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At least 343 records · Page 19Linked to original sources
PubMed1984

Effects of glucocorticoids on endocrine function in the dog.

There are a multitude of possible side effects when using high levels of or chronic administration of glucocorticoid treatment. Several of the studies referred to in this discussion used large amounts of glucocorticoids for rather lengthy periods. The endocrine, as well as nonendocrine, effects of glucocorticoids are minimized when the lowest effective doses are used, when treatment is terminated as soon as reasonably possible, and when an alternate-day therapy schedule is followed. However, an occasional individual may appear with a particular susceptibility to one or more of the side effects of glucocorticoid treatment even when these measures are followed.

Adrenal Cortex Neoplasms↗
PubMed1994

Responsiveness to corticotropin-releasing hormone and vasopressin in canine Cushing's syndrome.

Corticotropin-releasing hormone (CRH) and vasopressin are the most important hypothalamic factors regulating adrenocorticotropic hormone (ACTH) secretion. In this study we have investigated the responsiveness of the pituitary-adrenocortical axis to intravenous administration of CRH or lysine vasopressin (LVP) in 16 control dogs, 22 dogs with pituitary-dependent hyperadrenocorticism and five dogs with hyperadrenocorticism due to an adrenocortical tumor, using doses of CRH and LVP that caused equivalent ACTH responses in the control dogs. After CRH administration, the increment in plasma ACTH was significantly (p < 0.05) lower in dogs with pituitary-dependent hyperadrenocorticism (221 +/- 53 ng/l) than that in control dogs (279 +/- 41 ng/l). In the dogs with pituitary-dependent hyperadrenocorticism, the relative increases in ACTH after CRH were significantly (p < 0.05) lower than those after LVP. Despite the absence of an increase in ACTH following LVP administration in dogs with hyperadrenocorticism due to an adrenocortical tumor, there was a significant increase in plasma cortisol, the increment (790 +/- 238 nmol/l) being not statistically different from that in the control dogs (412 +/- 37 nmol/l). We conclude that in spite of the changes inherent to pituitary-dependent hyperadrenocorticism, i.e. neoplastic transformation of corticotropic cells and hypercortisolism, there is persistence of responsiveness to hypophysiotropic hormones. The ACTH secretion by corticotropic cells in pituitary-dependent hyperadrenocorticism was relatively less sensitive to stimulation with CRH than with LVP. Adrenocortical tumors develop an aberrant sensitivity to LVP.

Adrenal Cortex Neoplasms↗
PubMed1989

Hyperfunctioning and nonhyperfunctioning benign adrenal cortical lesions: characterization and comparison with MR imaging.

The authors evaluated the potential of magnetic resonance (MR) imaging at 0.35 T to permit differentiation of nine hyperfunctioning adrenal cortical lesions from 21 nonhyperfunctioning adrenal cortical adenomas. Both qualitative data (visual assessment) and quantitative data (signal intensity ratios, T1, and T2) were used for tissue characterization. With a 2,000/56-100 sequence (repetition time msec/echo time msec), the majority of lesions were visually isointense to liver. Of 34 quantitative measures, only lesion-liver and lesion-kidney intensity ratios at 2,000/150 showed statistically significant differences among nonhyperfunctioning adenomas, aldosterone-producing lesions, and corticosteroid-producing lesions; however, the authors question the significance of these differences because of the abundant noise associated with the 2,000/150 sequence. The results suggest that nonhyperfunctioning adrenal cortical adenomas cannot be distinguished from benign hyperfunctioning cortical lesions with use of MR imaging at 0.35 T.

Adenoma↗
PubMed1986

Diagnosis and pathophysiology of Cushing's syndrome.

Cushing's syndrome is the consequence of a sustained overproduction of cortisol (hydrocortisone) by the adrenal cortex. This may be due to excessive secretion of cortisol by functioning adrenocortical tumors or to "nontumorous" adrenocortical hyperfunction. The latter may be a result of stimulation of the adrenal cortex by increased release of corticotropin (ACTH) from a small pituitary tumor or from nonpituitary nonadrenal tumor. Carcinoids or carcinomas of the lung or pancreas, and even pheochromocytomas have caused the syndrome of ectopic ACTH production. The problems involved in the diagnosis of Cushing's syndrome are establishing its presence and determining the underlying cause. Treatment is then dependent upon the underlying pathogenetic lesion.

Adenoma↗
PubMedDate not supplied

[The function of the hypothalamo-hypophyseal-adrenal system in Itsenko-Cushing syndrome].

Altogether 28 patients with adrenocortical tumors (corticosteromas and corticoandrosteromas) were examined using a radioimmunoassay to determine the concentration of corticotropin, cortisol, blood cyclic nucleotides, the circadian rhythm and time course of corticotropin and cortisol levels against a background of insulin hypoglycemia. In patients with Itsenko-Cushing's syndrome the basel level of cortisol was notably raised, that of corticotropin was sharply decreased. The circadian rhythm of the levels of corticotropin and cortisol was disturbed, a response of the hypophyseal-adrenal system to a stressor was suppressed. The concentration of blood cyclic nucleotides was increased, and these changes were dependent on the nature of adrenal pathology.

Adrenal Cortex Neoplasms↗
PubMed2002

[Differential diagnosis and medical treatment in Cushing's disease].

Cushing's disease remains a difficult diagnosis in spite of new technical procedures such as pituitary MRI, selective bilateral petrosal or cavernous sampling, (111)In pentreotide scan and 18 Flurodeoxyglucose pituitary PET scan. In this article, we review biological diagnostic procedures of Cushing's disease and corticotroph adenomas. According to our experience and the literature, we summarize the approach in medical treatment of Cushing's disease.

ACTH Syndrome, Ectopic↗
PubMed1992

Structure and dynamics of adrenal mitochondria following stimulation with corticotropin releasing hormone.

The mitochondria of rat adrenals were investigated qualitatively and quantitatively in different functional states of the adrenal cortex. Following stimulation of the animals with corticotropin releasing hormone (CRH), the corticosterone serum levels reached a maximum 1 hour after stimulation with CRH. The amount of inner mitochondrial membrane within the zona fasciculata increased showing a biphasic time course, with a first maximum 2 hours and a second maximum 8 hours after stimulation. In contrast, a significant rise of mitochondrial volume occurred only 24 hours after CRH stimulation. Therefore, the dense vesicularization of mitochondrial cristae may constitute an early process to enhance the steroidogenic capacity of these cells. Within cells of the transition zone between zona glomerulosa and zona fasciculata, we could depict a special type of mitochondria with characteristic crescent-like cristae only seen after stimulation with CRH. This type of mitochondria may represent an intermediate form between mitochondria of zona glomerulosa and zona fasciculata underlining the impressive transformational capacity of adrenocortical mitochondria. After hypophysectomy, zona fasciculata cells contained mitochondria with tubular inner membranes, representing a hypofunctional state. In contrast, the hypofunctional state after hypophysectomy and the hyperfunctional state after stimulation of the adrenal cortex via CRH injection did not appear to correlate with the morphology of mitochondria from the zona reticularis and adrenal medulla.

Adrenal Cortex↗
PubMed1991

Osmoregulation of systemic vasopressin release during long-term glucocorticoid excess: a study in dogs with hyperadrenocorticism.

In 9 dogs with pituitary-dependent hyperadrenocorticism and in 6 dogs with hyperfunctioning adrenocortical tumours, the osmoregulation of arginine vasopressin (AVP) release was investigated by iv infusion of 20% NaCl for 2 h at a rate of 0.03 ml per kg body weight. The responses were analysed in terms of sensitivity and threshold of the osmoregulation of AVP secretion. The sensitivity was normal in 6 dogs and lowered in 9. In 4 of the latter dogs there was complete absence of a response to hypertonicity. The osmotic threshold of AVP release was raised in 9 dogs and normal in 2 dogs, whereas in the four dogs without any response the term threshold was not applicable. The results were not different for dogs with pituitary-dependent hyperadrenocorticism and dogs with hyperfunctioning adrenocortical tumour. It is concluded that corticosteroid excess per se induces a marked impairment of the osmoregulation of AVP secretion. The loss of reactivity of the osmoreceptor system may contribute to the corticosteroid-induced polyuria, which is also the result of resistance to AVP in the kidney.

Adrenal Cortex↗