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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    be proved that splenic anaemia is due to a streptothrix infection. The resemblance of the disease to kala-azar suggests that some micro-organism allied to Leishmania is responsible for the sporadic cases of the disease in this country; possibly it is ultra-microscopic. In a recent case under the care of my colleague, Dr. James Collier, smears of the excised spleen, examined by Dr. E. L. Hunt, did not show any evidence of ultra-microscopic organisms. Since splenectomy cures the disease it is clear: (a) that the spleen is in some way responsible, and there is not any active haemic infection or intoxication at work ; and (6) that splenic inadequacy is not the cause of the anaemia. The spleen may be considered to give rise to anaemia in the following ways :— i. By increased haemolytic activity; this hypothesis is naturally suggested by enlargement of an organ which normally plays some part in the destruction of red-blood corpuscles. In 1902, Barr3 suggested that splenic anaemia is due to vasomotor paralysis of the splanchnic area, caused by disease of the sympathetic; and Sutherland and Burghard43 assumed a loss of vasomotor control in the splenic artery, leading to overfilling of the spleen with arterial blood and hyperplasia, a condition which they compared with that of the thyroid in Graves’ disease. Over-activity of the spleen was thought to cause excessive haemolysis. The enlarge¬ ment, however, is not a pure hypertrophy, but is largely due to fibrosis, and such a spleen should be less functionally active than a normal one. Further, the blood changes do not resemble those of pernicious anaemia or of haemolytic jaundice—conditions in which blood destruction is known to occur; and there is no pigmentation of the spleen or liver to support the view of increased haemolysis in the spleen. ii. The spleen may be the headquarters of a chronic infective or toxic process, conveyed by the blood stream and possibly derived from the alimentary tract; the poisons thus pioduced may cause the local changes in the spleen, and later inhibit blood formation, both erythroblastic and leucoblastic, so producing anaemia. This hypothesis has the great merit of explaining satisfactorily the subsequent appearance of hepatic cirrhosis. But there is no convincing evidence that the anaemia is due to inhibition of blood forma- b 2