Pathological examinations of the testicular biopsy specimens revealed hypospermatogenesis
, maturation arrest and germ cell aplasia in 34.4%, 31.2% and 34.4% of patients, respectively.
Three cases had normal spermatogenesis, two cases had hypospermatogenesis
, two cases had maturation arrest, two cases had testicular atrophy and sertoli cell syndrome on histopathology, in one case the biopsy was inadequate.
In a group of 135 men, sperm were found in 51% of men with Sertoli-cell-only pattern, 83% in men with maturation arrest, and 100% of men with hypospermatogenesis
First, the production of spermatozoa may not be enough to trigger apoptosis in men with hypospermatogenesis
. In this case, Fas-positive spermatogonia may escape the signal to undergo apoptosis.
Microdeletions in these three regions are associated with various spermatogenetic alterations including Sertoli cell-only syndrome (SCOS), maturation arrest, and hypospermatogenesis
. Specifically, microdeletion of AZFa is relevant to complete SCOS and azoospermia.
In this study, sperm recovery was confirmed in 20 out of 83 men with NOA (24%) within 12 months after varicocelectomy, including 10 of 27 patients 37% with maturation arrest (MA) and 9 of 13 (69%) with hypospermatogenesis
. Similarly, in a meta-analysis by Weedin et al.
In the cases where late pachytene substages were observed in this group, failure of spermatogenesis appeared as hypospermatogenesis
, with a reduction of all stages from spermatogonia to spermatids.
The histopathologic diagnoses of the testes according to the seminiferous tubule pathology were mixed atrophy (11 testes, 50%, 4 of which also showed hyalinized tubules); Sertoli cell-only tubules plus hyalinized tubules (4 testes, 18.2%); Sertoli cell-only tubules (3 testes, 13.6%); intratubular germ cell neoplasia (2 testes, 9%, 1 of which also showed intermingled hyalinized tubules); complete tubular hyalinization (1 testis, 4.5%); and tubular hyalinization plus some groups of tubules with hypospermatogenesis
(1 testis, 4.5%) (Table 1).
(10) However, any mutation in mitochondrial genome would ultimately affect the production of ATP, consequently may lead to abnormal spermatogenesis, impaired differentiation and hypospermatogenesis
In a previous study from our laboratory, we documented that raised ROS levels lead to both mitochondrial sequence variation and nuclear DNA damage, which results in impaired motility and hypospermatogenesis
which may be the underlying pathology in infertility and RSA (6, 7).
However, deletion of only AZFc region is found to be associated with a wide range of phenotypes ranging from hypospermatogenesis
to SCO II (isolated foci of spermatogenesis along with Sertoli cells) syndrome (9).