Objective: To evaluate whether defective cyclic adenosine monophosphate responsive element modulator (CREM) expression is the causative factor of spermatid maturation arrest (SMA).
Design: Comparative evaluation of the testicular histology in patients with SMA or normal spermatogenesis.
Setting: University clinic of andrology.
Patient(s): Azoospermic patients undergoing testicular biopsy.
Intervention(s): None.
Main outcome measure(s): Expression of CREMtau in quantitative immunohistochemistry analysis of testicular biopsy samples.
Result(s): Regular CREM expression was observed in the tubules with round, but not elongated, spermatids of patients with SMA (n = 9). Quantitative analysis showed that round spermatids of patients with SMA had a staining intensity similar to that observed in controls (n = 7).
Conclusion(s): Lack of spermatid elongation was not due to defective CREM expression. Therefore, CREM did not play a pathogenetic role in the onset of SMA in humans.