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SVR Can Prevent HCC & Other Complications
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SUSTAINED VIROLOGICAL RESPONSE IS ASSOCIATED WITH A LOWER RISK OF COMPLICATIONS AND HEPATOCELLULAR CARCINOMA IN PATIENTS WITH HCV RELATED CIRRHOSIS
Reported by Jules Levin
43rd Annual Meeting of the European Association for the Study of the Liver
April 23-27, 2008, Milan, Italy
From Jules: in a study from EASL I distributed by email yesterday, French researchers reported regression of cirrhosis (2 or more points by METAVIR) resulted in no patients developing HCC, no death, and no transplantation; followup was 10-15 yrs. Report is attached.
A.C. Cardoso1, R. Moucari1, N. Giuily1, C. Figueiredo-Mendes1, N. Boyer1, M.P. Ripault1, C. Castelnau1, T. Asselah1, M. Martinot-Peignoux2, S. Maylin2, P. Bedossa3, P. Marcellin1
1 Service d Hepatologie et INSERM U773-CRB3, 2 Service de Microbiologie, 3 Anatomie Pathologique, H™pital Beaujon, Clichy, France
Background and Aim: To evaluate the influence of antiviral therapy on the long-term outcome of chronic hepatitis C (CHC) patients with bridging fibrosis or cirrhosis.
Patients and Methods: 307 consecutive CHC patients with bridging fibrosis or cirrhosis were retrospectively evaluated. They had all received at least one treatment course with interferon (conventional or pegylated) with or without ribavirin for at least 12 weeks. Cumulative incidence of haemorrhage, ascites, and HCC were compared between patients who developed or not sustained virological response (SVR). 50-60 percent of patients had cirrhosis, 35% had moderate to severe necroinflammation, and 37 percent had severe liver steatosis. The average number of courses of treatment was 2 to 2.3, and followup was a mean of 4 years, range from 1 to 18 years.
Results:
The patients characteristics were: male gender (68%), mean age (55±10 years), mean BMI (26±4 kg/m2), mean serum HCV RNA level (5.7±0.6 log IU/ml), genotype 1 (60%), 2 (9%), 3 (16%), 4 (13%).
Median follow-up was 2.4 (1-18) years after treatment.
SVR developed in 34% of patients.
Patients with SVR developed less frequently complications than those who did not achieve SVR:
haemorrhage (1% vs. 7%, p = 0.02),
ascites (5% vs. 19%, p = 0.001), and
HCC (6% vs. 16%, p = 0.02).
Six patients have been transplanted, all were non SVRs.
The cumulative incidence of HCC was significantly lower in patients with than in those without SVR (p = <.001). HCC developed in 45 patients. Treatment failed in 39 patients; 6 patients attained SVR. The cumulative incidence of HCC was 0.6 in the group that did not attain SVR and 0.1 in the group that did attain SVR, a large difference.
HCC developed 1 to 12 years after therapy in patients without SVR and 2 to 4 years in patients with SVR. (from Jules: this suggests to me perhaps liver cancer had been present or undetectable previous to SVR and continued to progress demonstrating risk of deferring therapy).
By univariate analyses, HCC was associated with male gender, age >50 years, overweight, diabetes, and treatment failure.
By logistic regression, HCC was independently associated with: male gender (OR = 3.3), age >50 years (OR = 4.7) and non SVR status (OR = 2.7).
The 6 patients who developed HCC despite SVR were all male, diabetics
and significantly older than those who developed HCC without SVR (64±8 vs. 55±9 years, p = 0.04).
Ascites developed in 46 patients: treatment failed in 41 patients; 5 patients attained SVR (p<.001). The cumulative incidence of ascites in patients without SVR was about 0.65 and in 0.02 in patients with SVR, also quite a large difference.
10 patients underwent liver transplantation: treatment failed in all 10 patients before transplantation. 23 patients died: treatment failed in 20 of these patients; 3 attained SVR. Survival in patients without liver transplantation was about 98% in patients with SVR and about 60% in those without SVR, in this study (remember 55% had cirrhosis and 35% had moderate to severe necroinflammation); followup was 10 years.
Conclusion:
In CHC patients with bridging fibrosis (F3) or cirrhosis (F4), SVR is associated with a lower rate of complications of cirrhosis and HCC.
However, despite SVR, HCC occurred in 6% of patients up to 4 years after therapy. In those patients, male gender, old age and diabetes might be risk factors of HCC.
Therefore, surveillance should be maintained in patients F3/F4 and SVR.
HCC, ascites and liver transplantation were more likely to survive than those in whom treatment failed.
In this study 33% of CHC patients with bridging fibrosis or cirrhosis attained SVR after receiving antiviral therapy.
SVR is associated with improved long-term clinical outcomes and with lower rates of liver decompensation and HCC, resulting in improved survival.
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