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PubMed2002

Parathyroid hormone secretion in chronic human endogenous hypercortisolism.

Osteoporosis is a common manifestation of Cushing's syndrome, but the mechanisms responsible for this abnormality have not been defined. With the objective of analyzing parathyroid hormone (PTH) secretion in chronic hypercortisolism (CH), we evaluated 11 healthy subjects and 8 patients with CH, 6 with Cushing's disease and 2 with adrenal adenoma. These volunteers were submitted to tests of PTH stimulation through hypocalcemia (EDTA), PTH suppression through hypercalcemia (iv and oral calcium), and evaluation of bone mineral density (BMD) by DEXA. During the test of PTH stimulation, the calcium and magnesium concentrations of the normal and CH groups were similar. Patients with CH showed an increased PTH response to the hypocalcemic stimulus compared to controls. PTH values were significantly higher in the CH group at 70 (17.5 +/- 3.5 vs 10.2 +/- 1.3 pmol/l, P = 0.04), and 120 min (26.1 +/- 5.9 vs 11.3 +/- 1.9 pmol/l, P = 0.008) of EDTA infusion. The area under the curve for PTH during EDTA infusion was also significantly higher in patients with CH than in normal subjects (1867 +/- 453 and 805 +/- 148 pmol l(-1) 2 h(-1), P = 0.02). During the test of PTH suppression, calcium, magnesium and PTH levels of the patients with hypercortisolism and controls were similar. BMD was decreased in patients with hypercortisolism in the spine (0.977 +/- 0.052 vs 1.205 +/- 0.038 g/cm2 in controls, P<0.01). In conclusion, our results show that subjects with CH present decreased bone mass mainly in trabecular bone. The use of dynamic tests permitted the detection of increased PTH secretion in response to a hypocalcemic stimulus in CH patients that may probably be involved in the occurrence of osteoporosis in this state.

Adenoma↗
PubMed1975

Uptake ratio of (19-1311) cholesterol by adrenal glands as observed by a scintigraphic method.

The adrenal scintigram was performed after administration of [19-131I] cholesterol. A high/low ratio of both adrenal glands was calculated to evaluate whether there is a difference between the left and right sides in adrenal diseases. During scanning, information was stored in a 64 X 64 matrix and then punched out on a computer compatible paper tape. This paper tape was processed with a small digital computer. The areas of interest were selected over adrenal glands. The computer decided mean counts per unit area. After subtraction of background counts, a high/low ratio of adrenal gland was calculated. In five patients with Cushing's syndrome due to bilateral hyperplasia, a high/low ratio ranged from 1.0 to 2.0. In four patients with primary aldosteronism due to adenoma, a high/low ratio ranged from 1.33 to 4.0. This method may be useful to differentiate bilateral hyperplasia from unilateral adrenocortical adenoma.

Adenoma↗
PubMed1980

Plasma concentrations of 18-hydroxy-11-deoxycorticosterone and 18-hydroxycorticosterone simultaneously measured in normal subjects and adrenocortical disorders.

A method for the simultaneous measurement of 18-hydroxy-11-deoxycorticosterone (18-OH-DOC) and 18-hydroxycorticosterone (18-OH-B) in human peripheral plasma has been developed. The present method consists of extracting plasma with dichloromethane, separating the 18-OH-DOC and 18-OH-B from other steroids on a Sephadex LH-20 column and quantitating each steroid by radioimmunoassay. The mean plasma level of 18-OH-DOC at 8:00 a.m. was 8.2 +/- 3.9 ng/100 ml (mean +/- S.D.) in normal males. It was 7.8 +/- 2.6 ng/100 ml in the follicular phase of normal females and 11.5 +/- 2.8 ng/100 ml in the luteal phase. The corresponding level of 18-OH-B in normal males was 10.3 +/- 4.2 ng/100 ml and in the follicular and luteal phases of normal females was 12.4 +/- 4.5 ng/100 ml and 13.8 +/- 4.1 ng/100 ml, respectively. No sex differences nor difference between the phases of the menstrual cycle was confirmed. Plasma levels of the two steroids were not rarely high in patients with Cushing syndrome due to adrenocortical hyperplasia and carcinoma, primary aldosteronism, idiopathic hyperaldosteronism and congenital 17 alpha-hydroxylase deficiency, while they were usually within the normal range in cases of Cushing syndrome due to adrenocortical adenoma. These steroid levels were significantly low in patients with Addison's disease.

18-Hydroxycorticosterone↗
PubMed1975

The pituitary-adrenal system of the genetically obese (ob/ob) mouse.

Adult genetically obese (ob/ob) mice which are characterized by adrenal hypertrophy and increased secretion of corticosteroids have considerably increased levels of ACTH in the pituitary gland. At 5 weeks of age there is no difference in the pituitary ACTH content of lean and obese animals and dietary restriction, sufficient to maintain body weight at normal values, reduces the pituitary ACTH content of adult obese mice from 14 times the level found in lean litter-mate controls to almost normal values. Using an in-vitro perifusion system, the release of ACTH from isolated pituitary glands was studied. Pituitaries from lean and obese mice responded similarly to stimulation with a crude extract of hypothalamic tissue containing coticotrophin releasing factor (CRF). The CRF content of the hypothalamus in both groups appears to be similar. In contrast with the high pituitary content, plasma values for ACTH in unstressed obese mice are not increased. The results are discussed in relation to other evidence for a hypothalamic disorder in ob/ob mice.

Adrenocortical Hyperfunction↗
PubMed1978

Hypothalamic corticotrophin releasing factor activity in dogs with pituitary-dependent hyperadrenocorticism.

Hypothalamic corticotrophin releasing factor (CRF) activity was determined in five dogs with spontaneous hyperadrenocorticism and in three control animals (one untreated, one treated with high doses of ACTH for 2 months and one treated with high doses of cortisone for 2 months). Hypothalamic CRF activity was low or undetectable in four dogs with Cushing's syndrome due to an adrenocortical tumour. The results are compatible with a pituitary origin for pituitary-dependent hyperadrenocorticism in the dog but are not conclusive; direct information about the rates of hypothalamic CRF secretion is required.

Adrenocortical Hyperfunction↗
PubMed1988

Effects of bromocriptine on corticotrophin, melanotrophin and corticosteroid secretion in dogs with pituitary-dependent hyperadrenocorticism.

Dogs with spontaneous pituitary-dependent hyperadrenocorticism were divided into two groups, one with normal plasma concentrations of alpha-MSH (normal alpha-MSH dogs, n = 26) and the other with high plasma concentrations of alpha-MSH (high alpha-MSH dogs, n = 14), on the presumption that high alpha-MSH concentrations indicated a parent cell of pars intermedia origin. The urinary corticoid/creatinine ratios of the high alpha-MSH dogs were significantly higher than those of the normal alpha-MSH dogs. The percentage decrease of the corticoid/creatinine ratios following dexamethasone administration was significantly higher in the normal alpha-MSH dogs than in the high alpha-MSH dogs. Dexamethasone resistance occurred in both the normal alpha-MSH dogs (4 out of 26) and the high alpha-MSH dogs (7 out of 14), indicating a relative rather than an absolute difference. The short-term effect of orally administered bromocriptine, at a dose (10 micrograms/kg body weight) known to be effective in lowering prolactin concentrations in dogs, was investigated by measuring concentrations of cortisol, ACTH and alpha-MSH in plasma at 4, 6 and 8 h after administration. Significant decreases were observed for cortisol in both groups and for alpha-MSH only in the high alpha-MSH dogs. The effect of 5 days of bromocriptine administration (10 micrograms at 12-h intervals) was assessed by measurements of urinary corticoid/creatinine ratios. Considering both groups as a whole, only the corticoid/creatinine ratios of the high alpha-MSH dogs decreased significantly on the first day of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex Hormones↗
PubMed1997

Residual pituitary function after transsphenoidal hypophysectomy in dogs with pituitary-dependent hyperadrenocorticism.

Pituitary function was assessed before and after transsphenoidal hypophysectomy in 39 dogs with pituitary-dependent hyperadrenocorticism (PDH). Anterior pituitary function was investigated using combined administration of four hypophysiotropic releasing hormones (corticotropin-releasing hormone (CRH), GHRH, GnRH, and TRH) with measurements of ACTH, cortisol, GH, LH, prolactin (PRL), and TSH Pars intermedia function was assessed by measurements of basal plasma alpha-MSH concentrations and adrenocortical function by baseline urinary corticoid/creatinine ratios. At eight weeks after hypophysectomy basal plasma ACTH, cortisol, GH, LH, PRL, and TSH concentrations were significantly lower than before surgery. In seven dogs with elevated alpha-MSH concentrations, the values returned to the normal level after surgery. In the combined anterior pituitary function test there were no plasma GH, LH, PRL, and TSH responses to stimulation, whereas plasma ACTH and cortisol responses were small but significant. Remission of hyperadrenocorticism was obtained in 35 dogs and recurrences occurred in 3 of these within 16 months postoperatively. At 8 weeks after hypophysectomy, these 3 dogs were not discernible, with respect to residual pituitary and adrenocortical function, from the 32 dogs with persisting remission. Urinary corticoid/creatinine ratios in the latter group of dogs did not increase during 22 months after hypophysectomy. In contrast to the presurgical findings, at 8 weeks after hypophysectomy there were significant positive correlations between baseline urinary corticoid/creatinine ratios and basal levels and responses for ACTH, indicating return to normal function of the pituitary-adrenocortical axis. It is concluded that among the adenohypophyseal cells present in the sella turcica after hypophysectomy, the corticotropes have a distinct behavior. Much more so than the other cell types, the unaffected corticotropes tend to remain functional, or a repressed reserve fraction of corticotropes may become functional. This may be due to the removal of the hypothalamic influence of a postulated corticotropin-release inhibiting factor or a diminished inhibitory influence of a postulated paracrine factor. The corticotropes may maintain normocorticism, but may also lead to mild recurrence after relatively long periods of remission.

Adrenocortical Hyperfunction↗
PubMed2001

Glucocorticoid and mineralocorticoid resistance/hypersensitivity syndromes.

Glucocorticoids and mineralocorticoids regulate diverse functions important to maintain central nervous system, cardiovascular, metabolic, and immune homeostasis. The actions of these hormones are mediated by their specific intracellular receptors: the glucocorticoid (GR) and mineralocorticoid (MR) receptors. Pathologic conditions associated with changes of tissue sensitivity to these hormones have been described. The syndrome of familial glucocorticoid resistance is characterized by hypercortisolism without Cushing's syndrome stigmata. The molecular defects of four kindreds and one sporadic case have been elucidated as inactivating mutations in the ligand-binding domain of GR. Two cases developed glucocorticoid resistance at the heterozygous state. In these patients, mutant receptors possessed transdominant negative activity upon the wild type receptor. Insensitivity to mineralocorticoids (which may also be caused by loss of function mutations of the MR gene) was found in one sporadic case and four autosomal dominant cases of Pseudohypoaldosteronism type 1. These included two frameshift mutations and a premature termination codon in exon 2, leading to gene products lacking the entire DNA- and ligand-binding domains, and a single base-pair deletion in the intron-5 splice donor site. Tissue hypersensitivity to glucocorticoids was recently hypothesized in patients with Human Immunodeficiency Virus (HIV) type-1 infection via the accessory proteins Vpr and Tat which enhance GR transactivation. Since HIV-1 long terminal repeat (LTR) and glucocorticoid-responsive promoters use the same set of coactivators, these proteins may stimulate HIV-1-LTR and glucocorticoid-inducible genes concurrently. The former may directly stimulate viral proliferation, while the latter may indirectly enhance viral propagation by suppressing the host immune system through glucocorticoid-mediated mechanisms.

Acquired Immunodeficiency Syndrome↗
PubMed2006

Plasma profiles of adrenocorticotropic hormone, cortisol, alpha-melanocyte-stimulating hormone, and growth hormone in dogs with pituitary-dependent hyperadrenocorticism before and after hypophysectomy.

The 6-h plasma profiles of adrenocorticotropic hormone (ACTH), cortisol, alpha-melanocyte-stimulating hormone (alpha-MSH), and GH were studied in 17 dogs with pituitary-dependent hyperadrenocorticism (PDH) before and after hypophysectomy. The aim of the study was to investigate the relation between the hormone profile characteristics and recurrence of PDH after surgery. The hormones were secreted in a pulsatile fashion. The basal plasma cortisol concentration and area under the curve (AUC) for cortisol were significantly higher in the PDH cases than in eight controls. The characteristics of the plasma profiles of ACTH and alpha-MSH were not significantly different between the PDH cases and the controls. In the PDH cases, less GH was secreted in pulses than in the controls, but the difference was not significant. The basal plasma cortisol concentration, the AUC for ACTH and cortisol, and the pulse frequency of ACTH and cortisol decreased significantly after hypophysectomy for the group of PDH cases. The basal plasma concentrations of ACTH and alpha-MSH, the AUC for alpha-MSH, and the characteristics of the plasma GH profiles of the PDH cases remained unchanged after hypophysectomy. No pulses of alpha-MSH were observed after hypophysectomy. The co-occurrence between the ACTH and cortisol pulses decreased significantly with hypophysectomy. The postoperative pulse frequency of ACTH was the only characteristic with predictive value for the recurrence of PDH after hypophysectomy. The results of this study demonstrate that ACTH, cortisol, alpha-MSH, and GH are secreted in a pulsatile fashion in dogs with PDH. Hypophysectomy effectively reduces the secretion of ACTH and cortisol. The presence of ACTH pulses after hypophysectomy is a risk factor for the recurrence of hyperadrenocorticism.

Adrenocortical Hyperfunction↗
PubMedDate not supplied

The efficacy of L-Deprenyl in dogs with pituitary-dependent hyperadrenocorticism.

Ten dogs with pituitary-dependent hyperadrenocorticism (PDH) received 2 mg/kg of L-Deprenyl once daily for 6 months. Monthly patient assessment consisted of evaluation of the owner's daily observation protocol, a standardized owner questionnaire, physical examination, CBC, biochemical profile, determination of the urine cortisol/creatinine ratio (UC/C), low-dose dexamethasone suppression (LDDS) test, corticotropin releasing hormone (CRH) test, and adrenal ultrasonography. At the beginning and the end of the study, an adrenocorticotropic hormone (ACTH) stimulation test and computed tomography also were performed. Two dogs developed neurologic signs and 2 dogs developed acute pancreatitis. An increase in activity, decrease in polyphagia, and decrease in panting were reported by 6, 4, and 2 owners, respectively. Seven owners believed that water intake decreased, but this was confirmed in only 3 dogs. Water intake increased in 2 dogs and remained unchanged in 5 dogs. The condition of the hair coat and skin improved in 2 dogs, worsened in 3, and remained unchanged in 5. Urine specific gravity, urine osmolality, ACTH test results, UC/C, and adrenal gland size did not change significantly throughout the study. In 4 of 8 dogs, LDDS was abnormal at the start of the study but normal at the end of the study, and in 2 dogs, the opposite occurred. Marked individual variation was noted in the CRH test, with a tendency for smaller increases in ACTH toward the end of the study. A marked increase in hypophyseal tumor size occured in 4 dogs. Treatment with L-Deprenyl resulted in improvement, deterioration, and stagnation of clinical signs in 2, 4, and 4 dogs, respectively. The results of this study indicate that L-Deprenyl cannot be recommended as the sole treatment for canine PDH.

Adrenal Glands↗
PubMedDate not supplied

Retrospective evaluation of urinary tract infection in 42 dogs with hyperadrenocorticism or diabetes mellitus or both.

A retrospective study was performed to determine the proportion of dogs with hyperadrenocorticism or diabetes mellitus or both that had urinary tract infection (UTI) and to describe clinical and laboratory findings. Dogs with these endocrine disorders were included if results of quantitative urine culture were available and dogs were not receiving antimicrobials. Dogs with positive urine cultures were considered to have UTI and dogs with negative urine cultures were used as controls. Information including history, clinical signs, physical examination findings, and results of laboratory tests and urine culture was extracted from all records. Findings in dogs with UTI were compared with control dogs. There were 101 dogs with hyperadrenocorticism or diabetes mellitus or both that met inclusion criteria; 42 (41.6%) had UTI and 59 (58.4%) did not. UTI was present in 46% of dogs with hyperadrenocorticism, 37% of dogs with diabetes mellitus, and 50% of dogs with both endocrine disorders. There was no association between endocrine group and occurrence of UTI. Escherichia coli was the most common bacteria isolated, and cultures from 29 dogs (69%) showed growth of this organism. Of dogs with UTI, <5% had stranguria, pollakiuria, or discolored urine, whereas 60% had pyuria and 69% had bacteriuria. We conclude that UTIs are common in dogs with hyperadrenocorticism, diabetes mellitus, or both diseases. Clinical signs of UTI, however, are uncommon and results of urinalysis may be normal. Therefore, it is appropriate to recommend urine culture as part of the evaluation of dogs with these endocrine disorders.

Adrenocortical Hyperfunction↗
PubMedDate not supplied

Trilostane therapy for treatment of pituitary-dependent hyperadrenocorticism in 5 cats.

Hyperadrenocorticism is a rare syndrome in cats. Current medical therapy is unsatisfactory and prognosis for long-term survival with surgical treatment is guarded. We report on 5 cats treated with the 3-beta hydroxysteroid dehydrogenase inhibitor trilostane. Diagnosis was confirmed in all cats by endocrine testing. Three cats had concurrent diabetes mellitus. Trilostane reduced clinical signs and improved endocrine test results in all cats, but insulin requirements did not change and all continued to have some signs of hypercortisolemia. Two died or were euthanized after 16 and 140 days, whereas 3 were still alive 6, 11, and 20 months after the start of trilostane therapy. Trilostane ameliorates clinical signs of feline hyperadrenocorticism, but more research is needed before it can be recommended for treatment.

3-Hydroxysteroid Dehydrogenases↗