The patient, aged 58 years, had prostatic carcinoma since 1969. Originally the tumourwas localised to the gland and seminal vesicles (T3); there was no elevation of the prostatic fraction of the serum acid phosphatase and there was no radiological evidence of bone deposits. The diagnosis was confirmed by histological examination of tissue resected torelieve outflow obstruction. In June 1974 he presented with metastases in the corpora cavernosa, producing painful priapism (Fig.). This caused obstruction by urethral compression; the urethra would not admit a 6F catheter. From 1969 he had been regularly taking Premarin, 2.5 mg t.d.s. with effective lowering of the plasma testosterone, the serum acid phosphatase remaining normal throughout. Until developing the penile metastases he had beenwell and symptom free. He was treated by intravenous Honvan without effect on the priapism; local external irradiation failed also. He developed urinary retention with overflow and permanent suprapubic cystostomy was considered. However, he was given cyproterone acetate, 100 mg t.d.s.: within 2 days the rock-hard penile deposit, originally 2 times 5 cm in size, had softened and he could void with a flow rate of 2 ml/min; after 7 days the priapism disappeared and the flow rate was 5 rnl/min. The present flow rate is I5 ml/min. Now heis symptom free and the metastasis can be felt only as a soft lesion 0.5 cm in size. There is no evidence of metastases elsewhere. The serum testosterone levels are as follows: Pre-treatment levels not available in 1969; 1972 while on Premarin, 100 nG/100 ml; after intravenous Honvan, 100 nG/100 ml; following cyproterone acetate 50 nG/100 ml. The patient had not been castrated or treated with pituitary irradiation.