We studied 648 hepatitis B surface antigen (HBsAg)– and/or anti-hepatitis C virus (HCV)–positive patients to evaluate the virologic and clinical characteristics of multiple hepatitis viral infection. We defined as Case B–C an HBsAg/anti–HCV positive patient and as Case b–C an anti–HCV/anti–HBc–positive, HBsAg/anti–HBs-negative patient. For each Case B–C we scheduled as Control–B an HBsAg positive and anti–HCV negative patient and as Control–C an HBsAg/anti–HBs/anti-hepatitis B core antigen (HBc)–negative and anti–HCV-positive patient. Control group C was used as the control also for Case group b–C. Serum HBV DNA by molecular hybridization was found more frequently in Control group B (54% of 161 patients) than in Case group B–C (35.7% of 84, P < .01). The prevalence of HBV wild type was similar in Case group B–C (14.3%) and in Control group B (17.4%), whereas the e–minus strain was less frequent in Case group B–C (10.7% vs. 33%; P < .01). HBV DNA by polymerase chain reaction (PCR) was detected in 40.8% of 71 patients in Case group b–C. HCV RNA was detected more frequently in Control group C (90.7% of 130 patients) than in Case group B–C (65.2% of 69, P < .0001). Moderate or severe chronic hepatitis or cirrhosis were more frequent in Case group B–C (62.9% of 65 patients) than in Control group B (46.7% of 90, P < .05) or C (40.8% of 98, P < .005), and in Case group b–C (71.1% of 76) than in Control group C. Thus, in multiple hepatitis we observed a reciprocal inhibition of the viral genomes and a more severe liver disease. In Case group b–C, serum HBV DNA was frequent and the clinical presentation was severe.

Approximately 3 million healthcare workers per year receive an injury with an occupational instrument, with around 2000000 exposures to hepatitis B virus (HBV) and 1000000 to hepatitis C virus (HCV). Although an effective HBV vaccine has been available since the early eighties, and despite the worldwide application of universal vaccination programs started in the early nineties, HBV still remains a prominent agent of morbidity and mortality. There is no vaccine to limit the diffusion of HCV infection, which progresses to chronicity in the majority of cases and is a major cause of morbidity and mortality worldwide due to a chronic liver disease. Healthcare workers are frequently exposed by a mucosal-cutaneous or percutaneous route to accidental contact with human blood and other potentially infectious biological materials while carrying out their occupational duties. Mucosal-cutaneous exposure occurs when the biological material of a potentially infected patient accidentally comes in contact with the mucous membranes of the eyes or mouth or with the skin of a healthcare worker. Percutaneous exposure occurs when an operator accidentally injures himself with a sharp contaminated object, like a needle, blade or other sharp medical instrument. About 75% of the total occupational exposure is percutaneous and 25% mucosal-cutaneous, the risk of infecting a healthcare worker being higher in percutaneous than in mucosal-cutaneous exposure. All healthcare workers should be considered for HBV vaccination and should meticulously apply the universal prophylactic measures to prevent exposure to HBV and HCV.

We enrolled 44 patients with hepatitis B virus (HBV) acute infection, 21 anti-hepatitis C virus (HCV)-positive for at least 1 year (case BC group), 20 anti-HCV-negative (control B group), and 3 with HBV/HCV acute concurrent infection. For each case BC, a subject with chronic HCV infection alone was selected (control C group). At the first observation, 85.7% of patients in case BC group and 85% of those in control B group were HBV-DNA-positive (polymerase chain reaction [PCR]), with a similar trend towards a decrease and negativization in about 20 days; in the case BC group, seroconversion to antibody to hepatitis B e antigen (anti-HBe) was more rapid. HCV-RNA (PCR) was undetectable in all case BC patients but 1, who shortly became negative, whereas 85.7% of subjects in control C group were positive (P < .001). Severe acute hepatitis was more frequent in the case BC group than in the control B group (28.6% vs. 0%, P < .05). Of the 14 patients in the case BC group and of the 16 in the control B group followed up for more than 6 months, 1 in the first and 1 in the second group became hepatitis B surface angiten (HBsAg) chronic carriers. Of the 13 patients in case BC group who recovered, 1 cleared both anti-HCV and HCV-RNA, 6 became HCV-RNA-positive, and 6 remained HCV-RNA-negative. In patients with HBV/HCV acute concurrent infection, HBV-DNA became undetectable in 15 days, and HCV-RNA and anti-HCV became positive at days 30 and 45, respectively; these patients developed HCV-RNA-positive chronic hepatitis. In conclusion, HBV superinfection in chronic HCV carriers has a severe clinical course and strongly and persistently depresses HCV.

Epidemiology of acute and chronic hepatitis B and delta over the last 5 decades in Italy

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. 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. 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. The study suggests that HBV occult infection, relatively frequent in anti-HIV-positive patients, is associated with hepatic flares.