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Hypotonia-cystinuria 2p21 deletion syndrome: Intrafamilial variability of clinical expression
Atif Towheed1, Christian L Hietanen1, Vasudeva G Kamath1
1Touro College of Osteopathic Medicine, Middletown, NY, 10940.
Insights
A rare genetic disorder, hypotonia-cystinuria 2p21 deletion syndrome, causes mitochondrial dysfunction in infants. Symptoms diverge later in childhood, showing significant intrafamilial phenotypic variability.
Area of Science:
- Genetics
- Pediatrics
- Biochemistry
Background:
- Congenital hypotonia, lactic acidosis, and failure to thrive are critical early indicators in infants.
- Cystinuria and nephrolithiasis in males, contrasted with chronic neurobehavioral disturbances in females, suggest complex genetic influences.
- Mitochondrial dysfunction, indicated by deficient cytochrome c oxidase activity, points to underlying metabolic derangements.
Abstract:
Two siblings presented similarly with congenital hypotonia, lactic acidosis, and failure to thrive. Later in childhood, the brother developed cystinuria and nephrolithiasis whereas the older sister suffered from cystinuria and chronic neurobehavioral disturbances. Biopsied muscle studies demonstrated deficient cytochrome c oxidase activities consistent with a mitochondrial disease. Whole exome sequencing (WES), however, revealed a homozygous 2p21 deletion involving two contiquous genes, SLC3A1 (deletion of exons 2-10) and PREPL (deletion of exons 2-14). The molecular findings were consistent with the hypotonia-cystinuria 2p21 deletion syndrome, presenting similarly in infancy with mitochondrial dysfunction but diverging later in childhood and displaying intrafamilial phenotypic variability.
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