THE MECHANISM OF HEMOLYSIS IN PAROXYSMAL COLD HEMOGLOBINURIA. II. OBSERVATIONS ON THE BEHAVIOR AND NATURE OF THE ANTIBODY 1

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Abstract
Erythrocytes from a patient with paroxysmal cold hemoglobinuria (PCH) were found to be agglutinable in antiglobulin serum (direct Coombs test). Although these erythrocytes had been "sensitized" in vivo, they were not hemolyzed when warmed with complement. The cells, however, were hemolyzed, both in vivo when the patient was chilled, and in vitro when they were chilled and warmed in PCH serum. The patient''s cells were no longer agglutinable in anti-globulin serum 6 hrs. after in vivo hemolysis. No concomitant change in either serum antibody or complement level was detected. Further characterization of the "cell antibody" responsible for agglutination in the direct Coombs test was not possible since the factor could not be demonstrated in eluates from the patient''s erythrocytes. The behavior of the abnormal antibody present in the sera of 2 patients with PCH was studied by using antiglobulin serum (indirect Coombs test) as well as the Donath-Landsteiner reaction. Antibody adsorbed in vitro from serum with a high antibody titer could be eluted from erythrocytes by heating the cells at 56[degree]C. The PCH serum factor which reacts with antiglobulin serum was identified as the PCH hemolysin. Fractionation of PCH serum in alcohol-water systems revealed that the PCH antibody is a water soluble (pseudoglobulin) gamma globulin and resembles most other human antibodies in this respect.