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FURTHER CONTRIBUTION TO THE PATHOGENESIS OF FIBROCONGESTIVE SPLENOMEGALY (BANTI SYNDROME)

PAOLO RAVENNA, M.D.

Arch Intern Med. 1943;72(6):786-794.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

It has been proved beyond a reasonable doubt that the Banti syndrome, a morbid condition characterized by chronic fibrous and congestive splenomegaly, secondary anemia and recurrent hematemeses, may occur independently of any obstruction to the portal circulation.¹ The splenic enlargement thus is not the result of circulatory disturbances in the portal bed, though portal sclerosis and thrombosis may secondarily complicate the picture. A drawback to the general acceptance of this concept lies in the fact that the same clinical and pathologic picture occurs in instances in which the presence of an important obstacle in the portal vessels suggests that the mechanism is passive hyperemia of the spleen. Depending on the nature of the obstruction in individual cases, this condition is termed thrombophlebitic splenomegaly,² portal phlebosclerosis³ or cavernomatous transformation of the portal vein.⁴ The current assumption⁵ that the splenomegaly is primary in some instances and secondary . . . [Full Text PDF of this Article]

Author Affiliations
CHICAGO

Footnotes
This work was aided by a grant from the A. B. Kuppenheimer Fund.

From the Department of Pathology, Michael Reese Hospital, Chicago. The department is in part supported by the Michael Reese Research Foundation.

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