PMC2994950

Insulin resistance was a better predictor of sustained virological response than steatosis or cirrhosis in multivariable models, and is the only non-invasive measure among the three correlated predict

Effect: improvement; IR model had smaller -2 log likelihood value than steatosis or cirrhosis models

Insulin resistance was a better predictor of sustained virological response than steatosis or cirrhosis in multivariable models, and is the only non-invasive measure among the three correlated predict

Effect: improvement; IR model had smaller -2 log likelihood value than steatosis or cirrhosis models

Insulin resistance was a better predictor of sustained virological response than steatosis or cirrhosis in multivariable models, and is the only non-invasive measure among the three correlated predict

Effect: improvement; IR model had smaller -2 log likelihood value than steatosis or cirrhosis models

Insulin resistance was a better predictor of sustained virological response than steatosis or cirrhosis in multivariable models, and is the only non-invasive measure among the three correlated predict

Effect: improvement; IR model had smaller -2 log likelihood value than steatosis or cirrhosis models

Insulin resistance was a better predictor of sustained virological response than steatosis or cirrhosis in multivariable models, and is the only non-invasive measure among the three correlated predict

Effect: improvement; IR model had smaller -2 log likelihood value than steatosis or cirrhosis models

Insulin resistance was a better predictor of sustained virological response than steatosis or cirrhosis in multivariable models, and is the only non-invasive measure among the three correlated predict

Effect: improvement; IR model had smaller -2 log likelihood value than steatosis or cirrhosis models

Insulin resistance was a better predictor of sustained virological response than steatosis or cirrhosis in multivariable models, and is the only non-invasive measure among the three correlated predict

Effect: improvement; IR model had smaller -2 log likelihood value than steatosis or cirrhosis models

Insulin resistance was a better predictor of sustained virological response than steatosis or cirrhosis in multivariable models, and is the only non-invasive measure among the three correlated predict

Effect: improvement; IR model had smaller -2 log likelihood value than steatosis or cirrhosis models

Insulin resistance was a better predictor of sustained virological response than steatosis or cirrhosis in multivariable models, and is the only non-invasive measure among the three correlated predict

Effect: improvement; IR model had smaller -2 log likelihood value than steatosis or cirrhosis models

Insulin resistance was a better predictor of sustained virological response than steatosis or cirrhosis in multivariable models, and is the only non-invasive measure among the three correlated predict

Effect: improvement; IR model had smaller -2 log likelihood value than steatosis or cirrhosis models

Insulin resistance was a better predictor of sustained virological response than steatosis or cirrhosis in multivariable models, and is the only non-invasive measure among the three correlated predict

Effect: improvement; IR model had smaller -2 log likelihood value than steatosis or cirrhosis models

Insulin resistance was a better predictor of sustained virological response than steatosis or cirrhosis in multivariable models, and is the only non-invasive measure among the three correlated predict

Effect: improvement; IR model had smaller -2 log likelihood value than steatosis or cirrhosis models

Insulin resistance was a better predictor of sustained virological response than steatosis or cirrhosis in multivariable models, and is the only non-invasive measure among the three correlated predict

Effect: improvement; IR model had smaller -2 log likelihood value than steatosis or cirrhosis models

Insulin resistance was a better predictor of sustained virological response than steatosis or cirrhosis in multivariable models, and is the only non-invasive measure among the three correlated predict

Effect: improvement; IR model had smaller -2 log likelihood value than steatosis or cirrhosis models

Insulin resistance was a better predictor of sustained virological response than steatosis or cirrhosis in multivariable models, and is the only non-invasive measure among the three correlated predict

Effect: improvement; IR model had smaller -2 log likelihood value than steatosis or cirrhosis models

Insulin resistance was a better predictor of sustained virological response than steatosis or cirrhosis in multivariable models, and is the only non-invasive measure among the three correlated predict

Effect: improvement; IR model had smaller -2 log likelihood value than steatosis or cirrhosis models

Insulin resistance was a better predictor of sustained virological response than steatosis or cirrhosis in multivariable models, and is the only non-invasive measure among the three correlated predict

Effect: improvement; IR model had smaller -2 log likelihood value than steatosis or cirrhosis models

Insulin resistance was a better predictor of sustained virological response than steatosis or cirrhosis in multivariable models, and is the only non-invasive measure among the three correlated predict

Effect: improvement; IR model had smaller -2 log likelihood value than steatosis or cirrhosis models

Insulin resistance was a better predictor of sustained virological response than steatosis or cirrhosis in multivariable models, and is the only non-invasive measure among the three correlated predict

Effect: improvement; IR model had smaller -2 log likelihood value than steatosis or cirrhosis models

Insulin resistance was a better predictor of sustained virological response than steatosis or cirrhosis in multivariable models, and is the only non-invasive measure among the three correlated predict

Effect: improvement; IR model had smaller -2 log likelihood value than steatosis or cirrhosis models

Insulin resistance was a better predictor of sustained virological response than steatosis or cirrhosis in multivariable models, and is the only non-invasive measure among the three correlated predict

Effect: improvement; IR model had smaller -2 log likelihood value than steatosis or cirrhosis models

Insulin resistance was a better predictor of sustained virological response than steatosis or cirrhosis in multivariable models, and is the only non-invasive measure among the three correlated predict

Effect: improvement; IR model had smaller -2 log likelihood value than steatosis or cirrhosis models

Insulin resistance was a better predictor of sustained virological response than steatosis or cirrhosis in multivariable models, and is the only non-invasive measure among the three correlated predict

Effect: improvement; IR model had smaller -2 log likelihood value than steatosis or cirrhosis models

Insulin resistance was a better predictor of sustained virological response than steatosis or cirrhosis in multivariable models, and is the only non-invasive measure among the three correlated predict

Effect: improvement; IR model had smaller -2 log likelihood value than steatosis or cirrhosis models

Insulin resistance was a better predictor of sustained virological response than steatosis or cirrhosis in multivariable models, and is the only non-invasive measure among the three correlated predict

Effect: improvement; IR model had smaller -2 log likelihood value than steatosis or cirrhosis models

Insulin resistance was a better predictor of sustained virological response than steatosis or cirrhosis in multivariable models, and is the only non-invasive measure among the three correlated predict

Effect: improvement; IR model had smaller -2 log likelihood value than steatosis or cirrhosis models

Insulin resistance was a better predictor of sustained virological response than steatosis or cirrhosis in multivariable models, and is the only non-invasive measure among the three correlated predict

Effect: improvement; IR model had smaller -2 log likelihood value than steatosis or cirrhosis models

Baseline insulin resistance (HOMA-IR >2) was independently associated with failure to achieve sustained virological response during pegIFN-α-2a and ribavirin retreatment of HIV/HCV co-infected patient

Effect: decline; AOR 0.17; CI: 95% CI 0.05–0.64

Baseline insulin resistance (HOMA-IR >2) was independently associated with failure to achieve sustained virological response during pegIFN-α-2a and ribavirin retreatment of HIV/HCV co-infected patient

Effect: decline; AOR 0.17; CI: 95% CI 0.05–0.64

Baseline insulin resistance (HOMA-IR >2) was independently associated with failure to achieve sustained virological response during pegIFN-α-2a and ribavirin retreatment of HIV/HCV co-infected patient

Effect: decline; AOR 0.17; CI: 95% CI 0.05–0.64

Baseline insulin resistance (HOMA-IR >2) was independently associated with failure to achieve sustained virological response during pegIFN-α-2a and ribavirin retreatment of HIV/HCV co-infected patient

Effect: decline; AOR 0.17; CI: 95% CI 0.05–0.64

Baseline insulin resistance (HOMA-IR >2) was independently associated with failure to achieve sustained virological response during pegIFN-α-2a and ribavirin retreatment of HIV/HCV co-infected patient

Effect: decline; AOR 0.17; CI: 95% CI 0.05–0.64

Baseline insulin resistance (HOMA-IR >2) was independently associated with failure to achieve sustained virological response during pegIFN-α-2a and ribavirin retreatment of HIV/HCV co-infected patient

Effect: decline; AOR 0.17; CI: 95% CI 0.05–0.64

Baseline insulin resistance (HOMA-IR >2) was independently associated with failure to achieve sustained virological response during pegIFN-α-2a and ribavirin retreatment of HIV/HCV co-infected patient

Effect: decline; AOR 0.17; CI: 95% CI 0.05–0.64

Baseline insulin resistance (HOMA-IR >2) was independently associated with failure to achieve sustained virological response during pegIFN-α-2a and ribavirin retreatment of HIV/HCV co-infected patient

Effect: decline; AOR 0.17; CI: 95% CI 0.05–0.64

Baseline insulin resistance (HOMA-IR >2) was independently associated with failure to achieve sustained virological response during pegIFN-α-2a and ribavirin retreatment of HIV/HCV co-infected patient

Effect: decline; AOR 0.17; CI: 95% CI 0.05–0.64

Baseline insulin resistance (HOMA-IR >2) was independently associated with failure to achieve sustained virological response during pegIFN-α-2a and ribavirin retreatment of HIV/HCV co-infected patient

Effect: decline; AOR 0.17; CI: 95% CI 0.05–0.64

Baseline insulin resistance (HOMA-IR >2) was independently associated with failure to achieve sustained virological response during pegIFN-α-2a and ribavirin retreatment of HIV/HCV co-infected patient

Effect: decline; AOR 0.17; CI: 95% CI 0.05–0.64

Baseline insulin resistance (HOMA-IR >2) was independently associated with failure to achieve sustained virological response during pegIFN-α-2a and ribavirin retreatment of HIV/HCV co-infected patient

Effect: decline; AOR 0.17; CI: 95% CI 0.05–0.64

Baseline insulin resistance (HOMA-IR >2) was independently associated with failure to achieve sustained virological response during pegIFN-α-2a and ribavirin retreatment of HIV/HCV co-infected patient

Effect: decline; AOR 0.17; CI: 95% CI 0.05–0.64

Baseline insulin resistance (HOMA-IR >2) was independently associated with failure to achieve sustained virological response during pegIFN-α-2a and ribavirin retreatment of HIV/HCV co-infected patient

Effect: decline; AOR 0.17; CI: 95% CI 0.05–0.64

Baseline insulin resistance (HOMA-IR >2) was independently associated with failure to achieve sustained virological response during pegIFN-α-2a and ribavirin retreatment of HIV/HCV co-infected patient

Effect: decline; AOR 0.17; CI: 95% CI 0.05–0.64

Baseline insulin resistance (HOMA-IR >2) was independently associated with failure to achieve sustained virological response during pegIFN-α-2a and ribavirin retreatment of HIV/HCV co-infected patient

Effect: decline; AOR 0.17; CI: 95% CI 0.05–0.64

Baseline insulin resistance (HOMA-IR >2) was independently associated with failure to achieve sustained virological response during pegIFN-α-2a and ribavirin retreatment of HIV/HCV co-infected patient

Effect: decline; AOR 0.17; CI: 95% CI 0.05–0.64

Baseline insulin resistance (HOMA-IR >2) was independently associated with failure to achieve sustained virological response during pegIFN-α-2a and ribavirin retreatment of HIV/HCV co-infected patient

Effect: decline; AOR 0.17; CI: 95% CI 0.05–0.64

Baseline insulin resistance (HOMA-IR >2) was independently associated with failure to achieve sustained virological response during pegIFN-α-2a and ribavirin retreatment of HIV/HCV co-infected patient

Effect: decline; AOR 0.17; CI: 95% CI 0.05–0.64

Baseline insulin resistance (HOMA-IR >2) was independently associated with failure to achieve sustained virological response during pegIFN-α-2a and ribavirin retreatment of HIV/HCV co-infected patient

Effect: decline; AOR 0.17; CI: 95% CI 0.05–0.64

Baseline insulin resistance (HOMA-IR >2) was independently associated with failure to achieve sustained virological response during pegIFN-α-2a and ribavirin retreatment of HIV/HCV co-infected patient

Effect: decline; AOR 0.17; CI: 95% CI 0.05–0.64

Baseline insulin resistance (HOMA-IR >2) was independently associated with failure to achieve sustained virological response during pegIFN-α-2a and ribavirin retreatment of HIV/HCV co-infected patient

Effect: decline; AOR 0.17; CI: 95% CI 0.05–0.64

Baseline insulin resistance (HOMA-IR >2) was independently associated with failure to achieve sustained virological response during pegIFN-α-2a and ribavirin retreatment of HIV/HCV co-infected patient

Effect: decline; AOR 0.17; CI: 95% CI 0.05–0.64