Document Detail


Stüve-Wiedemann syndrome: long-term follow-up and genetic heterogeneity.
MedLine Citation:
PMID:  20447141     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Stüve-Wiedemann syndrome (SWS, OMIM 601559) is a severe autosomal recessive condition caused by mutations in the leukemia inhibitory receptor (LIFR) gene. The main characteristic features are bowing of the long bones, neonatal respiratory distress, swallowing/sucking difficulties and dysautonomia symptoms including temperature instability often leading to death in the first years of life. We report here four patients with SWS who have survived beyond 36 months of age with no LIFR mutation. These patients have been compared with six unreported SWS survivors carrying null LIFR mutations. We provide evidence of clinical homogeneity of the syndrome in spite of the genetic heterogeneity.
Authors:
C Jung; N Dagoneau; G Baujat; M Le Merrer; A David; M Di Rocco; B Hamel; A Mégarbané; A Superti-Furga; S Unger; A Munnich; V Cormier-Daire
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Clinical genetics     Volume:  77     ISSN:  1399-0004     ISO Abbreviation:  Clin. Genet.     Publication Date:  2010 Mar 
Date Detail:
Created Date:  2010-05-07     Completed Date:  2010-07-06     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0253664     Medline TA:  Clin Genet     Country:  Denmark    
Other Details:
Languages:  eng     Pagination:  266-72     Citation Subset:  IM    
Affiliation:
Department of Genetics, Université Paris Descartes, Paris, France.
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MeSH Terms
Descriptor/Qualifier:
Abnormalities, Multiple / genetics*,  physiopathology
Female
Follow-Up Studies
Genes, Recessive
Genetic Heterogeneity*
Humans
Leukemia Inhibitory Factor Receptor alpha Subunit / genetics
Male
Osteochondrodysplasias / genetics*,  physiopathology
Syndrome
Chemical
Reg. No./Substance:
0/LIFR protein, human; 0/Leukemia Inhibitory Factor Receptor alpha Subunit

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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