Interleukin 10, but not tumor necrosis factor-alpha, gene variations are associated with factor VII inhibitor development.

Laboratory medicine Pub Date : 2024-01-06 DOI:10.1093/labmed/lmad026

Nahid Ramezanpour, Korosh Khanaki, Akbar Dorgalaleh, Mahmood Shams, Ali Elmi, Farhad Zaker

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Abstract

Objective: Development of alloantibodies against coagulation factor VII (FVII) is the main therapeutic challenge in severe congenital FVII deficiency. About 7% of patients with severe congenital FVII deficiency develop an inhibitor against FVII. In this research, the relationship between interleukin (IL)-10 and tumor necrosis factor-alpha (TNF)-α gene variants and inhibitor development was evaluated for a group of Iranian patients with severe congenital factor VII deficiency.

Methods: Patients with FVII deficiency were divided into 2 groups: 6 cases and 15 controls. Genotyping was performed using the amplification-refractory mutation system polymerase chain reaction.

Results: We found that IL-10 rs1800896 A>G gene variant is associated with the risk of FVII inhibitor development (OR = 0.077, 95% CI = 0.016-0.380, P = .001), whereas the TNFα-rs1800629G>A variant has no relation with inhibitor development in severe FVII deficiency.

Conclusion: The results show that the IL-10 rs1800896 A>G variant increases the risk of developing an inhibitor in patients with severe congenital FVII deficiency.

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白细胞介素 10（而非肿瘤坏死因子-α）基因变异与 VII 因子抑制剂的形成有关。

目的：凝血因子 VII（FVII）异体抗体的产生是严重先天性 FVII 缺乏症的主要治疗难题。约 7% 的严重先天性 FVII 缺乏症患者会产生 FVII 抑制剂。本研究评估了一组伊朗重度先天性 FVII 缺乏症患者的白细胞介素（IL）-10 和肿瘤坏死因子-α（TNF）-α 基因变异与抑制剂产生之间的关系：方法：将 FVII 缺乏症患者分为两组：6 例病例和 15 例对照。基因分型采用扩增-难治突变系统聚合酶链反应法进行：我们发现，IL-10 rs1800896 A>G 基因变异与 FVII 抑制剂的发生风险有关（OR = 0.077，95% CI = 0.016-0.380，P = .001），而 TNFα-rs1800629G>A 变异与严重 FVII 缺乏症抑制剂的发生无关：结论：研究结果表明，IL-10 rs1800896 A>G变异会增加严重先天性FVII缺乏症患者出现抑制因子的风险。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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Laboratory medicine

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