الفهرس 
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Abstract
Introduction: Hepatitis C virus (HCV) infection has acute and chronic forms with most of the morbidity through the development of chronic liver disease. In Egypt, HCV is one of the top five leading causes of death. Modern therapies are not affordable for the majority of HCV carriers worldwide. Silymarin is an extract of the milk thistle (Silybum marianum) . that inhibits hepatitis C virus (HCV) by displaying antioxidant, anti-inflammatory, and immunomodulatory actions that contribute to its hepatoprotective effects. There are several clinical studies on the use of herbal extracts, especially silymarin, for the treatment of patients with chronic hepatitis C, primarily in the belief that this drug improves response to antiviral agents and reduces adverse reactions.
Aim of the work:
This study was made to evaluate the impact of oral Silymarin 140 mg/d on HCV viremia when added to the known and well established conventional treatment (Peg-INF+ribavirin)
Results:
The study included 60 patients, the mean age was 37.6±7.9 years and 23 patents (38%) were females.
Basal ALT was 48.8±32 U/L, basal AST was 51.1±33, basal heamoglobin was 13.97±1.4 g/dL, basal platelet count was 243.7±67.8 ×1000/mm3, and basal white blood cells count was 6.1±1.3 ×1000/mm3. 12 weeks from starting therapy, ALT and AST decreased significantly (36.9±25, 33.2±24.1 U/L, p=0.011,<0.001 respectively), heamoglobin, platelet count and white blood cells count decreased significantly (10.8±1.1 g/dL, 151.9±56 ×1000/mm3, 3.3±1.04 ×1000/mm3, p<0.001, <0.001, <0.001, respectively).
There was no significant differences between patients who received silymarin and patients who did not regarding age, sex, history of Schistosomiasis, serum billirubin, ultrasonography proven enlarged liver, increased liver echogenicity, liver fibrosis, or portal vein size.
In addition, there was no significant difference between patients who took silymarin and patients who did not regarding basal ALT, basal AST, basal heamoglobin, basal platlet count, basal WBCs count, and basal PCR (2.72±2.8 vs. 2±1.74 ×103/mm5, p=0.404)
Interestingly, after 12 weeks from starting treatment course, patients who received silymarin had significantly lower ALT (29.5±15.7 vs. 44.4±30.4 U/L, p=0.544, figure 17), and AST (26.6±11.5 vs. 40±31 U/L, p=0.368, figure 18), higher platelet count (170.1±61.9 vs. 133.6±43 ×103/mm3, p=0.948, figure 19), and higher WBCs count (3.6±1.1 vs. 2.9±0.8 ×103/mm3, p=0.404, figure 20). Heamoglobin level, despite being relatively higher in patients who received silymarin, this did not reach statistical significance (11±1.1 vs. 10.6±0.9, p=0.1, figure 21)
Overall, 42 showed early virological response (Decided by negative PCR values at 12 weeks), of whom 24 patients received silymarin and 18 patients did not (p=0.09). Discontinuity of therapy occurred in 18 patients based on the finding of elevated positive PCR values during the 12 weeks visit after start of treatment (All: 1.05±1, silymarin: 1.13±1.6, no silymarin 1±0.7 ×105/mm3, p=0.813, figure 22). 6 of thee patients received silymarin and 12 did not (p=0.09). At 24 weeks of follow-up after treatment, 5 patients out of the 42 (12%) had relapse, decided by absence of SVR because of re-elevation of PCR, all of whom did not receive silymarin therapy, which was significantly higher than those who received silymarin (p=0.02). Finally, the overall number of patients who showed SVR (responders) after completion of treatment was 37 (62%), of whom 28 patients received silymarin and 13 patients did not (p=0.003).
It is worth noting that all patients who received silymarin and had EVR also showed SVR.