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Carbamazepine hypersensitivity syndrome triggered by a human herpes virus reactivation in a genetically predisposed patient.

机译:卡马西平超敏综合症是由遗传易感患者中的人疱疹病毒再激活引起的。

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摘要

A case of severe hypersensitivity syndrome, triggered by carbamazepine in the presence of a concomitant active human herpes virus (HHV) 6 and 7 infection is described. To further understand the molecular mechanism of this adverse reaction, analyses of the genetic variants of human leukocyte antigen (HLA) and of the epoxide hydrolase gene (EPHX1), previously associated with carbamazepine hypersensitivity, were performed. A lymphocyte transformation test (LTT) was conducted in order to detect drug-specific lymphocytes. In the hypersensitive patient, 2 genetic factors previously associated with intolerance to carbamazepine were detected: the allele HLA-A*3101 and homozygosity for the variant allele of SNP rs1051740 in EPHX1. Drug-specific lymphocytes could be detected by LTT when the HHV was active (positive PCR for viral DNA and increased anti-HHV 6 IgG titer), but not when it was no longer active. In conclusion, we document a case of severe carbamazepine hypersensitivity triggered by viral reactivation in a patient presenting the interaction of 2 unfavorable genetic factors.
机译:描述了卡马西平在伴有活动性人类疱疹病毒(HHV)6和7感染的情况下引发的严重超敏综合症。为了进一步了解这种不良反应的分子机制,进行了人类白细胞抗原(HLA)和环氧化物水解酶基因(EPHX1)的遗传变异的分析,这些变异先前与卡马西平超敏反应有关。进行了淋巴细胞转化试验(LTT),以检测药物特异性淋巴细胞。在这名过敏症患者中,检测到2个先前与卡马西平不耐受相关的遗传因素:EPHX1中的等位基因HLA-A * 3101和SNP rs1051740变异等位基因的纯合性。当HHV活跃时(病毒DNA的阳性PCR和增加的抗HHV 6 IgG滴度),LTT可以检测到药物特异性的淋巴细胞,但在不再活跃时则不能。总而言之,我们记录了一例由病毒再活化引发的严重卡马西平超敏反应的病例,该患者表现出2种不利遗传因素的相互作用。

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