We evaluated serum prostate specific antigen before and after radical prostatectomy. In 100 consecutive patients who underwent radical prostatectomy, preoperative prostate specific antigen levels tended to increase with the increasing severity of pathological stage. However, even at levels of greater than 10 ng. per ml. the positive and negative predictive values (78 and 61 per cent, respectively) of prostate specific antigen to predict extracapsular disease were not sufficient to make this test useful alone for staging. In theory, after radical prostatectomy prostate specific antigen should be zero if no remaining prostatic tissue is present. Tests of precision and analytical sensitivity in our laboratory using a commercial prostate specific antigen assay revealed that a value of 0.4 ng. per ml. or more is different from zero at a greater than 95 per cent confidence level. With this guideline we evaluated the meaning of prostate specific antigen levels 3 to 6 months after radical prostatectomy in 59 men. Among men whose prostate specific antigen level was less than 0.4 ng. per ml. only 9 per cent demonstrated recurrence as evidenced by the development of positive bone scan or progressively elevated prostate specific antigen levels within 6 to 50 months. Alternatively, in men whose 3 to 6-month prostate specific antigen level was 0.4 ng per ml. or more there was evidence of recurrence in 100 per cent within 6 to 49 months (p less than 0.0001). Progressively elevated (more than 0.4 ng. per ml.) prostate specific antigen levels preceded recurrence from 12 to 43 months in all 6 patients who had positive bone scans, while increasing prostate specific antigen levels since radical prostatectomy have continued from 9 to 65 months in the 11 patients who have no radiological evidence of recurrent disease to date. Prostatic acid phosphatase serum values after radical prostatectomy were not useful to predict persistent disease. Prostate specific antigen values 3 to 6 months after radical prostatectomy are a sensitive indicator of persistent disease after radical prostatectomy and often precede other evidence of this occurrence by many years. This fact may alter concepts about surgical results, and possibly shorten and sharpen clinical studies involving adjuvant therapy after radical prostatectomy.
Serum prostatic specific antigen and prostatic acid phosphatase levels were measured retrospectively and evaluated in 357 men with benign prostatic hypertrophy and in 209 men with various stages of prostatic carcinoma. Although prostatic specific antigen values were elevated in 21 per cent of the patients with benign prostatic hypertrophy, the elevations usually were low and did not interfere with clinical interpretation. Prostatic specific antigen was elevated in 98 per cent of 86 men with active stage D2 disease; in 22 per cent of the men prostatic specific antigen was the only elevated marker. In contrast, prostatic acid phosphatase was the only elevated marker in 1 per cent of the patients with stage D2 disease and neither marker was elevated in 2 per cent. Among 74 patients in whom prostatic specific antigen and prostatic acid phosphatase determinations were made before radical prostatectomy, prostatic specific antigen was elevated substantially (greater than 10 ng. per ml.) in 59 per cent (26 of 44) with extracapsular disease and in only 7 per cent (2 of 30) without extracapsular disease. More importantly, of those 28 patients with substantially elevated prostatic specific antigen levels 26 (93 per cent) had extracapsular disease. Serial serum measurements showed that prostatic specific antigen either reflected or predicted clinical status in more than 97 per cent of the patients. We conclude that prostatic specific antigen is an excellent serum tumor marker for monitoring patients with prostatic carcinoma and that it surpasses prostatic acid phosphatase in this regard. Prostatic specific antigen also may be useful in staging prostatic carcinoma and it may change our attitudes significantly about the therapeutic responses to this cancer.
The treatment of priapism has changed significantly because of better understanding of the physiology of erection and of the pathophysiology of the disease. Several operative procedures have been advised to provide better venous drainage to the corpora. Herein we describe our experience with 20 patients. In 7 cases a modification of the cavernospongiosum shunt was used. This shunt is done under direct vision at the level of the proximal glans, thus, providing a better cavernosum-spongiosum shunt.
We reviewed our experience with 68 consecutive Anderson-Hynes ureteropyeloplasties. The 64 infants, children and young adults ranged from 2 days to 28 years old (median age 2 years), and 28 were less than 1 year old. Intubation was used in only 4 patients: 2 who also underwent ureteral reimplantation for vesicoureteral reflux, 1 with stones in the renal pelvis and 1 with pyonephrosis. We successfully repaired 60 of 64 nonintubated renal units (93.4 per cent). Temporary postoperative ureteral stenting was required for extravasation from 8 renal units (12.5 per cent). Two patients later underwent repeat ureteropyeloplasty for recurrent obstruction. Nephrectomy was performed for pyonephrosis in 1 patient and for a nonfunctioning kidney that had exhibited poor function preoperatively in 1. Prolonged ileus necessitated extended hospitalization in 3 patients (4.6 per cent). We conclude that nonintubated dismembered ureteropyeloplasty for uncomplicated, primary ureteropelvic junction obstruction can be performed safely and successfully, and should be considered the standard treatment. Positioning of the Penrose drain is critical to avoid urinoma formation. When persistent urinary leakage occurs temporary diversion is easy and well tolerated. Hospital stay averaged 12.1 days for patients with extravasation compared to 4.3 days when no extravasation occurred. Immediate preoperative retrograde pyelography did not seem to contribute to postoperative urinary extravasation by causing edema of the ureteral orifice.
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