| Abstract: | Present evidence suggests that malacoplakia is the result of a functional defect in the mononuclear cells of the lesion caused by a deficiency of cyclic 3',5' guanosine monophosphate. This defect results in the impaired ability of the macrophage to release lysosomal enzymes necessary for the digestion of phagocytized bacteria. The persistent inflammatory reaction produces the characteristic granuloma of malacoplakia. Previous laboratory studies indicate that the phagocytic defect is reversible by cholinergic agonists, which led to the use of bethanechol chloride in the treatment of patients with malacoplakia. We report on 3 patients with vesical malacoplakia who were treated successfully with bethanechol chloride. |
