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American Journal of Pathology, Vol 148, 1689-1698, Copyright © 1996 by American Society for Investigative Pathology

REGULAR ARTICLES

Testicular dysgenesis does not affect expression of anti-mullerian hormone by Sertoli cells in premeiotic seminiferous tubules

R Rey, L al-Attar, F Louis, F Jaubert, P Barbet, C Nihoul-Fekete, JL Chaussain and N Josso
Unite de Recherches sur l'Endocrinologie du Developpement (INSERM), Montrouge, France.

Anti-Mullerian hormone (AMH) immunoreactivity was studied on paraffin sections obtained from archival testicular biopsies of 29 children with intersex disorders and of 22 controls. Strong AMH immunoreactivity was observed in Sertoli cell cytoplasm from 8 fetal weeks until puberty. During pubertal maturation, in both normal and intersex patients, AMH expression was present in premeiotic seminiferous tubules, but was no longer detected in neighboring tubules with meiotic development. AMH immunostaining was abolished in the testis of one patient with persistent Mullerian ducts due to a mutation of the AMH gene, but was conserved in the testes of two patients with mutations of the AMH receptor gene. Testicular dysgenesis usually results in sexual ambiguity, with low testosterone and AMH serum levels and persistence of Mullerian derivatives. AMH immunoreactivity was conserved in premeiotic seminiferous tubules of dysgenetic testes, and also in sex- cord cells of a gonadoblastoma. In patients with asymmetric gonadal differentiation, the streak gonad was AMH-negative. In conclusion, secretion of AMH is a constitutive feature of the immature Sertoli cell and its expression is altered only by mutations of the AMH gene, but not by gonadal dysgenesis. The degree of regression of Mullerian ducts and serum AMH levels reflect the number, not the functional value, of Sertoli cells present in the immature testis.

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