Hum. Reprod. Advance Access published online on January 5, 2006
Human Reproduction, doi:10.1093/humrep/dei444
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1 Department of Cell Biology, Georgetown University Medical Center, Washington DC USA
* To whom correspondence should be addressed. BACKGROUND: Adult patients with idiopathic hypogonadotropic hypogonadism (IHH) typically present absent puberty and therefore have prepubertal testes. IHH is recognized as one of the few curable causes of infertility and is often effectively treated with either gonadotropins or pulsatile GnRH therapy. The objective of study was to determine the structure of the testis prior to initiation of treatment. METHODS AND RESULTS: adult IHH patients with prepubertal testes (<4 ml), with no previous gonadotropin therapy and with no history cryptorchidism underwent open bilateral testicular biopsy prior to the initiation of hormonal treatment. The testes all patients showed seminiferous cords separated by interstitium composed of blood vessels, connective tissue and collagen fibres but typical adult Leydig cells were absent. The cords contained only Sertoli cells and early type spermatogonia. The spermatogonia mostly resided in the centre of the cords and were often large, typical of cytes. Sertoli cells appeared immature with ovoid nuclei devoid of infoldings and cytoplasm that lacked Tight junctional complexes commonly found connecting adult Sertoli cells were lacking. CONCLUSIONS: results demonstrate that the immature testes from patients with the severe form of IHH possess early spermatogonia that could possibly reinitiate spermatogenesis with appropriate hormone stimulation. Therefore, the immature of this IHH subset resembles those of prepubertal boys and may provide important biologic and genetic insights testicular development. *These authors are equal first authors of the article
Received September 19, 2005
Revised November 7, 2005
Accepted November 14, 2005
Article
Testis morphology in patients with idiopathic hypogonadotropic hypogonadism
Pananghat A. Kumar 1 *,
Nelly Pitteloud 2 *,
Peter A.M. Andrews 1,
Andrew Dwyer 2,
Frances Hayes 2,
William F. Crowley Jr 2,
and
Martin Dym 1 *
2 Reproductive Endocrine Unit, Massachusetts General Hospital and the Harvard Reproductive Endocrine Sciences Center, Boston MA USA
Martin Dym, E-mail: dymm{at}georgetown.edu
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