Published online Dec 26, 2017. doi: 10.4330/wjc.v9.i12.848
Peer-review started: March 24, 2017
First decision: July 17, 2017
Revised: August 28, 2017
Accepted: September 12, 2017
Article in press: September 12, 2017
Published online: December 26, 2017
Processing time: 273 Days and 6.5 Hours
Genetic analyses of patients with transposition of the great arteries have identified rare copy number variations, suggesting that they may be significant to the aetiology of the disease. This paper reports the identification of a 16p11.2 microduplication, a variation that has yet to be reported in association with transposition of the great arteries. The 16p11.2 microduplication is associated with autism spectrum disorder and developmental delay, but with highly variable phenotypic effects. Autism and attention deficit disorders are observed more frequently in children with congenital heart disease than in the general population. Neonatal surgery is proposed as a risk factor, but as yet unidentified genetic abnormalities should also be taken into account. Thus, congenital heart abnormalities may constitute a part of the phenotypic spectrum associated with duplications at 16p11.2. We suggest chromosomal microarray be considered part of the diagnostic work-up in patients with transposition of the great arteries.
Core tip: Rare copy number variations may be of significance to the aetiology of transposition of the great arteries. This paper reports, for the first time, the finding of a 16p11.2 microduplication in a patient with transposition of the great arteries. Recognizing a possible genetic association to transposition of the great arteries will spur investigations into associated phenotypic effects such as developmental delays, thus allowing for earlier identification and treatment. We recommend that chromosomal microarray be considered part of the diagnostic work-up in patients with transposition of the great arteries.