Tissue from the normal, hyperplastic and the cancerous human prostate as well as tissue from the human seminal vesicles are capable of metabolizing testosterone in vitro. By incubating minced tissue with 3H-testosterone for 2 hours at 37 degrees C the following radioactive metabolites were identified: testosterone (17 beta-hydroxyl-4-androsten-3-one), androstenedione (4-androstene-3,17-dione), androstanedione (5alpha-androstane-3,17-dione), 5alpha-dihydrostestosterone (17 beta-hydroxy-5alpha-androstane-3-one, DHT), 3alpha-androstanediol (5alpha-androstane-3alpha,17beta-diol), 3beta-androstanediol (5alpha-androstane-3beta-17beta-diol) and androsterone (3alpha-hydroxy-5alpha-androstane-17-one). When normal human prostatic tissue was incubated with 3H-testosterone approximately 40% of the hormone was metabolized and 30-35% of the metabolites were identified as DHT. There were apparently no differences in testosterone metabolism between the dorsal and lateral prostatic lobes. A much lower conversion of 3H-testosterone was observed in the seminal vesicles (24%). The same metabolites were formed by prostatic carcinoma tissue, although distinctive quantitative differences from the normal prostate were observed. Thus, only 23% of the testosterone was metabolized by cancerous tissue of which 15% was present as DHT. The formation of 17-keto metabolites and androstanediols in the prostatic carcinoma tissue was approximately the same as in the normal prostatic tissue. The most extensive metabolism of testosterone was found by incubation of tissue from benign nodular prostatic hyperplasia. About 65% of the testosterone was metabolized, and 40% of the metabolites were identified as DHT. Hyperplastic prostatic tissue also showed a significantly higher formation of 5alpha-androstanedoils and the other tissues examined. The high formation of DHT and 5alpha-androstanediols in benign nodular prostatic hyperplasia in comparison with normal and cancerous prostatic tissue and seminal vesicle tissue might indicate that these metabolites should be studied more closely as possible aetiological factors for prostatic hyperplasia. The very low metabolism of testosterone in prostatic carcinoma tissue should be examined further in relation to tumour differentiation and clinical effect of endocrine therapy.
An unusual type of prostatic carcinoma associated with crossed renal ectopia and dermatomyositis is reported in a young man. Infiltration by an epithelial tumor filled the enlarged prostate with soft papillary masses. Cystoprostatectomy and removal of a single large pelvic lymph node metastasis were done. Histologically, the tumor resembled endometrial carcinoma and may have arisen from paramesonephric tissue in the prostate. Large amounts of immunoglobulins were found in the tumor tissue. The patient has survived for more than 5 years, although a slow growing urethral recurrence has been noted.
The result of surgical correction of hydronephrosis caused by chronic obstruction at the pyeloureteral junction has been evaluated clinically as well as by urography and body background substracted renography performed preoperatively and up to 65 months postoperatively. The average follow-up period was 24 months. Twenty-eight patients (29 kidneys) were operated. Clinically 24 patients were improved. Urography showed regress of hydronephrosis and/or improved urinary pelvic drainage in 22 patients, whereas kidney function is judged from renography was improved in only 8 patients. Improvement in all parameters was generally most marked during the first postoperative months. Renographic improvement was seen much more often when the contralateral (non-operated) kidney was abnormal. Thus, kidney function in terms of effective renal plasma flow is rather uninfluenced by hydronephrosis surgery if the contralateral kidney is normal, whereas clinical improvement in urinary drainage is regularly obtained. This improvement in drainage is poorly registered by renography. It is concluded that renography is an important complementary method to urography, but the method cannot replace the radiological methods in the follow-up of hydronephrosis surgery.
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