| Literature DB >> 20635403 |
Oliver Bartsch1, Eberhard Schneider, Natalja Damatova, Roger Weis, Maria Tufano, Raffaele Iorio, Alischo Ahmed, Vera Beyer, Ulrich Zechner, Thomas Haaf.
Abstract
We report on a 4-year-old girl with severe developmental delay, absent speech, and chromosome 22q13.3 deletion (Phelan-McDermid syndrome), karyotype 46,XX.ish del(22)(q13.31qter)(ARSA-,N85A-,SHANK3-). At the age of 3 years, she needed an emergency liver transplantation because of fulminant hepatic failure, most likely caused by hyperacute autoimmune hepatitis triggered by a viral infection. This is the second report of a patient with 22q13.3 deletion and fulminant liver failure. By array-CGH we identified in this patient a 5.675 Mb terminal deletion (22q13.31 --> qter; including approximately 55 genes; from NUP50 to RABL2B) and in the previous patient a 1.535 Mb deletion (22q13.32 --> qter; including approximately 39 genes; from BRD1 to RABL2B). PIM3 is a prime candidate gene for the fulminant hepatic failure in the two patients; SHANK3/PROSAP2 could be another candidate gene. We recommend liver function tests and array-CGH in the management of patients with Phelan-McDermid syndrome. This patient showed a developmental catch-up following the liver transplantation, possibly suggesting that chronic hepatic disease could contribute to the developmental delay in a subset of these patients.Entities:
Mesh:
Year: 2010 PMID: 20635403 DOI: 10.1002/ajmg.a.33542
Source DB: PubMed Journal: Am J Med Genet A ISSN: 1552-4825 Impact factor: 2.802