Reappraisal of the Role of Anti‐i in Haemolytic Anaemia in Infectious Mononucleosis

Abstract
Summary. Current literature implies that haemolytic anaemia in infectious mononucleosis is regularly caused by the temporary production of high thermal amplitude cold agglutinins of anti‐i specificity. More recently, Capra et al (1969) suggested interaction between IgG anti‐i and anti‐IgG antibodies as the cause of haemolytic anaemia in infectious mononucleosis. A detailed serologic evaluation of three patients during moderate to severe haemolytic anaemia in infectious mononucleosis revealed high thermal amplitude anti‐i in only one. This patient's direct antiglobulin test (DAT) was negative using anti‐IgG but was 3 + using anti‐C3 and ‐C4. The serum antibody titre against cord or adult Oi cells was 512 at 4°C and 4 at 31°C. The anti‐i was inhibited by mercaptoethanol, and anti‐IgG was not found in the patient's serum. Patient 2 had a negative DAT and patient 3 had a 2 + DAT using anti‐C3 and anti‐C4. Anti‐i was present only in low titre at 4°C and was unreactive at 20°C. It was inhibited by mercaptoethanol. These patients' sera contained anti‐IgG antibodies. In none of our patients were warm autoantibodies detected. This data demonstrates that haemolytic anaemia in infectious mononucleosis is not necessarily associated with high thermal amplitude anti‐i. Further, since the anti‐i antibodies in patients 2 and 3 were of low titre, were inhibited by mercaptoethanol, and did not react at physiologic temperatures, the mechanism of haemolysis in these patients does not seem related to the interaction of anti‐IgG and IgG anti‐i antibodies. Further work is necessary to clarify the mechanism of haemolytic anaemia in infectious mononucleosis.