Literature DB >> 24140492

Novel α-galactosidase A mutation in patients with severe cardiac manifestations of Fabry disease.

Giovanni Duro1, M Beatrice Musumeci2, Paolo Colomba1, Carmela Zizzo1, Giuseppe Albeggiani1, Vittoria Mastromarino2, Massimo Volpe2, Camillo Autore3.   

Abstract

Fabry disease (FD) is a hereditary metabolic disorder caused by the partial or total inactivation of α-galactosidase A (α-gal A), a lysosomal hydrolase. This inactivation is responsible for the accumulation of undegraded glycosphingolipids in the lysosomes with subsequent cellular and microvascular dysfunction. Fabry is considered a rare disease, with an incidence of 1:40,000; however, there are good reasons to believe that it is often seen but rarely diagnosed. To date, more than 600 mutations have been identified in human GLA gene that are responsible for FD. We describe the case of a 54-year-old male patient, who presented with left ventricular hypertrophy, chronic renal failure and acroparaesthesias, which are considered to be specific features of FD. Clinical and instrumental investigations showed several cardiovascular manifestations. The molecular analysis of GLA gene revealed a novel mutation in the fifth exon, called N249K, and the enzymatic analysis showed no α-galactosidase A activity. Family screening detected the same mutation in some relatives and also the enzymatic analysis confirmed the diagnosis of FD. In conclusion, these data suggest that the N249K mutation may be associated with cardiac manifestations of FD combined with other classical features of the disease.
© 2013 Elsevier B.V. All rights reserved.

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Keywords:  Akt; Bp; CT; DNA complementary to RNA; ERK; FSGD; Fabry disease; GH; GHR; High resolution melting; Hypertrophic cardiomyopathy; JAK; Janus kinase; Mutation N249K; PI3K; PRLR; RACE; RT-PCR; SEM; SLR; STAT; TBE; UTR; base pair; cDNA; extracellular signal-regulated kinase; fish specific genome duplication; growth hormone; growth hormone receptor; mRNA; messenger RNA; nt; nucleotide; phosphatidylinositide 3-kinase; prolactin receptor; protein kinase B; rapid amplification of cDNA ends; reverse transcription polymerase chain reaction; signal transducer and activator of transcription; somatolactin receptor; standard error of the mean; threshold cycle number; tris–borate–ethylenediaminetetraacetic acid; untranslated region; α-Galactosidase A

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Year:  2013        PMID: 24140492     DOI: 10.1016/j.gene.2013.09.058

Source DB:  PubMed          Journal:  Gene        ISSN: 0378-1119            Impact factor:   3.688


  4 in total

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Journal:  Immun Ageing       Date:  2014-12-20       Impact factor: 6.400

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Journal:  BMC Med Genet       Date:  2016-10-24       Impact factor: 2.103

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Journal:  BMC Med Genet       Date:  2018-12-27       Impact factor: 2.103

4.  Functional evaluation of a novel GLA causative mutation in Fabry disease.

Authors:  Ping Li; Lijuan Zhang; Qiuhong Xiong; Zhe Wang; Xiaodong Cui; Yong-An Zhou; Yuxian Wang; Han Xiao; Changxin Wu
Journal:  Mol Genet Genomic Med       Date:  2019-07-18       Impact factor: 2.183

  4 in total

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