Testicular growth after varicocele surgery was evaluated in 116 boys 9 to 20 years old. A total of 88 boys was available for followup testicular examination 3 to 60 months after successful varicocele repair (mean 25). Left testicular volume loss of 2 cc or greater was present preoperatively in 72 of the 88 patients. The Palomo procedure was performed in 36 cases and repair using artery sparing techniques was done in 36. Mean relative left testicular volume increased 18% in the artery sparing group and 21% in the Palomo group. The increase in relative testicular volume compared to preoperative volumes was statistically significant in both groups (p < 0.05). There was no significant difference in testicular growth between the groups and no postoperative testicular atrophy was observed. A comparison group of 8 boys with uncorrected varicoceles demonstrated a mean relative volume increase of 3% (mean followup 22 months). The increase in testis volume in successfully corrected cases was statistically different (p < 0.05) from that of uncorrected cases. We conclude that reversal of varix induced testicular growth failure occurs only after successful surgical correction. The Palomo procedure resulted in equivalent testicular growth compared to the artery sparing techniques with fewer complications and no testicular atrophy despite intentional ligation of the testicular artery. Based on our data, we believe that the Palomo procedure should be the procedure of choice for adolescent varicocele correction.

The use of pelvic CT and bone scans for clinical staging in patients with a PSA level of < or = 20 ng/mL should not be advocated because they have a very low yield and are not cost effective. We question the role of a modified pelvic lymphadenectomy for staging purposes, either by an open or laparoscopic procedure, because the yield of positive diagnoses is very low.

Platelet eicosanoid metabolism resulting from tumor-cell-induced platelet aggregation (TCIPA) was examined in a homologous in vitro system. Rat Walker 256 carcinosarcoma cells induced the aggregation of rat platelets via a thrombin-dependent mechanism with concomitant production of eicosanoid metabolites (e.g., 12-HETE, TXA2). TCIPA was dependent on the concentration of tumor cells inducing aggregation, as well as cyclooxygenase and lipoxygenase products. Cyclooxygenase inhibitors, but not lipoxygenase inhibitors, blocked platelet aggregation induced in vitro by a low concentration of agonist. At a high agonist concentration, neither cyclooxygenase nor lipoxygenase inhibitors alone affected platelet aggregation; however, the combined inhibition of both the cyclooxygenase and lipoxygenase pathways resulted in subsequent inhibition of platelet aggregation regardless of agonist concentration. The extent of platelet TXA2 and 12-HETE biosynthesis was likewise dependent on and correlated with agonist concentration. The inhibitors used in this study did not significantly inhibit protein kinase C activity at the doses tested. Platelet surface glycoprotein alpha IIb beta 3 play an important role in platelet aggregation. The effect of platelet cyclooxygenase and lipoxygenase inhibition in regulating alpha IIb beta 3 surface expression was examined by flow cytometric analysis. Thrombin stimulation of washed rat platelets resulted in significantly increased surface expression of platelet alpha IIb beta 3 integrin complex. The enhanced surface expression was not inhibited by a cyclooxygenase inhibitor (aspirin), a thromboxane synthase inhibitor (CGS-14854) or a thromboxane receptor antagonist (SQ 29,548), nor was it stimulated by a thromboxane A2 mimic (pinane-thromboxane A2). However, alpha IIb beta 3 expression was blocked by lipoxygenase inhibition and stereospecifically increased by the platelet lipoxygenase metabolite 12(S)-HETE. These results suggest that both the platelet lipoxygenase and cyclooxygenase pathways are important for TCIPA but that different mechanisms of action are involved.