The Banti syndrome is still an unsolved problem. The question of cardinal importance is whether the splenomegaly is primary or secondary to portal or hepatic changes.
Banti1 stated the belief that the trouble lay primarily in the spleen and that the portal and hepatic changes were dependent on the splenic ones. The idea that the splenomegaly was the consequence of circulatory disturbances was put forward by Dock and Warthin2 and further developed with the description of the thrombophlebitic splenomegaly.3 This theory occupied a position of definite advantage when it was recognized that the structure of Banti splenomegaly was chiefly congestive4 and that the pressure in the splenic vein was highly increased.5 But these same signs of portal hypertension were found to be present when an obstructive factor was missing. This fact was responsible for the widest gap in the support of the theory of venous congestion as the causative agent
RAVENNA P. BANTI SYNDROME (FIBROCONGESTIVE SPLENOMEGALY): DEFINITION, CLASSIFICATION AND PATHOGENESIS. Arch Intern Med (Chic). 1940;66(4):879–892. doi:10.1001/archinte.1940.00190160098008
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