The Rôle of Congestion (Portal Hypertension) in So-Called Banti's Syndrome

Idiopathic Portal Hypertension and Its Pathology

“…In 1928, a spleen clinic was founded in the Columbia Presbyterian Hospital, New York, where many patients with splenomegaly came to be evaluated and treated. When Rousselot 4 analyzed 31 splenectomized patients, 11 had cirrhosis, 2 schistosomiasis, 2 splenic vein thrombosis, 1 cavernous transformation (extrahepatic portal obstruction), and 15 no demonstrable obstructive pathology along the portal vein system. In 1945, when Whipple 5 analyzed 17 years of clinical experience, which included 1,189 cases of splenopathy, Banti's disease had nearly been replaced by the concept of portal hypertension as the cause of congestive splenomegaly.…”

The pathogenesis of idiopathic portal hypertension (so-called Banti's disease). An experimental study.

“…This so-called Banti's disease (or syndrome) is a poorly defined clinical entity of obscure etiology, and its existence has long been disputed. Rousselot (1936) pointed out the clinical importance of portal hypertension for the development of Banti's syndrome. The spleen changes were found to be no different from those seen in liver cirrhosis and Banti's syndrome became synonymous with congestive splenomegaly.…”

Noncirrhotic portal hypertension—Historical perspectives bring clarity to the entity and its management

“…Cauchois in 1908 assuredly refuted Banti’s concept when he described a similar group of patients in whom the cause was identified as a portal or splenic vein thrombosis, thereby airing the initial descriptions of another etiology for NCPH, namely portal vein thrombosis, which he called extrahepatic portal vein obstruction or EHPVO 13 . This was further consolidated by various investigators who described Banti’s disease complex in many patients with “pyelithrombotic phlebitis,” which led to the conclusion that splenic enlargement, subsequent hematological aberrations, and development of PHT were due to obstruction in the portal vasculature leading to “congestive splenomegaly” with greatly increased pressure in the splenic vein 14 . Investigators found that clinical and histopathologic features described by Banti were also associated with various other disease conditions, some even in the absence of portal venous system obstruction 15,16 .…”

“…[13] This was further consolidated by various investigators who described Banti's disease complex in many patients with "pyelithrombotic phlebitis," which led to the conclusion that splenic enlargement, subsequent hematological aberrations, and development of PHT were due to obstruction in the portal vasculature leading to "congestive splenomegaly" with greatly increased pressure in the splenic vein. [14] Investigators found that clinical and histopathologic features described by Banti were also associated with various other disease conditions, some even in the absence of portal venous system obstruction. [15,16] Thus, the term Banti's disease was discarded and a more appreciable terminology, "Banti syndrome," took its place.…”

“…[17,18] Initial descriptions and classification of NCPH-Banti's syndrome-were mainly founded on the morphologic bases of splenic histology and segregated into fibrous/fibroadenic variants (Banti's classification). This congestive type included chronic thrombotic occlusion of splenic or portal vein or that associated with cirrhosis, [14,19,20] or a siderotic type (Gamna's) of splenic disorder. [14,19,20] Further classifications were based on the affected primary organ tissue, including Naegeli's, McNee's, and Michel-Minot's descriptions featuring infections, granulomatous diseases, diseases affecting myeloid and lymphatic structures, reticuloendothelial system, vascular system, and various malignancies.…”