Raffaella Pisapia

Impact of occult hepatitis B virus infection in HIV patients naive for antiretroviral therapy.

Objective:To study the impact of occult hepatitis B virus (HBV) infection in 115 consecutive anti-HIV-positive, hepatitis B surface antigen-negative patients, naive for antiretroviral treatment. Methods:Of these 115, 86 patients were followed for at least 6 months (range 6–36) with serial determinations of HIV RNA and HBV DNA by polymerase chain reaction and other laboratory tests. Results:Of the 86 patients having a follow-up, plasma HBV DNA was detected in 17 (19.8%), 13 on admission and four during follow-up. HBV DNA was more frequently found in patients with isolated anti-hepatitis B core (HBc; 35.5% of 31 cases) than in those lacking anti-HBc and anti-hepatitis B surface (8.8% of 41, P < 0.005), or showing both (21.4% of 14). Twenty-eight patients (32.5%) experienced a hepatic flare during the follow-up; this event was more frequent in the 17 HBV-DNA-positive patients than in the 69 negative (64.7% versus 24.6%, P < 0.005). Of the 13 HBV-DNA-positive patients on admission, 11 receiving HAART containing lamivudine became HBV-DNA negative, but two of these again became positive and experienced a hepatic flare during treatment and two both during and after lamivudine treatment. A hepatic flare also occurred under lamivudine treatment in two of the four patients in whom HBV DNA became detectable during follow-up. The role of immune reconstitution inflammatory syndrome and HAART in inducing a hepatic flare was found to be marginal in 49 patients with no HBV or hepatitis C virus marker. Conclusion:The study suggests that HBV occult infection, relatively frequent in anti-HIV-positive patients, is associated with hepatic flares.

Improvement in the aetiological diagnosis of acute hepatitis C: A diagnostic protocol based on the anti-HCV-IgM titre and IgG Avidity Index

BACKGROUND The gold standard for the diagnosis of acute hepatitis C (AHC) is seroconversion to anti-HCV/HCV-RNA positivity, an occurrence frequently missed in clinical practice. OBJECTIVES This study aims to diagnose AHC by the combined use of the HCV Avidity Index (HCV-AI) and HCV-IgM titre. STUDY DESIGN We enrolled 45 patients with AHC diagnosed by seroconversion to anti-HCV/HCV-RNA positivity and 36 with exacerbation of chronic hepatitis C (e-CHC) diagnosed at least 1 year earlier. HCV-IgM titres were determined by a commercial enzyme-linked immunosorbent assay (ELISA) and HCV-AI by an ELISA for detection of HCV IgG with a partial modification. For each test, specific cut-off values at four selected checking points were established during the observation (<10 days, 11-15 days, 16-20 days and >20 days from the onset of symptoms): for the HCV-IgM assay, the highest value in e-CHC +5% and for HCV-AI assay, the lowest value in e-CHC -5%. RESULTS Around 90% of patients with AHC or e-CHC were correctly diagnosed at all checking points by combining the results of both tests. This practice afforded an improvement in sensitivity for the diagnosis of AHC, with the highest values at first and third checking points (92.3% and 92.6%, respectively) and an improvement in negative predictive value (NPV), with the highest value at first checking point (92.6%). CONCLUSIONS The diagnosis of AHC, made by seroconversion to anti-HCV/HCV-RNA positivity, was confirmed in more than 90% of patients by combining the results of IgG Avidity Index (IgG-AI) and HCV-IgM obtained in a single serum sample.

Factors affecting the changes in molecular epidemiology of acute hepatitis B in a Southern Italian area.

Summary.  To explore changes in molecular epidemiology of acute viral hepatitis B (AVH‐B), hepatitis B virus (HBV) genotypes were determined by direct sequencing of the Pre‐S‐S region in 123 consecutive patients, with AVH‐B observed in Naples or its surroundings in the last decade (group AVH‐B) and in 123 HBV chronic carriers [chronic carrier of HBV (CC‐B) group] from the same areas, who had been hepatitis B surface antigen‐positive for more than 10 years. Genotype D was less frequently detected in patients with AVH‐B than in those in the CC‐B group (76.4%vs 97.5%, P < 0.0001). In the AVH‐B group, intravenous drug addiction (IVDA) was the prevalent risk factor (55.3%) for acquiring HBV in the 94 patients with HBV genotype D, but it was rarely recorded (6.9%) in the 29 patients with genotypes non‐D (P < 0.0001); unsafe sexual intercourse was prevalent in patients with genotype non‐D (72.3%) and less frequent in those with genotype D (28.8%, P < 0.005). In the AVH‐B group, the prevalence of non‐D genotypes increased during the observation period from 11.1% in 1999–2003 to 41.1% in 2004–2008 (P < 0.0005), paralleling the increase in the prevalence of patients with unsafe sexual intercourse; similarly, the progressive decrease in IVDA paralleled the decrease in the prevalence of genotype D (from 88.3% in 1999–2003 to 11.7% in 2004–2008). The prevalence of HBV non‐D genotypes recorded in the last 10 years in AVH‐B in this area shows a progressive increase, most probably because of recent changes in HBV epidemiology, namely, the HBV mass vaccination campaign and increased immigration from areas with high HBV endemicity.

Clinical and Virological Improvement of Hepatitis B Virus-Related or Hepatitis C Virus-Related Chronic Hepatitis with Concomitant Hepatitis A Virus Infection

BACKGROUND We evaluated the clinical and virological characteristics of hepatitis A virus infection in persons concomitantly infected with hepatitis B virus (HBV) or hepatitis C virus (HCV). METHODS We enrolled 21 patients with acute hepatitis A and chronic hepatitis with no sign of liver cirrhosis, 13 patients who were positive for hepatitis B surface antigen (case B group), 8 patients who were anti-HCV positive (case C group), and 21 patients with acute hepatitis A without a preexisting liver disease (control A group). Two control groups of patients with chronic hepatitis B (control B group) or C (control C group) were also chosen. All control groups were pair-matched by age and sex with the corresponding case group. RESULTS Fulminant hepatitis A was never observed, and hepatitis A had a severe course in 1 patient in the case B group and in 1 patient in the control A group. Both patients recovered. On admission, HBV DNA was detected in 1 patient in the case B group (7.7%) and in 13 patients (50%) in the control B group; HCV RNA was found in no patient in the case C group and in 16 patients (81.2%) in the control C group. Of 9 patients in the case B group who were followed up for 6 months, 3 became negative for hepatitis B surface antigen and positive for hepatitis B surface antibody, 2 remained positive for hepatitis B surface antigen and negative for HBV DNA, and 4 became positive for HBV DNA with a low viral load [corrected] Of 6 patients in the case C group who were followed up for 6 months, 3 remained negative for HCV RNA, and 3 had persistently low viral loads. CONCLUSION Concomitant hepatitis A was always self-limited, associated with a marked inhibition of HBV and HCV genomes, and possibly had a good prognosis for the underlying chronic hepatitis.