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Case Reports in Urology
Volume 2012, Article ID 648643, 5 pages
http://dx.doi.org/10.1155/2012/648643
Case Report

Leydig Cell Tumor Associated with Testicular Adrenal Rest Tumors in a Patient with Congenital Adrenal Hyperplasia due to 11 -Hydroxylase Deficiency

1Endocrinology Department, Hedi Chaker Hospital, Sfax 3029, Tunisia
2Department of Radiology, Hedi Chaker Hospital, Sfax 3029, Tunisia
3Department of Urology, Habib Bourguiba Hospital, Sfax 3029, Tunisia
4Anatomic Pathology Department, Habib Bourguiba Hospital, Sfax 3029, Tunisia

Received 15 October 2011; Accepted 24 November 2011

Academic Editors: S. K. Hong and S. Srinivas

Copyright © 2012 Nadia Charfi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Congenital adrenal hyperplasia (CAH) describes a group of inherited autosomal recessive disorders characterized by enzyme defects in the steroidogenic pathways that lead to the biosynthesis of cortisol, aldosterone, and androgens. Chronic excessive adrenocorticotropic hormone (ACTH) stimulation may result in hyperplasia of ACTH-sensitive tissues in adrenal glands and other sites such as the testes, causing testicular masses known as testicular adrenal rest tumors (TARTs). Leydig cell tumors (LCTs) are make up a very small number of all testicular tumors and can be difficult to distinguish from TARTs. This distinction is interesting because LCTs and TARTs require different therapeutic approaches. Hereby, we present an unusual case of a 19-year-old patient with CAH due to 11β-hydroxylase deficiency, who presented with TARTs and an epididymal Leydig cell tumor.