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Results for “ADRENAL CORTEX HYPERFUNCTION”

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At least 253 records · Page 14Linked to original sources
PubMed1998

Adrenocortical responsiveness to adrenocorticotropic hormone is enhanced in chronically food-restricted rats.

Chronic food restriction (FR) of rats and mice results in moderate hyperadrenocorticism, which may play a role in activating cellular mechanisms that retard aging. Previously, we reported that the FR-induced hyperadrenocorticism is not due to an activated hypothalamo-pituitary unit. Therefore, we investigated in a series of experiments whether adrenal responsiveness to adrenocorticotropic hormone (ACTH), in vitro and in vivo, is enhanced by FR. Three mo-old male Fischer 344 rats were either given free access to food (AL rats) or restricted to 60% of food consumed by AL rats (FR rats) from 6 wk of age. They were killed by decapitation in the morning (AM) and afternoon (PM) when endogenously circulating corticosterone levels are at their nadir and peak, respectively. In vitro, adrenal glands from FR rats (1.5 mo FR) produced more corticosterone per mg at all doses of ACTH than those from AL rats in both the AM and PM (diet main effect, P < 0.001). FR (1.5 to 2.5 mo) also enhanced adrenal responsiveness to physiologic (diet main effect, P < 0.05) and superphysiologic (diet main effect, P < 0.001) levels of ACTH administered in vivo to dexamethasone-treated rats. ACTH-receptor (ACTH-R) mRNA, normalized to adrenal mass or to total RNA, was not influenced by FR (1.5 mo). However, adrenal ACTH-R mRNA, as well as adrenal mass, per unit body weight was greater in FR than in AL rats (diet main effect, P < 0.001). These results indicate that enhanced adrenocortical responsiveness to ACTH plays a major role in the hyperadrenocortical state of chronically FR rats.

Adrenal Cortex↗
PubMed1997

Mitotane (o,p'-DDD) treatment in a cat with hyperadrenocorticism.

An 11-year-old male castrated Persian cat with spontaneous hyperadrenocorticism was presented. Both adrenals were grossly enlarged and calcified. A diagnosis of pituitary-dependent hyperadrenocorticism was made. Signs of hyperadrenocorticism resolved with long-term mitotane treatment. Concurrent diabetes mellitus resolved after 220 days of therapy. No severe adverse drug reactions were noted.

Adrenal Cortex↗
PubMed1988

An alternative protocol for the medical management of canine pituitary-dependent hyperadrenocorticism.

As an alternative to the o,p'-DDD treatment aimed at the selective destruction of the adrenal cortices, the authors have introduced a protocol aimed at the complete destruction of the adrenal cortices. It consists of a longer period of daily treatment with o,p'-DDD and lifelong substitution for primary hypoadrenocorticism. The results obtained in 41 dogs, with a minimum follow-up period of one year, indicate that this approach has advantages over lifelong maintenance therapy with o,p'-DDD.

Adrenal Cortex↗
PubMed1992

Pituitary dependent hyperadrenocorticism in a cat.

A cat that was suspected some insulin resistance was diagnosed as pituitary dependent hyperadrenocorticism from an adrenocorticotropic hormone (ACTH) stimulation test, dexamethasone suppression test and measure of endogenous plasma ACTH concentration. Histopathological examination revealed chromophobe adenoma in pituitary gland and hyperplasia in adrenal cortex.

Adenoma, Chromophobe↗
PubMed2004

Macronodular adrenocortical hyperplasia in a postmenopausal woman.

This case report describes the diagnosis of Cushing's syndrome due to macronodular adrenal hyperplasia in an elderly woman who presented with fatigue, muscle weakness and oedema, and recent excessive bruising. Long-standing disease and comorbidity precluded adrenalectomy. Despite treatment with metyrapone and diuretics, the patient died after two months hospitalisation. Postmortal examination revealed overexpression of luteinising hormone (LH) receptors in the adrenal glands, suggesting that the postmenopausal rise in LH may have a role in adrenal hyperplasia and hypercortisolism.

Adrenal Cortex↗
PubMed1991

Changes induced in newborn piglets by the trichothecene toxin T-2.

Three pregnant sows, being in the last quarter of gestation, were used in an experiment to study the changes induced in newborn piglets by T-2 toxin. One sow was used as control (C). The other two received 24 mg (sow A) and 6 mg (sow B) T-2 toxin, respectively, mixed in the feed, daily, up to the time of farrowing. The piglets of sow A became ill by 48-72 h after birth, while the litters of sow B and C remained healthy. The clinical symptoms included faintness, diarrhoea, decreased blood glucose level, and collapse followed by death. The milk and urine of sow A and the stomach contents of affected and dead piglets contained T-2 toxin and its metabolites. Pathological changes seen at necropsy included acute enteritis, degeneration of the liver and kidneys, and oedema of the mesentery. The stomach was filled with clotted milk. Histopathological and electron-microscopic findings consisted of reduced glycogen content and pathological simple fatty infiltration of the liver cells, lymphocyte depletion and necrosis in the lymphoid follicles of the intestinal mucosa, atrophy of the thymic cortex, and hyperfunction of the adrenal and thyroid glands compared to the control.

Animals↗