Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA.
Clin Exp Med. 2024 Jan 27;24(1):17. doi: 10.1007/s10238-023-01259-y.
Activated phosphoinositide 3-kinase delta syndrome (APDS) is a rare genetic disorder that presents clinically as a primary immunodeficiency. Clinical presentation of APDS includes severe, recurrent infections, lymphoproliferation, lymphoma, and other cancers, autoimmunity and enteropathy. Autosomal dominant variants in two independent genes have been demonstrated to cause APDS. Pathogenic variants in PIK3CD and PIK3R1, both of which encode components of the PI3-kinase, have been identified in subjects with APDS. APDS1 is caused by gain of function variants in the PIK3CD gene, while loss of function variants in PIK3R1 have been reported to cause APDS2. We conducted a review of the medical literature and identified 256 individuals who had a molecular diagnosis for APDS as well as age at last report; 193 individuals with APDS1 and 63 with APDS2. Despite available treatments, survival for individuals with APDS appears to be shortened from the average lifespan. A Kaplan-Meier survival analysis for APDS showed the conditional survival rate at the age of 20 years was 87%, age of 30 years was 74%, and ages of 40 and 50 years were 68%. Review of causes of death showed that the most common cause of death was lymphoma, followed by complications from HSCT. The overall mortality rate for HSCT in APDS1 and APDS2 cases was 15.6%, while the mortality rate for lymphoma was 47.6%. This survival and mortality data illustrate that new treatments are needed to mitigate the risk of death from lymphoma and other cancers as well as infection. These analyses based on real-world evidence gathered from the medical literature comprise the largest study of survival and mortality for APDS to date.
活化的磷酯酰肌醇 3-激酶 δ 综合征(APDS)是一种罕见的遗传性疾病,临床上表现为原发性免疫缺陷。APDS 的临床表现包括严重、反复感染、淋巴组织增生、淋巴瘤和其他癌症、自身免疫和肠病。已经证明两种独立基因中的常染色体显性变异可导致 APDS。APDS 患者中已鉴定出编码 PI3-激酶成分的 PIK3CD 和 PIK3R1 的致病性变异。APDS1 是由 PIK3CD 基因的功能获得性变异引起的,而 PIK3R1 的功能丧失性变异已被报道可引起 APDS2。我们对医学文献进行了回顾,确定了 256 名具有 APDS 分子诊断和最后报告年龄的个体;193 名 APDS1 患者和 63 名 APDS2 患者。尽管有可用的治疗方法,但 APDS 患者的生存似乎比平均寿命缩短。APDS 的 Kaplan-Meier 生存分析显示,20 岁时的条件生存率为 87%,30 岁时为 74%,40 岁和 50 岁时为 68%。对死亡原因的回顾表明,最常见的死亡原因是淋巴瘤,其次是 HSCT 的并发症。APDS1 和 APDS2 病例中 HSCT 的总死亡率为 15.6%,而淋巴瘤的死亡率为 47.6%。这些生存和死亡率数据表明,需要新的治疗方法来降低淋巴瘤和其他癌症以及感染的死亡风险。这些基于从医学文献中收集的真实世界证据的分析是迄今为止对 APDS 进行的最大规模的生存和死亡率研究。