Sheen I S, Liaw Y F, Lin D Y, Chu C M
Liver Research Unit, Chang-Gung Memorial Hospital, Taipei, Taiwan.
J Hepatol. 1996 May;24(5):525-31. doi: 10.1016/s0168-8278(96)80136-x.
BACKGROUND/METHODS: To examine the incidence, predisposing factors, clinicopathological characteristics and implications of acute exacerbations in chronic hepatitis C, a consecutive series of 194 biopsy-verified, anti-HCV-positive and hepatitis B surface antigen-negative patients were followed up and studied for the events of acute exacerbations, sustained biochemical resolution and development of cirrhosis.
During a mean period of 6.2 +/- 3.5 (1.0-14.0) years, 151 episodes of acute exacerbations were recorded in 78 patients (40.2%). The estimated annual incidence of acute exacerbations was 11.9%. Fifty-five percent of acute exacerbations were asymptomatic. Histological study of acute exacerbations showed mild to moderate lobular inflammatory activities without bridging hepatic necrosis in all and periportal piecemeal in 23 (42.6%). The clinicopathological features of acute exacerbations in patients with chronic hepatitis C were less severe than those in patients with chronic hepatitis B. The route of infection, sex, age, mode of clinical presentation and the initial histology did not influence the occurrence of acute exacerbations. Only those with alanine aminotransferase > or = 300 U/l at entry tended to develop acute exacerbations more frequently (p < 0.001, odds ratio = 3.6, 95% confidence interval: 1.9-6.5). Acute exacerbations per se did not influence the subsequent development of cirrhosis or sustained biochemical resolution. Cirrhosis developed more frequently in patients with chronic active hepatitis at entry (p < 0.001, odds ratio = 6.5, 95% confidence interval: 2.6-16.0). Compared with baseline HCV-RNA level, HCV-RNA increased in 61% of acute exacerbations but the genotype remained unchanged in 75%.
These results suggest that acute exacerbations also occur frequently in patients with chronic hepatitis C. They are clinically indolent, histologically less severe and not likely to be followed by sustained remission or development of cirrhosis.
背景/方法：为了研究慢性丙型肝炎急性加重的发生率、诱发因素、临床病理特征及影响，对194例经活检证实抗-HCV阳性且乙肝表面抗原阴性的患者进行了连续随访，观察急性加重事件、生化指标持续缓解情况及肝硬化的发生情况。
在平均6.2±3.5（1.0 - 14.0）年的随访期间，78例患者（40.2%）发生了151次急性加重事件。急性加重的年发生率估计为11.9%。55%的急性加重事件无症状。急性加重的组织学研究显示，所有患者均有轻度至中度小叶炎症活动，无桥接性肝坏死，23例（42.6%）有门周碎屑样坏死。慢性丙型肝炎患者急性加重的临床病理特征不如慢性乙型肝炎患者严重。感染途径、性别、年龄、临床表现方式及初始组织学情况均不影响急性加重的发生。仅入院时丙氨酸氨基转移酶≥300 U/L的患者更易发生急性加重（p < 0.001，比值比 = 3.6，95%置信区间：1.9 - 6.5）。急性加重本身并不影响随后肝硬化的发生或生化指标的持续缓解。入院时为慢性活动性肝炎的患者更易发生肝硬化（p < 0.001，比值比 = 6.5，95%置信区间：2.6 - 16.0）。与基线HCV-RNA水平相比，61%的急性加重事件中HCV-RNA升高，但75%的患者基因型未变。
这些结果表明，慢性丙型肝炎患者也经常发生急性加重。它们在临床上较为隐匿，组织学表现较轻，不太可能导致持续缓解或肝硬化的发生。
