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利血生治疗酒精性肝硬化伴血小板减少或白细胞减少的疗效。

The therapeutic effect of leucogen in treating alcoholic liver cirrhosis with thrombocytopenia or leukopenia.

作者信息

Su Min, He Mengwen, Yang Wu-Cai, Wang Jianjun, Guo Chang, Fu Yi-Ming, Li Shuyao, Ji Dong, Chen Hong-Yan

机构信息

From the Senior Department of Hepatology, The Fifth Medical Center of the People's Liberation Army, General Hospital, Beijing, China.

From the Senior Department of Hepatology, Peking University, 302 Clinical Medical School, Beijing, China.

出版信息

Ann Saudi Med. 2025 Jan-Feb;45(1):9-17. doi: 10.5144/0256-4947.2025.9. Epub 2025 Feb 6.

DOI:10.5144/0256-4947.2025.9
PMID:39929792
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11810874/
Abstract

BACKGROUND

Thrombocytopenia and leukopenia are common complications of alcoholic liver cirrhosis (ALC) and are associated with an increased risk of bleeding, infection and mortality.

OBJECTIVES

Evaluate the effectiveness and safety of leucogen, a cysteine derivative that increases platelet (PLT) and white blood cell (WBC) counts in ALC patients.

DESIGN

Retrospective.

SETTING

Department of hepatology, general hospital.

PATIENTS AND METHODS

Patients with ALC who had thrombocytopenia and/or leukopenia were enrolled between 2022 and 2023 and were divided into two groups based on their treatment: the leucogen group (20 mg, three times per day) and the non-leucogen group.

MAIN OUTCOME MEASURES

The primary endpoint was an increase in PLT or WBC of ≥5% from baseline.

SAMPLE SIZE

413 patients (320 patients in the final analysis).

RESULTS

In this retrospective study, 320 patients were analyzed post-propensity score matching: 160 patients each in the leucogen and non-leucogen groups. Following 3 months of treatment, the leucogen group experienced a median increase in PLT levels of 1.0×10/L versus a decrease of 3.0×10/L in the non-leucogen group (=.003), and a median increase in WBC counts of 0.1×10/L compared to a decrease of 0.1×10/L (=.006). The changes in ALT, AST, and TBIL levels were not significantly different between groups. A higher proportion of patients in the leucogen group experienced increases in both PLT (46.9% vs. 32.5%, =.012) and WBC counts (50.0% vs. 36.2%, =.018), and 28.1% of patients in the leucogen group had increases in both parameters, compared to 15.6% in the non-leucogen group (=.01). The leucogen group also demonstrated greater increases in PLT (OR 1.833; =.009) and WBC counts (OR 1.759; =.013) compared to the non-leucogen group. The safety profile of leucogen was favorable, with no significant adverse events reported. Leucogen was particularly beneficial for patients younger than 60 years and those with lower baseline ALT and AST levels, showing significant improvements in both PLT and WBC counts in these subgroups.

CONCLUSIONS

Leucogen effectively increased PLT and WBC counts in patients with ALC, showing a favorable safety profile.

LIMITATIONS

Retrospective study.

摘要

背景

血小板减少症和白细胞减少症是酒精性肝硬化(ALC)的常见并发症,与出血、感染及死亡风险增加相关。

目的

评估利血生(一种半胱氨酸衍生物)对提高ALC患者血小板(PLT)和白细胞(WBC)计数的有效性及安全性。

设计

回顾性研究。

地点

综合医院肝病科。

患者与方法

纳入2022年至2023年间患有血小板减少症和/或白细胞减少症的ALC患者,并根据治疗情况将其分为两组:利血生组(20毫克,每日三次)和非利血生组。

主要观察指标

主要终点为PLT或WBC较基线水平增加≥5%。

样本量

413例患者(最终分析320例患者)。

结果

在这项回顾性研究中,对320例患者进行倾向得分匹配后分析:利血生组和非利血生组各160例患者。治疗3个月后,利血生组PLT水平中位数增加1.0×10⁹/L,而非利血生组下降3.0×10⁹/L(P = 0.003);利血生组WBC计数中位数增加0.1×10⁹/L,非利血生组下降0.1×10⁹/L(P = 0.006)。两组间谷丙转氨酶(ALT)、谷草转氨酶(AST)和总胆红素(TBIL)水平变化无显著差异。利血生组中PLT增加(46.9%对32.5%,P = 0.012)和WBC计数增加(50.0%对36.2%,P = 0.018)的患者比例更高,利血生组28.1%的患者两项指标均增加,而非利血生组为15.⑥%(P = 0.01)。与非利血生组相比,利血生组PLT(比值比[OR]1.833;P = 0.009)和WBC计数(OR 1.759;P = 0.013)增加幅度更大。利血生的安全性良好,未报告显著不良事件。利血生对年龄小于60岁以及基线ALT和AST水平较低的患者尤其有益,在这些亚组中PLT和WBC计数均有显著改善。

结论

利血生有效提高了ALC患者的PLT和WBC计数,安全性良好。

局限性

回顾性研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98ef/11810874/92e31a5aae9e/0256-4947.2025.9-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98ef/11810874/05c37681b227/0256-4947.2025.9-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98ef/11810874/c82b2aff2f75/0256-4947.2025.9-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98ef/11810874/c576e8df1ace/0256-4947.2025.9-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98ef/11810874/7ed2fb6ebd6e/0256-4947.2025.9-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98ef/11810874/b05d96beb5f3/0256-4947.2025.9-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98ef/11810874/92e31a5aae9e/0256-4947.2025.9-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98ef/11810874/05c37681b227/0256-4947.2025.9-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98ef/11810874/c82b2aff2f75/0256-4947.2025.9-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98ef/11810874/c576e8df1ace/0256-4947.2025.9-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98ef/11810874/7ed2fb6ebd6e/0256-4947.2025.9-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98ef/11810874/b05d96beb5f3/0256-4947.2025.9-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98ef/11810874/92e31a5aae9e/0256-4947.2025.9-fig6.jpg

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