Lazăr Călin, Grigorescu-Sido Paula, Manasia Rodica, Mireştean Stefan, Skorka Cristina, Neculoiu Daniela, Molnar Geza, Cocean Stela
Axente Iancu, 1st Pediatric Clinic, Iuliu Moldovan Institute of Hygine, Cluj-Napoca, Romania.
Rom J Gastroenterol. 2005 Sep;14(3):219-24.
In chronic infection with hepatitis virus B the fact that HBeAg becomes negative does not always mean suppression of viral replication.
HBV replication was assessed in 74 patients with chronic hepatitis or viral B cirrhosis, in whom diagnosis was made according to clinical, biological, and histological criteria. The patients were divided into two groups: group I (36 patients with interferon- therapy, 3 million U/m 2/ dose, 3 doses/week over a period of 4-6 months) and group II (control group of 38 patients who did not undergo interferon therapy). After a follow up period of 6 years in which patients underwent clinical, biochemical and serologic monitorization, HBV DNA was detected by the hybridization method on solid medium.
During evolution the levels of transaminases became normal in both groups. The HBe Ag/Ab seroconversion rate at the end of the interferon therapy was 52.8% and the spontaneous HBe Ag/Ab seroconversion rate was 72.7% in group II after an average evolution of 6 years. HBs Ag/Ab seroconversion was not detected in any patient. Assessment of viral replication by HBV DNA testing at the end of the follow up period showed higher levels as compared to the HBeAg testing (69.4% vs. 25% in group I, 55.2% vs. 7.9% in group II). The absence of viral replication (HBV DNA negative) had similar rates in both groups (30.6% in group I vs. 44.8% in group II, p>0.9) and HBV DNA titers in the two groups were not significantly different at the end of the follow up period. In both groups, HBV DNA titers were significantly higher in patients with positive HBeAg. The concordance between the two viral markers was 100%.
Because of the fluctuating evolution, long-term follow up and monitorization (including HBV DNA testing) of patients with chronic hepatitis B and of inactive HBsAg carriers are necessary.
在慢性乙型肝炎病毒感染中,HBeAg转为阴性并不总是意味着病毒复制受到抑制。
对74例慢性肝炎或乙型病毒性肝硬化患者的HBV复制情况进行评估,这些患者根据临床、生物学和组织学标准进行诊断。患者分为两组:第一组(36例接受干扰素治疗的患者,300万U/m²/剂量,每周3次,共4 - 6个月)和第二组(38例未接受干扰素治疗的对照组患者)。在6年的随访期内,患者接受临床、生化和血清学监测,采用固相介质杂交法检测HBV DNA。
在疾病进展过程中,两组患者的转氨酶水平均恢复正常。干扰素治疗结束时,HBeAg/Ab血清转换率为52.8%,第二组在平均6年的病程后自发HBeAg/Ab血清转换率为72.7%。未检测到任何患者发生HBsAg/Ab血清转换。随访期末通过HBV DNA检测评估病毒复制情况,结果显示与HBeAg检测相比水平更高(第一组为69.4%对25%,第二组为55.2%对7.9%)。两组中病毒复制阴性(HBV DNA阴性)的发生率相似(第一组为30.6%,第二组为44.8%,p>0.9),随访期末两组的HBV DNA滴度无显著差异。两组中,HBeAg阳性患者的HBV DNA滴度均显著更高。两种病毒标志物之间的一致性为100%。
由于病情演变波动,对慢性乙型肝炎患者和HBsAg携带者进行长期随访和监测(包括HBV DNA检测)是必要的。