The Wiskott-Aldrich syndrome. Results of transfer factor therapy.
12 patients with Wiskott-Aldrich syndrome were treated with therapeutic doses of transfer factor in an attempt to induce cellular immunity. Clinical improvement was noted after transfer factor therapy in 7 of the 12 patients treated. Because this disease has a variable course and temporary spontaneous improvement can occur, the observed improvement cannot necessarily be attributed to the transfer factor. However, in two patients repeated remissions consistently followed transfer factor administration on repeated occasions. This included freedom from infections, regression of splenomegaly, and clearing of eczema. An unexpected finding was a decrease in bleeding in 3 of the 10 patients who had bleeding. Conversion of skin reactivity was obtained in all seven patients who clinically seemed to respond to transfer factor. In vitro studies performed after the administration of transfer factor demonstrated that the lymphocytes of the patients now produced migration inhibitory factor in response to appropriate test antigens, but did not undergo increased radioactive thymidine incorporation in response to the same antigens. A defect in the monocyte IgG receptors has been found in certain patients with the disease, and the current study shows that all patients with defective monocyte IgG receptors responded to transfer factor, whereas only one patient with normal receptors showed any response. This test may thus prove to be useful in predicting the results of transfer factor therapy in patients with Wiskott-Aldrich syndrome, although evaluation of a larger series of patients will be necessary to confirm this point. We conclude that cellular immunity can be induced, that there appears to be clinical benefit in certain patients with Wiskott-Aldrich syndrome by the use of transfer factor, and that this mode of therapy warrents trial in these patients and others with defects of cellular immunity.
D002464:Cell Migration Inhibition; D004247:DNA / Q000096:biosynthesis; D004485:Eczema / Q000628:therapy; D006470:Hemorrhage / Q000628:therapy; D006801:Humans; D007111:Immunity, Cellular; D007112:Immunity, Maternally-Acquired; D007074:Immunoglobulin G; D007167:Immunotherapy; D007239:Infections / Q000628:therapy; D008214:Lymphocytes / Q000276:immunology; D008264:Macrophages; D011955:Receptors, Drug; D012075:Remission, Spontaneous; D012882:Skin Tests; D013163:Splenomegaly / Q000628:therapy; D013936:Thymidine / Q000378:metabolism; D014923:Wiskott-Aldrich Syndrome / Q000276:immunology / Q000628:therapy*
D007074:Immunoglobulin G; D011955:Receptors, Drug; D004247:DNA; D013936:Thymidine