Hepatitis B surface antigen serum levels help to distinguish active from inactive hepatitis B virus genotype D carriers.

BACKGROUND & AIMS: The accurate identification of inactive (serum HBV-DNA persistently or=20,000 IU/mL (AC2): 883 (0.5-7838) vs 4233 (164-82,480) IU/mL, P=.002. HBV infection was less productive in IC and AC1 than AC2 (log10 HBV-DNA/HBsAgsl ratios 0.25 and 0.49 vs 2.06, respectively, P<.001) and in chronic hepatitis than cirrhosis (1.97 vs 2.34, respectively; P=.023). The combined single point quantification of HBsAg (<1000 IU/mL) and HBV-DNA (

Severe liver disease is caused by HBV rather than HCV in children with hematological malignancies.

UNLABELLED: Patients receiving chemotherapy experience exacerbations of chronic hepatitis B (HBV) or hepatitis C (HCV) viral infections. We examined the pattern of liver disease induced by these infections in 92 children and adolescents with elevated transaminases (median age: 9 years). This included 76 with hematological malignancies (55 ALL, 15 NHL and six Hodgkin's disease) and 16 with thalassemia major. Liver disease was graded: A--occasional hypertransaminemia, B--persistent hypertransaminemia, C--severe hepatitis without encephalopathy, D--fulminant hepatic failure (FHF) and death. Screening included HBsAg, anti-HCV antibody, HBV-DNA and HCV-RNA: 26 had liver biopsies. A total of 60 (79%) patients with malignancies were HBsAg and/or HBV-DNA(+)(genotype D-E) and 47 (62%) were anti-HCV and/or HCV-RNA(+); 33 were coinfected with HBV and HCV. Grade A (n=24) included 16 with HCV and 12 with HBV (six coinfected); 18 with HBV and 11 with HCV (10 coinfected) were graded B (n=22). All grade C (n=25) had HBV with 16 HCV coinfected. FHF and death occurred in five HBV-DNA(+) patients, in four within a month of i.v. methotrexate. Patterns C and D were associated with HBsAg and HBV-DNA (P=0.001 and P<0.001, respectively). In all, 70% of HBV-infected children suffered chemotherapy-associated flares. None of the thalassemics had severe hepatitis exacerbations; 94% had HCV markers with none HBV-DNA(+). One died of progressive cirrhosis. CONCLUSIONS: Children with hematological malignancies have worse liver disease when associated with chronic HBV. FHF occurred in HBsAg/HBV-DNA(+) children following i.v. methotrexate. Early recognition of hepatic dysfunction in HBV carriers is essential in order to reduce incidence of life-threatening complications.

Viral load 1 week after liver transplantation, donor age and rejections correlate with the outcome of recurrent hepatitis C.

BACKGROUND: Early identification of patients at a higher risk of rapidly progressive recurrent hepatitis post liver transplantation (LT) could help to tailor antiviral therapy. METHODS: We studied the correlation between early post-LT viral load and the histological and clinical outcomes of 49 consecutive patients (34 males, median age 55 years) in whom viraemia was monitored at days 0, 1, 7, 30, 180 and 365 after LT. RESULTS: Hepatitis C recurred at histology in 38 of 42 (90.5%) patients. Early viral load after LT was higher in patients with rapidly progressive hepatitis C recurrence (day 7 median HCV-RNA levels: 5.84 vs 4.93 Log(10) IU/ml, P=0.003). Day 7 HCV-RNA levels >/=2.5 x 10(5) IU/ml, donor age >60 years and rejection episodes were independently associated with progression to cirrhosis within one year post-LT [P=0.018, odds ratio (OR) 27.59; P=0.043, OR 13.85 and P=0.048, OR 9.95, respectively]. Day 7 viraemia and rejection episodes were independently associated with 5-years survival. Day 7 viraemia, in combination with acute hepatitis and/or donor age, showed 80% sensitivity, 94% specificity and 90.5% diagnostic accuracy to identify severe recurrence. CONCLUSIONS: Early post-LT HCV-RNA correlates with the severity of hepatitis C recurrence and in combination with donor age (>60 years) and rejections, identifies patients with a high risk of severe recurrence and candidates of cost-effective pre-emptive antiviral therapy.

Longitudinal evaluation reveals a complex spectrum of virological profiles in hepatitis B virus/hepatitis C virus-coinfected patients.

Hepatitis B virus (HBV) and hepatitis C virus (HCV) coinfection is often associated with severe forms of liver disease. However, comprehensive studies are lacking, and scant information is available regarding the virological behavior over time in coinfected patients. This study enrolled 133 untreated HBV/HCV-positive patients (male/female = 102/31; median age 51 years [range: 22-83 years]) who were longitudinally followed up for 1 year with bimonthly evaluation of HBV/HCV viremia levels and liver biochemistry. Thirty of these patients had triple infection with hepatitis Delta virus (HDV), while 103 patients were HDV-negative. In the HDV-negative group, active infection with both HBV and HCV was revealed in 24 cases, inactive infection by both viruses was seen in 15 cases, active HBV/inactive HCV was seen in 15 cases, and inactive HBV/active HCV was seen in 49 cases. However, 32 subjects (31%) presented dynamic virological profiles characterized by fluctuation of HBV and/or HCV viremia levels that at different time points were over or under the cutoff limits. Consequently, a correct diagnosis could be performed in these subjects only by serially repeating the virological tests 1 year apart. Similarly, 15 of the 30 HDV-positive subjects showed active HBV and/or HCV infection, with fluctuating virological patterns in 8 cases. In conclusion, this study showed that the virological patterns in HBV/HCV coinfection are widely divergent and have dynamic profiles. A careful longitudinal evaluation of the viremia levels of both viruses is essential for making a correct diagnosis and tailoring the appropriate therapeutic schedule in coinfected patients.