Banti's Syndrome Research Articles

Hepatoportal arteriovenous fistula.

One of the most hazardous types of bleeding from the gastrointestinal tract is that occurring from esophageal or gastric varices. Such varices usually arise following an obstruction to the return of portal blood to the systemic venous system. There are two common types of portal obstruction: that occurring in the liver—the so-called intrahepatic type—and that seen in splenomegaly (Banti's syndrome), in which the portal vein is obstructed. The latter is referred to as the extrahepatic type. In addition Linton has described portal hypertension occurring secondary to a combination of the above two lesions. We would like to suggest that the lesion presented by the patient in this report represents an additional situation in which portal hypertension may develop, i. e., secondary to an arteriovenous fistula between the hepatic artery and portal vein. This case is the second to be recorded in the literature. The first was reported by Strickler, Lufkin,

The roentgen demonstration of cirrhosis of the liver with fatty metamorphosis: report of a case due to congenital fibrocystic disease.

The diagnosis of cirrhosis of the liver ordinarily cannot be made on the basis of the routine roentgen examination. In those cases in which there is a large spleen associated with varices of the esophagus, the diagnosis of cirrhosis may be suspected on the basis of the roentgen examination, particularly if the liver is also enlarged. However, there are other diseases, such as Banti's syndrome and portal vein thrombosis, which may present the same roentgen findings. We are reporting a case of congenital fibrocystic disease with associated cirrhosis in which the diagnosis of cirrhosis was established entirely on the basis of the plain roentgenogram of the abdomen. Case History The patient was a male child first seen in the University of California Fibrocystic Clinic, Dec. 22, 1949, at the age of twenty-six months. He was referred to the clinic because of a diagnosis of fibrocystic disease. Two siblings had died of conditions which resembled fibrocystic disease. The patient had been followed by the referring...

Clinical Studies on the Genesis of Anemia in Banti's Syndrome

Clinical Studies on the Genesis of Anemia in Banti's Syndrome

Chronic ulcers of the leg associated with blood dyscrasias.

BLOOD dyscrasias, particularly the congenital hemolytic anemias, 1 are of primary importance in a consideration of the possible causes of chronic recurrent ulcers of the leg. An association of leg ulcers with sickle cell anemia is generally better appreciated than the relationship of this symptom to other forms of congenital hemolytic anemia, e. g., congenital hemolytic icterus (familial acholuric jaundice, spherocytic anemia) and Mediterranean disease (Cooley's anemia, thalassemia). In a review of the subject of indolent ulcers of the leg in diseases of the blood, in addition to the conditions already mentioned, Gendel 2 lists the following: Banti's syndrome, thrombocytopenic purpura, Gaucher's disease, pernicious anemia, and chronic hemolytic polycythemia. The latter was presented before the Royal Society of Medicine by Rau, Pulvertaft and Humble. 3 Gendel 2 did not include polycythemia vera (erythremia, Osler-Vaquez disease). However, ulcerations of the lower extremities 4 and peripheral vascular complications have

The surgical treatment of Banti's syndrome.

The surgical treatment of Banti's syndrome.

The results of splenectomy in Banti's syndrome.

Article1 June 1951THE RESULTS OF SPLENECTOMY IN BANTI'S SYNDROMEROBERT H. DURHAM, M.D., F.A.C.P.ROBERT H. DURHAM, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-34-6-1372 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe clinical concept of Banti's disease has undergone an evolutionary transition found in few other diseases. Concurrent with this changing knowledge, the original name Banti's disease has been supplanted by a succession of other terms. Osler was among the first to challenge Banti's original interpretations. After observing cases without any apparent hepatic involvement, Osler suggested that this type of case should more appropriately be calledsplenic anemia. This term has since become obsolete.Banti's syndromelater came into use as a general descriptive term and continues to be used by many clinicians. As the rôle of the spleen became better...Bibliography1. Whipple AO: Recent studies in the circulation of the portal bed and of the spleen in relation to splenomegalia, Tr. and Stud., Coll. Physicians, Philadelphia 8: 203, 1941. Google Scholar2. Rousselot LM: The late phase of congestive splenomegaly (Banti's syndrome) with hematemesis but without cirrhosis of the liver, Surgery 8: 34, 1940. Google Scholar3. Rousselot LM: Congestive splenomegaly, Bull. New York Acad. Med. 15: 188, 1939. MedlineGoogle Scholar4. ThompsonCougheyWhippleRousselot WPJLAOLM: Splenic vein pressure in congestive splenomegaly (Banti's syndrome), J. Clin. Investigation 16: 571, 1937. CrossrefMedlineGoogle Scholar5. LimarziJonesPaulPoncher LRRMJTHG: Sternal marrow in Banti's syndrome and other splenomegalic states, Am. J. Clin. Path. 13: 231, 1943. CrossrefGoogle Scholar6. Howells L: The treatment of splenic anaemia in Banti's syndrome, Lancet 1: 1320, 1938. CrossrefGoogle Scholar7. Pemberton Jd: Splenectomy: Indications and results, South. Med. and Surg. 102: 46, 1940. Google Scholar8. EliasonJohnson ELJ: Splenectomy, Surgery 2: 823, 1937. Google Scholar9. Diamond LK: Indications for splenectomy in childhood, Am. J. Surg. (New Series) 39: 400, 1938. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Detroit, Michigan*Presented at the Thirty-first Annual Session of the American College of Physicians, Boston, Massachusetts, April 19, 1950.Received for publication December 6, 1950.From the Department of Medicine, Division of General Medicine, Henry Ford Hospital, Detroit, Michigan. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byRole of the spleen in liver fibrosis in rats may be mediated by transforming growth factor beta-1Leber und intrahepatische Gallenwege, PfortaderkreislaufIndikationen zur Splenektomie bei BlutkrankheitenDer Einfluß der Splenektomie auf die Leberfunktion bei LebereirrhosenAnhang: Milzvenenstenose, hämodynamische MilzdekompensationThrombocytopathienRelation of hemorrhage from varices to mortality in cirrhosisBlood volume in patients with Laennec's cirrhosis of the liver as determined by radioactive chromium-tagged red cellsHaematological Findings in Splenomegaly�ber Indikation und Wirkung der Milzentfernung mit Ligatursperre der kardialen Venen bei Hypertonie im Pfortaderkreislauf 1 June 1951Volume 34, Issue 6Page: 1372-1381KeywordsAnemiaHospital medicineSpleenSplenectomy ePublished: 1 December 2008 Issue Published: 1 June 1951 PDF downloadLoading ...

A Contribution to the Knowledge of Banti's Syndrome

RésuméA la suite d'un compte rendu de la notion: «Syndrome de Ranti» on rapporte une série de cas personnels: 7 cas appartenant au groupe cirrhose hépatique splénomégalique et 7 appartenant au groupe de ras prouvés ou probables d'engorgement de la veine porte.Le diagnostic diffdréntiel entre ces deux groupes est discuté. Dans le premier le symptôme de lésion au foie domine; dans le dernier ce sont des hémorragies dans le tube digestif notaniment des varices oesophagiennes. Une sédimentation accélérée indique la cirrhose hépatique, il y a cependant des cas transitoires entre les deux groupes.Lo traitement est avant tout dirigé contre l'hypertension de la circulation portale et ses conséquences c.à.d. les hémorragies des varices oesophagiennes.La splénectomie ne produit habituellement qu'une amédlioration de courte durée. Tous les cas du deuxième gronpe du matériel présenté ont été traités par la splénectomie et tous ont eu des récidives d'hémorragies.Les auteurs exposent les nouvelles méthodes chirurgicales et communiquent les expériences de 4 cas (dont un adulte). En cas d'hypertension de la circulation portale on ne doit pas conseiller la splénectomie sans projeter en même temps un anastomose entre les systèmes porte et cave. II faut cependant remettre une appréciation définitive de la valeur des nouvelles méthodes jusqu'à cc qu'on ait acquis une plus grande expérience et qu'on ait eu un plus long temps d'observation.ZusammenfassungNach einer Erklärung des Begriffes, Bantis Syndrom, wird eine Serie eigener Fäille mitgeteilt, von denen 7 zu der Gruppe tier splenomegalen Lebercirrhosen und 7 zu der Gruppe der Fälle mit nachgewiesenem oder wahrscheinlichem Hindernis in der Vena portae gehören.Die Differentialdiagnose zwischen diesen beiden Gruppen wird besprochen. Bei der ersteren herrschen die Symptome der Leberschädigung, bei dor letzteren Blutungen von Seiten des Digesbionstraktes besonders Oesophagusvaricen vor. Eine erhöhte Senkungsreaktion spricht für Lebercirrhose. Es gibt jedoch Übergangsfälle zwischen diesen beiden Gruppen.Die Behandlung richtet sich zunachst gegen die Portahypertension und deren Folgen, d. h. die Blutungen von Seiten der Oesophagusvaricen.Splenektomie gibt gewöhnlich nur kurzdauernde Verbesserung. Sämtliche der zweiten Gruppe zugehörigen Fälle des vorliegenden Materiales wurden splenektomiert und alle hatten Recidive ihrer Blutungen.Die Verfasser beschreiben die neueren chirurgischen Methoden und teilen ihre Erfahrungen in 4 Fäillen (darunter ein Erwachsener) mit. Splenektomio soll nicht angeraten werden in Fällen von Portahypertension ohne dass gleichzeitig eine entlastende Anastomose zwischen Porta‐ und Cavasystem geplant wird. Ein sicheres Urteil über den Wert der neueren Methoden muss jedoch aufgeschoben werden, bis man grossere Erfahrung gewonnen und langere Beobachtungszeit gehabt hat.ResumenSiguiendo una exposición del témino «síndrome de Banti», se informa sobre una serie de casos, do los cuales siete pertenecen al grupo de cirrosis esplenomegala hepática y siete al de casos con obstrucción establecida o probable en is vena portal.Se discute la diagnosis diferencial entre estos dos grupos. En el primer grupo dominan los síntomas de lesiones del hígado, mientras que en el segundo domina la hemorragia del tracto digestivo, especialmente de varices esofágicas. El aumento del grado de sedimentación eritrocítica habla en favor de la cirrosis hepática. Hay, sin embargo, casos intermedios entre los dos grupos.El tratamiento se dirige ante todo a impedir la hipertensión portal y sus consecuencias, es decir, la hemorragia de varices esofágicas.La esplenectomia corriente ocasiona sólo mejoría momentánea. Todos los casos del segundo grupo eran casos esplenactomizados y con recaídas en la hemorragia.Los autores informan sobre los nuevos métodos quirúrgicos y sobre las experiencias obtenidas en cuatro de los casos (uno de ellos de adulto). La esplenectomia no se recomienda en los casos de hipertensión portal sin una preparación simultánea de anastomosis de alivio entre los sistemas portaly caval. Es necesario sin embargo, dejar para mas adelante, liasta que se hayan realizado más experiencias y el período de observación haya sido más largo, un juicio más definitivo sobre el valor de los nuevos métodos.

A METHOD FOR CONTROL OF BLEEDING FROM ESOPHAGEAL VARICES

ONE OF the most dramatic and hazardous types of bleeding from the gastrointestinal tract is that from esophageal varices. Esophageal varices commonly occur in association with cirrhosis of the liver. In such instances the dilated esophageal vessel is a reflection of increased tension in the portal system. Several methods have been devised for controlling hemorrhage from varices, most of them being a direct attack on the varix itself. In 1939 Crafoord and Frenckner1described the nonsurgical treatment of varicose veins by injection of a sclerosing solution under direct vision. Phemister2in 1947 reported 1 case with treatment by total gastrectomy and 1 with treatment by esophagogastric resection for bleeding esophageal varices in Banti's syndrome. None of these methods attempt to control the cause of the varix but, rather, attempt to treat the varix itself by removal of the dilated veins or by an attempt to cause clotting within

ESOPHAGEAL VARICES

ESOPHAGEAL varices with repeated severe hemorrhages are due usually to varying degrees of portal vein obstruction. The increased portal vein pressure forces blood into the esophageal veins. The veins in the submucosa of the esophagus are poorly supported by loose connective tissue. Thus varicosities may develop. The sucking effect of respiration accentuates this. There is evidence that Banti's syndrome of splenomegaly, anemia, leukopenia and esophageal varices, with hemorrhage and at times ascites, is due not to primary disease of the spleen but rather to varying degrees of obstruction in the portal system. Whipple 1 and his co-workers, by blocking the portal vein experimentally, were able to produce Banti's syndrome. The term congestive splenomegaly suggested by Larrabee in 1934 is more descriptive of this condition. Portal hypertension may be due to intrahepatic or extrahepatic block. The former is usually the result of cirrhosis. Extrahepatic block may be due to fibrous

Venous Calcification in Banti's Syndrome

Venous calcification within the abdominal cavity, with the exception of phlebolith formation, is an extremely rare condition. Roentgen evidence of its occurrence is not to be found in the literature, although arterial changes have been frequently described. The few reported instances of venous calcification do not include radiographic studies, the changes having been found at autopsy or surgery. The occurrence of venous sclerosis in Banti's syndrome is especially interesting in view of the evidence that portal bed obstruction is probably the etiologic agent. Because of these features and the definite and striking roentgen picture, the following case was thought to be worthy of presentation. Case History L. L. B., a 49-year-old white male, was admitted to the Medical Service of the Wadsworth General Hospital, July 14, 1946. From 1919 to 1929, he had severe and repeated gastric hemorrhages, for which he was frequently hospitalized. He had been told that he had an enlarged spleen. In 1929, at another hospital, a splenectomy was done. Records obtained from that hospital are essentially unrevealing. A clinical diagnosis of Banti's or Gaucher's disease was made but there was no pathological examination. Following splenectomy, the patient remained well until May 1946, when he had a severe gastrointestinal hemorrhage, vomiting bright red blood and passing tarry stools. This occurred while he was on his honeymoon, and he was taken to a local hospital, where he had several more severe hemorrhages. He was later treated with multiple transfusions and was told he had a bleeding duodenal ulcer, shown radiographically. Three weeks later, while en route to the West Coast, he had another severe hemorrhage and one week before admission he had still another. He was hospitalized twice, en route, because of recurrent hemorrhage. On admission, the patient appeared rather thin and very pale. The physical examination was essentially negative except for a left upper rectus scar, a liver which was palpable two finger-breadths below the costal margin on deep inspiration, and internal hemorrhoids. Occult blood was found in the stool. The erythrocyte count was 3,100,000 with 56 per cent hemoglobin. The platelet count, prothrombin time, and fragility tests were normal. The urine examination revealed three-plus albumin, numerous red and white blood cells, and a low specific gravity. The urea nitrogen was 31.8 mg. per cent. The patient had several hemorrhages while on the Medical Service, the erythrocyte count at one time falling to 1,300,000 with 26 per cent hemoglobin. He was treated with multiple transfusions and was seen in surgical consultation. It was felt that his condition was too poor for any major surgical procedure at this time and conservative therapy and repeated transfusions were therefore recommended. When he improved he was transferred to the Surgical Service.

THE HEMORRHAGIC TENDENCY IN CONGESTIVE SPLENOMEGALY (BANTI'S SYNDROME)

This paper is an exposition of some concepts of the mechanism of the hemorrhagic disorder encountered in Banti's syndrome (congestive splenomegaly, portal hypertension), of means for the recognition of its manifestations and of methods found useful in the control or amelioration of the tendency to bleed. The discussion that follows rests on observations made on 22 patients for whom a diagnosis of Banti's syndrome seemed indicated and who had had bleeding in one form or another. In 9 of the patients evidence of cirrhosis was obtained clinically, at operation or at necropsy. From the histories, it was probable that splenomegaly had preceded the manifestations of cirrhosis. Hematemesis or melena was the form of bleeding in 17 patients. Epistaxis, hematuria, vaginal bleeding, purpura and hemothorax were some of the other forms. The incidence of hemorrhagic complications in patients with this syndrome is difficult to estimate. Except for a brief mention of

PRINCIPAL INDICATIONS FOR SPLENECTOMY DURING CHILDHOOD

THE THERAPEUTIC value of splenectomy in certain blood dyscrasias has become more widely recognized during the past twenty-five years. Despite the fact that splenic function is not fully understood, sufficient progress has been made as a result of both clinical and hematologic investigation to permit of definite conclusions as to treatment. Splenic dysfunction occurs in congenital hemolytic icterus, thrombocytopenic purpura and Banti's syndrome. In such diseases splenectomy is especially beneficial. It is the purpose of this paper to present the principal indications for splenectomy in children and to evaluate results obtained. Splenectomy was performed on 55 children at the University Hospital between September 1933 and August 1946. The youngest child was 30 days old and the oldest 12 years. Among the indications for operation were congenital hemolytic icterus (20 children), thrombocytopenic purpura (22 children) and the Banti syndrome (7 children). In the remaining 6, splenectomy was performed for rarer disturbances,

Alterations de la retine en rapport avec les affections generales. Atlas ophthalmoscopique II.

This report on retinal disorders related to systemic diseases was presented to the<i>Societé française d'ophthalmologie</i>on May 15 1947, and is the work of Paul Bonnet, professor at the ophthalmic clinic in Lyons. This is part 2 of the ophthalmoscopic atlas, of which part 1, on diseases of the retina, by Gabriel Renard, was published in 1946 and previously reviewed in theArchives(<b>38:</b>129 [July] 1947). The general diseases studied in this book are those of the blood. The retinal conditions enumerated are cyanosis of the retina, intracranial aneurysm, various types of leukemia, malignant Hodgkin's disease (lymphogranulomatosis), anemias, angiomatosis (Rendu-Osler disease), hemolytic jaundice, Banti's syndrome (splenomegaly of undetermined origin), hemorrhagic diathesis, the effects of thorium X, general infections and certain forms of diabetes. The discussion of each condition is prefaced by a short introduction on the fundamental medical illness, followed by a description of the ophthalmoscopic picture and

BANTI'S SYNDROME WITH MULTIPLE ANEURYSMS AND THROMBOSES OF THE SPLENIC BLOOD VESSELS

Excerpt Confusion still exists concerning the pathogenesis and pathologic picture of the disease complex called Banti's syndrome. Two opposing views are held concerning its development. Banti2and h...

Surgery of Banti's Syndrome

Surgery of Banti's Syndrome

Two Cases of Banti's Syndrome: Hepatomegaly with Anæmia

Two Cases of Banti's Syndrome: Hepatomegaly with Anæmia

Splenomegaly and hepatomegaly in an adolescent simulating Banti's syndrome

Splenomegaly and hepatomegaly in an adolescent simulating Banti's syndrome

SPLENOPORTAL VENOUS OBSTRUCTION WITHOUT SPLENOMEGALY

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 phlebosclerosis 3 or cavernomatous transformation of the portal vein. 4 The current assumption 5 that the splenomegaly is primary in some instances and secondary

PRIMARY PORTAL PHLEBOSCLEROSIS

Although of the portal system is recognized as a entity, its definition is obscure and its pathogenesis and etiology require further investigation. Since its occurrence has been adequately established, 1 it should be more carefully sought for at autopsy. It is the purpose of this paper to indicate how it may be clinically identified more frequently. It is also proposed to employ henceforth the name primary portal phlebosclerosis for clarification and uniformity. Up to 1928, 2 29 cases were reported in children, but few in adults. The exact number is difficult to ascertain in view of the existing confusion. In many of these cases the condition appeared to resemble Banti's syndrome, as it did in my case. However, on further study or at autopsy, the question of some obstruction of the portal circulation, with or without coexisting thrombosis or sclerosis of either the splenic or the portal

LIVER AND BILIARY TRACT

As in previous reviews, no attempt has been made to give either an inclusive or a comprehensive survey of the literature dealing with diseases of the liver and the biliary tract during 1940. Instead I have selected topics that have been the subject of special advances or particular study during the year. In many cases detailed reviews have been published elsewhere, and I have referred to them instead of attempting to give a comprehensive bibliography in this article. PORTAL HYPERTENSION AND CONGESTIVE SPLENOMEGALY— BANTI'S DISEASE The literature dealing with the syndrome of portal hypertension and its role in the production of congestive splenomegaly and the so-called Banti syndrome has been reviewed by Greene, Plotz and Localio. 1 The importance of portal hypertension in producing congestive splenomegaly has been emphasized further by Whipple 2 and Rousselot. 3 Thompson 4 has recently summarized the experience of investigators at Presbyterian Hospital in New