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DNA Damage and Oxidative DNA Damage in Inflammatory Bowel Disease

2016-04-19Journal article Restricted access
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dc.contributor.authorPereira, Cristiana
dc.contributor.authorCoelho, Rosa
dc.contributor.authorGrácio, Daniela
dc.contributor.authorDias, Cláudia
dc.contributor.authorSilva, Marco
dc.contributor.authorPeixoto, Armando
dc.contributor.authorLopes, Pedro
dc.contributor.authorCosta, Carla
dc.contributor.authorTeixeira, João Paulo
dc.contributor.authorMacedo, Guilherme
dc.contributor.authorMagro, Fernando
dc.date.accessioned2016-10-20T14:31:28Z
dc.date.available2017-05-01T00:30:11Z
dc.date.issued2016-04-19
dc.description.abstractBackground and aims: Inflammation has long been regarded as a major contributor to cellular oxidative damage and to be involved in the promotion of carcinogenesis. Methods: We aimed to investigate the oxidative damage in inflammatory bowel disease [IBD] patients through a case–control and prospective study involving 344 IBD patients and 294 healthy controls. DNA damage and oxidative DNA damage were measured by comet assay techniques, and oxidative stress by plasmatic lipid peroxidation, protein carbonyls, and total antioxidant capacity. Results: Higher DNA damage [p < 0.001] was found both in Crohn’s disease [CD] (9.7 arbitrary units [AU]; interquartile range [IQR]: 6.2–14.0) and ulcerative colitis [UC] [7.1 AU; IQR: 4.4–11.7], when compared with controls [5.4 AU; IQR: 3.8–6.8], and this was also the case with oxidative DNA damage [p < 0.001] [CD: 3.6 AU; IQR: 1.8–6.8; UC: 4.6 AU; IQR: 2.4–8.1], when compared with controls: 2.3 AU; IQR: 1.2–4.2]. Stratifying patients into groups according to therapy (5-aminosalicylic acid [5-ASA], azathioprine, anti-TNF, and combined therapy [azathioprine and anti-TNF]) revealed significant between-group differences in the level of DNA damage, both in CD and UC, with the combined therapy exhibiting the highest DNA damage levels [11.6 AU; IQR: 9.5–14.3, and 12.4 AU; IQR: 10.6–15.0, respectively]. Among CD patients, disease behaviour [B1 and B2], and age at diagnosis over 40 years [A3] stand as risk factors for DNA damage. For UC patients, the risk factors found for DNA damage were disease activity, treatment, age at diagnosis under 40 years [A1 + A2] and disease locations [E2 and E3]. Conclusions: In IBD there is an increase in DNA damage, and treatment, age at diagnosis and inflammatory burden seem to be risk factors.pt_PT
dc.description.sponsorshipThis work was supported by a grant from GEDII [Portuguese Study Group for Inflammatory Bowel Disease].pt_PT
dc.identifier.citationJ Crohns Colitis. 2016 Apr 19. pii: jjw088. doi.10.1093/ecco-jcc/jjw088pt_PT
dc.identifier.doi10.1093/ecco-jcc/jjw088pt_PT
dc.identifier.issn1873-9946
dc.identifier.urihttp://hdl.handle.net/10400.18/4064
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherOxford University Press/European Crohn’s and Colitis Organisation (ECCO)pt_PT
dc.relation.publisherversionhttp://ecco-jcc.oxfordjournals.org/content/early/2016/05/13/ecco-jcc.jjw088.longpt_PT
dc.rights.urihttp://creativecommons.org/licenses/by-nc/4.0/pt_PT
dc.subjectInflammatory Bowel Diseasept_PT
dc.subjectDNA damagept_PT
dc.subjectRisk Factorspt_PT
dc.titleDNA Damage and Oxidative DNA Damage in Inflammatory Bowel Diseasept_PT
dc.typejournal article
dcterms.subjectInfecções Gastrointestinais
dspace.entity.typePublication
oaire.citation.titleJournal of Crohn's and Colitispt_PT
rcaap.rightsembargoedAccesspt_PT
rcaap.typearticlept_PT

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