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缬更昔洛韦抑制来氟米特免疫抑制期间的 EBV 再激活。

Valganciclovir suppressed Epstein Barr virus reactivation during immunosuppression with alemtuzumab.

机构信息

Department of Medicine, Queen Mary Hospital, Hong Kong.

Department of Medicine, Queen Mary Hospital, Hong Kong.

出版信息

J Clin Virol. 2014 Apr;59(4):255-8. doi: 10.1016/j.jcv.2014.01.005. Epub 2014 Jan 18.

DOI:10.1016/j.jcv.2014.01.005
PMID:24507802
Abstract

BACKGROUND

Reactivation of latent herpes viruses occurs with immunosuppression. Alemtuzumab is an antibody targeting CD52, which is expressed on all B- and T-cells. Treatment with alemtuzumab leads to profound T-cell suppression, and reactivation of cytomegalovirus (CMV) and Epstein-Barr virus (EBV) occurs. Valganciclovir is used as an anti-CMV prophylaxis during alemtuzumab therapy.

OBJECTIVE

To determine if EBV reactivation is decreased with valganciclovir prophylaxis.

STUDY DESIGN

Plasma EBV DNA was serially quantified by quantitative polymerase chain reaction with a World Health Organization EBV standard in patients receiving alemtuzumab therapy with valganciclovir as anti-CMV prophylaxis.

RESULTS

Twenty-nine patients were studied. A total of 258 samples were quantified, at a median of 7 (3-25) specimens per patient. Twenty-four patients never had any quantifiable EBV DNA. Five patients (17%) developed EBV reactivation. Two patients had EBV reactivation at very low levels of about 10(3)IU/mL, 3-4 logs lower than those typically found in post-transplant lymphoproliferative diseases. Three patients had EBV reactivation at higher levels of 10(4)IU/mL, which only occurred after two courses of alemtuzumab were administered. EBV reactivation subsided spontaneously in four cases. One patient developed EBV-positive Hodgkin lymphoma, but he had also received previously another potent T-cell suppressing drug fludarabine.

CONCLUSION

Valganciclovir suppressed EBV reactivation during alemtuzumab therapy. It might be a useful prophylaxis in immunocompromized patient populations at high risk of EBV reactivation.

摘要

背景

潜伏的疱疹病毒会在免疫抑制时被激活。阿仑单抗是一种靶向 CD52 的抗体,CD52 表达于所有 B 细胞和 T 细胞上。阿仑单抗治疗会导致 T 细胞严重抑制,从而导致巨细胞病毒(CMV)和 EBV 被激活。缬更昔洛韦被用作阿仑单抗治疗期间的 CMV 预防药物。

目的

确定缬更昔洛韦预防是否能降低 EBV 的激活。

研究设计

在接受阿仑单抗治疗并使用缬更昔洛韦进行 CMV 预防的患者中,通过定量聚合酶链反应(qPCR)用世界卫生组织 EBV 标准连续定量检测血浆 EBV DNA。

结果

共 29 例患者入组。每位患者的中位数为 7(3-25)份样本,共检测了 258 份样本。24 例患者从未检测到任何可定量的 EBV DNA。5 例患者(17%)出现 EBV 激活。2 例患者 EBV 激活水平非常低,约为 10(3)IU/mL,比移植后淋巴组织增生性疾病中通常发现的水平低 3-4 个对数级。3 例患者 EBV 激活水平较高,为 10(4)IU/mL,仅在接受了两个疗程的阿仑单抗治疗后才出现。4 例 EBV 激活病例自发消退。1 例患者发展为 EBV 阳性霍奇金淋巴瘤,但他此前还接受了另一种强效的 T 细胞抑制药物氟达拉滨治疗。

结论

缬更昔洛韦抑制了阿仑单抗治疗期间的 EBV 激活。对于 EBV 易激活的高危免疫抑制患者群体,它可能是一种有用的预防药物。

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