Clearance of hepatitis B surface antigen and risk of hepatocellular carcinoma in a cohort chronically infected with hepatitis B virus

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http://www3.interscience.wiley.com/journal/123194749/abstract?CRETRY=1 & SRETRY=0

Hepatology

Early View (Articles online in advance of print)

Published Online: 30 Nov 2009

American Association for the Study of Liver Diseases

Viral Hepatitis

Clearance of hepatitis B surface antigen and risk of hepatocellular carcinoma in

a cohort chronically infected with hepatitis B virus

phine Simonetti 1, Bulkow 2, J. McMahon 1 2 *, Chriss Homan 1,

Snowball 1, Negus 1, 1, E. Livingston 1

1Liver Disease & Hepatitis Program, Alaska Native Tribal Health Consortium,

Anchorage, AK

2Arctic Investigations Program, National Center for Preparedness, Detection and

Control of Infectious Diseases, Centers for Disease Control and Prevention,

Anchorage, AK

email: J. McMahon (bdm9@...)

*Correspondence to J. McMahon, Liver Disease and Hepatitis Program, Alaska

Native Tribal Health Consortium, 4315 Diplomacy Drive, Anchorage, AK 99508

Potential conflict of interest: Nothing to report.

fax: 907-729-3429.

Funded by:

Liver Disease and Hepatitis Program

Alaska Native Tribal Health Consortium

Anchorage

Native American Research Centers for Health; Grant Number: 1 U26 94 00005

Abstract

Some individuals who are chronically infected with hepatitis B virus (HBV)

eventually lose hepatitis B surface antigen (HBsAg). Hepatocellular carcinoma

(HCC) has been demonstrated to occur in a few patients after loss of HBsAg.

Neither factors associated with loss of HBsAg nor the incidence of HCC

thereafter have been clearly elucidated. We performed a prospective

population-based cohort study in 1,271 Alaska Native persons with chronic HBV

infection followed for an average of 19.6 years to determine factors associated

with loss of HBsAg and risk of developing HCC thereafter. HBsAg loss occurred in

158 persons for a rate of HBsAg clearance of 0.7%/year. Older age, but not sex,

was associated with clearance of HBsAg, and loss of HBsAg was not associated

with any particular HBV genotypes (A, B, C, D, and F) found in this population.

Participants were followed for an average of 108.9 months after HBsAg loss. Six

patients, two with cirrhosis and four without, developed HCC a mean of 7.3 years

after HBsAg clearance (range, 2.0-15.5 years). The incidence of HCC after

clearance of HBsAg was 36.8 per 100,000 per year (95% CI 13.5-80.0) which was

significantly lower than the rate in those who remained HBsAg-positive (195.7

cases per 100,000 person-years of follow-up [95% CI 141.1-264.5; P < 0.001]).

After loss of HBsAg, HBV DNA was detected in the sera of 28 (18%) of those who

cleared a median of 3.6 years after clearance. Conclusion: HCC can occur in

persons with chronic hepatitis B who have lost HBsAg, even in the absence of

cirrhosis. These persons should still be followed with periodic liver ultrasound

to detect HCC early. (HEPATOLOGY 2010.)

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Received: 1 June 2009; Accepted: 24 October 2009

Digital Object Identifier (DOI)

10.1002/hep.23464