|Four studies were performed to test the hypothesis that gonadotrophic hormones, and particularly luteinizing hormone (LH), play a role in the pathogenesis of hyperadrenocorticism in ferrets:
(I) adrenal glands of ferrets with hyperadrenocorticism were studied immunohistochemically to detect LH receptors;
(II) gonadotrophin-releasing hormone (GnRH) stimulation tests were performed in 10 neutered ferrets, with measurement of androstenedione, 17Ã¡-hydroxyprogesterone and cortisol as endpoints;
(III) GnRH stimulation tests were performed in 15 ferrets of which 8 had hyperadrenocorticism, via puncture of the vena cava under anaesthesia; and
(IV) urinary corticoid/creatinine ratios were measured at 2-week intervals for 1 year in the same ferrets as used in study II.
Clear cells in hyperplastic or neoplastic adrenal glands of hyperadrenocorticoid ferrets stained positive with the LH receptor antibody.
Plasma androstenedione and 17Ã¡-hydroxyprogesterone concentrations increased after stimulation with GnRH in 7 out of 8 hyperadrenocorticoid ferrets but in only 1 out of 7 healthy ferrets.
Hyperadrenocorticoid ferrets had elevated urinary C/C ratios during the breeding season.
The observations support the hypothesis that gonadotrophic hormones play a role in the pathogenesis of hyperadrenocorticism in ferrets. This condition may be defined as a disease resulting from the expression of LH receptors on sex steroid-producing adrenocortical cells.
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