Positive Direct Antiglobulin Tests and Immune Hemolytic Anemia in Patients Receiving Procainamide

Abstract

To characterize the autoimmune phenomena in patients receiving procainamide, we studied the prevalence of positive direct antiglobulin (Coombs') tests and immune hemolytic anemia in 100 such patients and compared them with 100 age-matched and sex-matched controls. There was a significant increase in the frequency of positive direct antiglobulin tests in patients receiving procainamide (21 vs. 10 per cent, P = 0.05). The mechanism of red-cell sensitization in patients receiving procainamide was the production of red-cell autoantibody, which was serologically indistinguishable from that seen in warm autoimmune hemolytic anemia. In contrast, positive direct antiglobulin tests in control patients were due to the presence of complement components. Red-cell autoantibody production secondary to procainamide was not correlated with a higher-than-expected frequency of antinuclear antibodies or the clinical syndrome of drug-induced lupus erythematosus. In the series of 100 patients receiving procainamide, we identified three cases of immune hemolytic anemia. In two of the three cases, the anemia resolved after the medication was discontinued and did not require steroid therapy. We conclude that procainamide often results in the production of red-cell autoimmune phenomena.

Drug-Induced Immune Hemolytic Anemia

“…126,127 The following hypotheses have been proposed for the induction of autoantibody production by procainamide: 126,127 The following hypotheses have been proposed for the induction of autoantibody production by procainamide:…”

Modulation of procainamide toxicity by selenium-enriched yeast in rats

“…Procainamide and its oxidized derivatives suppress incorporation of [3H] thymidine into DNA, produce massive DNA strand breaks, and, at high doses, are lethal to cultured leukocytes (Rubin et al 1987). There also have been reports of immune hemolytic anemia in patients with diagnosed procainamide-induced lupus (Kleinman et al 1984).…”

Immune hemolytic anemia caused by sensitivity to a metabolite of etodolac, a nonsteroidal anti‐inflammatory drug

“…This type of antibody can be detected by showing that it reacts with RBCs treated with drug and then washed. A second type of hemolysis (Type II), associated with sensitivity to drugs such as α‐methyldopa 16 and procainamide, 17 is characterized by RBC‐specific autoantibodies that do not require drug to be present in order to bind to RBCs and cause their destruction 3,16,18 . Type I and Type II drug‐induced immune hemolysis is usually mild, sometimes even subclinical.…”