Abstract
If we summarize our observations, we see that the capacity for antibody formation as a response to Brucella endotoxin stimulation is well preserved especially in acute leukemia, chronic myelosis, and in myelofibrosis. It is significantly decreased only in chronic lymphadenosis. A decrease, but lacking statistical significance, was further observed in reticulosarcoma and lymphosarcoma, Hodgkin’s disease, and myeloma, i.e., in affections in which the RES is mainly involved.
The very frequent infectious complications affecting patients with acute leukemia cannot in most cases be ascribed to deficient capacity to form antibodies, as often erroneously claimed, but rather to other factors which will be dealt with elsewhere. In contrast to this, in chronic lymphadenosis the frequent infectious complications are very probably due to impaired antibody formation together with relatively frequent hypogammaglobulinemia.
Chemotherapy, corticoid and x-ray treatment in the usual clinical doses doses were not found to inhibit antibody formation as a response to an antigenic stimulus.
Even changes in the leukocyte count—leukocytosis, neutropenia or lymphopenia—did not seem to inhibit the capacity for antibody formation to Brucella endotoxin.
In 2 patients with idiopathic chronic agranulocytosis, who were examined for comparison, we found a strikingly high titer of circulating antibodies to the Brucella endotoxin. It is suggested that, in chronic agranulocytosis, the capacity for circulating antibody formation may be enhanced to compensate for the decrease in the number of polymorphonuclears.
