Vasopressin levels in Cushing's disease: inferior petrosal sinus assay, response to corticotrophin‐releasing hormone and comparison with patients without Cushing's disease

Abstract

The results of this study show that patients with Cushing's disease and poor surgical outcome had the highest AVP levels in our series. CRH administration caused different effects on AVP levels: it increased them in 35% of patients whereas there was no response in the remaining patients. On the basis of these findings, it is hypothesized that AVP might be involved in the persistence of ACTH hypersecretion in a subset of patients poorly responsive to surgery.

Overexpression of vasopressin (V3) and corticotrophin‐releasing hormone receptor genes in corticotroph tumours

“…It is generally assumed that the chronic hypercortisolism of Cushing's disease restrains the hypothalamic drive and deprives the pituitary tumour from endogenous CRH stimulation. The situation with vasopressin seems different: whereas CRH is undetectable in inferior petrosal sinus (Friedman et al, 1996), vasopressin is readily detected and increases further after exogenous CRH administration (Pieters et al, 1983;Colao et al, 1996;Friedman et al, 1996). On this basis a pathophysiological role for vasopressin has been proposed (Wittert et al, 1990) which could be reinforced by our results, suggesting the overexpression of its receptor.…”

“…The situation with vasopressin seems different: whereas CRH is undetectable in inferior petrosal sinus (Friedman et al, 1996), vasopressin is readily detected and increases further after exogenous CRH administration (Pieters et al, 1983;Colao et al, 1996;Friedman et al, 1996). The situation with vasopressin seems different: whereas CRH is undetectable in inferior petrosal sinus (Friedman et al, 1996), vasopressin is readily detected and increases further after exogenous CRH administration (Pieters et al, 1983;Colao et al, 1996;Friedman et al, 1996).…”

Inferior petrosal sinus ACTH and prolactin responses to CRH in ACTH-dependent Cushing’s syndrome: a single centre experience from the United Kingdom

“…It has long been recognised that in addition to ACTH, intersinus gradients for prolactin, growth hormone, thyrotrophin-secreting hormone, alpha-human chorionic gonadotrophin and beta-endorphin [14][15][16][17][18] can be detected in blood samples from inferior petrosal sinuses of patients with surgically and histologically confirmed Cushing's disease in the basal unstimulated state. Moreover, stimulation with CRH has been shown to induce further increases in the concentrations of prolactin, growth hormone, thyroid-stimulating hormone, alpha-subunit, tumour necrosis factor-alpha, alpha-melanocyte stimulating hormone and arginine vasopressin [14,[19][20][21][22][23][24][25][26] in blood from the dominant inferior petrosal sinus (the petrosal sinus with the maximal ACTH response), although these paradoxical responses of other hormones are not consistently seen [27]. It is also possible that corticotroph cells are capable of secreting prolactin but not able to store this hormone or that CRH used for stimulation during IPSS is contaminated with peptide fragments that can release pituitary hormones other than ACTH.…”

Increased prevalence of thyroid autoimmunity in patients successfully treated for Cushing's disease

“…The diagnosis of CD was based on the following criteria: (1) increased excretion of daily urinary cortisol with inappropriately high plasma ACTH concentrations; (2) increased serum cortisol concentrations with lack of physiological circadian rhythm; (3) failure of urinary and serum cortisol suppression after low dose but a greater than 50% decrease after high dose dexamethasone test. A pituitary adenoma was documented in all patients by computed tomography, magnetic resonance imaging or inferior petrosal sinus sampling, performed as previously described (Oldfield et al ., 1991; Colao et al ., 1996; Colao et al ., 1998). Cure of CD was established on the basis of the following criteria: (1) plasma ACTH concentrations and daily urinary cortisol excretion below or within the normal range; (2) serum cortisol concentrations below or within the normal range with restoration of circadian rhythm; (3) suppression of urinary and serum cortisol concentrations after low‐dose dexamethasone test (Colao et al ., 1999b).…”