Key result
Whole-exome sequencing identifies a novel ALPK3 frameshift mutation in an infant with congenital cardiomyopathy.
Case Report (n=1)
No
Identifies a novel homozygous frameshift mutation in ALPK3 associated with congenital cardiomyopathy, expanding the genetic spectrum of the disease.
Expands ALPK3 spectrum in congenital cardiomyopathy; leaves open validation before informing genetic testing or practice.
Primary cardiomyopathy is one of the most common inherited cardiac diseases and harbors significant phenotypic and genetic heterogeneity. Because of this, genetic testing has become standard in treatment of this disease group. Indeed, in recent years, next-generation DNA sequencing has found broad applications in medicine, both as a routine diagnostic tool for genetic disorders and as a high-throughput discovery tool for identifying novel disease-causing genes. We describe a male infant with primary dilated cardiomyopathy who was diagnosed using intrauterine echocardiography and found to progress to hypertrophic cardiomyopathy after birth. This proband was born to a nonconsanguineous family with a past history of a male fetus that died because of cardiac abnormalities at 30 wk of gestation. Using whole-exome sequencing, a novel homozygous frameshift mutation (c.2018delC; p.Gln675SerfsX30) in ALPK3 was identified and confirmed with Sanger sequencing. Heterozygous family members were normal with echocardiographic examination. To date, only two studies have reported homozygous pathogenic variants of ALPK3, with a total of seven affected individuals with cardiomyopathy from four unrelated consanguineous families. We include a discussion of the patient's phenotypic features and a review of relevant literature findings.
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Çağlayan et al. (2017) conducted a case report in Congenital cardiomyopathy (n=1). Whole-exome sequencing was evaluated on Identification of disease-causing genetic variant. Whole-exome sequencing identified a novel homozygous frameshift mutation (c.2018delC; p.Gln675SerfsX30) in the ALPK3 gene in a male infant with congenital cardiomyopathy.
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