Gao Haiqing, Zhao Ying, Chen Shengan, Zhang Zhen, Yang Fanping, Chen Zihua, Wang Lanting, Yang Jin, He Shan, Tang Chang, Zheng Shenyuan, Guan Chenggong, Xu Yu, Tang Lin, Zhang Aiyuan, Maurer Marcus, Lee Dylan, Ma Li, Luo Xiaoqun
Department of Allergy & Immunology, Department of Dermatology, Huashan Hospital, Fudan University, 12 Middle Urumqi Road, Shanghai, 200040, P.R. China.
Research Center of Allergy and Disease, Fudan University, Shanghai, 200040, P.R. China.
J Clin Immunol. 2025 Aug 23;45(1):124. doi: 10.1007/s10875-025-01912-z.
Hereditary angioedema with normal C1 inhibitor (HAE-nC1-INH) is a rare and genetically heterogeneous disorder with an incomplete molecular understanding. This study aimed to identify novel genetic variants associated with HAE-nC1-INH, characterize their clinical manifestations, and evaluate real-world treatment responses. Whole-exome sequencing of 27 HAE patients, including eight with HAE-nC1-INH, identified four previously unreported MYOF variants and additional pathogenic variants in KNG1 and HS3ST6, expanding the genetic spectrum of the disease. MYOF variants were associated with recurrent edema episodes, often with prolonged duration. The HS3ST6 variant was linked to refractory angioedema with non-resolving lower extremity involvement, highlighting atypical, persistent clinical phenotypes beyond the classical self-limiting presentation of HAE. Lanadelumab effectively reduced attack frequency in most patients; however, the variability in treatment response, particularly in MYOF and HS3ST6 carriers, highlights the need for individualized therapeutic approaches. These findings provide new insights into the genetic and clinical complexity of HAE-nC1-INH and emphasize the importance of genetic testing in refining diagnosis and optimizing treatment strategies, contributing to a more precise understanding of hereditary angioedema.
C1抑制剂正常的遗传性血管性水肿(HAE-nC1-INH)是一种罕见的、基因异质性疾病,对其分子机制的了解尚不完整。本研究旨在鉴定与HAE-nC1-INH相关的新型基因变异,描述其临床表现,并评估实际治疗反应。对27例HAE患者进行全外显子测序,其中包括8例HAE-nC1-INH患者,鉴定出4个先前未报道的MYOF变异以及KNG1和HS3ST6中的其他致病变异,扩大了该疾病的基因谱。MYOF变异与复发性水肿发作相关,发作时间通常较长。HS3ST6变异与难治性血管性水肿及下肢受累不缓解有关,突出了HAE经典自限性表现之外的非典型、持续性临床表型。在大多数患者中,lanadelumab可有效降低发作频率;然而,治疗反应的变异性,尤其是在MYOF和HS3ST6携带者中,凸显了个体化治疗方法的必要性。这些发现为HAE-nC1-INH的遗传和临床复杂性提供了新的见解,并强调了基因检测在完善诊断和优化治疗策略中的重要性,有助于更精确地了解遗传性血管性水肿。