Blood, 1953, Vol. 8, No. 1, pp. 16-25.
© 1953 American Society of Hematology, Inc.
The Mechanism of Quinidine Purpura
ROGER K. LARSON M.D.1
1 Department of Internal Medicine, Kern General Hospital, Bakersfield, Calif.
A case of thrombocytopenic purpura was studied and evidence of a specific
hypersensitivity mechanism was found. The following experimental observations
and their conclusions were discussed.
1. A rapid fall in circulating platelets occurred in the patient after a test dose
of the drug. This fall was too rapid to be accounted for by inhibition of the bone
marrow megakaryocytes alone.
2. Inhibition of clot retraction could be produced in the patient's blood by the
addition of minute quantities of quinidine in vitro. This was assumed to demonstrate a specific peripheral action of quinidine on this patient's platelets.
3. No inhibition of clot retraction could be produced by the addition of
quinine (an optical isomer of quinidine) to the blood of this patient in vitro.
This was further evidence of the marked specificity of the reaction.
4. Complete inhibition of clot retraction could be produced in the blood of a
normal individual by the addition of serum from the patient together with
quinidine. No inhibition occurred if one or the other was added alone. This was
assumed to demonstrate that quinidine did not effect the platelets directly but
did so through a combined action with some other element in platelet-free serum.
It was felt that this was strong support for an antigen-antibody type of reaction.
5. No significant fall in platelet concentration by the addition of quinidine
in vitro could be demonstrated. This was interpreted as evidence against a
complete lysis of the platelets as the method of destruction. The disparity between the platelet counts at the end of 2 hours in vivo and in vitro suggested
that the platelets were injured in such a manner as to effect their rate of removal
by the reticulo-endothelial system and their ability to produce clot retraction.
Submitted on June 30, 1952
Accepted on October 8, 1952
