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Article: Corticotropin releasing hormone (CRH) promoter polymorphisms in various ethnic groups of patients with rheumatoid arthritis

TitleCorticotropin releasing hormone (CRH) promoter polymorphisms in various ethnic groups of patients with rheumatoid arthritis
Authors
KeywordsChemicals And Cas Registry Numbers
Issue Date2000
PublisherDr Dietrich Steinkopff Verlag. The Journal's web site is located at http://www.link.springer.de/link/service/journals/00393/index.htm
Citation
Zeitschrift Fur Rheumatologie, 2000, v. 59 n. 1, p. 29-34 How to Cite?
AbstractThe regulatory region of the corticotropin releasing hormone (CRH) is highly conserved and plays a crucial role in the response of the organism to stress. Release of CRH initiates a cascade of events leading to the release of cortisone and the regulation of inflammatory and immune events. Objective: Since it has been postulated that the impaired corticotropin releasing hormone (CRH) response to stress in patients with rheumatoid arthritis (RA) has a genetic basis, we investigated the distribution of CRH alleles in a cohort of UK patients as well as in South African RA patients. Methods: Restriction fragment length polymorphism of PCR amplified DNA products of the CRH promoter. We compared the allele frequencies in the RA patients with the respective healthy control population described previously. Results: As in the control populations we found two biallelic polymorphic sequences (named A1 and A2 and B1 and B2, respectively) in the CRH promoter which could be assigned to compound alleles. The A2B1 compound allele was protective against development of RA in a large group of UK Caucasoid patients (p=0.03; odds ratio 0.43, 95% confidence interval 0.21-0.88). In contrast, A1B1 was positively associated with RA in a cohort of black South African RA patients (p=0.05; odds ratio 1.78, 95% confidence interval 1.01-3.15). Conclusion: Taken together, these findings support the hypothesis that CRH promoter polymorphism represents a new genetic marker for RA susceptibility and may prove useful for the prediction of RA risk in the future when further genetic and environmental risk factors are determined.
Persistent Identifierhttp://hdl.handle.net/10722/91442
ISSN
2015 Impact Factor: 0.569
2015 SCImago Journal Rankings: 0.166
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorBaerwald, CGOen_HK
dc.contributor.authorMok, CCen_HK
dc.contributor.authorPanayi, GSen_HK
dc.contributor.authorLanchbury, JSen_HK
dc.contributor.authorTickly, Men_HK
dc.contributor.authorLau, CSen_HK
dc.contributor.authorWordsworth, BPen_HK
dc.contributor.authorOllier, Ben_HK
dc.date.accessioned2010-09-17T10:19:28Z-
dc.date.available2010-09-17T10:19:28Z-
dc.date.issued2000en_HK
dc.identifier.citationZeitschrift Fur Rheumatologie, 2000, v. 59 n. 1, p. 29-34en_HK
dc.identifier.issn0340-1855en_HK
dc.identifier.urihttp://hdl.handle.net/10722/91442-
dc.description.abstractThe regulatory region of the corticotropin releasing hormone (CRH) is highly conserved and plays a crucial role in the response of the organism to stress. Release of CRH initiates a cascade of events leading to the release of cortisone and the regulation of inflammatory and immune events. Objective: Since it has been postulated that the impaired corticotropin releasing hormone (CRH) response to stress in patients with rheumatoid arthritis (RA) has a genetic basis, we investigated the distribution of CRH alleles in a cohort of UK patients as well as in South African RA patients. Methods: Restriction fragment length polymorphism of PCR amplified DNA products of the CRH promoter. We compared the allele frequencies in the RA patients with the respective healthy control population described previously. Results: As in the control populations we found two biallelic polymorphic sequences (named A1 and A2 and B1 and B2, respectively) in the CRH promoter which could be assigned to compound alleles. The A2B1 compound allele was protective against development of RA in a large group of UK Caucasoid patients (p=0.03; odds ratio 0.43, 95% confidence interval 0.21-0.88). In contrast, A1B1 was positively associated with RA in a cohort of black South African RA patients (p=0.05; odds ratio 1.78, 95% confidence interval 1.01-3.15). Conclusion: Taken together, these findings support the hypothesis that CRH promoter polymorphism represents a new genetic marker for RA susceptibility and may prove useful for the prediction of RA risk in the future when further genetic and environmental risk factors are determined.en_HK
dc.languageengen_HK
dc.publisherDr Dietrich Steinkopff Verlag. The Journal's web site is located at http://www.link.springer.de/link/service/journals/00393/index.htmen_HK
dc.relation.ispartofZeitschrift fur Rheumatologieen_HK
dc.subjectChemicals And Cas Registry Numbersen_HK
dc.subject.meshAdulten_HK
dc.subject.meshAfrican Continental Ancestry Group - geneticsen_HK
dc.subject.meshAllelesen_HK
dc.subject.meshArthritis, Rheumatoid - ethnology - geneticsen_HK
dc.subject.meshAsian Continental Ancestry Group - geneticsen_HK
dc.subject.meshCohort Studiesen_HK
dc.subject.meshCorticotropin-Releasing Hormone - geneticsen_HK
dc.subject.meshEnglanden_HK
dc.subject.meshEuropean Continental Ancestry Group - geneticsen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGene Frequency - geneticsen_HK
dc.subject.meshGenetics, Populationen_HK
dc.subject.meshGenotypeen_HK
dc.subject.meshHLA-DR4 Antigen - geneticsen_HK
dc.subject.meshHong Kongen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshPolymerase Chain Reactionen_HK
dc.subject.meshPolymorphism, Restriction Fragment Lengthen_HK
dc.subject.meshPromoter Regions, Genetic - geneticsen_HK
dc.subject.meshReference Valuesen_HK
dc.subject.meshSouth Africaen_HK
dc.titleCorticotropin releasing hormone (CRH) promoter polymorphisms in various ethnic groups of patients with rheumatoid arthritisen_HK
dc.typeArticleen_HK
dc.identifier.emailLau, CS:cslau@hku.hken_HK
dc.identifier.authorityLau, CS=rp01348en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid10769420-
dc.identifier.scopuseid_2-s2.0-0034058719en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034058719&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume59en_HK
dc.identifier.issue1en_HK
dc.identifier.spage29en_HK
dc.identifier.epage34en_HK
dc.identifier.isiWOS:000086114100002-
dc.publisher.placeGermanyen_HK
dc.identifier.scopusauthoridBaerwald, CGO=7003454641en_HK
dc.identifier.scopusauthoridMok, CC=34668219600en_HK
dc.identifier.scopusauthoridPanayi, GS=7102074348en_HK
dc.identifier.scopusauthoridLanchbury, JS=7004804446en_HK
dc.identifier.scopusauthoridTickly, M=6505737336en_HK
dc.identifier.scopusauthoridLau, CS=14035682100en_HK
dc.identifier.scopusauthoridWordsworth, BP=7005895666en_HK
dc.identifier.scopusauthoridOllier, B=6701769237en_HK

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