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    The incidence and prevalence of systemic lupus erythematosus in Thrace, 2003-2014: A 12-year epidemiological study
    (Sage Publications Ltd, 2016) Pamuk, O. N.; Balci, M. A.; Donmez, S.; Tsokos, G. C.
    Background We estimated the prevalence and incidence, clinical features, treatment, and prognosis of systemic lupus erythematosus (SLE) patients in the Thrace region of Turkey. Methods We retrospectively evaluated 331 patients (307 female, 24 male, mean age 38.5 years) diagnosed with SLE between 2003 and 2014. Clinical features, treatments, and response to various treatment modalities were recorded. Our hospital has been the only tertiary referral center for rheumatological diseases for a mixed rural and urban population of 620,477 people (306,036 females, 314,411 males) for more than 16 years. Results The mean annual incidence of SLE was 4.44/100,000 (females, 8.4/100,000; males, 0.6/100,000). The overall prevalence of SLE was 51.7/100,000 (females, 97.7/100,000; males, 7/100,000). Major organ involvement was present in the following percentages: neurologic involvement: 20.1%; renal involvement: 28.2%; autoimmune hemolytic anemia: 9.6%; thrombocytopenia: 14.7%. Seventeeen SLE patients (13 females, four males) died at a median follow-up of 48 months. The five-year survival was 94.5%, and the ten-year survival was 89.9%. According to Kaplan-Meier survival analysis, poor prognostic factors were: male gender (p=0.015); smoking (p=0.02); pleural involvement (p=0.011); thrombocytopenia (p=0.021); myocarditis (p=0.028); renal involvement (p=0.037); treatment with cyclophosphamide (p=0.011); and an initial high SLEDAI score (>4) (p=0.02). Lymphopenia at the time of diagnosis appeared as a favorable prognostic factor (p=0.008). Cox regression analysis revealed myocarditis (OR: 20.4, p=0.018) and age at diagnosis (OR: 1.11, p=0.035) to be poor, and lymphopenia at the time of diagnosis to be good prognostic factors (OR:0.13, p=0.031). Conclusions The annual incidence and prevalence of SLE in the Thrace region of Turkey is lower than those reported in North America, however they are similar to those reported for European countries. Clinical manifestations appear to be milder, whereas survival was similar to those recorded in Western countries.
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    Spleen tyrosine kinase (Syk) inhibitor fostamatinib limits tissue damage and fibrosis in a bleomycin-induced scleroderma mouse model
    (Clinical & Exper Rheumatology, 2015) Pamuk, O. N.; Can, G.; Ayvaz, S.; Karaca, T.; Pamuk, G. E.; Demirtas, S.; Tsokos, G. C.
    Objective. The pathogenesis of fibrosis in scleroderma (SSc) is unknown. TGF-beta and platelet-derived growth factor are important in the development of fibrosis and tyrosine kinases are involved in these pathways. The possible antifibrotic effects of various kinase inhibitors in SSc have been studied before. Spleen tyrosine kinase (Syk) is a protein tyrosine kinase which activates intracellular signal transduction pathways; and has been claimed to be involved in the pathogenesis of systemic autoimmune diseases. Inhibition of Syk suppresses IgE-and IgG-associated FcR signal activation in various cell types; and suppresses experimental arthritis and skin and kidney disease in lupus-prone mice. We investigated the ability of a small drug, the Syk inhibitor, fostamatinib, to protect mice from bleomycin-induced SSc. Methods. Four study groups of BALB/c mice were included into this study: control, bleomycin (administered subcutaneously to BALB/c mice for 21 days), bleomycin and fostamatinib (mice fed with chow containing a Syk inhibitor for 21 days), and fostamatinib alone groups. Skin and lung tissue specimens were obtained and evaluated histologically. Results. Treatment with fostamatinib significantly reduced skin thickness and fibrosis. Mice treated with fostamatinib also displayed less fibrosis and inflammation in the lung tissue. Following fostamatinib treatment, Syk, phospho-Syk, and TGF-beta expression decreased in both skin and lung tissues. Conclusion. The Syk inhibitor fostamatinib prevented bleomycin-induced fibrosis and inflammation in the skin and in the lung. The anti-fibrotic effect of fostamatinib is linked to reduced Syk phosphorylation and TGF-beta expression. The Syk pathway appears as a potential molecular target for therapeutic intervention in SSc.