Browsing by Author "Oygur, Cagdas Sahap"

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    Behcet's: A Disease or a Syndrome? Answer from an Expression Profiling Study
    (2016) Oguz, Ali Kemal; Yilmaz, Seda Tasir; Oygur, Cagdas Sahap; Candar, Tuba; Sayin, Irmak; Kilicoglu, Sibel Serin; Ergun, Ihsan; Ates, Askin; Ozdag, Hilal; Akar, Nejat; 26890122
    Behcet's disease (BD) is a chronic, relapsing, multisystemic inflammatory disorder with unanswered questions regarding its etiology/pathogenesis and classification. Distinct manifestation based subsets, pronounced geographical variations in expression, and discrepant immunological abnormalities raised the question whether Behcet's is "a disease or a syndrome". To answer the preceding question we aimed to display and compare the molecular mechanisms underlying distinct subsets of BD. For this purpose, the expression data of the gene expression profiling and association study on BD by Xavier et al (2013) was retrieved from GEO database and reanalysed by gene expression data analysis/visualization and bioinformatics enrichment tools. There were 15 BD patients (B) and 14 controls (C). Three subsets of BD patients were generated: MB (isolated mucocutaneous manifestations, n = 7), OB (ocular involvement, n = 4), and VB (large vein thrombosis, n = 4). Class comparison analyses yielded the following numbers of differentially expressed genes (DEGs); B vs C: 4, MB vs C: 5, OB vs C: 151, VB vs C: 274, MB vs OB: 215, MB vs VB: 760, OB vs VB: 984. Venn diagram analysis showed that there were no common DEGs in the intersection "MB vs C" boolean AND "OB vs C" boolean AND "VB vs C". Cluster analyses successfully clustered distinct expressions of BD. During gene ontology term enrichment analyses, categories with relevance to IL-8 production (MB vs C) and immune response to microorganisms (OB vs C) were differentially enriched. Distinct subsets of BD display distinct expression profiles and different disease associated pathways. Based on these clear discrepancies, the designation as "Behcet's syndrome" (BS) should be encouraged and future research should take into consideration the immunogenetic heterogeneity of BS subsets. Four gene groups, namely, negative regulators of inflammation (CD69, CLEC12A, CLEC12B, TNFAIP3), neutrophil granule proteins (LTF, OLFM4, AZU1, MMP8, DEFA4, CAMP), antigen processing and presentation proteins (CTSS, ERAP1), and regulators of immune response (LGALS2, BCL10, ITCH, CEACAM8, CD36, IL8, CCL4, EREG, NFKBIZ, CCR2, CD180, KLRC4, NFAT5) appear to be instrumental in BS immunopathogenesis.
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    Long-Term Results of Kidney Transplantation in Patients with Familial Mediterranean Fever
    (2023) Bitik, Berivan; Hatipoglu, Bugra; Sayin, Burak; Kanbur, Aysenur Yalcintas; Bursa, Nurbanu; Oygur, Cagdas Sahap; Ozdemir, Handan; Colak, Turan; Haberal, Mehmet; Yucel, Ahmet Eftal; 0000-0001-5803-915X; 0000-0002-7528-3557; 0000-0002-3462-7632; 0000-0002-0168-2993; 36544375; AAI-9195-2021; X-8540-2019; AAJ-8097-2021
    IntroductionLong-term kidney transplantation (KT) results in patients with familial Mediterranean fever (FMF)-related amyloidosis are not well studied. This study reviewed the long-term survival outcomes of FMF patients who underwent KT. MethodsWe compared the outcomes of 31 patients who underwent (KT) for biopsy-proven amyloidosis secondary to FMF with 31 control patients (five with diabetes mellitus and 26 with nondiabetic kidney disease) undergoing KT between 1994 and 2021 at Baskent University Hospital. All data were recorded retrospectively from patients' files. Results: The median age (quartile deviationQD) at the time of KT in the FMF and control group were 31 (6.7) and 33 (11), respectively. The median follow-up period (QD) after KT was 108 (57) months in the FMF and 132 (72) months in the control group. In the FMF group, graft and patient survivals were 71% and 84% at 5 years and 45% and 48% at 10 years, respectively. In the control group, graft and patient survivals were 79% and 100% at 5 years and 63% and 71% at 10 years, respectively. Patient survival in the FMF group at 5 years was significantly lower than in the control group (p = .045). There was no statistically significant difference between the FMF and control groups in terms of graft and patient survival, and serum creatinine levels at 10 years. All patients were given triple immunosuppressive treatment with cyclosporine, mycophenolate mofetil, and prednisolone. Three patients received anakinra and one received canakinumab in addition to colchicine treatment. One FMF patient also underwent heart transplantation due to AA amyloidosis. Of the FMF patients, 11 died during follow-up. ConclusionWe have found that the long-term outcome of KT in patients with FMF amyloidosis is numerically worse but not statistically different from the control group. However, short- and long-term complications still need to be resolved.