The diagnosis and pathogenesis of clinical variants in viral hepatitis.
The heterogeneity of the clinical responses to hepatitis A and B infection is well known, and may in part relate to different etiologic agents (hepatitis A, B, "C", etc.) as well as to the individual hosts' immune responses. The spectrum of disease ranges from anicteric asymptomatic infections to fulminant hepatic necrosis with hepatic failure and death. Although the clinical presentation is varied, there are essentially two patterns of necrosis that can be seen histologically during the first few weeks of clinical symptoms. The more common pattern is focal, and necrosis is scattered throughout the hepatic lobule. Less commonly, zones of necrosis that bridge between the portal--portal or portal--central areas of the lobule develop. When the latter process (bridging necrosis) is extensive, confluent lobules may be destroyed. Patients with focal patterns of necrosis eventually recover without sequelae, whereas a sizable proportion (30-60%) of patients who have bridging or multilobular necrosis progress to chronic active hepatitis, postnecrotic cirrhosis, or progressive hepatocellular failure. There is increasing evidence that these widely differing clinical and histologic responses to hepatitis infection may be related to differences in the immune response.
D000208:Acute Disease; D002353:Carrier State / Q000453:epidemiology; D002779:Cholestasis / Q000150:complications; D002908:Chronic Disease; D014644:Genetic Variation; D006506:Hepatitis A / Q000209:etiology; D006509:Hepatitis B / Q000209:etiology; D006525:Hepatitis, Viral, Human / Q000175:diagnosis* / Q000209:etiology / Q000473:pathology; D006801:Humans; D007565:Jaundice / Q000150:complications; D009336:Necrosis; D013997:Time Factors; D014481:United States