Effect Of Obstruction To Sperm Egress On The Male Testis And Epididymis

Abstract

Objective: The effects of obstructive azoospermia on the testis and epididymis have been studied in vasectomized subjects. However, effects of obstruction to sperm egress in primary obstructive azoospermia on the testes and epididymis have not been extensively reported. The present study on fifty patients of primary obstructive azoospermia focuses on the local immune response and its effect on the testis and epididymis. This was a prospective study in a tertiary hospital setting comparing epididymal histology and epididymal fluid antisperm antibody in men with primary obstructive infertility with those in men with proven fertility. Material and Methods: Fifty males with primary obstructive infertility in the study group and ten subjects with proven fertility as controls were included in the study. While performing vasoepididymostomy on such patients, testicular and epididymal tissues were taken, and epididymal fluid was aspirated for estimation of antisperm antibodies. Testicular and epididymal histologies were studied under light microscopy for evidence of cellular immune response to obstruction. Antisperm antibodies in epididymal fluid were assayed by ELISA. Result(s): No effects of obstruction were evident on spermatogenesis or the testicular histology. Epididymal epithelial flattening with local or diffuse loss of cilia (n=25); pigment in the epithelial cells as a remnant of sperm ingestion (n=20); intraductal macrophages (n=29) with sperm ingestion in 62%; breach of epithelium with sperm extravasation (n=20) were considered as evidence of effects of obstruction leading to proximal ductal dilatation and damage. Presence of plasma cells and lymphocytes (n=31) and macrophages (n=11) in the interstitium were considered effects of antigenic sperm extravasation in the interstitium. These effects could be a local cell mediated immune response. Significant ELISA for antisperm antibodies was found in 29 patients; all patients with inflammatory cell infiltrate in the interstitium had significant ELISA for antisperm antibodies in the epididymal fluid. The cellular immune response as assessed by the presence of interstitial inflammatory cells and macrophages in epididymal histology was found in 12/20 patients. Testicular biopsies in all patients were normal. Humoral immune response as assessed by significant titres of antisperm antibodies in epididymal fluid was found in 14/20 patients. Evidence of local immune response (cellular or humoral or both) was found in 17/20 patients. Conclusion(s): We believe that intermittent exposure to small amounts of extravasated sperms in the epididymal interstitium would be sufficient to produce a local cell mediated immune response with its attendant effects on the epididymis, the primary site of sperm maturation, producing irreversible changes in its structure.