Analysis of thrombophilic genetic mutations in patients with Sheehan's syndrome: is thrombophilia responsible for the pathogenesis of Sheehan's syndrome?

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dc.contributor.authorGokalp, Deniz
dc.contributor.authorTuzcu, Alpaslan
dc.contributor.authorBahceci, Mithat
dc.contributor.authorAyyildiz, Orhan
dc.contributor.authorYurt, Murat
dc.contributor.authorCelik, Yusuf
dc.contributor.authorAlpagat, Gulistan
dc.date.accessioned2024-04-24T16:02:19Z
dc.date.available2024-04-24T16:02:19Z
dc.date.issued2011
dc.departmentDicle Üniversitesien_US
dc.description.abstractThe gene mutations of Factor V R506Q (FV-Leiden), prothrombin (FII G20210A), methylene tetrahydrofolate reductase (MTHFR) C677T and A1298C and PAI-1 4G/5G are well-established risk factors for thrombosis. We aimed to investigate the prevalence of these gene mutations and their possible impact on the development of pathogenesis in patients with Sheehan's syndrome (SS). 40 female patients with SS compared to a control group of 45 healthy women. The presence of FV-Leiden, FII G20210A, MTHFR C677T, MTHFR A1298C and PAI-1 4G/5G gene mutations were assessed by polymerase chain reaction analysis with a light cycler analyzer. An odds ratio of greater than one is considered to increase the risk of SS disease as found in Factor V Leiden, FII G20210A, MTHFR C677T, MTHFR A1298C and PAI-1 4G/5G polymorphism, as follows respectively: 1.13, 1.85, 6.00, 8.14 and 1.45. MTHFR C677T and MTHFR A1298C polymorphism were found significantly higher in SS patients than the control group (P < 0.001), however FV-Leiden, FII G20210A and PAI-1 4G/5G polymorphism showed no significant difference (P > 0.05). The level of plasma total homocysteine (tHcy) was significantly higher in patients with SS than in the control group (P < 0.001). We suggest that the genetic mutations of FV-Leiden, FII G20210A, MTHFR C677T, MTHFR A1298C and PAI-1 4G/5G increase the risk of SS. Also, high plasma tHcy levels may be a risk factor for the development of SS.en_US
dc.identifier.doi10.1007/s11102-010-0276-x
dc.identifier.endpage173en_US
dc.identifier.issn1386-341X
dc.identifier.issue2en_US
dc.identifier.pmid21107737
dc.identifier.scopus2-s2.0-79958125205
dc.identifier.scopusqualityQ2
dc.identifier.startpage168en_US
dc.identifier.urihttps://doi.org/10.1007/s11102-010-0276-x
dc.identifier.urihttps://hdl.handle.net/11468/14739
dc.identifier.volume14en_US
dc.identifier.wosWOS:000290586500010
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoenen_US
dc.publisherSpringeren_US
dc.relation.ispartofPituitary
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectSheehan Syndromeen_US
dc.subjectThrombofilic Factorsen_US
dc.titleAnalysis of thrombophilic genetic mutations in patients with Sheehan's syndrome: is thrombophilia responsible for the pathogenesis of Sheehan's syndrome?en_US
dc.titleAnalysis of thrombophilic genetic mutations in patients with Sheehan's syndrome: is thrombophilia responsible for the pathogenesis of Sheehan's syndrome?
dc.typeArticleen_US

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