Severe thrombocytopenia following intralesional BCG therapy

Of eight patients we have seen with disseminated BCG infection (BCGosis) following BCG injection into primary melanomas, all eight have developed a significant decrease in platelet count of 33 to 99% mean ∓ 1 SE = 63 ∓ 9%) from the preinjection values. A concomitant randomized control group with melanoma not receiving BCG did not show a significant platelet depression. Two patients receiving BCG developed a profound thrombocytopenia (platelet count less than 2,000) that persisted for two weeks. These patients had both received approximately 5 × 10⁸ viable BCG organisms intralesionally and required isoniazid therapy for the BCGosis that developed. BCGosis was documented by the presence of granulomas in liver and/or bone marrow of both patients, and the growth of BCG from bone marrow and liver biopsies in one patient. Both severely affected patients had short platelet survival but evidence of normal platelet production in that megakaryocytes were plentiful in the bone marrow. Using sera from before, during and after the severe thrombocytopenic episode in both patients With and without added BCG, immunolo‐gic evidence for an antiplatelet antibody could not be substantiated by complement fixation and serotonin release studies. After ethambutol, rifampin and prednisolone therapy was instituted in both patients, fevers due to BCGosis disappeared within a day, but platelet counts did not begin to rise for 11 and 14 days, respectively. Severe thrombocytopenia can occur following BCG administration and should be recognized as a potential life‐threatening complication in all patients receiving intralesional BCG therapy.