To clarify the pathophysiology of maturation arrest (MA), one of the most important causes of male infertility, by examining testicular morphology and biophysical and endocrine profiles of azoospermic patients with MA.

Thirty azoospermic men were assessed; 10 were found to have Sertoli‐cell only syndrome or chromosomal abnormalities, and 20 to have MA on biopsy. The second group had their clinical variables and findings analysed retrospectively after the diagnosis of MA (mean age 32.1 years, sd 5.2). Johnsen's score, serum hormone levels (follicle stimulating hormone, FSH, luteinizing hormone, LH, testosterone, prolactin and oestradiol), testicular volume, and the diameter of the seminiferous tubules, were evaluated. Patients were categorized into groups according to Johnsen score, i.e. group 1 (<4), group 2 (≥4 and <6) or group 3 (≥6). The clinical variables were compared in each group.

Hormone levels in almost all patients were in the normal range. FSH was related to the stage of MA; the difference in FSH between groups 1 and 3 was significant (P = 0.006). Serum levels of LH, testosterone, prolactin or oestradiol were similar in all groups. The diameter of the seminiferous tubules was less in group 1 than in group 3 (r = 0.881, P < 0.001) and there was an inverse and linear correlation between the FSH concentration and the diameter of the seminiferous tubules (r = −0.661, P = 0.0028).

FSH is the most useful variable for evaluating the severity of MA, even when it is within the normal range. The finding that gonadal hormone concentrations are normal in patients with MA suggests that an abnormality other than a disturbance in the hypothalamo‐pituitary‐testicular axis is responsible for MA.