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Association between RAS gene polymorphisms (ACE I/D, AGT M235T) and Henoch-Schönlein purpura in a Turkish population.
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MedLine Citation:
PMID:  23151617     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Henoch-Schönlein purpura (HSP) is a small-vessel vasculitis of autoimmune hypersensitivity, and renin-angiotensin system (RAS) regulates vascular homeostasis and inflammation with activation of cytokine release. Thus, we aimed to investigate the association between HSP and ACE I/D and AGT M235T polymorphisms. Genotyping was determined by allele specific PCR and PCR-RFLP. We obtained a significant difference in genotype distribution (p=0.003) and allele frequencies (p<0.001) of ACE I/D polymorphism between patients and controls, while no significant association was detected in genotype distribution (p> 0.05) and allele frequencies (p> 0.05) of the AGT M235T polymorphism. Risk assessment showed significant risk for HSP in the subjects both with the ID + DD genotype (p=0.019, OR: 2.288, 95% CI: 1.136-4.609) and D allele (OR: D vs. I: 2.0528, 95% CI: 1.3632-3.0912, p=0.001) while no significant risk was obtained for HSP in the subjects both with the MT + TT genotype (p=0.312, OR: 1.3905, 95% T vs. M: 1.065, 95% CI: 0.7326-2.6391) and T allele (OR: patients were stratified by the presence of certain systemic complications of HSP, no significant association was detected with ACE I/D, and AGT M235T polymorphisms. Our findings suggest that ACE I/D polymorphism is significantly associated with HSP susceptibility.
Authors:
Sinem Nalbantoglu; Yılmaz Tabel; Sevgi Mir; Erkin Serdaroğlu; Afig Berdeli
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Disease markers     Volume:  34     ISSN:  1875-8630     ISO Abbreviation:  Dis. Markers     Publication Date:  2013  
Date Detail:
Created Date:  2012-12-18     Completed Date:  2013-05-28     Revised Date:  2013-12-30    
Medline Journal Info:
Nlm Unique ID:  8604127     Medline TA:  Dis Markers     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  23-32     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Adolescent
Adult
Amino Acid Substitution
Angiotensinogen / genetics*
Case-Control Studies
Child
Child, Preschool
DNA Mutational Analysis
Female
Gene Frequency
Genetic Association Studies
Genetic Predisposition to Disease
Humans
INDEL Mutation*
Male
Middle Aged
Peptidyl-Dipeptidase A / genetics*
Polymorphism, Single Nucleotide*
Purpura, Schoenlein-Henoch / enzymology,  genetics*
Renin-Angiotensin System / genetics*
Risk Factors
Turkey
Young Adult
Chemical
Reg. No./Substance:
0/AGT protein, human; 11002-13-4/Angiotensinogen; EC 3.4.15.1/ACE protein, human; EC 3.4.15.1/Peptidyl-Dipeptidase A

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

Full Text
Journal Information
Journal ID (nlm-ta): Dis Markers
Journal ID (iso-abbrev): Dis. Markers
Journal ID (publisher-id): DM
ISSN: 0278-0240
ISSN: 1875-8630
Publisher: IOS Press
Article Information
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Copyright © 2013 Hindawi Publishing Corporation.
Received Day: 12 Month: 11 Year: 2012
Accepted Day: 12 Month: 11 Year: 2012
Print publication date: Year: 2013
Electronic publication date: Day: 17 Month: 12 Year: 2012
Volume: 34 Issue: 1
First Page: 23 Last Page: 32
PubMed Id: 23151617
ID: 3810110
Article Id: 624757
DOI: 10.3233/DMA-2012-120946

Association between RAS Gene Polymorphisms (ACE I/D, AGT M235T) and Henoch-Schönlein Purpura in a Turkish Population
Sinem Nalbantoglu1*
Yılmaz Tabel2
Sevgi Mir3
Erkin Serdaroğlu4
Afig Berdeli1
1Molecular Medicine LaboratoryChildren’s HospitalFaculty of MedicineEge UniversityBornovaIzmirTurkey
2Department of PediatricsFaculty of MedicineInonu UniversityMalatyaTurkey
3Division of Pediatric NephrologyDepartment of PediatricsFaculty of MedicineEge UniversityBornovaIzmirTurkey
4Izmir Dr. Behcet Uz Children's HospitalIzmirTurkey
Correspondence: *Sinem Nalbantoglu: nalbantoglusinem@gmail.com


Article Categories:
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Keywords: Henoch-Schönlein purpura (HSP), ACE I/D, AGT M235T, Single Nucleotide Polymorphism (SNP), organ involvements, Genotype-phenotype correlation.

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