Chronic splenic anæmia and Banti's Disease / by H.D. Rolleston.

  • Rolleston, Humphry Davy, Sir, 1862-1944.
Date:
[1914?]
Catalogue details

Licence: In copyright

Credit: Chronic splenic anæmia and Banti's Disease / by H.D. Rolleston. Source: Wellcome Collection.

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    Banti’s disease. Since 1894, w^en he first described 11 splenomegaly with cirrhosis ” as a definite disease,2 Banti has several times elaborated and defended his thesis. The following is a summary of Banti’s conception of the disease which goes by his name, and of which he has now studied 50 cases.3 There are three stages :—(i) The pre-ascitic, characterized by splenomegaly, without enlargement of the lymphatic glands or much alteration in the general health. There may or may not be anaemia, and at any rate the splenomegaly pre¬ cedes the anaemia. This stage usually lasts 3 to 5 years, but may be longer, as the splenomegaly is generally con¬ siderable when the patient first comes under observation, (ii) The intermediate or transitional stage shows definite though moderate anaemia, leucopenia with relative increase of the mononuclear leucocytes, and a low colour index. The skin is pale and at times slightly icteric, and the liver somewhat enlarged. The urine is scanty and high-coloured. The general health is impaired, and gastro-intestinal dis¬ turbance, especially diarrhoea, and sometimes piles appear. This stage lasts from 12 to 18 months, (iii) In this stage, which may rightly be called Banti’s disease, ascites appears, the liver is cirrhotic and gets smaller, the general health fails, the patient wastes, and gastro-intestinal and other haemorrhages occur ; in short, the picture of ordinary cirrhosis. This stage is often short, a few months to a year. This division into three stages is perhaps too sharp, and the first two stages especially run into each other. Its claim to be regarded as a disease, namely as a definite and constant sequence of pathological events not due to any other recog¬ nized cause, with a correlated group of clinical manifestations, has been much discussed and contested. Gilbert and Lere- boullet,22 and others deny its existence except as a syndrome, or group of symptoms, which may be produced by several different morbid changes. Undoubtedly, some conditions, such as cirrhosis, syphilis of the spleen and liver, and thrombosis of the splenic and portal veins, may almost exactly imitate it, but it appears to me that it is impossible to deny the existence of cases corresponding more or less accurately to those described by Banti, in which no other causal factor