Li Jiayue, Gao Jie, Wang Lin, Li Yanhua, Zhang Ming, Pan Xietian, Guo Xinhong
Department of Cardiovascular Medicine, the Sixth Medical Center, PLA General Hospital, Beijing 100853, China.
Zhonghua Yi Xue Yi Chuan Xue Za Zhi. 2024 May 10;41(5):596-600. doi: 10.3760/cma.j.cn511374-20230401-00184.
To explore the genetic etiology for a patient with Alström syndrome (ALMS) presenting as dilated cardiomyopathy.
A 41-year-old male patient who had presented at the Sixth Medical Center of PLA General Hospital on October 20, 2021 was selected as the study subject. Clinical and laboratory examinations were carried out. Whole exome sequencing (WES) was employed for genetic testing, and candidate variants were validated by Sanger sequencing and pathogenicity analysis.
The patient had a 14-year medical history characterized by dilated cardiomyopathy, complete atrioventricular block, visual impairment, sensorineural hearing loss, truncal obesity, insulin resistance, type 2 diabetes, hypertension, renal dysfunction, and paranoid delusions. Genetic testing revealed that he has harbored compound heterozygous variants of the ALMS1 gene, namely c.6823C>T (p.Arg2275Ter) and c.9442_9445dup (p.Ser3149LysfsTer2). Sanger sequencing confirmed that they were inherited from his father and mother, respectively. Based on the guidelines from the American College of Medical Genetics and Genomics (ACMG), both variants were predicted to be pathogenic (PVS1_VeryStrong+PM2_Supporting+PM3+PP3, PVS1_VeryStrong+PM2_Supporting+PM3). Literature review indicated that the complete atrioventricular block in the patient was a phenotype unreported previously.
The c.6823C>T (p.Arg2275Ter) and c.9442_9445dup (p.Ser3149LysfsTer2) compound heterozygous variants of the ALMS1 gene probably underlay the pathogenesis in this patient. Above findings have expanded the phenotypic spectrum of ALMS and provided insights for clinicians dealing with similar cases.
探讨以扩张型心肌病为表现的阿尔斯特伦综合征(ALMS)患者的遗传病因。
选取2021年10月20日就诊于解放军总医院第六医学中心的一名41岁男性患者作为研究对象。进行了临床和实验室检查。采用全外显子组测序(WES)进行基因检测,并通过桑格测序和致病性分析对候选变异进行验证。
该患者有14年病史,特征为扩张型心肌病、完全性房室传导阻滞、视力障碍、感音神经性听力损失、躯干肥胖、胰岛素抵抗、2型糖尿病、高血压、肾功能不全和偏执妄想。基因检测显示,他携带ALMS1基因的复合杂合变异,即c.6823C>T(p.Arg2275Ter)和c.9442_9445dup(p.Ser3149LysfsTer2)。桑格测序证实它们分别遗传自他的父亲和母亲。根据美国医学遗传学与基因组学学会(ACMG)的指南,这两个变异均被预测为致病性变异(PVS1_VeryStrong+PM2_Supporting+PM3+PP3,PVS1_VeryStrong+PM2_Supporting+PM3)。文献复习表明,该患者的完全性房室传导阻滞是此前未报道过的一种表型。
ALMS1基因的c.6823C>T(p.Arg2275Ter)和c.9442_9445dup(p.Ser3149LysfsTer2)复合杂合变异可能是该患者发病机制的基础。上述发现扩展了ALMS的表型谱,并为临床医生处理类似病例提供了思路。