الفهرس 
HEPATITIS C VIRUSOnly 14 pages are availabe for public view
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Abstract
To this day, hepatitis C virus infection represents a global burden. The long term impact of HCV infection is highly variable, ranging from minimal effects to severe extra-hepatic complications including CVD. HCV treatment has been transformed by the availability of DAAs, which achieve >90% SVR rates.
The optimal method for CVD risk assessment in HCV infected persons is currently unknown. Total cholesterol, LDL, and hsCRP, which are routinely used, are reduced in the setting of HCV-associated chronic liver disease and hence underestimate CVD risk in these patients. Non-hepatic CVD markers such as Lp-PLA2 may be better CVD risk predictors in this setting. In addition, successful HCV treatment may reduce CVD risk and improve levels of non-hepatic CVD biomarkers.
The aim of this study was to measure the level of serum Lipoprotein associated phospholipase A2 (Lp-PLA2) and serum lipids, in chronic HCV infected patients, before and after treatment with DAAs, to identify change in risk of cardiovascular disease in relation to HCV clearance.
This prospective study was conducted on 90 chronic HCV infected patients, with no underlying CVD, eligible for antiviral treatment with DAAs. 45 patients (50%) had
received SOF/DCV while the other 45 received SOF/DCV/RBV. 86/90 patients achieved SVR, 12 weeks after the end of treatment. Of the total studied subjects, 22 patients were found to have liver cirrhosis. Amongst cirrhotic patients, 9/22 were Child A5, 12/22 were Child A6 and 1/22 was Child B7 as per Child-Pugh score. Furthermore, our study included 18 smokers (20%), 15
hypertensive patients (16.7%), 7 diabetic patients (7.8%)
and 13 pre-diabetic patients (14.4%).
All patients were assessed at baseline and week 12 with laboratory workup including lipid profile and Lp- PLA2 concentration, Framingham CVD risk score analysis, ultrasonography and transient elastography.
Lipid profile was found to be low or optimal at baseline, being significantly lower in cirrhotic patients. Total Cholesterol, LDL, HDL and Triglyceride levels were shown to increase in patients who achieved SVR with no significant change in the non-SVR group. Framingham score calculated for all patients demonstrated no significant difference in value or risk stratification before and after treatment. In addition, as per Framingham score, 70% were defined as low-risk patients.
On the other hand, baseline Lp-PLA2 levels were significantly high, classifying 82% of patients as having
high risk for CVD, and demonstrated a significant decline in patients after SVR, with no correlation to liver stiffness score.
Interpretation of changes in Lp-PLA2 is hindered by the lack of validation of the biomarker for CVD risk prediction in HCV infection, and inability to correlate biomarker levels with hard outcomes such as CVD events. Despite this, our data warrants further investigation into determining the predictive power of both non-hepatic and hepatic CVD biomarkers in HCV infected patients.