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Gilbert's syndrome: protective effect on endothelial dysfunction

dc.contributor.authorSertoglu, Erdim
dc.contributor.authorTapan, Serkan
dc.contributor.authorDogru, Teoman
dc.contributor.authorAcar, Ramazan
dc.contributor.authorDogan, Tolga
dc.contributor.authorInce, Selami
dc.contributor.authorBilgi, Cumhur
dc.date.accessioned2026-10-09T21:51:24Z
dc.date.issued2016
dc.departmentYüksek İhtisas Üniversitesi
dc.description.abstractObjective: Gilbert's syndrome (GS), is a benign condition characterized by unconjugated hyperbilirubinemia related to a decreased hepatic glucuronidating activity without symptoms and signs of liver disease or overt hemolysis. In the present study, we aimed to assess circulating levels of asymmetric dimethylarginine (ADMA), pentraxin-3 (PTX-3) and high sensitivity C-reactive protein (hs-CRP) between patients with GS and controls and determine the correlation of unconjugated bilirubin (UCB) levels with these molecules as prognostic factors for vascular risk stratification and endothelial dysfunction. Methods: Forty two patients with GS and 37 age and sex matched control subjects were enrolled in this study. The diagnosis of GS was made by unconjugated hyperbilirubinemia (1 mg/dL or > 17.1 mu mol/L) on at least two occasions with normal values of other liver function tests, normal hepatic imaging, and absence of hemolysis. Results: Serum ADMA, PTX-3 and hs-CRP levels were significantly lower in GS than the healthy controls (p = 0.037, p = 0.025 and p = 0.040, respectively). In correlation analysis, UCB was negatively correlated with ADMA, PTX-3 and hs-CRP (r = -0.239, p = 0.034; r = -0.280, p = 0.012 and r = -0.224, p = 0.047, respectively). Discussion and conclusion: The present study showed for the first time that decreased levels of ADMA, PTX-3 and hs-CRP may prove the protective effects of hyperbilirubinemia on the endothelial dysfunction.
dc.identifier.doi10.1515/tjb-2016-0150
dc.identifier.endpage458
dc.identifier.issn0250-4685
dc.identifier.issn1303-829X
dc.identifier.issue6
dc.identifier.scopus2-s2.0-85007158174
dc.identifier.scopusqualityQ3
dc.identifier.startpage451
dc.identifier.trdizinid215007
dc.identifier.urihttps://doi.org/10.1515/tjb-2016-0150
dc.identifier.urihttps://search.trdizin.gov.tr/tr/yayin/detay/215007
dc.identifier.urihttps://hdl.handle.net/20.500.12794/3831
dc.identifier.volume41
dc.identifier.wosWOS:000393197500010
dc.identifier.wosqualityQ4
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakTR-Dizin
dc.indekslendigikaynak.digerScience Citation Index Expanded (SCI-EXPANDED)
dc.language.isoen
dc.publisherWalter de Gruyter Gmbh
dc.relation.ispartofTurkish Journal of Biochemistry-Turk Biyokimya Dergisi
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.relation.sdgGoal-03: Good Health and Well-Being
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_WoS_20260922
dc.subjectGilbert'S Syndrome
dc.subjectEndothelial Dysfunction
dc.subjectAsymmetric Dimethylarginine
dc.subjectPentraxin-3
dc.subjectHigh Sensitivity C-Reactive Protein
dc.titleGilbert's syndrome: protective effect on endothelial dysfunction
dc.title.alternativeGilbert sendromu: Endotel disfonksiyonu üzerinde koruyucu etkisi
dc.typeArticle

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