Effect of Danazol in Immune Thrombocytopenic Purpura

Danazol and vinblastine are effective in many patients with chronic immune thrombocytopenic purpura (ITP). To evaluate the mechanism of action of these drugs, we studied six consecutive patients with chronic ITP treated with danazol and one treated with vinblastine. All the patients responded clinically without a notable change in the level of platelet-associated IgG. Instead, the clinical response to therapy was associated with a decrease in the number of monocyte binding sites for monomeric IgG (Fc receptors). In one patient, clinical relapse was associated with a spontaneous 2.7-fold increase in the number of monocyte Fc (IgG) receptors, without a change in the level of platelet-associated immunoglobulin. A decrease in the number of monocyte Fc (IgG) receptors following vinblastine infusion was associated with a clinical remission. We conclude that the clinical course of ITP may be influenced by the expression of monocyte or macrophage Fc (IgG) receptors. Danazol and vinblastine may mediate their clinical effect, at least in part, by influencing the number of available Fc (IgG) receptors on phagocytic cells. (N Engl J Med 1987; 316:503–8.) MANY patients with chronic immune thrombocytopenic purpura (ITP) can be treated successfully with danazol, 1 a synthetic analogue of androgenic steroids and progesterone, and with vinblastine. 2 However, the mechanism of action of these drugs in ITP is uncertain. ITP is caused by antiplatelet antibodies, which are frequently of the IgG class. 3 4 5 6 The levels of IgG on the platelet surface are generally elevated in patients with ITP, and a change in the level of platelet-bound IgG in a given patient is often associated with a change in the platelet count. Danazol and vinblastine may induce remissions in ITP by decreasing the production . . .