In 1898 Banti postulated that increased splenic blood flow could cause profound changes in the portal system.1 He felt that the increased flow led to splenomegaly, portal phlebosclerosis and eventually cirrhosis. When it later became apparent that obstruction to flow rather than its increase was the usual cause of portal hypertension in liver disease, Banti's concept fell into disfavor.
In recent years, however, portal hypertension which could be attributed to increased portal flow has been described in a number of nonhepatic diseases. Listed among the diseases are myeloproliferative disorders, leukemia, Hodgkin's disease, tropical splenomegaly, and systemic-portal arteriovenous fistulae. A new addition to the list of "forward-flow" conditions is osteopetrosis with splenomegaly, reported in the current issue of the Archives of Internal Medicine.2
Until recently, there has been a scarcity of hemodynamic data on patients with forward-flow portal hypertension because of limitations of the various methods for studying portal