The objective of this study was to determine the need for repeat prostatic biopsies in men whose initial biopsy results revealed no evidence of cancer or atypia. We evaluated 1,136 men who underwent 1 or more prostatic biopsies in a longitudinal prostate specific antigen (PSA) based prostate cancer screening study that called for biopsy if the serum PSA level was greater than 4.0 ng./ml. (Hybritech assay) and findings on rectal examination or ultrasonography were abnormal or suspicious for cancer. Of the 1,136 men who underwent prostatic biopsy 391 (34%) had prostate cancer on the initial biopsy. Of 427 men who had negative initial biopsy results, a persistent serum PSA level of greater than 4.0 ng./ml. and abnormal rectal or ultrasound examination findings 82 (19%) had cancer on biopsy 2. Of 203 men with persistent abnormalities 16 (8%) had cancer on biopsy 3 and 6 of 91 (7%) had cancer on biopsy 4 or later. Thus, 96% of the cancers were detected through either biopsy 1 or 2. The median initial PSA level, followup PSA levels and the yearly rate of change in PSA were significantly greater in men whose cancer was detected compared with those of men whose cancer was not detected (6.4 versus 5.4 ng./ml., 7.4 versus 6.6 ng./ml. and 1.1 versus 0.7 ng./ml. per year, respectively). There was a trend for a higher percentage of tumors detected through serial screening to be pathologically organ confined with those detected through initial screening (73% versus 62%, p = 0.07). We conclude that men with a persistently elevated serum PSA value after an initial negative prostatic biopsy should routinely undergo at least 1 repeat biopsy to exclude adequately the presence of detectable prostate cancer.

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We concluded that the pathological features of most prostatic carcinomas detected via PSA based screening do not resemble those of autopsy cancers, and that most prostatic cancers detected in screening programs are likely to be clinically important.

Men with a family history of prostate cancer are at a significantly increased risk for prostate cancer, especially if the affected relative had early onset of cancer. Prostate cancer does not seem to be associated with a higher incidence of other cancers in family members.

Extracorporeal shock wave lithotripsy (ESWL not equal to) is the optimal therapy for renal calculi less than 2 cm. in diameter and for proximal ureteral calculi. Controversy continues over the initial approach to distal ureteral calculi (that is below the bony pelvis): in situ ESWL versus ureteroscopy. Since February 1990, 76 distal ureteral calculi were treated at our institution using either in situ ESWL (Dornier HM3 ESWL with a Stryker frame modification in 27 patients or Siemen's Lithostar electromagnetic ESWL in 22) or ureteroscopy (27 patients). Patient age and stone size were similar among the groups. All ESWL treatments were performed with the patient under intravenous sedation and on an outpatient basis. Stone-free rates were 96% for the HM3 device, 84% for the Lithostar and 100% for ureteroscopy. Retreatment was required in 3 Lithostar cases (14%) and 1 HM3 case (4%). When compared to ESWL ureteroscopy for distal ureteral stones was more time-consuming, entailed routine placement of a ureteral stent, often required general anesthesia, more often led to hospitalization and doubled the convalescence period. From a cost standpoint, ESWL on an HM3 unit was a few hundred dollars more expensive than ureteroscopy. In summary, we believe that in situ ESWL provides optimal first line therapy for distal ureteral calculi, while ureteroscopy is better reserved as a salvage procedure should ESWL fail.

Nonbacterial prostatitis is a common clinical entity which is often difficult to diagnose and treat. Little is known with regard to the etiology and pathogenesis of this disease process. To develop an animal model and characterize the immune parameters of nonbacterial prostatitis, we harvested the prostates from SJL, AJ, Balb/c, C57bl/6 and C57bl/6 lpr mice. These prostates were homogenized and injected into syngeneic mice. Controls were injected with Freund's complete adjuvant only. Mice from each group were sacrificed 30 days after injection, and the prostates were harvested. Prostatic tissue was examined histologically for degree of inflammation. None of the Balb/c mice exhibited prostatic inflammation. The SJL and AJ mice exhibited varying degrees of prostatic inflammation. All of the C57bl/6 mice were found to have lymphocytic infiltration of the stroma and periglandular region. The C57bl/6 lpr mice did not appear to be more susceptible than the parental strain. Adoptive transfer studies demonstrated the prostatic inflammation to be at least in part immune mediated. We conclude that injection of syngenic prostate antigen induces prostatic inflammation similar to clinical nonbacterial prostatitis. Nonbacterial prostatitis may be an autoimmune process.

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