-
A Gramenzi,
E Loggi, L Micco,
C Cursaro,
S Fiorino,
S Galli,
S Gitto,
C Galli,
G Furlini,
M Bernardi,
P Andreone
[show abstract]
[hide abstract]
ABSTRACT: Serum hepatitis B virus surface antigen (HBsAg) levels have been suggested to predict interferon response in chronic hepatitis B. A few data are available on the role of HBsAg measurement in nucleos(t)ide analogues (NA) treatment. We retrospectively investigated the relation between HBsAg changes and main treatment outcomes during long-term lamivudine treatment in hepatitis e antigen (HBeAg)-negative chronic hepatitis B. A total of 42 HBeAg-negative patients were consecutively enrolled in an open-label study on long-term lamivudine monotherapy (150 mg/die). Serum HBsAg levels were quantified every 6 months by Architect assay (Abbott Diagnostics). HBV-DNA was quantified quarterly by real-time PCR (Roche Diagnostics). The median duration of lamivudine treatment was 66 months (20-153). One patient (2%) was a primary nonresponder, 35 (83%) developed virological breakthrough (VB) and the remaining six patients (14%) were classified as long-term on-treatment responders. During treatment, HBsAg levels decreased only in long-term on-treatment responders, while no changes were observed in resistant patients. Failure to achieve a decrease of 0.7 log(10) IU/mL in serum HBsAg at month six of lamivudine had a positive predictive value of developing VB of 90% and a negative predictive value of 100%. These high predictive values were also maintained in the subgroup of patients negative for HBV-DNA at month six. The results of this study with a small sample size suggest a role of on-treatment HBsAg quantification in the management of lamivudine-treated patients. If validated prospectively in a larger patient cohort, HBsAg measurements would be a useful adjunct to optimize antiviral therapy.
Journal of Viral Hepatitis 10/2011; 18(10):e468-74. · 4.09 Impact Factor
-
A Gramenzi,
F Conti,
F Felline,
C Cursaro,
A Riili,
M Salerno,
S Gitto, L Micco,
A Scuteri,
P Andreone,
M Bernardi
[show abstract]
[hide abstract]
ABSTRACT: Chronic hepatitis C virus (HCV) infection has been poorly investigated in the elderly. The aim of this study was to identify the age-specific characteristics of chronic hepatitis C by comparing patients > or =65 years with those <65 years. A cross-sectional study was performed on data collected from consecutive outpatients referred for the first time to two tertiary outpatient clinics for liver diseases located in Bologna (Northern Italy) and Paola, Cosenza (Southern Italy) over a two-year period. A total of 560 anti-HCV and HCV-RNA positive patients were enrolled, of whom 174 (31%) were 65 years or older. The proportion of older patients was significantly higher in the Southern Italy centre, accounting for more than 40%. Comparison of younger and older groups showed that 51% patients > or =65 years had advanced liver disease (liver cirrhosis or hepatocellular carcinoma) compared with 26% younger patients (P < 0.0001). About half of the patients > or =65 years were not aware of their anti-HCV positive status, even if they tended to be more symptomatic than the younger group. By multivariate analysis, age > or = 65 years, alcohol consumption and diabetes were independently associated with advanced liver disease. Overall, 34 out of 174 patients (20%) > or =65 years had received antiviral treatment compared with 122 out of 386 (32%) younger patients (P = 0.003). Our results further emphasize the notion that chronic hepatitis C is becoming a disease of the elderly and that elderly patients with chronic HCV infection often have severe and underestimated disease.
Journal of Viral Hepatitis 09/2009; 17(5):360-6. · 4.09 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Due to their high prevalence in the general population, alcohol use and abuse can be associated with hepatitis B and C virus infections and it has been demonstrated that alcohol plays a role as a co-morbid factor in the development of liver disease. There is evidence that alcohol abuse accelerates the progression of liver fibrosis and affects the survival of patients with chronic hepatitis C. The mechanism by which alcohol worsens hepatitis C virus-related liver disease has not been fully clarified, but enhanced viral replication, increased oxidative stress, cytotoxicity and impairment of immune response could play a relevant role. Alcohol abuse also seems to reduce both sensitivity to interferon and adherence to treatment. It sounds reasonable to presume that the mechanisms enhancing liver damage in patients affected by hepatitis B are similar to those involved in hepatitis C virus infection. However, more studies are warranted to improve our knowledge about the interaction between alcohol intake and hepatitis B virus infection. In conclusion alcohol abuse is associated with an accelerated progression of liver injury, leading to an earlier development of cirrhosis, higher incidence of hepatocellular carcinoma, and higher mortality. Abstinence could reverse some of these deleterious effects.
Digestive and Liver Disease 08/2008; 41(1):67-70. · 3.05 Impact Factor
