By studying the clearance of autologous labeled antibody-coated or heat-damaged erythrocytes, we showed that reversible blockade of the splenic component of reticuloendothelial function existed in 14 of 15 patients referred for treatment of nephritis or vasculitis. In 10 patients treated by plasma exchange--alone in three and combined with steroids and cytotoxic drugs in six--reversal of splenic blockade followed in nine, and in the three patients treated solely by plasma exchange this reversal was demonstrated to occur within 48 hours of the procedure. Only gradual reversal of splenic blockade was found in three of five patients treated by steroids with or without cytotoxic drugs; no change in splenic function was observed in two. When circulating immune complexes were detected by a C1q-binding assay, there was, in serial studies, an approximate inverse correlation between splenic function and the level of C1q-binding material, though hyposplenism was also a feature of patients in whom the C1q-binding assay was negative.

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Summary Daily rifampicin in a single dose of 600 mg, combined with other drugs, usually streptomycin and isoniazid, was given to forty-nine patients for 3 months. It was planned to continue for another 15 months with twice-weekly rifampicin 1200 mg plus isoniazid 900 mg, but the high incidence of side effects led to cessation of the intermittent regimen when only two patients had completed 18 months. Though there was no serious problem with daily treatment, eleven patients (22%) were unable to continue rifampicin on the intermittent regimen. In eight (16%) a pyrexial syndrome occurred. In one of these patients there was also temporary renal failure and in another, precipitous thrombocytopenia led to epistaxis and bleeding into the tongue and lips. Symptomless thrombocytopenia developed in two other patients, making three cases (6%) of thrombocytopenia in all. In sixteen (33%) of the forty-nine patients antibodies to rifampicin were detected in the blood. Side-effects occurred in nine (56%) of these, including the three developing thrombocytopenia, but in only two (6%) of the thirty-three patients with no antibodies detected. This association of toxic reactions with antibodies is highly significant (P < 0·001).

The name ofJohn Dacie has been so inextricably bound with the development of knowledge about the autoimmune haemolytic anaemias (AIHA), that it is diflicult in a short paper to acknowledge all his contributions to the subject. Probably his frnest single achievement was the compilation of his book, The Haemolytic Anaemias in 1954; in the second edition one volume, part 11, published in 1962, is devoted exclusively to the autoimmune haemolytic anaemias. This volume not only reviewed the world literature up to that date, but also provided a summary of Dacie's experience with 175 cases of autoimmune haemolytic anaemia, many of whose sera and red cells he had investigated personally. It is still the standard reference text for all who are interested in AIHA.John Dacie is essentially a laboratory worker at heart and in this paper we will attempt to summarize some of his contributions to the serology of AIHA and review the current state of knowledge. This will be done under the following headings: the direct antiglobulin test, warm autoantibodies, cold autoantibodies, sub-divided into high-titre cold agglutinins and the Donath-Landsteiner antibody and, finally, classification of AIHA. THE DIRECT ANTIGLOBULIN TESTAlthough it was suggested at the turn of the century that some haemolytic anaemias were caused by antibodies produced by the patient against their own red-cell antigens, it was not until the rediscovery of the antiglobulin (Coombs) test by Coombs, Mourant & Race in 1945 and the application of this test to the red cells of patients suffering from these disorders by Boorman, Dodd & Loutit, and Loutit & Mollison in 1946, that this concept came to be generally accepted. The usefulness of the direct antiglobulin test in the diagnosis of AIHA is mentioned in the first edition of Practical Haematology in 1950, on page 103, and by 1951 Dacie had already studied these positive reactions in some detail. He demonstrated that there were at least two different components in antiglobulin serum; one which could be inhibited by 7-globulin and another which could not be inhibited. He showed that the positive direct reactions of red cells from patients with warm AIHA, like the reactions of red cells sensitized with incomplete anti-D, were inhibited by 7-globulin, while the positive direct reactions of red cells from patients with cold AIHA, like the reactions of red cells sensitized by normal incomplete cold antibody (described by Dacie earlier in the same year), were not inhibited. He suggested that the former type of antibody was composed of 7-globulin while the latter type of antibody