Impaired spermatogenesis in testes at risk of torsion

Abstract

The oligospermia observed after unilateral torsion of the spermatic cord could reflect immunological damage to the opposite testis. An alternative explanation, that there may be a pre‐existing defect in spermatogenesis, was tested in 20 post‐pubertal males with acute torsion. In a prospective study the contralateral testis was biopsied at operation and the histological appearances were related to subsequent testicular function as assessed by seminal analysis 3 months later. Thirteen patients had biopsy evidence of partial maturation arrest in spermatogenesis which was either mild (6), moderate (4) or severe (3), and ten of these were oligospermic ( < 20 × 10⁶/ml). By contrast all seven patients with normal histology had a sperm concentration gt; 25 × 10⁶/ml. Histological grading of spermatogenesis by the Johnsen technique gave a higher score in patients with a normal biopsy (median 9·01, semi‐quartile range 8·96–9·21) than in those with abnormal histology (median 8·28, semi‐quartile range 7·98–8·45, P < 0·001) and correlated with the log of the sperm concentration 3 months later (r = 0·79, P < 0·001). There was minimal anti‐sperm and no anti‐testis antibody formation following torsion. Serum FSH levels were raised in 6 of 10 oligospermic patients, while all those with a normal sperm count had FSH concentrations within the normal range. Thus many patients who develop testicular torsion have an underlying defect in spermatogenesis, which correlates closely with poor postoperative exocrine function.