Value of Testicular Biopsy in Nonobstructive Azoospermia

Abstract

One of the first problems that arise in the study of the azoospermic patient is to determine if he has a blockage of the spermatic ducts, obstructive azoospermia, or otherwise there is a primary failure in spermatogenesis, i.e., nonobstructive azoospermia (NOA). The testicular volume, FSH, and inhibin B may be normal in patients with NOA. In these cases only a testicular biopsy can make a final differential diagnosis of obstructive and nonobstructive azoospermia. NOA incidence is estimated at 60 % of azoospermic patients. Patients with NOA have severe spermatogenesis failures that do not obey to a single etiology. Up to 20 % of NOA cases have a detectable chromosomal abnormality; the remaining 80 % are considered idiopathic azoospermias. Of the hundreds of genes causing infertility in mice, only a few mutations (HSF2, SYCP3, PRM1, PRM2, SOHLH1, NR5A1, and TEX11) caused azoospermia in men. Testicular biopsy is also the basis for the classification of these lesions, the starting point to know whether other genes are involved in spermatogenesis, and the evaluation of noninvasive techniques such as detection of germ cell-specific mRNA traces in seminal plasma to predict the state of spermatogenesis. The most common histologic lesions in patients with NOA include tubular hyalinization, Sertoli cell-only syndrome, mixed atrophy, hypospermatogenesis, and maturation arrest.