| Literature DB >> 28945313 |
Théa Venet1, Emmanuelle Masson2,3, Cécile Talbotec4, Kareen Billiemaz1, Renaud Touraine5, Claire Gay6, Sylvie Destombe6, David N Cooper7, Hugues Patural1, Jian-Min Chen2,8,9, Claude Férec2,3,8,9.
Abstract
Exocrine pancreatic insufficiency (EPI) is rare in children, with most if not all cases occurring as part of syndromic conditions such as cystic fibrosis and Shwachman-Diamond syndrome. Here we report two cases, both presenting with severe EPI around 5 months of age. Characterized by diffuse pancreatic lipomatosis, they otherwise exhibited no remarkable deficiencies in other organs. Novel non-identical homozygous variants (a deletion removing the entire SPINK1 gene and an insertion of a full-length inverted Alu element into the 3'-untranslated region of the SPINK1 gene) resulting in the complete functional loss of the SPINK1 gene (encoding pancreatic secretory trypsin inhibitor) were identified in each patient. Having correlated our findings with current knowledge of SPINK1's role in exocrine pancreas pathophysiology, we propose that complete and partial functional losses of the SPINK1 gene are associated with quite distinct phenotypes, the former causing a new pediatric disease entity of severe infantile isolated EPI.Entities:
Keywords: Alu insertion; SPINK1 gene; chronic pancreatitis; exocrine pancreatic insufficiency; pancreatic lipomatosis
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Year: 2017 PMID: 28945313 DOI: 10.1002/humu.23343
Source DB: PubMed Journal: Hum Mutat ISSN: 1059-7794 Impact factor: 4.878