Yazar "Idilman, R." seçeneğine göre listele

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    Adefovir treatment of entecavir resistance in patients with lamivudine-refractory chronic hepatitis B
    (Elsevier Science Bv, 2008) Yurdaydin, C.; Idilman, R.; Cevik, E.; Akarca, U. S.; Kaymakoglu, S.; Bozdayi, A. M.
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    ENTECAVIR AND TENOFOVIR MONOTHERAPY IN TREATMENT-NAIVE PATIENTS WITH CHRONIC HEPATITIS B: A MULTICENTER TURKISH STUDY IN CLINICAL PRACTICE
    (Elsevier Science Bv, 2014) Idilman, R.; Keskin, O.; Gunsar, F.; Koruk, M.; Meral, C. E.; Tuzun, A.; Gulsen, M.; Elhan, A. H.; Akarca, U. S.; Yurdaydin, C.
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    Historical epidemiology of hepatitis C virus (HCV) in selected countries
    (Wiley, 2014) Bruggmann, P.; Berg, T.; Ovrehus, A. L. H.; Moreno, C.; Brandao Mello, C. E.; Roudot-Thoraval, F.; Marinho, R. T.; Sherman, M.; Ryder, S. D.; Sperl, J.; Akarca, U.; Balik, I.; Bihl, F.; Bilodeau, M.; Blasco, A. J.; Buti, M.; Calinas, F.; Calleja, J. L.; Cheinquer, H.; Christensen, P. B.; Clausen, M.; Coelho, H. S. M.; Cornberg, M.; Cramp, M. E.; Dore, G. J.; Doss, W.; Duberg, A. S.; El-Sayed, M. H.; Ergor, G.; Esmat, G.; Estes, C.; Falconer, K.; Felix, J.; Ferraz, M. L. G.; Ferreira, P. R.; Frankova, S.; Garcia-Samaniego, J.; Gerstoft, J.; Giria, J. A.; Goncales, F. L., Jr.; Gower, E.; Gschwantler, M.; Guimaraes Pessoa, M.; Hezode, C.; Hofer, H.; Husa, P.; Idilman, R.; Kaberg, M.; Kaita, K. D. E.; Kautz, A.; Kaymakoglu, S.; Krajden, M.; Krarup, H.; Laleman, W.; Lavanchy, D.; Lazaro, P.; Marotta, P.; Mauss, S.; Mendes Correa, M. C.; Muellhaupt, B.; Myers, R. P.; Negro, F.; Nemecek, V.; Ormeci, N.; Parkes, J.; Peltekian, K. M.; Ramji, A.; Razavi, H.; Reis, N.; Roberts, S. K.; Rosenberg, W. M.; Sarmento-Castro, R.; Sarrazin, C.; Semela, D.; Shiha, G. E.; Sievert, W.; Starkel, P.; Stauber, R. E.; Thompson, A. J.; Urbanek, P.; van Thiel, I.; Van Vlierberghe, H.; Vandijck, D.; Vogel, W.; Waked, I.; Wedemeyer, H.; Weis, N.; Wiegand, J.; Yosry, A.; Zekry, A.; Van Damme, P.; Aleman, S.; Hindman, S. J.
    Chronic infection with hepatitis C virus (HCV) is a leading indicator for liver disease. New treatment options are becoming available, and there is a need to characterize the epidemiology and disease burden of HCV. Data for prevalence, viremia, genotype, diagnosis and treatment were obtained through literature searches and expert consensus for 16 countries. For some countries, data from centralized registries were used to estimate diagnosis and treatment rates. Data for the number of liver transplants and the proportion attributable to HCV were obtained from centralized databases. Viremic prevalence estimates varied widely between countries, ranging from 0.3% in Austria, England and Germany to 8.5% in Egypt. The largest viremic populations were in Egypt, with 6358000 cases in 2008 and Brazil with 2106000 cases in 2007. The age distribution of cases differed between countries. In most countries, prevalence rates were higher among males, reflecting higher rates of injection drug use. Diagnosis, treatment and transplant levels also differed considerably between countries. Reliable estimates characterizing HCV-infected populations are critical for addressing HCV-related morbidity and mortality. There is a need to quantify the burden of chronic HCV infection at the national level.
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    Long-term entecavir or tenofovir disoproxil fumarate therapy in treatment-naive chronic hepatitis B patients in the real-world setting
    (Wiley-Blackwell, 2015) Idilman, R.; Gunsar, F.; Koruk, M.; Keskin, O.; Meral, C. E.; Gulsen, M.; Elhan, A. H.; Akarca, U. S.; Yurdaydin, C.
    The aim of this study was to determine the long-term efficacy of entecavir (ETV) and tenofovir disoproxil fumarate (TDF) on the natural course of disease in chronic hepatitis B patients (CHB) with/without cirrhosis in clinical practice. A total of 355 treatment-naive CHB patients were enrolled into the study. The primary outcome measure was viral suppression as defined by serum HBV DNA level <20IU/mL. A secondary outcome measure was to determine the development of Hepatocellular carcinoma (HCC). Virological and biochemical responses were similar between the two treatment groups over time. The presence of cirrhosis and hepatitis B e antigen (HBeAg) positivity did not appear to impact viral suppression. The cumulative probability of HBeAg loss was 41% at 4years of therapy. Hepatitis B surface antigen (HBsAg) loss occurred in four patients. Model for End-Stage Liver Disease score was significantly improved from baseline to week 48 and 96 under antiviral therapy (P=0.013, P=0.01). HCC was diagnosed in 17 patients (4.8%). The cumulative probability of the development of HCC was 3.3% at 1year and 7.3% at 4years of therapy. The development of HCC was independently associated with older age (P=0.031) and the presence of cirrhosis (P=0.004). Serum creatinine levels and creatinine clearance remained stable over time. ETV and TDF effectively maintained virological and biochemical responses in long-term follow-up of CHB patients with/without cirrhosis. HCC may still develop, although at a lower rate, and is more likely to develop in patients with cirrhosis, especially in older patients.
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    Long-term entecavir or tenofovir disoproxil fumarate therapy in treatment-naive chronic hepatitis B patients in the real-world setting
    (Wiley-Blackwell, 2015) Idilman, R.; Gunsar, F.; Koruk, M.; Keskin, O.; Meral, C. E.; Gulsen, M.; Elhan, A. H.; Akarca, U. S.; Yurdaydin, C.
    The aim of this study was to determine the long-term efficacy of entecavir (ETV) and tenofovir disoproxil fumarate (TDF) on the natural course of disease in chronic hepatitis B patients (CHB) with/without cirrhosis in clinical practice. A total of 355 treatment-naive CHB patients were enrolled into the study. The primary outcome measure was viral suppression as defined by serum HBV DNA level <20IU/mL. A secondary outcome measure was to determine the development of Hepatocellular carcinoma (HCC). Virological and biochemical responses were similar between the two treatment groups over time. The presence of cirrhosis and hepatitis B e antigen (HBeAg) positivity did not appear to impact viral suppression. The cumulative probability of HBeAg loss was 41% at 4years of therapy. Hepatitis B surface antigen (HBsAg) loss occurred in four patients. Model for End-Stage Liver Disease score was significantly improved from baseline to week 48 and 96 under antiviral therapy (P=0.013, P=0.01). HCC was diagnosed in 17 patients (4.8%). The cumulative probability of the development of HCC was 3.3% at 1year and 7.3% at 4years of therapy. The development of HCC was independently associated with older age (P=0.031) and the presence of cirrhosis (P=0.004). Serum creatinine levels and creatinine clearance remained stable over time. ETV and TDF effectively maintained virological and biochemical responses in long-term follow-up of CHB patients with/without cirrhosis. HCC may still develop, although at a lower rate, and is more likely to develop in patients with cirrhosis, especially in older patients.
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    Long-term entecavir or tenofovir disoproxil fumarate therapy in treatment-naive chronic hepatitis B patients in the real-world setting
    (Wiley-Blackwell, 2015) Idilman, R.; Gunsar, F.; Koruk, M.; Keskin, O.; Meral, C. E.; Gulsen, M.; Elhan, A. H.; Akarca, U. S.; Yurdaydin, C.
    The aim of this study was to determine the long-term efficacy of entecavir (ETV) and tenofovir disoproxil fumarate (TDF) on the natural course of disease in chronic hepatitis B patients (CHB) with/without cirrhosis in clinical practice. A total of 355 treatment-naive CHB patients were enrolled into the study. The primary outcome measure was viral suppression as defined by serum HBV DNA level <20IU/mL. A secondary outcome measure was to determine the development of Hepatocellular carcinoma (HCC). Virological and biochemical responses were similar between the two treatment groups over time. The presence of cirrhosis and hepatitis B e antigen (HBeAg) positivity did not appear to impact viral suppression. The cumulative probability of HBeAg loss was 41% at 4years of therapy. Hepatitis B surface antigen (HBsAg) loss occurred in four patients. Model for End-Stage Liver Disease score was significantly improved from baseline to week 48 and 96 under antiviral therapy (P=0.013, P=0.01). HCC was diagnosed in 17 patients (4.8%). The cumulative probability of the development of HCC was 3.3% at 1year and 7.3% at 4years of therapy. The development of HCC was independently associated with older age (P=0.031) and the presence of cirrhosis (P=0.004). Serum creatinine levels and creatinine clearance remained stable over time. ETV and TDF effectively maintained virological and biochemical responses in long-term follow-up of CHB patients with/without cirrhosis. HCC may still develop, although at a lower rate, and is more likely to develop in patients with cirrhosis, especially in older patients.
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    The present and future disease burden of hepatitis C virus (HCV) infection with today's treatment paradigm
    (Wiley, 2014) Razavi, H.; Waked, I.; Sarrazin, C.; Myers, R. P.; Idilman, R.; Calinas, F.; Vogel, W.; Mendes Correa, M. C.; Hezode, C.; Lazaro, P.; Akarca, U.; Aleman, S.; Balik, I.; Berg, T.; Bihl, F.; Bilodeau, M.; Blasco, A. J.; Brandao Mello, C. E.; Bruggmann, P.; Buti, M.; Calleja, J. L.; Cheinquer, H.; Christensen, P. B.; Clausen, M.; Coelho, H. S. M.; Cramp, M. E.; Dore, G. J.; Doss, W.; Duberg, A. S.; El-Sayed, M. H.; Ergor, G.; Esmat, G.; Falconer, K.; Felix, J.; Ferraz, M. L. G.; Ferreira, P. R.; Frankova, S.; Garcia-Samaniego, J.; Gerstoft, J.; Giria, J. A.; Goncales, F. L., Jr.; Gower, E.; Gschwantler, M.; Guimaraes Pessoa, M.; Hindman, S. J.; Hofer, H.; Husa, P.; Kaberg, M.; Kaita, K. D. E.; Kautz, A.; Kaymakoglu, S.; Krajden, M.; Krarup, H.; Laleman, W.; Lavanchy, D.; Marinho, R. T.; Marotta, P.; Mauss, S.; Moreno, C.; Murphy, K.; Negro, F.; Nemecek, V.; Ormeci, N.; Ovrehus, A. L. H.; Parkes, J.; Pasini, K.; Peltekian, K. M.; Ramji, A.; Reis, N.; Roberts, S. K.; Rosenberg, W. M.; Roudot-Thoraval, F.; Ryder, S. D.; Sarmento-Castro, R.; Semela, D.; Sherman, M.; Shiha, G. E.; Sievert, W.; Sperl, J.; Starkel, P.; Stauber, R. E.; Thompson, A. J.; Urbanek, P.; Van Damme, P.; van Thiel, I.; Van Vlierberghe, H.; Vandijck, D.; Wedemeyer, H.; Weis, N.; Wiegand, J.; Yosry, A.; Zekry, A.; Cornberg, M.; Muellhaupt, B.; Estes, C.
    The disease burden of hepatitis C virus (HCV) is expected to increase as the infected population ages. A modelling approach was used to estimate the total number of viremic infections, diagnosed, treated and new infections in 2013. In addition, the model was used to estimate the change in the total number of HCV infections, the disease progression and mortality in 2013-2030. Finally, expert panel consensus was used to capture current treatment practices in each country. Using today's treatment paradigm, the total number of HCV infections is projected to decline or remain flat in all countries studied. However, in the same time period, the number of individuals with late-stage liver disease is projected to increase. This study concluded that the current treatment rate and efficacy are not sufficient to manage the disease burden of HCV. Thus, alternative strategies are required to keep the number of HCV individuals with advanced liver disease and liver-related deaths from increasing.
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    Recurrence and occurrence of hepatocellular carcinoma following ledipasvir and sofosbuvir treatment for chronic hepatitis C in patients with advanced liver disease: Turkish multi-center early access program
    (Elsevier Science Bv, 2018) Idilman, R.; Demir, M.; Aladag, M.; Kaymakoglu, S.; Erol, C.; Cavus, B.; Iliaz, R.; Akarca, U. S.; Koklu, S.; Cakaloglu, Y.; Sahin, M.; Koksal, I.; Ozgenel, M.; Toka, B.; Karasu, Z.; Ersoz, G.; Kiyici, M.; Akdogan, M.; Turkey, E. A. P.
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    Strategies to manage hepatitis C virus (HCV) disease burden
    (Wiley, 2014) Wedemeyer, H.; Duberg, A. S.; Buti, M.; Rosenberg, W. M.; Frankova, S.; Esmat, G.; Ormeci, N.; Van Vlierberghe, H.; Gschwantler, M.; Akarca, U.; Aleman, S.; Balik, I.; Berg, T.; Bihl, F.; Bilodeau, M.; Blasco, A. J.; Brandao Mello, C. E.; Bruggmann, P.; Calinas, F.; Calleja, J. L.; Cheinquer, H.; Christensen, P. B.; Clausen, M.; Coelho, H. S. M.; Cornberg, M.; Cramp, M. E.; Dore, G. J.; Doss, W.; El-Sayed, M. H.; Ergor, G.; Estes, C.; Falconer, K.; Felix, J.; Ferraz, M. L. G.; Ferreira, P. R.; Garcia-Samaniego, J.; Gerstoft, J.; Giria, J. A.; Goncales, F. L., Jr.; Guimaraes Pessoa, M.; Hezode, C.; Hindman, S. J.; Hofer, H.; Husa, P.; Idilman, R.; Kaberg, M.; Kaita, K. D. E.; Kautz, A.; Kaymakoglu, S.; Krajden, M.; Krarup, H.; Laleman, W.; Lavanchy, D.; Lazaro, P.; Marinho, R. T.; Marotta, P.; Mauss, S.; Mendes Correa, M. C.; Moreno, C.; Muellhaupt, B.; Myers, R. P.; Nemecek, V.; Ovrehus, A. L. H.; Parkes, J.; Peltekian, K. M.; Ramji, A.; Razavi, H.; Reis, N.; Roberts, S. K.; Roudot-Thoraval, F.; Ryder, S. D.; Sarmento-Castro, R.; Sarrazin, C.; Semela, D.; Sherman, M.; Shiha, G. E.; Sperl, J.; Starkel, P.; Stauber, R. E.; Thompson, A. J.; Urbanek, P.; Van Damme, P.; van Thiel, I.; Vandijck, D.; Vogel, W.; Waked, I.; Weis, N.; Wiegand, J.; Yosry, A.; Zekry, A.; Negro, F.; Sievert, W.; Gower, E.
    The number of hepatitis C virus (HCV) infections is projected to decline while those with advanced liver disease will increase. A modeling approach was used to forecast two treatment scenarios: (i) the impact of increased treatment efficacy while keeping the number of treated patients constant and (ii) increasing efficacy and treatment rate. This analysis suggests that successful diagnosis and treatment of a small proportion of patients can contribute significantly to the reduction of disease burden in the countries studied. The largest reduction in HCV-related morbidity and mortality occurs when increased treatment is combined with higher efficacy therapies, generally in combination with increased diagnosis. With a treatment rate of approximately 10%, this analysis suggests it is possible to achieve elimination of HCV (defined as a >90% decline in total infections by 2030). However, for most countries presented, this will require a 3-5 fold increase in diagnosis and/or treatment. Thus, building the public health and clinical provider capacity for improved diagnosis and treatment will be critical.