Disease relevance of Adrenocortical Hyperfunction

• On the other hand, noncachectic mice with Meth A fibrosarcoma gained weight, which was somewhat less than the control, and had neither hypoglycemia nor hypercorticism, although some mild disorders of hepatic functions were found [1].
• Until the end of this review, we will conveniently refer to these variants of adrenocortical hyperactivity as "hypercortisolism." In addition, rather than using the term "hypercortisolism" for the rat, we will use "hyperadrenocorticism" (as they secrete corticosterone, rather than cortisol) [2].
• These results suggest that preoperative impairment of anterior pituitary hormone secretion is secondary to hyperadrenocorticism and that ACTH hypersecretion by a primary pituitary adenoma is the primary etiology in Cushing's disease [3].
• It has many abnormalities, including hyperphagia, hyper-insulinemia, insulin resistance, low cerebral glucose utilization and an overactive hypothalamo-pituitary adrenal (HPA) axis with resulting hypercorticism [4].
• Abnormal results on oral dexamethasone suppression tests, clinical findings, and bilateral adrenal hyperplasia found on necropsy of one of the cats suggested concurrent hyperadrenocorticism [5].

Psychiatry related information on Adrenocortical Hyperfunction

• Alzheimer's disease is often characterized by an increase in plasma cortisol without clinical evidence of hypercorticism [6].

High impact information on Adrenocortical Hyperfunction

• Thus, besides polycystic ovaries, the bLHbeta-CTP mice provide a useful model for studying human disorders related to elevated LH secretion and adrenocortical hyperfunction [7].
• LH receptor (LHR) expression and activity were also elevated in adrenals from female TG mice, but gonadectomized TG females showed no increase in corticosterone, suggesting that the dysfunctional ovaries of the intact TG females promote adrenocortical hyperfunction [7].
• Physiologic doses of hydrocortisone induced hepatic TAT activity, but pair-weighed control animals with the same degree of hypercorticism as was found in tumor-bearing animals had normal TAT activity in liver tissue [8].
• In conclusion, metabolic disturbances elicited by a type 2 diabetes syndrome (insulin and/or leptin resistance, but not hypercorticism) appear to suppress type 1 diabetes development in NOD-Lepr(db-5J)/Lt by inhibiting activation of T-effector cells [9].
• ACTH-independent macronodular adrenal hyperplasia (AIMAH) is an uncommon cause of Cushing's syndrome characterized by bilateral nodular adrenocortical hyperfunction in the presence of suppressed ACTH levels [10].

Chemical compound and disease context of Adrenocortical Hyperfunction

• She had high urinary free cortisol levels (711 micrograms/day) and a positive response to metyrapone and suppression with 8 mg dexamethasone, suggesting pituitary ACTH-dependent adrenocortical hyperfunction [11].
• Analysis of binding data indicated that increased binding in patients treated with prednisone was due to an ncrease in receptor concentration, whereas in patients with adrenocortical hyperfunction, it was due to an increase in receptor affinity [12].
• The inhibition of cholesterol cleavage by metyrapone (26 and 62%, at 0.1 and 1.0 mM concentrations, respectively) was also demonstrable in adrenal mitochondria from a patient with hypercorticism resulting from an ACTH-independent adrenal adenoman (AA) [13].
• Serum concentrations of dehydroepiandrosterone sulfate (DHEA-S) were measured in patients with hyperadrenocorticism [14].
• Hypercorticism secondary to steroid treatment has been associated with a thrombophilic state and the presence of a reduced fibrinolytic potential in particular [15].

Biological context of Adrenocortical Hyperfunction

• It is suggested that elevation of plasma non-protein bound 11-OHCS, resulting from impaired metabolism and reduced protein binding of cortisol in patients with hepatic disease, may explain the features of endogenous hypercorticism seen in such patients [16].
• During the initial period, worsening hyperadrenocorticism resulted in a rise of atrial natriuretic factor and an inhibition of renin activity, consistent with an increase of cortisol and plasma volume [17].
• Osmoregulation of systemic vasopressin release during long-term glucocorticoid excess: a study in dogs with hyperadrenocorticism [18].
• Thus, in a substantial number of patients with hypercorticism, the renin angiotensin system may be an important factor in the pathogenesis of hypertension, whereas in patients with low PRA values other factors like oversecretion of mineralocorticoids may be responsible for the observed blood pressure increases [19].

Anatomical context of Adrenocortical Hyperfunction

• In the present study cerebrospinal fluid (CSF) CRH levels and levels of ACTH and cortisol in CSF and plasma were measured in clinically healthy dogs, in dogs with pituitary-dependent hyperadrenocorticism (PDH), and in dogs with hyperadrenocorticism due to an adrenocortical tumor (ATH) [20].
• OBJECTIVE: To investigate the role of hypercorticism in the development of compromised beta-adrenergic signalling in adipocytes of mature C57BL/6J-ob/ob mice [21].
• Besides the direct effect of the thyroid hormones on the kidney, our findings indicate that the excess of triiodothyronine and thyroxine stimulates the activity of adrenals indirectly and evokes hyperadrenocorticism which could be related to the action of adrenal steroids on kidney function and kidney growth [22].
• A case of adrenal gland dependent hyperadrenocorticism with mitotane therapy in a Yorkshire terrier dog [23].
• The conclusions has been drawn that a short-term raising of hydrocortisone level stimulates and prolonged hypercorticism inhibits peroxidase activity in neutrophils and, consequently, their function [24].

Gene context of Adrenocortical Hyperfunction

• It is concluded that continuous hyperstimulation of pituitary corticotropes with hypothalamic CRH is probably not the cause of excessive ACTH secretion in dogs with pituitary-dependent hyperadrenocorticism [20].
• However, with regard to group II, the CRH-induced ACTH increase 1 week after selective adenomectomy indirectly supports the concept of CRH deficiency during hypercorticism and thus, in these patients as well as in group I, a pituitary origin of the disease [25].
• (The nocturnal increment in plasma prolactin concentrations in these patients with hypercorticism compared with that of normal subjects was reduced, P less than .02) [26].
• In pituitary-dependent hyperadrenocorticism (Cushing's disease), the disturbed regulation of ACTH secretion is associated with neoplastic transformation of corticotropic cells [27].
• The aim of this study is to investigate the effects of ghrelin and GH-releasing peptide-6 (GHRP-6) on the release of growth hormone (GH), adrenocorticotrophic hormone (ACTH), and cortisol in dogs with pituitary-dependent hyperadrenocorticism (PDH) and in healthy dogs of comparable age [28].

Analytical, diagnostic and therapeutic context of Adrenocortical Hyperfunction

• For the diagnosis of hyperadrenocorticism itself, the measurement of the concentration of corticosteroids in a single sample of plasma obtained 8 h after intravenous injection of 0.01 mg dexamethasone/kg was sufficient [29].
• Efficacy of cobalt 60 radiotherapy in dogs with pituitary-dependent hyperadrenocorticism [30].
• PROCEDURE: Hyperadrenocorticism was diagnosed on the basis of clinical signs; physical examination findings; and results of ACTH stimulation test, low-dose dexamethasone suppression test, or both [31].
• Although high-dosage dexamethasone suppression tests often are useful in the differential diagnosis of hyperadrenocorticism, a lack of suppression of plasma cortisol does not necessarily exclude pituitary-dependent hyperadrenocorticism [32].
• A retrospective study on stored plasma from normal dogs and dogs with pituitary dependent hyperadrenocorticism (PDH), pituitary dependent hyperadrenocorticism controlled by mitotane (o,p'-DDD),* iatrogenic hyperadrenocorticism, and hypoadrenocorticism was conducted to determine if alterations in aldosterone production exist in these disorders [33].

References