Bianchi Chloé, Margot Henri, Fernandes Helder, Pasquet Marlène, Priqueler Laurence, Roy-Peaud Frédérique, Bauduer Frédéric, Bayart Sophie, Garnier Nathalie, Fain Olivier, Van Gils Julien, Joly Sandrine Baron, Rialland Fanny, Paillard Catherine, Deparis Marianna, Lambilliotte Anne, Leblanc Thierry, Fahd Mony, Leverger Guy, Héritier Sébastien, Geneviève David, Rieux-Laucat Frédéric, Picard Capucine, Neyraud Caroline, Aladjidi Nathalie
Pediatric Haemato-Immunology, CIC1401, INSERM CICP, National Reference Center for Autoimmune Cytopenias in Children (CEREVANCE), Bordeaux University Hospital, Bordeaux, France.
Department of Medical Genetics, MRGM INSERM U1211, Bordeaux University Hospital, University of Bordeaux, Bordeaux, France.
Br J Haematol. 2024 May;204(5):1899-1907. doi: 10.1111/bjh.19387. Epub 2024 Mar 3.
Kabuki syndrome (KS) is now listed in the Human Inborn Errors of Immunity (IEI) Classification. It is a rare disease caused by KMT2D and KDM6A variants, dominated by intellectual disability and characteristic facial features. Recurrently, pathogenic variants are identified in those genes in patients examined for autoimmune cytopenia (AIC), but interpretation remains challenging. This study aims to describe the genetic diagnosis and the clinical management of patients with paediatric-onset AIC and KS. Among 11 patients with AIC and KS, all had chronic immune thrombocytopenic purpura, and seven had Evans syndrome. All had other associated immunopathological manifestations, mainly symptomatic hypogammaglobinaemia. They had a median of 8 (5-10) KS-associated manifestations. Pathogenic variants were detected in KMT2D gene without clustering, during the immunological work-up of AIC in three cases, and the clinical strategy to validate them is emphasized. Eight patients received second-line treatments, mainly rituximab and mycophenolate mofetil. With a median follow-up of 17 (2-31) years, 8/10 alive patients still needed treatment for AIC. First-line paediatricians should be able to recognize and confirm KS in children with ITP or multiple AIC, to provide early appropriate clinical management and specific long-term follow-up. The epigenetic immune dysregulation in KS opens exciting new perspectives.
歌舞伎综合征(KS)现已被列入人类先天性免疫缺陷(IEI)分类中。它是一种由KMT2D和KDM6A基因变异引起的罕见疾病,主要特征为智力残疾和特殊面容。最近,在接受自身免疫性血细胞减少症(AIC)检查的患者中,这些基因被鉴定出致病性变异,但解读仍具有挑战性。本研究旨在描述儿童期发病的AIC和KS患者的基因诊断及临床管理情况。在11例AIC和KS患者中,所有患者均患有慢性免疫性血小板减少性紫癜,7例患有伊文氏综合征。所有患者均有其他相关的免疫病理表现,主要为症状性低丙种球蛋白血症。他们的KS相关表现中位数为8(5 - 10)项。在3例AIC免疫检查过程中,在KMT2D基因中检测到致病性变异,但无聚集现象,并强调了验证这些变异的临床策略。8例患者接受了二线治疗,主要是利妥昔单抗和霉酚酸酯。中位随访时间为17(2 - 31)年,10例存活患者中有8例仍需要接受AIC治疗。一线儿科医生应能够识别并确诊患有ITP或多种AIC的儿童中的KS,以便提供早期适当的临床管理和特定的长期随访。KS中的表观遗传免疫失调开启了令人兴奋的新前景。