Postnecrotic cirrhosis is considered, in the United States, almost always to be a residual of infectious or homologous serum hepatitis, although in occasional instances, exposure to toxic chemicals may be blamed.1 In the tropics, malnutrition is believed to be an important etiologic factor. Whatever the basic cause, all appear to have in common the ability to produce the diffuse hepatocellular necrosis required in the pathogenesis of postnecrotic cirrhosis.
During and since World War II, there has been a high incidence of hepatitis throughout the world. This has stimulated great interest in the possible residuals of that disease. In our experience and in that of others,2,3 there also has recently been an increase in the frequency of postnecrotic cirrhosis, and it is natural to associate the two conditions. There have been, however, a number of patients in whom postnecrotic cirrhosis appears to have developed de novo.4,5 Not only