道丙型肝炎病毒相关肝细胞癌(CLD-C)患者的血小板减少发生率高于乙型肝炎病毒相关肝细胞癌(CLD-B)患者。本研究旨在通过肝纤维化和脾肿大调整,探讨 CLD-B 和 CLD-C 患者血小板减少的潜在差异。

方法

本研究纳入了 102 例 CLD-B 患者和 143 例 CLD-C 患者。采用瞬时弹性成像技术测量肝硬度,该技术与肝纤维化程度具有良好的相关性。

结果

协方差分析显示,调整肝硬度后,CLD-C 患者的血小板计数较 CLD-B 患者低。进一步对肝硬度进行分层后发现,CLD-C 患者的血小板减少程度较 CLD-B 患者更严重,且肝硬度较高;而两组患者的脾肿大程度无显著差异。对于肝硬度较高的患者,CLD-B 和 CLD-C 患者的血小板生成素水平无差异,且 CLD-C 患者的未成熟血小板计数较低,尽管这些患者的血小板减少更严重。

结论

即使脾肿大程度相同,肝纤维化程度较高的 CLD-C 患者的血小板减少程度也较 CLD-B 患者严重。CLD 患者血小板减少的机制可能是血小板生成受损而非破坏增强。

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