RESIDUAL PITUITARY-FUNCTION AFTER TRANSSPHENOIDAL HYPOPHYSECTOMY IN DOGS WITH PITUITARY-DEPENDENT HYPERADRENOCORTICISM

Pituitary function was assessed before and after transsphenoidal hypop hysectomy in 39 dogs with pituitary-dependent hyperadrenocorticism (PD H). Anterior pituitary function was investigated using combined admini stration of four hypophysiotropic releasing hormones (corticotropin-re leasing hormone (CRH), GHRH, GnRH, and TRH) with measurements of ACTH, cortisol, GH, LH, prolactin (PRL), and TSH. Pars intermedia function was assessed by measurements of basal plasma alpha-MSH concentrations and adrenocortical function by baseline urinary corticoid/creatinine r atios. At eight weeks after hypophysectomy basal plasma ACTH, cortisol , GH, LH, PRL, and TSH concentrations were significantly lower than be fore surgery. In seven dogs with elevated alpha-MSH concentrations,the values returned to the normal level after surgery. In the combined an terior pituitary function test there were no plasma GH, LH, PRL, nd TS H responses to stimulation, whereas plasma ACTH and cortisol responses were small but significant. Remission of hyperadrenocorticism was obt ained in 35 dogs and recurrences occurred in 3 of these within 16 mont hs postoperatively. At 8 weeks after hypophysectomy, these 3 dogs were not discernible, with respect to residual pituitary and adrenocortica l function, from the 32 dogs with persisting remission. Urinary cortic oid/creatinine ratios in the latter group of dogs did not increase dur ing 22 months after hypophysectomy. In contrast to the presurgical fin dings, at 8 weeks after hypophysectomy there were significant positive correlations between baseline urinary corticoid/creatinine ratios and basal levels and responses for ACTH, indicating return to normal func tion of the pituitary-adrenocortical axis. It is concluded that among the adenohypophyseal cells present in the sella turcica after hypophys ectomy, the corticotropes have a distinct behavior. Much more so than the other cell types, the unaffected corticotropes tend to remain func tional, or a repressed reserve fraction of corticotropes may become fu nctional. This may be due to the removal of the hypothalamic influence of a postulated corticotropin-release inhibiting factor or a diminish ed inhibitory influence of a postulated paracrine factor. The corticot ropes may maintain normocorticism, but may also lead to mild recurrenc e after relatively long periods of remission.