Thrombocytopenic purpura caused by hypersensitivity to quinine.

Abstract

Abstract Studies are reported on a patient who developed thrombocytopenic purpura on two separate occasions after ingestion of Bromoseltzer and Bromoquinine, the latter containing quinine hydrobromide. After recovery from the second acute episode, test doses with acetanilid, a constituent of Bromoseltzer, failed to produce a significant platelet reduction, whereas 5 mg. of quinine hydrobromide caused a systemic reaction, a marked reduction in platelets, and prolongation of bleeding time. Marked thrombocytopenic purpura with a prolonged bleeding time and petechiae was produced in a normal volunteer after concomitant oral ingestion of quinine hydrobromide and intravenous injection of plasma from the quinine-sensitive patient. No change in platelet counts was observed in the same volunteer when quinine or plasma from the patient was given alone. Platelet agglutinin tests done on plasma from the recipient were negative. In vitro platelet agglutinin tests were consistently positive only when quinine hydrobromide was added to the patient's serum. The serum factor remained active after 199 days' storage at −10 °C. In the presence of quinine, a high panagglutinin titer could still be demonstrated in the patient's blood drawn 203 days after recovery from the second acute episode of thrombocytopenic purpura. No conclusive platelet agglutinins were demonstrable when sodium bromide, acetanilid, or Bromoseltzer were added to the patient's serum. Passive transfer tests using patient's serum and quinine were negative. It is suggested: (a) that the immune mechanism responsible for the thrombocytopenia causes both a peripheral destruction of platelets and transient damage to megakaryocytes, and (b) that the antigen to which antibody is produced is a complex composed of a union between the drug and platelets.