Kerkeni E, Sakka R, Sfar S, Bouaziz S, Ghedira N, Ben Ameur K, Ben Hmida H, Chioukh F-Z, Ghédira E S, Gribaa M, Monastiri K
Research Unit 01/UR/08-14, Faculty of medicine of Monastir, University of Monastir, Monastir, Tunisia; Department of intensive care and neonatal medicine, CHU Fattouma Bourguiba, Monastir, Tunisia.
Research Unit 01/UR/08-14, Faculty of medicine of Monastir, University of Monastir, Monastir, Tunisia; Department of intensive care and neonatal medicine, CHU Fattouma Bourguiba, Monastir, Tunisia.
Arch Pediatr. 2015 Sep;22(9):951-5. doi: 10.1016/j.arcped.2015.06.003. Epub 2015 Jul 29.
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.
桑贾德 - 萨卡蒂综合征(SSS)(OMIM 241410)是一种罕见的常染色体隐性疾病,其特征为先天性甲状旁腺功能减退,并伴有生长发育迟缓和智力障碍,同时伴有癫痫发作和特征性面容。已证明SSS的分子病理学是由1号染色体q42 - q43上的TBCE基因突变所致。所有阿拉伯裔的患病患者在该基因外显子3中均为12个碱基对(155 - 166del)缺失的纯合子。我们报告了一名患有SSS的突尼斯儿童,其为155 - 166del突变的纯合子。我们的研究结果为阿拉伯患者中TBCE基因外显子3常见的(155 - 166del)缺失奠基者效应提供了额外支持。这种突变很可能起源于中东,并由巴努·希拉尔入侵者引入突尼斯。