Reticuloendothelial Cell Function in a‐Methyldopa‐Induced Hemolytic Anemia

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Abstract
Two patients having .alpha.-methyldopa [for control of hypertension]-induced hemolytic anemia were followed sequentially using an in vitro assay of autologous monocyte-macrophage activity to determine if their RES function was abnormal and thus could be related to the mechanism of lysis. RES function was evaluated while the patients were actively hemolyzing and during remission, following discontinuance of the drug. RES activity apparently is normal in patients having hemolytic anemia due to .alpha.-methyldopa administration. Also, following cessation of drug therapy, the patients'' IgG-coated red cells interacted significantly for a prolonged period (4-5 mo.) with autologous or normal allogeneic monocyte-macrophages. This was associated with a concurrent reticulocytosis and indicates a persistent low-level hemolytic phase throughut this period, even though Hb and hematocrit values remained within the normal ranges. Although levels of IgG sensitizing the patients red cells were essentially constant during the hemolytic phase and when the patients were in complete remission, significant monocyte-macrophage activity was only evident during the hemolytic period. In an attempt to explain this phenomenon, it is postulated that hemolysis in patients receiving .alpha.-methyldopa is related to the interaction of drug with red cell membrane proteins which results in a variably expressed altered antigen which is recognized by autoantibody. The proper expression of the Fc portion of the Ig molecule to result in specific recognition by receptors on monocyte-macrophages depends upon the extent of the antigen alteration by .alpha.-methyldopa. if the drug does not result in appropriate antigen alteration, then, although autoantibody may still bind to the red blood cell, its Fc region is not readily recognized by monocyte-macrophages and little or no erythrophagocytosis occurs.