Predictors of Response to HCV Tretment Clinical Trial
Official title:
Very Rapid and Rapid Virological Response as Predictors of Response to Sofosbuvir / Daclatasvir Treatment of HCV Related Liver Disease
assessment of very rapid virological response and rapid virological response as predictors of response to sofosbuvir and daclatasvir in treatment of cirrhotic and non-cirrhotic patients with HCV, eligible to treatment.
Chronic hepatitis C infection (CHC) is a global health problem, with an estimated 120 to 130
million chronic hepatitis C virus (HCV) carriers worldwide Therefore, early recognition and
effective management of the disease can modify its natural history
. There is a growing body of evidence that suggests that treatment will help reduce liver
inflammation, may reverse liver damage (scarring),slow down disease progression and improve
symptoms and quality of life. All of these factors are important reasons to seek HCV medical
treatment Identifying host-viral factors that predict the likelihood of SVR prior to
initiating therapy would be a very useful clinical tool that could help reduce costs and
avoid unnecessary exposure to therapy with significant side effects Little is known about
predictors of failure to achieve SVR with DAAs. Although numerous clinical parameters
predicted poor response to pegylated IFN treatment , none of them have been shown to be
associated with virological relapse after DAA based therapy
Treatment response terms:
The ultra rapid virological response (uRVR) is a new endpoint that we defined as an
undetectable serum HCV RNA at the end of 1st week of therapy.
The very rapid virologic response( vRVR )defined as undetectable serum HCV RNA level at week
2.
The rapid virological response (RVR) defined as undetectable serum HCV RNA after 4 weeks of
treatment sustained virological response (SVR), which is defined by the undetectable serum
HCV RNA 12-24 weeks after the end of treatment Relapser was defined as undetectable viral
load at the end of DAA treatment but subsequent detectable viral load at 12 weeks after
treatment end.
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