An analysis of the clinical characteristics of patients with chronic hepatitis B superinfected with acute hepatitis E / 中华实验和临床病毒学杂志

ABSTRACT

<p><b>OBJECTIVE</b>To investigate clinical features of the patients with hepatitis B superinfected with acute hepatitis E (AHE).</p><p><b>METHODS</b>Totally 625 consecutive patients enrolled from Dec 2002 to Dec 2006 were studied retrospectively. All of the patients were subclassified into acute hepatitis E group (AHE=437 cases) and Superinfected Group (S=188 cases), and S group was further divided into the group of chronic hepatitis B superinfected with acute hepatitis E (CHB+AHE, 130 cases) and the group of liver cirrhosis and hepatitis B superinfected with acute hepatitis E (LCB+AHE, 58 cases). In 32 of the 188 superinfected patients the effects of HEV on HBV were observed by comparing the levels of HBV DNA in acute vs. convalescence stages.</p><p><b>RESULTS</b>Compared with the patients with AHE, the superinfected patients had a higher level of total bilirubin (TBil), an elevated frequency of fulminate hepatitis, mortality and a longer period of the mean hospital stay for the cured patients but significantly lower levels of alanine aminotransferase (ALT), serum albumin and prothrombin activity (PA). Furthermore, the group of LCB+AHE had a higher level of TBil and higher incidences of complications such as ascites, peritonitis, hepatic encephalopathy and disturbance in glycometabolism than the group of CHB+AHE. The follow-up for the superinfected patients showed that 20 of 32 patients (62.5 percent) had decreased copies of HBV DNA during the recovery phase compared with the acute phase, and the mean decrease of HBV DNA was 2.1 log10. The HBV DNA was in a persistently undetectable level in 6 of 32 (18.8 percent) superinfected patients. However, 4 of 32 patients (12.5 percent) showed an unchanged levels of HBV DNA and 2 cases (6.2 percent) had a slightly increased HBV DNA levels.</p><p><b>CONCLUSION</b>Superinfection with AHE in patients with chronic hepatitis B leads to a more severe hepatic damage and the replication of HBV DNA can be transiently inhibited.</p>