The incidence, clinicopathological features and etiolo'gy of acute exacerbation occurring in patients with chronic type B hepatitis were 888e88ed prospectively among 385 patients who had HBeAg and 279 who had anti-HBe in serum. During an average follow-up of 23.5 months, acute exacerbations occurred in 197 HBeAgpositive patients and in 56 anti-HBe positive patients, with a calculated annual incidence of 28.6 and 10.3%, respectively (p < 0.001). The clinical and laboratory findings of acute exacerbations were similar in the HBeAg-positive and anti-HBe positive patients. The mean serum bilirubin and a-fetoprotein levels were higher in anti-HBe positive patients (p < 0.01). but actual differences were small. The histologic features of acute exacerbations were also similar in the HBeAgpositive patients and anti-HBe positive patients. Lobular alterations were the main histologic findings; in addition, one-fourth of patients had bridging necrosis and one-fourth had piecemeal necrosis. Spontaneous reactivation of hepatitis B was the major cause of these exacerbations in both HBeAg-positive patients (91.5%) as well as anti-HBe positive patients (62.5%). Hepatitis delta virus superinfection accounted for a higher percentage of exacerbations in anti-HBe positive patients (14.3%) than in HBeAg-positive cases (6.5%). Hepatitis A and possibly non-A, non-B virus superinfections also contributed to some episodes of exacerbation. Thus, acute exacerbations of disease occurred more frequently in HBeAg-positive patients than in anti-HBe positive patients with chronic type B hepatitis, but the clinicopathological features and etiologies were similar.
Studies on the natural history of chronic type B hepatitis have shown that acute exacerbations occur frequently in patients who have HBeAg in serum (1,2), and that loss of HBeAg and seroconversion to anti-HBe is usually accompanied by remission of the disease and fall of serum transaminase levels into the normal range (3, 4). However, such seroconversion does not always signal a permanent resolution of chronic type B hepatitis, since subsequent spontaneous reactivation may occur (2,5,6).