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Editorial Board: Emmet B. Keeffe, MD (Chair);
Anna Lok, MD; Brian McMahon,
MD; Albert Min, MD; Myron Tong, MD; Naoky Tsai, MD; Bruce Tung, MD
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HBV
Watch™
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Timely Information for Practicing Physicians
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MAY 2005
HBV VACCINATION
Protection after 15 years of follow-up. Alaska Natives have a high prevalence of
chronic HBV infection that is primarily acquired during early childhood. Brian McMahon and
colleagues report data on persistence of anti-HBs and protection afforded by
HBV vaccination of an Alaska Native population after 15 years of follow-up. Between
November 1981 and May 1982, 1,578 Alaska Natives aged 6 months or older
residing in 15 villages received 3 doses of plasma-derived hepatitis B vaccine.
This cohort was followed annually
for the first 11 years, and 841 (53%) of the participants were tested at 15
years. Mean plasma levels of anti-HBs decreased from 822 mIU/mL after vaccination to 27 mIU/mL
at 15 years. A longitudinal linear mixed model analysis identified initial
anti-HBs level, age >4 years at vaccination, and male sex to be associated
with the persistence of higher anti-HBs levels at 15 years. Asymptomatic
breakthrough infection developed in only 16 participants and occurred more
frequently in vaccination nonresponders than in responders (P = 0.01); serum HBV DNA was detected in
6 of these participants. Two persons
were infected with wild-type HBsAg and 4 persons were infected with both
wild-type HBsAg and HBsAg variants.
These data demonstrated that HBV vaccination provided good protection
against infection for at least 15 years. In this population, antibody levels were
found to decrease the most in persons immunized at 4 years of age or younger. (McMahon BJ, et al. Ann
Intern Med. 2005;142:333–341)
HBV-RELATED ACUTE LIVER FAILURE
(HBV-ALF)
Virologic
characteristics. C-T Wai
and others
from
the US Acute Liver Failure Study Group studied 34 consecutive patients with
HBV-ALF. Of these, 23 patients (68%) survived (14 after liver transplantation,
and 9 without transplantation). Forward logistic regression analysis identified
only older age to be an independent predictor of poor outcome (P=0.011). Precore stop and core promoter
dual variants were found in 32% and 44%, respectively, of 25 patients with
detectable serum HBV DNA. Comparison with a cohort of 530 patients with chronic
HBV infection from the US HBV Epidemiology Study (Chu CJ, et al. Gastroenterology. 2003;125:444–451),
patients with HBV-ALF were more likely to be non-Asians (P= 0.005) and to be infected with genotype D (P<0.01). A higher prevalence of HBV genotype D among HBV-ALF
patients persisted after matching for race and HBeAg status (P=0.007). These findings suggest that
HBV genotype D may be associated with an increased risk of an aggressive
clinical course. Further studies are needed to determine the role of HBV
genotype in the outcome of acute HBV infection. (Wai
C-T, et al. J Viral Hepat.
2005;12:192–198)
INTERFERON ALFA (IFNa) THERAPY
Impact on
liver fibrosis progression.
GV Papatheodoridis and coworkers evaluated 147 patients with
HBeAg-negative chronic hepatitis B who had at least 2 liver biopsies and had
been treated with IFNa (n = 120) or had been followed without treatment (n =
27). A blinded analysis of the liver biopsies was conducted by a single
histopathologist and scored using the Ishak classification. Fibrosis improved
in 17.5% of IFNa-treated patients and in 4% of untreated patients; it worsened
in 34% of IFNa-treated patients and in 70% of untreated patients (P=0.002). The annual rate of fibrosis
progression was higher in the untreated group than in the treated group (P=0.001). However, further analysis
showed that the fibrosis progression rate in the untreated group was similar to
that in the treated patients who did not achieve a sustained biochemical
response to IFNa. Multivariate analysis identified older age, worse baseline
grading score, lower baseline fibrosis, and lack of sustained response to IFNa
to be associated with a worse fibrosis progression rate. These data indicate
that the rate of fibrosis progression is reduced in patients with
HBeAg-negative chronic HBV who achieve a sustained biochemical response to IFNa
therapy. (Papatheodoridis
GV, et al. J Viral Hepat.
2005;12:199–206)
HEPATOCELLULAR CARCINOMA (HCC)
HBV
reactivation. The clinical course of cytotoxic chemotherapy treatment of
cancer patients who are HBV carriers may be complicated by HBV reactivation. In
China, more than 80% of patients with HCC are HBV carriers.
Winnie Yeo and colleagues at the Prince of Wales
Hospital in Hong
Kong
prospectively studied 102 patients with unresectable HCC who were
HBsAg-positive and were to receive systemic chemotherapy. The patients were
followed during the chemotherapy course and for 8 weeks after the completion of the
chemotherapy. In total, 37 patients (36%) developed hepatitis due to HBV
reactivation. The severity of hepatitis was moderate in 20 patients and severe
in 14 patients. HBV reactivation was the primary cause of death in 12 of the
patients. Patients with HBV reactivation had higher ALT levels at baseline than
did patients who did not undergo HBV reactivation (P=0.04). The incidence rates of chemotherapy interruption and
median survival times were similar between patients with and without HBV reactivation.
These findings demonstrate that HBV reactivation is a common cause of hepatitis
in HBsAg-positive HCC patients who undergo systemic chemotherapy. Pre-emptive antiviral therapy should be considered for all
HBsAg-positive patients prior to initiation of cancer chemotherapy and be continued
for at least 2 months after completion of chemotherapy. (Yeo W, et al. Ann
Oncol. 2004;15;1661–1666)
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