丁型肝炎患者肝组织HDAg和HBsAg/HBcAg的免疫组化检测

HDAG AND HBSAG/HBCAG EXPRESSION IN LIVER TISSUES FROM PATIENTS WITH HEPATITIS D BY IMMUNOHISTOCHEMICAL TECHNIQUE

目的 探讨HDAg和HBsAg/HBcAg在丁型肝炎患者肝组织中表达及关系。方法 应用免疫组化双重染色,检测79例丁型肝炎患者肝组织HDAg、HBsAg和HBcAg表达,以52例乙型肝炎作对照。结果 丁型肝炎HBsAg、HBcAg检出率(81％、71％)较乙型肝炎(94％、92％)低(P<0.05或0.01)。HDAg以肝细胞核表达为主,HBsAg以肝细胞浆表达为主,HDAg和HBsAg表达强度及阳性细胞分布呈一致性,且均与肝组织的炎症活动和病理损害程度相关(P<0.01)。HBcAg以肝细胞核表达为主,阳性细胞主要呈单个细胞或点状分布,且HBcAg阳性细胞明显少于HDAg阳性细胞。结论 HDV感染会抑制HBV病毒抗原(HBcAg)表达;HDV致病机制中既有HDV的直接细胞毒性作用,也有HBV和HDV的协同作用。

Objective To explore the relationship between expression of hepatitis D virus antigen(HDAg)and HBsAg/HBcAg in liver tissues of the patients with hepatitis D(HD). Methods HDAg and HBsAg/HBcAg in paraffin-embedded liver tissues from 79 liver biopsies of autopsy samples from the patients with hepatitis D virus (HDV) and hepatitis B virus(HBV)superinfection and from 52 patients with hepatitis B virus infection alone were studied by immunihistochemical double labelling techniques. Results The detection rates for HBsAg and HBcAg HD in patients were 81% and 71%,lower than that of hepatitis B( 94% ,92%) (P<0.05 or 0.01) . HDAg was mainly expressed in nuclei and cytoplasm of hepatocyte,HDAg positive cells were obviously aggregated in periportal region,especially at the edges of piecemeal necrosis, moreover, strong expression of HDAg was shown in the bollooning degeneration hepa-tocytes and hepatocytes near piecemeal necrosis region. HBsAg was mainly expressed in cytoplasm of hepatocytes,and positive cells distribution were similar to that of HDAg positive cells. HBcAg was mainly expressed in unclei of hepatocytes, positive cells distribution were alone of focal type(3 - 5 cells). Double labelling studies showed that HDAg and HBsAg were mostly expressed in the same hepatocytes,and positive cells of HDAg and HBsAg were mostly found to locate in the same area of liver tissus,but HDAg seldom coexisted with HBcAg, respectively the expression degrees and positive cells distribution of HDAg and HBsAg were all obviously associated with the grades of pathological damage of liver tissues and necroinflammatory activity (P < 0.01) . Conclusion HDV infection can inhibit replication of HBV genome or expression of HBcAg. Besides of interactions beteween HBV and HDV, it is possible that direct cyto-toxicity of HDV may play an impotant pathogenetic role in pathogenetic mechanisms of HDV.