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This version published online on November 7, 2006
Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2006-1216
A more recent version of this article appeared on February 1, 2007
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Submitted on June 6, 2006
Accepted on November 1, 2006

ANTIPITUITARY ANTIBODIES AGAINST GONADOTROPIN-SECRETING CELLS IN ADULT MALE PATIENTS WITH APPARENTLY IDIOPATHIC HYPOGONADOTROPIC HYPOGONADISM

Annamaria De Bellis*, Antonio Agostino Sinisi, Marisa Conte, Concetta Coronella, Giuseppe Bellastella, Dario Esposito, Daniela Pasquali, Giuseppe Ruocco, Antonio Bizzarro, and Antonio Bellastella

Chair of Endocrinology and Chair of Immunology - Department of Clinical and Experimental Medicine and Surgery "F. Magrassi, A. Lanzara", Second University of Naples, Italy

* To whom correspondence should be addressed. E-mail: annamaria.debellis{at}unina2.it.

Context: Hypogonadotropic Hypogonadism (HH) can occur at any stage of life as an isolated congenital or acquired abnormality or within a more generalized pituitary or hypothalamic impairment. However, the defect in patients with idiopathic HH is still unknown.

Objective: Aim of this study was to investigate in a group of HH patients with or without Kallmann's syndrome (KS) the prevalence of antipituitary antibodies (APA) and to characterize their pituitary target.

Design: We conducted a cross-sectional cohort study.

Setting: The study was performed at the Endocrinology Unit of 2nd University of Naples.

Patients: Twenty-one HH patients with normal sense of smell (group 1), 10 with KS (group 2), 13 with HH associated with other pituitary hormone deficiencies (group 3) and 50 normal controls were studied.

Main outcome measures: APA were evaluated in patients and in controls by indirect immunofluorescence. Moreover, a magnetic resonance imaging (MRI) of hypothalamic-pituitary region was performed in all 3 groups of patients.

Results: APA were detected at high titer in 8 out of 21 patients in group 1 (38%) and in 5 of 13 in group 3 (38.4%) and at low titers in 2 out of 10 in group 2 (20%) and in 3 of 50 controls (6%). In patients of group 1 APA immunostained selectively gonadotropin-secreting cells while in those of group 3 they immunostained also other pituitary hormone-secreting cells. None of patients in group 1 showed alterations on MRI, while all patients in group 2 showed aplasia/hypoplasia of the olfactory bulbs/tracts and/or of olfactory sulci. Among the 5 APA positive patients in group 3, 3 had normal MRI, 1 findings of empty sella and 1 of autoimmune hypophysitis.

Conclusions: Our results suggest that some apparently idiopathic cases of HH, both isolated and associated to other pituitary impairment, can be caused by an autoimmune process at pituitary level, early involving the gonadotrophs. Future longitudinal studies are needed to clarify the natural history of this process and the possible effect of early corticosteroid therapy.
Key words: antipituitary antibodies • hypogonadotropic hypogonadism • antibodies to gonadotropin-producing cells • Kallmann's syndrome




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