MP43-20 TESTICULAR HYPOPLASIA IS DRIVEN BY DEFECTIVE VASCULAR FORMATION

Abstract

You have accessJournal of UrologyPediatrics: Testis, Varicocele & Stones1 Apr 2016MP43-20 TESTICULAR HYPOPLASIA IS DRIVEN BY DEFECTIVE VASCULAR FORMATION Pankaj Dangle, Dr. Cláudia Salgado, Miguel Reyes-Mugica, Rajeev Chaudhry, Francis Schneck, Michael Ost, and Sunder Sims-lucas Pankaj DanglePankaj Dangle More articles by this author , Dr. Cláudia SalgadoDr. Cláudia Salgado More articles by this author , Miguel Reyes-MugicaMiguel Reyes-Mugica More articles by this author , Rajeev ChaudhryRajeev Chaudhry More articles by this author , Francis SchneckFrancis Schneck More articles by this author , Michael OstMichael Ost More articles by this author , and Sunder Sims-lucasSunder Sims-lucas More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2016.02.229AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES A testicular “nubbin” or vanishing testis is considered to be secondary to a neo-natal torsion event and is evidenced by a definable hemosiderin deposit. We hypothesize that a, “vanishing testis” is a fault in embryological development as a result of arrest in endothelial cells migration rather than secondary to a random physical torsion/twist. Endothelial cell migration and testicular cord formation are interdependent processes, involving rearrangement of migrating endothelial cells from the mesonephric vascular plexus. We therefore sought to determine whether the testicular microvasculature is underdeveloped in “nubbin” testis compared with age matched healthy testicles from cadaveric specimens. METHODS Cases of testicular nubbin excision [average age 9.5 (range 2-12) months] were compared with age-matched controls [5.14, (2- 12 months)] from cadaveric testes without known genitourinary pathology. Testicular samples were serially sectioned and sampled appropriately at selected levels for vascular labeling. To elucidate the testis microvasculature we performed immunohistochemistry (IHC) using an automated staining platform with controlled and standardized conditions and positive and negative controls. We used CD34 which in the testis stains the endothelium, stem cells and interstitium; CD31 to stain the endothelium; and D2-40 to stain lymphatic endothelium. Whole slide digital images were subsequently scanned and morphometric analysis was carried out, the percentage of the total tissue with CD31 and CD34 positive stain was assessed and the number of the lymphatic vessels (D2-40) per mm2 was counted. RESULTS Seven patients were found to have vanishing testis on the left side. Of the 10 cases stained, 4 had evidence of hemosiderin deposit and calcification. The average testicular volume in these 4 cases was 2.2 compared to 4.8 cm3 in others with diagnosis of testicular atrophy (p=0.103). The percentage (%) distribution of CD34 in controls was higher, 14.4±4.5 (mean ±SD) compared to nubbin cases 7.5±3.8 (p=0.002). The % distribution of CD31 was 3.2±1.7 in controls and trended to be less in nubbin testis (2.2±1.0) (p=0.152). The lymphatic distribution was unchanged in both case and control. These findings elucidate that the testis microvasculature is mis-patterned in nubbin cases, while the lymphatic endothelium distribution is unaffected. CONCLUSIONS This histopathological study suggests that disturbances in endothelial malformation may be a contributing factor leading to testicular hypoplasia and a resultant nubbin testis independent of a physical torsion event. © 2016FiguresReferencesRelatedDetails Volume 195Issue 4SApril 2016Page: e586 Advertisement Copyright & Permissions© 2016MetricsAuthor Information Pankaj Dangle More articles by this author Dr. Cláudia Salgado More articles by this author Miguel Reyes-Mugica More articles by this author Rajeev Chaudhry More articles by this author Francis Schneck More articles by this author Michael Ost More articles by this author Sunder Sims-lucas More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...