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静脉注射免疫球蛋白治疗对血小板生成的影响。

Influence of Intravenous Immunoglobulin Treatment on Thrombopoiesis.

作者信息

Meyer Oliver, Winter Oliver, Salama Abdulgabar

机构信息

Institut für Transfusionsmedizin, Charité - Universitätsmedizin Berlin, Germany.

出版信息

Transfus Med Hemother. 2012 Jun;39(3):217-220. doi: 10.1159/000339258. Epub 2012 May 15.

DOI:10.1159/000339258
PMID:22851938
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3375129/
Abstract

AIM

The mechanisms by which intravenous immunoglobulins (IVIg) result in an increase in platelet counts in most patients with autoimmune thrombocytopenia (ITP) have not yet been fully explained. One of these mechanisms may be related to stimulation of thrombopoiesis. METHODS: A total of 13 adult patients who received IVIg were studied: 11 patients with primary ITP, 1 patient with ITP related to common variable immunodeficiency (CVID), and 1 patient with uncharacterized thrombocytopenia. IVIg (0.5-1.5 g/kg body weight) was administered on consecutive days (days 1-3). Endogenous thrombopoietin (eTPO) was measured prior to and at least 1 day following treatment. In addition, IL-6 was measured in 5 of the treated patients. RESULTS: In 10 of 13 patients, IVIg treatment resulted in an increase in platelet counts. eTPO remained unchanged or elevated in almost all cases where the platelet count remained low (<100 × 10(3)/μ0. In all cases with normal or increased platelet counts (>100 × 10(3)/μ0, the eTPO concentration decreased. Furthermore, IVIg induced IL-6 synthesis in all 5 examined patients. CONCLUSION: Our data indicate that the induction of eTPO synthesis by IL-6 may be a potential mechanism in which IVIg may stimulate thrombopoiesis. Further studies are required to characterize this mechanism.

摘要

目的

静脉注射免疫球蛋白(IVIg)使大多数自身免疫性血小板减少症(ITP)患者血小板计数增加的机制尚未完全阐明。其中一种机制可能与刺激血小板生成有关。方法:共研究了13例接受IVIg治疗的成年患者:11例原发性ITP患者,1例与常见可变免疫缺陷(CVID)相关的ITP患者,以及1例血小板减少症未明确的患者。连续数日(第1 - 3天)给予IVIg(0.5 - 1.5 g/kg体重)。在治疗前及治疗后至少1天测量内源性血小板生成素(eTPO)。此外,对5例接受治疗的患者测量了白细胞介素-6(IL-6)。结果:13例患者中有10例,IVIg治疗使血小板计数增加。在几乎所有血小板计数仍低(<100×10³/μl)的病例中,eTPO保持不变或升高。在所有血小板计数正常或升高(>100×10³/μl)的病例中,eTPO浓度降低。此外,IVIg在所有5例接受检查的患者中均诱导了IL-6的合成。结论:我们的数据表明,IL-6诱导eTPO合成可能是IVIg刺激血小板生成的一种潜在机制。需要进一步研究来阐明这一机制。

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本文引用的文献

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