Mitomycin-induced hemolytic uremic syndrome (HUS) is a life-threatening complication of this therapy, and increased levels of circulating immune complexes and hypocomplementemia have been found in some patients. We further characterize the role of immune complexes in mitomycin-HUS by showing that removal of these complexes by immunoadsorption with staphylococcal protein A columns correlates with temporal improvement in the microangiopathic hemolytic anemia in this disorder. Two immune complexes bound to the protein A column were identified: an 11S platelet-aggregating protein and a 15S non-platelet-aggregating protein. In addition, the patient had anaphylactoid reactions at the onset of immunoadsorption similar to first-use dialysis reactions that correlated with increases in complement 3a and 5a, interleukin-1 (IL-1), IL-6, and tumor necrosis factor levels. This case suggests that platelet-aggregating and complement-fixing circulating immune complexes are, in part, a proximate cause for mitomycin C-induced HUS. Therapy for mitomycin (HUS) with protein A columns should continue until circulating immune complexes reach undetectable levels and serum complement levels return to the normal range.

We have noted what other preliminary reports have also described as a new specificity of the MY4 monoclonal antibody from Coulter Immunology which previously was designated to only have myelogenous CD14 specificity. The MY4 marker appears to characterize a subpopulation of some B-lymphocytic malignancies that are CD19, CD20, surface immunoglobulin as well as MY4 positive. The results occurred when other myelogenous markers such as CD11b, CD13 and CD33 were unreactive. Another monoclonal antibody marker of CD14 specificity, MO2, did not demonstrate a similar reactivity. Various other monoclonal antibodies of the same IgGI subclass as MY4 were also not reactive and thereby excludes non-specific adsorption as an explanation of the results. The six patients described in this report represented five non-Hodgkin's lymphoma cases and one chronic lymphocytic leukemia case. Fifteen B-lymphocytic leukemias and 30 other B-lymphocytic non-Hodgkin's lymphomas analysed during the same period were not MY4 positive. In reviewing the clinical course of the six patients compared to the general behavior of these types of malignancies and making a speculative generalization from the small group of cases, the MY4 antigen appeared to be expressed by low to intermediate grade B-lymphocytic malignancies of a type that were more rapidly progressive and/or had a greater tendency to undergo a transformation of their malignancy. Two of the three transformed cases were proceeded by chronic lymphocytic leukemia.