| Literature DB >> 26231322 |
E Kerkeni1, R Sakka2, S Sfar3, S Bouaziz3, N Ghedira3, K Ben Ameur2, H Ben Hmida2, F-Z Chioukh2, E S Ghédira4, M Gribaa5, K Monastiri2.
Abstract
Sanjad-Sakati syndrome (SSS) (OMIM 241410) is a rare autosomal recessive disorder characterized by congenital hypoparathyroidism with growth and mental retardation associated with seizures and a characteristic physiognomy. SSS molecular pathology has been shown to be due to mutations in the TBCE gene on chromosome 1q42-q43. All affected patients of Arab origin are homozygous for a 12-bp (155-166del) deletion in exon 3 of this gene. We report on a Tunisian child with SSS who was homozygous for the 155-166del mutation. Our findings provide additional support of the common (155-166del) deletion founder effect in exon 3 of the TBCE gene in Arab patients. It is very likely that this mutation originated in the Middle East and was introduced in Tunisia by the Banu Hilal invaders.Entities:
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Year: 2015 PMID: 26231322 DOI: 10.1016/j.arcped.2015.06.003
Source DB: PubMed Journal: Arch Pediatr ISSN: 0929-693X Impact factor: 1.180