Nature of anaemia in rheumatoid arthritis. II. Survival of transfused erythrocytes in patients with rheumatoid arthritis.

In a recent report, Roy, Alexander, and Duthie (1955) reviewed the literature on the characteristics of anaemia in rheumatoid arthritis and described abnormalities of iron metabolism in this disease. It was shown that the anaemia did not present the typical features of iron-deficiency and that there was no evidence of impaired absorption of iron from the gut in the majority of cases. Decreased survival of erythrocytes transfused from healthy donors to patients with active rheumatoid arthritis had been observed, and it was suggested that a reduced lifespan of the patient's own red cells might be a factor in the production of anaemia. There are few reports on the fate of transfused red cells in rheumatoid arthritis. Brown, Hayward, Powell, and Witts (1944) found that cell survival was normal in one patient with "severe disease". It was not made clear if this implied that evidence of active inflammation was still present. Mollison and Paterson (1949) gave two transfusions to each of two patients suffering from rheumatoid arthritis. Cells used for the first transfusion in each case were incubated in vitro with serum containing Rh-blocking antibody and in both instances survival of the transfused cells was markedly reduced. Both patients were transfused again with cells which had not been exposed to blocking antibody. In one case rapid destruction was again observed, but in the other, cell survival was of normal duration. Since the start of the present investigation two further reports have appeared. Freireich, Ross, Bayles, Emerson, and Finch (1954) measured the survival of transfused cells in patients with rheumatoid arthritis and found it to be decreased, destruction being most marked in patients with active disease. Bunim (1954), who used 51Cr. to measure the survival of patient's own red cells, stated that an increased rate of destruction was recorded in patients with active rheumatoid arthritis. The present study was designed to investigate more thoroughly the possibility that abnormal destruction of red cells might be a factor in the causation of anaemia in rheumatoid arthritis. The first part of the report deals with studies of the survival of cells from healthy donors in patients with active disease and varying degrees of anaemia. It was felt that abnormally rapid destruction of healthy red cells might not necessarily imply that the patients' own red cells were being destroyed at the same rate. The second part of the report records the results of experiments designed to compare the survival of cells from a rheumatoid patient with that of cells from a healthy donor in the same recipient; recipients with clear-cut evidence of active rheumatoid disease were closen. Such a comparison does not provide any measure of the life-span of the recipient's own red cells, but it was considered important to ascertain whether any difference existed between the survival of healthy cells and rheumatoid cells in the rheumatoid patient. In addition, a comparison has been made of the survival of healthy red cells before and during the administration of ACTH to rheumatoid patients. Similar observations have been recorded before and during haematological improvement induced by the administration of iron by the intravenous route.