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PubMed1984

Adrenocortical hyperactivity in newly admitted alcoholics: prevalence, course and associated variables.

After initial screening of 269 consecutive Psychiatry Service admissions suggested adrenal stimulation in alcoholics, 52 consecutive newly-admitted alcoholics were intensively studied in order to determine the extent of adrenal hyperactivity, how quickly it resolved and the factors associated with it. While 21% failed to show suppression of cortisol at either 0800 or 1600 hr the day following administration of dexamethasone (1 mg) at 2300 hr, no patient showed both clinical and biochemical evidence of alcoholic pseudo-Cushing's syndrome, and all patients suppressed normally eight days later. Analysis of a variety of variables, including several measures of recent alcohol consumption, alcohol withdrawal and depression failed to show significant association with nonsuppression. The DST should be interpreted cautiously in alcohol abusers during the first 10-14 days following admission. Persistent nonsuppression, however, is probably not due to alcohol abuse.

Adrenocortical Hyperfunction↗
PubMed1989

Is cortisol involved in upper-body obesity?

Obesity is a major health problem that can be defined as an excess of body fat, associated with hypertension, diabetes and coronary heart disease. Several groups have evaluated the clinical significance of variations in fat cell distribution on these complications. A frequently used index of fat cell distribution is the waist to hips ratio (W/H). A high W/H ratio is said to reflect upper body fat cell distribution while a low waist to hips ratio reflects a lower body type fat cell distribution. Studies have shown that those whose W/H ratio indicate upper body fat cell distribution had a higher prevalence of diabetes and hypertension than those with the lower type. Over the years cortisol has attracted considerable interest as a possible factor in the development and maintenance of obesity. The clinical findings associated with upper body type of obesity are in many ways similar to those of the hypercortisol state. Our hypothesis is that upper body obesity forms a unique subgroup of the obese population and their regional fat distribution is associated with mild cortisol excess. In humans, studies have reported that some obese subjects hypersecrete cortisol and have an increase in the cortisol production rate. Although recent studies would tend to discount any influence of cortisol in human obesity, several factors should be taken into consideration. It is difficult to measure cortisol economy in obese subjects because among other things the measurements are less than precise; and cortisol secretion changes during the day and in response to outside stimuli. Further, obesity is a heterogeneous disorder and not all obese subjects may have the same disorder.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdomen↗
PubMed1984

Hormonal, metabolic and morphologic studies of aged C57BL/6J obese mice.

Genetically obese mice (C57BL/6J-ob/ob), fed ad libitum, demonstrated a precipitous increase in the spontaneous death rate after 50 weeks. The first signs of morbidity were a ruffled hair coat and a progressive motor ataxia. Necropsy revealed that obese mice had pale and fatty livers, urolithiasis and grossly distended bladders. Microscopically, the hepatocellular changes observed in all aged obese mice included: a loss of orientation of hepatocytes, an enormous variability in the size of both hepatocytes and their nuclei, and an extensive deposition of both large and small lipid droplets, confirmed by an increase content of triacylglycerols. A subacute-to-chronic, multifocal, necrotizing hepatitis was also present. Kidneys from aged obese mice contained hypertrophied glomeruli and increased PAS-stained material. Tubular dilation with compaction of the tubular cells was also seen. There were no significant alterations in the microanatomy or mineralization of femurs from obese mice, yet there was a significant increase in plasma alkaline phosphatase activity. In obese mice at 62-63 weeks of age, hyperglycemia was present even in spite of hyperinsulinemia. Pituitary immunoreactive ACTH and its molar ratio to pituitary immunoreactive beta-endorphin were also increased in obese mice at this age. Even though the etiology of the decreased lifespan of genetically obese mice remains uncertain, the possibility is discussed that an overall defect in the central nervous system may be involved.

Adrenocortical Hyperfunction↗
PubMed1995

Urinary excretion of glucocorticoids in the diagnosis of hyperadrenocorticism in cats.

In dogs and humans, the measurement of urinary corticoid excretion has become a standard screening test for the diagnosis of hyperadrenocorticism. Mainly because the urinary excretion of cortisol was considered to be very low in cats, its measurement was not used in the diagnosis of hyperadrenocorticism in this species. We therefore studied the urinary excretion of [3H]cortisol and measured the corticoid/creatinine (C/C) ratio in healthy cats and in cats with hyperadrenocorticism in order to evaluate the applicability of this measurement in the diagnosis of feline hyperadrenocorticism. The median urinary excretion of intravenously administered [3H]cortisol was 1.85% (measured as excreted 3H; range, 1.56 to 1.99; n = 4). High-performance liquid chromatography analysis showed a small peak of cortisol and a large peak consisting primarily of conjugates of cortisol and/or its metabolites. The 2.5 and 97.5 percentiles of the urinary C/C ratio in healthy cats were 2 x 10(-6) to 36 x 10(-6) (n = 42). The C/C ratio was significantly higher in six cats with pituitary-dependent hyperadrenocorticism (median, 122 x 10(-6); range 51 x 10(-6) to 272 x 10(-6)). The administration of a high dose of dexamethasone (0.1 mg/kg thrice daily per os) led to marked suppression of the C/C ratio in healthy cats (median suppression of the average of the C/C ratio of the first two consecutive days was 92%; range, 74 to 96%; n = 12), as well as in five cats with pituitary-dependent hyperadrenocorticism.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocortical Hyperfunction↗
PubMed1991

Treatment of major depression with steroid suppressive drugs.

The hypercorticism frequently observed in major depression, unaccompanied by signs of Cushing's syndrome, is still poorly understood. One suicidal young woman, with very high cortisol levels and unusual resistance to dexamethasone suppression, is described. She was successfully treated with steroid suppressive drugs (aminoglutethimide, metyrapone), had a prompt and complete remission and has remained well for more than two years on no medication. This success prompted an on-going clinical trial of this therapy. The available drugs and a working hypothesis of their action are discussed.

Adrenocortical Hyperfunction↗
PubMed1993

The pathogenesis of adrenal and extra adrenal hyperandrogenism.

The data reviewed in this paper suggest that a factor other than ACTH which is suppressible by treatment with glucocorticoid, plays an essential role in the regulation of adrenal androgen production. Adrenal androgen biosynthesis probably takes place exclusively in specific androgen-secreting cells. That availability of androgen substrate alone e.g. 17OH-progesterone, is not sufficient to lead to hyperandrogenaemia is clear from data which was obtained from treated patients with the 21 hydroxylase deficiency type of congenital adrenal hyperplasia. In pituitary ACTH excess, cortisol production is relatively greater than that of androgens. In contrast, in some patients with ectopic ACTH production, the excess production of androgens is relatively greater than that of cortisol. Taken together, these observations suggest that a factor closely related to ACTH, i.e. a POMC fragment other than ACTH, plays an important role in the regulation of adrenal androgen production, that in Cushing's disease the ratio of ACTH to the androgen-stimulating fragment increases, and that in some patients with ectopic ACTH syndrome the ratio of ACTH to the alternative fragment may be decreased. In addition, the data reviewed are consistent with a model for the pathogenesis of idiopathic hirsutism and polycystic ovary syndrome whereby mild adrenal androgen excess is primary to the development of these disorders. However, the identity of the putative adrenal androgen stimulating hormone has yet to be established.

Adrenal Hyperplasia, Congenital↗
PubMed1995

Expression of hsp90 beta messenger ribonucleic acid in patients with familial glucocorticoid resistance--correlation to receptor status.

We have previously shown an increased specific DNA-binding of liganded unactivated glucocorticoid receptor (GR) to the LTR-region of MMTV DNA in a patient with primary cortisol resistance and receptor thermolability indicating a defective interaction of GR with hsp90. In some patients, however, no apparent receptor abnormality was found in spite of a characteristic phenotype. mRNA expression levels of hsp90 beta were analysed in cultured fibroblasts from patients with known receptor defects, such as thermolability, decreased ligand binding affinity and low receptor expression levels, and from patients with a cortisol resistant phenotype but no detected receptor alteration. Fibroblasts from patients with GR defects expressed higher hsp90 beta mRNA levels as compared to patients with no receptor defects or to healthy controls. These data indicate that GR defects are associated with increased hsp90 beta mRNA levels.

Adrenocortical Hyperfunction↗
PubMedDate not supplied

Comparative dermatology--canine endocrine dermatoses.

Endocrine diseases in the dog commonly manifest with dermatological lesions. Hypothyroidism is the most common endocrinopathy and usually presents with alopecia in areas of wear, seborrhea, and recurrent infections. Common clinical signs associated with hyperadrenocorticism include polyuria, polydipsia, and polyphagia. The most common dermatological manifestation of hyperadrenocorticism is bilaterally symmetrical alopecia sparing the head and distal extremities. Pyoderma is a common finding associated with immunosuppression. Less commonly, calcinosus cutis may occur. Sex hormone excess, primarily hyperestrogenism and hyperandrogenism, may also be associated with dermatological signs. Usually, dogs are intact, and the excess production is due to testicular or ovarian neoplasia.

Adrenocortical Hyperfunction↗
PubMed2006

Suspected case of hyperadrenocorticism in a golden hamster (Mesocricetus auratus).

Dermatologic disease is a common problem in pet rodents. This article describes the case of a pet golden hamster (Mesocricetus auratus) with dermatologic and other clinical signs (polyuria, polydypsia) similar to those found in other mammalian species with hyperadrenocorticism. Among other diagnostic tests, the urine cortisol/creatinine ratio was measured and was found to be increased, which appeared to support the diagnosis. Treatment with ketoconazole was initiated, without apparent success.

Adrenocortical Hyperfunction↗
PubMed2005

Feline endocrinopathies.

Feline endocrinopathies (excluding diabetes mellitus) include hyperthyroidism, hypothyroidism, acromegaly, hyposomatotropism, diabetes insipidus, hyperadrenocorticism, primary sex hormone-secreting adrenal tumors, primary hyperaldosteronism, pheochromocytoma, hypoadrenocorticism, hyperparathyroidism, and hypoparathyroidism. Each of these conditions will be discussed including their prevalence, cause, clinical signs, diagnosis, treatment options, and prognosis.

Acromegaly↗
PubMed2006

Update on drugs used to treat endocrine diseases in small animals.

Drug therapy for the endocrine system is implemented to replace a hormone deficiency or to prevent or reduce the formation or effects of excess hormone. Treatment of endocrine disorders covers diseases of the pituitary, adrenal, parathyroid, and thyroid glands as well as the endocrine pancreas. This article focuses on new therapies currently available for specific diseases. Administration of trilostane for treatment of hyperadrenocorticism and use of insulin glargine, protamine zinc insulin (PZI), and porcine Lente insulin for diabetes mellitus are discussed. In addition, transdermal methimazole therapy for treatment of feline hyperthyroidism and administration of progestins for pituitary dwarfism are considered.

Adrenocortical Hyperfunction↗
PubMed2004

Urinary glucocorticoid excretion in the diagnosis of hyperadrenocorticism in ferrets.

Hyperadrenocorticism in ferrets is usually associated with unaltered plasma concentrations of cortisol and adrenocorticotropic hormone (ACTH), although the urinary corticoid/creatinine ratio (UCCR) is commonly elevated. In this study the urinary glucocorticoid excretion was investigated in healthy ferrets and in ferrets with hyperadrenocorticism under different circumstances. In healthy ferrets and in one ferret with hyperadrenocorticism, approximately 10% of plasma cortisol and its metabolites was excreted in the urine. High-performance liquid chromatography (HPLC) revealed one third of the urinary corticoids to be unconjugated cortisol; the other peaks mainly represented cortisol conjugates and metabolites. In 21 healthy sexually intact ferrets, the UCCR started to increase by the end of March and declined to initial values halfway the breeding season (June). In healthy neutered ferrets there was no significant seasonal influence on the UCCR. In two neutered ferrets with hyperadrenocorticism the UCCR was increased, primarily during the breeding season. In 27 of 31 privately owned ferrets with hyperadrenocorticism, the UCCR was higher than the upper limit of the reference range (2.1 x 10(-6)). In 12 of 14 healthy neutered ferrets dexamethasone administration decreased the UCCR by more than 50%, whereas in only 1 of the 28 hyperadrenocorticoid ferrets did the UCCR decrease by more than 50%. We conclude that the UCCR in ferrets primarily reflects cortisol excretion. In healthy sexually intact ferrets and in ferrets with hyperadrenocorticism the UCCR increases during the breeding season. The increased UCCR in hyperadrenocorticoid ferrets is resistant to suppression by dexamethasone, indicating ACTH-independent cortisol production.

Adrenocortical Hyperfunction↗
PubMed2005

Hyperadrenocorticism in a dog due to ectopic secretion of adrenocorticotropic hormone.

Spontaneous hyperadrenocorticism in dogs is known to be the result of excessive secretion of adrenocorticotropic hormone (ACTH) by the pituitary gland or excessive autonomous glucocorticoid secretion by an adrenocortical tumor. Here, we report on an 8-year-old German shepherd dog in which ACTH-dependent hyperadrenocorticism was a result of ectopic ACTH secretion and could be related to an abdominal neuroendocrine tumor. Hyperadrenocorticism was diagnosed on the basis of the history, clinical signs, and elevated urinary corticoid/creatinine ratios (UCCRs; 236 and 350 x 10(-6); reference range < 10 x 10(-6)). The UCCR remained elevated (226 x 10(-6)) after three oral doses of dexamethasone (0.1 mg/kg body weight) at 8-h intervals. Ultrasonography revealed two equivalently enlarged adrenal glands, consistent with adrenocortical hyperplasia. Plasma ACTH concentration was clearly elevated (159 and 188 ng/l; reference range 5-85 ng/l). Computed tomography (CT) revealed that the pituitary was not enlarged. These findings were interpreted as indicating dexamethasone-resistant pituitary-dependent hyperadrenocorticism. Transsphenoidal hypophysectomy was performed but within 2 weeks after surgery, there was exacerbation of the clinical signs of hyperadrenocorticism. Plasma ACTH concentration (281 ng/l) and UCCRs (1518 and 2176 x 10(-6)) were even higher than before surgery. Histological examination of the pituitary gland revealed no neoplasia. Stimulation of the pituitary with corticotropin-releasing hormone did not affect plasma ACTH and cortisol concentrations. Treatment with trilostane was started and restored normocorticism. CT of the pituitary fossa, 10 months after hypophysectomy, revealed an empty sella. Hence, it was presumed that there was ectopic secretion of ACTH. CT of the abdomen revealed a mass in the region of the pancreas and a few nodules in the liver. Partial pancreatectomy with adjacent lymph node extirpation was performed and the liver nodules were biopsied. Histological examination revealed a metastasized neuroendocrine tumor. Abdominal surgery was not curative and medical treatment with trilostane was continued. At 18 months after the abdominal surgery, the dog is still in good condition. In conclusion, the combination of (1) severe dexamethasone-resistant hyperadrenocorticism with elevated circulating ACTH levels, (2) definitive demonstration of the absence of pituitary neoplasia, and (3) an abdominal neuroendocrine tumor allowed the diagnosis of ectopic ACTH secretion.

ACTH Syndrome, Ectopic↗
PubMed2005

Na(+), K(+)-ATPase content in skeletal muscle of dogs with pituitary-dependent hyperadrenocorticism.

Several hormones regulate Na(+), K(+)-ATPase content in the muscle cell membrane, which is essential for maintaining muscle cell excitability. Chronic glucocorticoid excess is associated with muscle weakness and reduced endurance. We hypothesized that chronic glucocorticoid excess affects Na(+), K(+)-ATPase content in canine skeletal muscle, and contributes to reduced endurance and muscle weakness associated with pituitary-dependent hyperadrenocorticism (PDH) in dogs. Therefore, Na(+), K(+)-ATPase content in skeletal muscle was evaluated before and after hypophysectomy and hormone replacement (cortisone and l-thyroxin) in dogs with PDH (n=13), and in healthy controls (n=6). In addition, baseline and exercise-induced changes in plasma electrolyte concentrations and acid-base balance were evaluated before and after hypophysectomy in dogs with PDH. Na(+), K(+)-ATPase content of gluteal muscle in dogs with PDH was significantly lower than in control dogs (201+/-13pmol/g versus 260+/-8pmol/g wet weight; P<0.01). Similar differences were found in palatine muscle. After hypophysectomy and on hormone replacement, Na(+), K(+)-ATPase was increased (234+/-7pmol/g wet weight). Both plasma pH and base excess in dogs with PDH (7.44+/-0.01; 1.7+/-0.6mmol/l, respectively) were significantly higher (P<0.05) than after hypophysectomy and hormone replacement (7.41+/-0.01; -0.2+/-0.4mmol/l, respectively). Exercise induced respiratory alkalosis, but did not result in hyperkalemia in dogs with PDH. In conclusion, chronic glucocorticoid excess in dogs with PDH is associated with decreased Na(+), K(+)-ATPase content in skeletal muscle. This may contribute to reduce endurance in canine PDH, although dogs with PDH did not exhibit exercise-induced hyperkalemia. Na(+), K(+)-ATPase content normalized to values statistically not different from healthy controls after hypophysectomy and hormone replacement.

Adrenocortical Hyperfunction↗
PubMed2005

Cortisol, aldosterone, cortisol precursor, androgen and endogenous ACTH concentrations in dogs with pituitary-dependant hyperadrenocorticism treated with trilostane.

Trilostane is thought to be a competitive inhibitor of the 3beta-hydroxysteroid dehydrogenase (3beta-HSD), an essential enzyme system for the synthesis of cortisol, aldosterone and androstenedione. Due to its reliable clinical efficacy, trilostane is increasingly used to treat dogs with pituitary-dependant hyperadrenocorticism (PDH). The objective of our study was to investigate the effect of trilostane on precursor concentrations located before (17alpha-OH-pregnenolone, dehydroepiandrostenedione) and after (17alpha-OH-progesterone, androstenedione, 11-deoxycortisol, 21-deoxycortisol) the proposed enzyme inhibition, on end products of steroid biosynthesis (cortisol and aldosterone) and on endogenous adrenocorticotrophic hormone (ACTH) concentrations in dogs with PDH. Hormones of the steroid biosynthesis pathway were evaluated in 15 dogs before and 1h after injection of synthetic ACTH prior to (t(0)), in weeks 1-2 (t(1)) and in weeks 3-7 (t(2)) of trilostane treatment. Endogenous ACTH concentrations were measured at the same time points before performing the ACTH stimulation test. During trilostane treatment baseline and post-stimulation cortisol concentrations decreased significantly. Baseline serum aldosterone levels showed a significant increase; post-stimulation values decreased. Baseline and post-stimulation 17alpha-OH-pregnenolone and dehydroepiandrostenedione concentrations increased significantly. 17alpha-OH-progesterone and androstenedione levels did not change. Post-stimulation 21-deoxycortisol concentrations decreased significantly, baseline 11-deoxycortisol concentrations increased significantly. Endogenous ACTH levels showed a significant increase. The significant increase in 17alpha-OH-pregnenolone and dehydroepiandrostenedione concentrations confirms an inhibitory effect of trilostane on the 3beta-HSD. Since 17alpha-OH-progesterone concentrations did not change, but cortisol concentrations markedly decreased, trilostane seems to influence additional enzymes of the hormone cascade, like the 11beta-hydroxylase and possibly the 11beta-hydroxysteroid dehydrogenase.

17-alpha-Hydroxypregnenolone↗