Literature DB >> 15028849

Twin pairs showing discordance of phenotype in adult Gaucher's disease.

R H Lachmann1, I R Grant, D Halsall, T M Cox.   

Abstract

BACKGROUND: Non-neuronopathic (type 1) Gaucher's disease, a recessive disorder caused by glucocerebrosidase deficiency, shows marked variability in the severity and extent of clinical expression: many individuals who harbour two mutant alleles remain mildly affected or asymptomatic. Despite much effort, it is not possible accurately to predict disease severity from the genotype, or to identify those patients destined to develop severe disease and meriting early treatment. AIM: To determine the degree to which variance in Gaucher disease is determined by non-heritable factors.
DESIGN: Case reports of monozygotic and dizygotic twin pairs.
RESULTS: For the monozygotic twin pair, homozygous for the frequent N370S glucocerebrosidase allele, there was no evidence that significant lipid storage was ever initiated in the unaffected twin. In contrast, pathological storage of glucocerebroside has been present in the macrophages of both members of the dizygotic twin pair (compound heterozygotes for the N370S and L444P alleles) from an early age but, by the age of 57 years, only one has developed symptoms. DISCUSSION: Non-heritable factors influence Gaucher disease expression in genetically predisposed individuals. Understanding the interactions between heritable and non-heritable factors will be critical for an analysis of pathogenesis, and the treatment of individuals predisposed to Gaucher disease.

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Year:  2004        PMID: 15028849     DOI: 10.1093/qjmed/hch036

Source DB:  PubMed          Journal:  QJM        ISSN: 1460-2393


  55 in total

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3.  Histone deacetylase inhibitors prevent the degradation and restore the activity of glucocerebrosidase in Gaucher disease.

Authors:  Jie Lu; Chunzhang Yang; Masako Chen; Donald Y Ye; Russell R Lonser; Roscoe O Brady; Zhengping Zhuang
Journal:  Proc Natl Acad Sci U S A       Date:  2011-12-12       Impact factor: 11.205

4.  Ultrasensitive in situ visualization of active glucocerebrosidase molecules.

Authors:  Martin D Witte; Wouter W Kallemeijn; Jan Aten; Kah-Yee Li; Anneke Strijland; Wilma E Donker-Koopman; Adrianus M C H van den Nieuwendijk; Boris Bleijlevens; Gertjan Kramer; Bogdan I Florea; Berend Hooibrink; Carla E M Hollak; Roelof Ottenhoff; Rolf G Boot; Gijsbert A van der Marel; Herman S Overkleeft; Johannes M F G Aerts
Journal:  Nat Chem Biol       Date:  2010-10-31       Impact factor: 15.040

5.  Decreased glucocerebrosidase activity in Gaucher disease parallels quantitative enzyme loss due to abnormal interaction with TCP1 and c-Cbl.

Authors:  Jie Lu; Jeffrey Chiang; Rajiv R Iyer; Eli Thompson; Christine R Kaneski; David S Xu; Chunzhang Yang; Masako Chen; Richard J Hodes; Russell R Lonser; Roscoe O Brady; Zhengping Zhuang
Journal:  Proc Natl Acad Sci U S A       Date:  2010-11-22       Impact factor: 11.205

6.  Disease severity in sibling pairs with type 1 Gaucher disease.

Authors:  Deborah Elstein; Ayelet Gellman; Gheona Altarescu; Aya Abrahamov; Irith Hadas-Halpern; Mici Phillips; Maya Margalit; Ehud Lebel; Menachem Itzchaki; Ari Zimran
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9.  The non-lysosomal β-glucosidase GBA2 is a non-integral membrane-associated protein at the endoplasmic reticulum (ER) and Golgi.

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Journal:  J Biol Chem       Date:  2012-12-17       Impact factor: 5.157

10.  Potential efficacy of enzyme replacement and substrate reduction therapy in three siblings with Gaucher disease type III.

Authors:  J Cox-Brinkman; M J van Breemen; B T van Maldegem; L Bour; W E Donker; C E M Hollak; F A Wijburg; J M F G Aerts
Journal:  J Inherit Metab Dis       Date:  2008-10-15       Impact factor: 4.982

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