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PubMed1990

Effects of repetitive administration of corticotropin-releasing hormone combined with lysine vasopressin on plasma adrenocorticotropin and cortisol levels in secondary adrenocortical insufficiency.

To examine the functioning of the hypothalamo-pituitary-adrenocortical axis in secondary adrenocortical insufficiency, we administered 100 micrograms synthetic human CRH, iv, plus 10 U lysine-8-vasopressin (LVP), im, three times daily for 3 consecutive days. The changes in plasma ACTH and cortisol levels during the administration and the response to an insulin tolerance test (ITT) conducted before and after the administration were determined. In three patients with isolated ACTH deficiency, basal plasma ACTH and cortisol levels were undetectablly low, and there was no response noted in the ITT or during CRH-LVP administration throughout the observation period. In four patients with adrenocortical insufficiency who had undergone successful transsphenoidal microadenomectomy for Cushing's disease and in six patients who had undergone curative unilateral adrenalectomy for Cushing's syndrome, basal plasma ACTH levels were low, but responded considerably to both stimulation tests. Along with the 3 days of CRH-LVP stimulation, however, neither the peak nor the time-integrated ACTH response was significantly enhanced, because of the variability of the responses among the patients. Compared with the ACTH response on the last day of CRH-LVP stimulation, the subsequent ITT tended to induce a lower ACTH response in the post-Cushing's disease patients and a higher response in the post-Cushing's syndrome patients. Regarding the plasma cortisol levels, the basal, peak, and integrated responses tended to increase daily during CRH-LVP administration. Conversely, the ITT after repetitive CRH-LVP administration induced a higher cortisol response than the test before CRH-LVP administration in the post-Cushing's disease patients. No serious complications were noted in any of the patients during or after the treatment. The present findings indicate that 1) repetitive administration of CRH in combination with LVP is a safe and valuable provocation test to examine the pituitary ACTH reserve and the integrity of the pituitary-adrenocortical axis; 2) isolated ACTH deficiency is usually due to a defect at the pituitary level; 3) with respect to adrenocortical responsiveness, post-Cushing's disease patients show a better accumulation of the provocative effect than do post-Cushing's syndrome patients; and 4) both hypothalamic and pituitary dysfunction are responsible for adrenal hypofunction in patients after hypercortisolemia, but post-Cushing's syndrome patients (especially those with a short period of hypercortisolemia) appeared to have less impairment of hypothalamic ACTH-releasing activity than post-Cushing's disease patients.

Adrenal Cortex↗

PubMedDate not supplied

[Addison's disease: principal clinical associations and description of natural history of the disease].

From 1967 to 1988 we studied 75 cases of Addison's disease (AD). An autoimmune etiology was found in 68%, while previous tubercular infection was demonstrated in 21% of the cases; minor causes were involved in 3%, and in 8% of the cases the disease remained of unknown origin. Autoimmune adrenalitis has become the most frequent cause of AD as a consequence of decreased tubercular infection. Autoimmune AD prevailed in children or in young people, and tubercular AD in adults. The finding of calcifications in adrenals and/or other organs was the specific diagnostic sign for the identification of tubercular forms. On the other hand, the finding of circulating adrenal autoantibodies (AA) and/or other organ specific autoantibodies was the fundamental diagnostic marker of autoimmune forms. In 72% of the cases autoimmune AD is associated with other organ-specific autoimmune diseases. Subjects with AA but without clinical signs of hypoadrenalism were considered to have "potential AD", because they showed a high risk of developing clinical hypoadrenalism. This condition develops over a long period characterized by different stages of subclinical adrenal hypofunction. Steroid cell autoantibodies (StCA) are frequently detectable in patients with autoimmune AD, in whom they are markers of autoimmune premature ovarian failure. The study of StCA-positive cases without hypogonadism will be important to clarify whether or not these autoantibodies could be markers of potential autoimmune hypogonadism.

Addison Disease↗

PubMed1998

Adrenal insufficiency in an adult on inhaled corticosteroids; recovery of adrenal function with inhaled nedocromil sodium.

BACKGROUND: Whereas oral corticosteroids and high-dose inhaled corticosteroids may be associated with suppression of the hypothalamic-pituitary-adrenal axis, medium-dose inhaled corticosteroids have not been reported to be associated with clinically significant adrenal insufficiency in the adult. OBJECTIVE: A case study of adrenal responsiveness after prolonged medium-dose inhaled corticosteroids and after replacement of steroid therapy by inhaled nedocromil sodium is described. METHODS: Standard 250-microg dose ACTH (cosyntropin) stimulation tests were followed after replacement of inhaled triamcinolone acetonide therapy by nedocromil sodium. RESULTS: A 55-year-old woman who had been on inhaled triamcinolone acetonide, 1600 microg/day for 12 years, presented with symptoms of adrenal hypofunction upon inhaled corticosteroid taper. An ACTH stimulation test confirmed adrenal insufficiency. She was switched to inhaled nedocromil sodium with improvement in her clinical syndrome and normalization of her ACTH stimulation test. CONCLUSION: Withdrawal from prolonged use of inhaled medium-dose corticosteroids may be associated with clinically significant adrenal insufficiency in adults. Steroid sparing agents may be considered for those on long-term inhaled corticosteroid therapy.

Administration, Inhalation↗

PubMed1986

Corticosteroids for rheumatic disease. 1. Physiology, pharmacology, and therapeutic strategies.

Of the corticosteroid preparations available, the intermediate-acting agents are the preparations most commonly used in the rheumatic diseases. Careful tailoring of dosage is important to avoid adrenal atrophy and signs of adrenocortical hypofunction. The best regimen in a given patient depends on the amount of antiinflammatory and immunosuppressive activity required. The therapeutic strategies in use include pulse therapy, daily high-dose therapy, daily low-dose therapy, and alternate-day dosing. The latter two methods are preferable because of the decreased likelihood of adverse reactions, yet are not sufficient in cases of fulminant systemic inflammatory processes.

Adrenal Cortex↗

PubMed1979

Adrenocortical suppression in dogs on daily and alternate-day prednisone administration.

Three groups of eight normal dogs each were orally given prednisone at doses of 0.22 mg/kg of body weight/day, 0.55 mg/kg/day, or 1.1 mg/kg on alternate mornings. Four dogs served as nontreated controls. Samples were obtained from members of each group to determine baseline serum cortisol and ACTH-stimulated cortisol values and histologic features in the lateral thoracic skin before prednisone administration, and after 1, 2, 3, and 4 weeks of administration. Some animals from each group were necropsied after 1, 2, 3, and 4 weeks of prednisone administration. Each course of prednisone administration resulted in adrenocortical atrophy and hypofunction, but adrenocortical suppression was less severe and slower in onset in the group given prednisone on alternate days. Extra-adrenal effects observed were atrophy of the skin and focal, fatty change of the liver. These changes were most evident in dogs given daily pharmacologic doses of prednisone (0.55 mg/kg/day). Fewer extra-adrenal effects were observed in dogs given alternate-day therapy. There were no extra-adrenal lesions in the dogs given equivalent glucocorticoid replacement doses (0.22 mg/kg/day).

Administration, Oral↗

PubMed2003

Dynamic evaluation of adrenal hypofunction.

The diagnosis of adrenal hypofunction is suggested by clinical features and confirmed by biochemical testing. The characteristic features of acute primary adrenal insufficiency include orthostatic hypotension, fever, and hypoglycemia. By contrast, patients with chronic primary adrenal insufficiency have a longer history of malaise, as well as fatigue, anorexia, diarrhea, weight loss, joint and back pain, and darkening of the skin. While the clinical presentation of secondary adrenal insufficiency is similar to that of primary adrenal insufficiency, there is no hyperpigmentation, and hypotension and orthostasis are less pronounced. As a result, patients often present with vague, non-specific symptoms and the diagnosis may not be entertained. There is considerable debate regarding the best dynamic test for the diagnosis of adrenal hypofunction. Optimally, a screening test would be economic, convenient and safe. It would have high sensitivity and specificity based on consensus criteria for interpretation. Unfortunately, to date no test meets all of these criteria. Measurement of basal cortisol is an inexpensive and convenient screening test that can include (< 3 microg/dl; 83 nmol/l) or exclude (> 19 microg/dl; 524 nmol/l) adrenal insufficiency. However, most patients will have intermediate values and will require dynamic testing. This review discusses the use of metyrapone, insulin, CRH and synthetic ACTH 1-24 as provocative agents for cortisol secretion. Although the insulin and metyrapone stimulation tests have the advantage of testing the entire hypothalamic-pituitary-adrenal axis, they are cumbersome and carry more risk than the other tests. The 250 microg ACTH test works well to identify primary adrenal hypofunction, but can only detect secondary adrenal hypofunction when there is sufficient time for the glands to atrophy because of reduced endogenous ACTH stimulation. The 1 microg ACTH test has been advocated in the setting of possible secondary adrenal insufficiency, but its widespread use has been mitigated by the lack of a commercial preparation of this small dose and controversy regarding diagnostic criteria. Ultimately, the choice of test should be individualized for each patient, with knowledge of the available reference assays and the vagaries of each test.

Adrenal Cortex Function Tests↗

PubMed1976

The function of the anterior pituitary-adrenal cortex axis in hyperemesis gravidarum.

In order to study the function of the pituitary-adrenal axis, serum ACTH and cortisol levels were estimated before and after insulin induced hypoglycaemia in nine women with hyperemesis gravidarum, seven women in normal early pregnancy and in eight non-pregnant controls. Before hypoglycaemia, the basal ACTH level in the hyperemesis group (102-4+/-62-9 pg/ml) was higher than in normal early pregnancy (67-5+/-19-2 pg/ml; p less than 0-05) or in non-pregnant controls (54-8+/-25-2 pg/ml; less than 0-01). Correspondingly, the mean cortisol value in hyperemesis (0-47+/-0-16 mumol/l) was higher than in normal early pregnancy (0-39+/-0-10 mumol/l; p greater than 0-05) or in non-pregnant controls (0-32+/-0-13 mumol/l; p less than 0-01). After insulin the elevation of ACTH (p greater than 0-05) and cortisol (p less than 0-01) was observed in every group. The level of ACTH and cortisol was highest in hyperemesis group. Our results do not support the idea that hypofunction of the pituitary-adrenal axis contributes to the aetiology or pathogenesis of hyperemesis gravidarum. The high ACTH level might be evidence of the psychia instability of hyperemesis gravidarum patients.

Adolescent↗

PubMedDate not supplied

Congenital and non-congenital depigmentation.

The hypofunction of melanocytes results in congenital and noncongenital depigmentation. Congenital depigmentation can be further divided into two groups; the first is depigmentation caused by loss of melanization in premelanosomes represented by oculocutaneous albinism; the second group is congenital decrease of melanocytes represented by nevus dipigmentosus. In contrast, acquired progressive depigmentation represented by vitiligo vulgaris and Sutton's leukoderma is characterized by the loss of premelanosome synthesis. The pathogenesis of these three major types of melanogenic defects has been further discussed with the current clinical, biological and immunological view of melanogenesis.

Adrenal Cortex Hormones↗

PubMed1988

[Functions of the sympathetic-adrenomedullar system and adrenocortex in patients with vibration syndrome. Investigations of plasma and urine catecholamine and plasma cortisol during cold exposure].

Much discussion has been made as to whether vibration syndrome is a peripheral or systemic disorder. We studied plasma and urine norepinephrine and epinephrine, and plasma cortisol under resting and cold exposure conditions (7 degrees C cold room for 30 min). The subjects were 20 patients with vibration syndrome and with a history of Raynaud's phenomenon, 20 patients with vibration syndrome without a history of Raynaud's phenomenon, and 20 healthy controls. They were all males and the three groups were matched by age. The following results were obtained. 1. Mean temperatures of finger skin in the patient groups under resting and cold exposure conditions were lower than in the control group. Mean systolic and diastolic blood pressures in the patient groups under both conditions were higher than in the control group. Mean values of blood pressure change produced by cold exposure in the patient groups were lower than in the control group. Some of these differences were statistically significant (p less than 0.05 or p less than 0.01). 2. Mean levels of plasma norepinephrine in the patient groups under resting and cold exposure conditions were significantly higher (p less than 0.01 or p less than 0.05) than in the control group. This finding indicates that the patients with vibration syndrome had hyperfunction of the sympathetic nervous system. Mean levels of urine norepinephrine in the patient groups were not significantly different from the control group. 3. Mean levels of plasma epinephrine in the patient groups under resting and cold exposure conditions were lower than in the control group. The differences between the patient groups and the control group were significant (p less than 0.05 or p less than 0.01) in the cold exposure condition. This finding suggests that the patients with vibration syndrome had hypofunction of the adrenomedullar system. Urine epinephrine in the patient groups was not significantly different from the control group. 4. Mean levels of cortisol in the patient groups were higher than in the control group. The difference in cortisol level between the group of patients without Raynaud's phenomenon and the control group was significant (p less than 0.01) in the resting condition. This finding may suggest that the patients with vibration syndrome had hyperfunction of the adrenocortex. The foregoing data support the hypothesis that vibration syndrome is a systemic dysfunction, which includes disorders of the sympathetic-adrenomedullar system and adrenocortex.

Adrenal Cortex↗

PubMed2003

Ectopic adrenocorticotropin (ACTH) and corticotropin-releasing hormone (CRH) production in the adrenal gland: basic and clinical aspects.

The hypothalamic-pituitary-adrenal (HPA) axis is integrated in the human stress system and controls the metabolism of many cell systems in the body. Therefore, hypofunction or hyperfunction of the HPA axis potentially threatens the life of the whole organism. Noncontrolled overproduction of its key regulators, CRH and ACTH, causes dysfunction of the stress system. Ectopic secretion of these compounds may be part of extraadrenal paraneoplastic syndromes caused by various benign or malignant tumors. However, ectopic ACTH and CRH may originate from the adrenal itself. A local CRH/ACTH system exists in the normal human adrenal medulla. Overproduction of CRH and ACTH has been documented in pheochromocytomas causing Cushing's syndrome. Finally, ectopic production of ACTH causing Cushing's syndrome has also been demonstrated in adrenocortical cells. This suggests a marked plasticity within the HPA axis and the neuroendocrine cell system.

Adrenal Cortex Neoplasms↗

PubMed2000

Deletion of tyrosine hydroxylase gene reveals functional interdependence of adrenocortical and chromaffin cell system in vivo.

Catecholamines are produced in the medulla of the adrenal gland and may participate in the intraglandular regulation of its cortex. We analyzed the adrenal structure and function of albino tyrosine hydroxylase-null (TH-null) mice that are deficient in adrenal catecholamine production. Adrenal catecholamines were markedly reduced, and catecholamine histofluorescence was abrogated in 15-day-old TH-null mice. Chromaffin cell structure was strikingly altered at the ultrastructural level with a depletion of chromaffin vesicles and an increase in rough endoplasmic reticulum compared with wild-type mice. Remaining chromaffin vesicles lined up proximally to the cell membrane in preparation for exocytosis providing a "string-of-pearls" appearance. There was a 5-fold increase in the expression of proenkephalin mRNA (502.8 +/- 142% vs. 100 +/- 17.5%, P = 0.016) and a 2-fold increase in the expression of neuropeptide Y (213.4 +/- 41.2% vs. 100 +/- 59.9%, P = 0.014) in the TH-null animals as determined by quantitative TaqMan (Perkin-Elmer) PCR. Accordingly, immunofluorescence for met-enkephalin and neuropeptide tyrosine in these animals was strongly enhanced. The expression of phenylethanolamine N-methyl transferase and chromogranin B mRNA was similar in TH-null and wild-type mice. In TH-null mice, adrenocortical cells were characterized by an increase in liposomes and by tubular mitochondria with reduced internal membranes, suggesting a hypofunctional state of these steroid-producing cells. In accordance with these findings, plasma corticosterone levels were decreased. Plasma ACTH levels were not significantly different in TH-null mice. In conclusion, both the adrenomedullary and adrenocortical systems demonstrate structural and functional changes in catecholamine-deficient TH-null mice, underscoring the great importance of the functional interdependence of these systems in vivo.

Adrenal Glands↗

PubMed2001

[Hypothalamo-hypophyseal-adrenal hypofunction caused by the use of bleaching cosmetics in Senegal].

Cosmetic use of bleaching agents to clear skin is widespread among black West African women. In Dakar, most products used for whole body applications contain highly potent corticosteroids. Whereas cutaneous adverse effects are well described, little is known about possible systemic consequences. In order to assess transcutaneous absorption of glucocorticoids, hypothalamo-pituitary-adrenal axis functionality can be tested. We measured plasma cortisol concentration at 8 h and 1 h after intramuscular injection of 250 micrograms of cosyntropin (Synacthen) in 12 women with a more than 10 years use of bleaching agents. Cortisol at 8 H was also measured in 9 non exposed women without disease or treatment able to disturb glucocorticoids metabolism. All controls had 8 H cortisol concentration (mean = 521 +/- 113 nmol/l) above the minimal normal level considered by our laboratory. The 8 H cortisol concentrations were under the minimal normal level in 9 exposed women and the overall mean value was significantly lower than the one observed in controls (264 +/- 81 nmol/l; p < 0.001). After cosyntropin, cortisol concentrations were elevated among all exposed women (469 +/- 196 nmol/l), and less so in 3 of them. Most of the bleaching agents users present a functional inertia of hypothalamo-pituitary adrenal axis. While there is no absolute evidence for risk of stress-induced adrenal insufficiency, our results show conclusively that an excessive corticosteroids charge among users who could be exposed to systemic adverse effects.

Absorption↗

PubMed1991

[Mycoses and adrenocortical function. New pathogenetic aspects of adrenal hypofunction].

Three aspects of the possible relationships between adrenocortical function and mycoses are considered: a) abnormal steroid hormone concentrations that may favour onset and/or clinical course of mycotic diseases; b) presence of granulomas in the adrenal glands during systemic mycoses; c) effects of antifungal drugs on steroidogenesis. Glucocorticoids are potent inhibitors of T-lymphocyte proliferation, in that they affect both the production of IL-1 from monocytes/macrophages and IL-2 from activated T-lymphocytes. Consequently opportunistic fungal infections are frequently observed in patients with chronic hypercortisolism (Cushing's syndrome) and in particular in those under chronic treatment with corticoids. On the other hand, mucocutaneous candidiasis is a prominent feature of the autoimmune polyglandular syndrome type I, characterized by adrenal insufficiency, hypoparathyroidism and mucocutaneous candidiasis. Its onset is usually at childhood, first with symptoms and signs of the fungal infection and then with those of endocrine failure. It is a complex disorder, familiar or sporadic, not linked to particular HLA haplotype, potentially associated with other autoimmune diseases (endocrine and not), thus forming the so called candidiasis endocrinopathy syndrome (CES). Adrenal involvement is very frequent in systemic mycoses, such as histoplasmosis (Histoplasma capsulatum), cryptococcosis (Cryptococcus neoformans), and paracoccidioidomycosis. From the pathogenetic view point, corticostatins-defensins may play a role. They are a family of recently discovered cationic peptides, that are able to inhibit adrenal steroidogenesis by interfering with ACTH at the specific receptor level. The pharmacological effects of ketoconazole on adrenal (and gonadal) steroidogenesis are a focus of great interest. This compound has been demonstrated to be a potent inhibitor of cytochrome P450-dependent enzymes.(ABSTRACT TRUNCATED AT 250 WORDS)

Acquired Immunodeficiency Syndrome↗

PubMed2000

Dietary protein restriction stress in the domestic chicken (Gallus gallus domesticus) induces remodeling of adrenal steroidogenic tissue that supports hyperfunction.

The stress of dietary protein restriction in the immature domestic turkey (Meleagris gallopavo) induces adrenal steroidogenic hypofunction that is associated with an alteration in the proportion of density-dependent subpopulations of steroidogenic cells within the adrenal gland. In contrast, when imposed on immature chickens, this nutritional stressor induces long-term enhancement of adrenal steroidogenic function. However, whether this alteration in function is accompanied by a remodeling of chicken adrenal steroidogenic tissue as in the turkey is not known. To address this question, immature cockerels (2 weeks old) were fed established isocaloric synthetic diets containing either 20% (control) or 8% (restriction) soy protein for 4 weeks. Adrenal glands were processed for the isolation of defined, density-separable, adrenal steroidogenic cell subpopulations: three low-density adrenal steroidogenic cell subpopulations [LDAC-1 (rho = 1.0285-1.0430 g/ml), LDAC-2 (rho = 1. 0430-1.0485 g/ml), and LDAC-3 (rho = 1.0485-1.0500 g/ml)] and one high-density subpopulation [HDAC (rho = 1.0510-1.0840 g/ml)]. The steroidogenic function of these cell subpopulations was assessed. Protein restriction consistently, but differentially, enhanced maximal ACTH-induced corticosterone production by the subpopulations: values of LDAC-1, -2, and -3 and HDAC from protein restricted birds were, respectively, 116, 43, 33, and 20% greater than those of corresponding cell subpopulations from control birds. However, it had contrasting influences on maximal ACTH-induced aldosterone production by the cell subpopulations. Whereas the value of LDAC-1 from protein-restricted birds was 70% greater than that from control birds, the values for LDAC-2 and -3 were not different from those of the control, and the value for HDAC was 22% less than that of the control. Protein restriction also altered the cell subpopulation composition of the adrenal gland: compared to control, it increased the proportion of LDAC-1 by 46% and decreased the proportion of LDAC-3 and HDAC by 34 and 20%, respectively. Thus, dietary protein restriction increased the proportion of cells (i.e., LDAC-1) having the greatest enhancement in corticosteroid production. This pattern of remodeling of chicken adrenal steroidogenic tissue in response to dietary protein restriction contrasts sharply with the pattern that occurs in another galliform species, the domestic turkey.

Adrenal Cortex Hormones↗

PubMed2002

Adrenal gland hypofunction in active polymyalgia rheumatica. effect of glucocorticoid treatment on adrenal hormones and interleukin 6.

OBJECTIVE: To evaluate hypothalamic-pituitary-adrenal (HPA) axis function in patients with recent onset polymyalgia rheumatica (PMR) not previously treated with glucocorticoids; and to detect possible correlations between adrenal hormone levels, interleukin 6 (IL-6), and other acute phase reactants at baseline and during 12 months of glucocorticoid treatment. METHODS: Forty-one PMR patients of both sexes with recent onset disease and healthy sex and age matched controls were enrolled into a longitudinal study. Patients were monitored for serum cortisol, dehydroepiandrosterone sulfate (DHEAS), androstenedione (ASD), and clinical and laboratory measures of disease activity such as C-reactive protein and IL-6 concentrations at baseline and after 1, 3, 6, 9 and 12 months of glucocorticoid treatment. To assess dynamic HPA axis function, serum cortisol and plasma adrenocorticotropic hormone (ACTH) levels were evaluated in another 8 patients with recent onset PMR not treated with glucocorticoid in comparison to controls after challenge with ovine corticotropin releasing hormone (oCRH) test. In addition, serum cortisol and 17-hydroxyprogesterone (17-OHP) levels were evaluated after stimulation with low dose (1 microg) intravenous ACTH. RESULTS: Serum cortisol and ASD levels of all PMR patients at baseline did not differ from controls. During followup, cortisol levels dipped at one and 3 months. Serum DHEAS levels in all patients were significantly lower than in controls at baseline. In female PMR patients a significant correlation was found at baseline between cortisol levels and duration of disease. Serum concentrations of IL-6 at baseline were significantly higher in PMR patients than in controls. During 12 months of glucocorticoid treatment IL-6 levels dropped significantly at one month; thereafter they remained stable and did not increase again despite tapering of the glucocorticoid dose. After oCRH stimulation, a similar cortisol response was found in patients and controls. After ACTH administration, a significant cortisol peak was detected in patients and controls, whereas no significant difference in cortisol area-under-the-curve (AUC) was found between the groups. In contrast, ACTH induced a significantly higher (p < 0.05) peak of 17-OHP and AUC in PMR patients than in controls. CONCLUSION: This study found reduced production of adrenal hormones (cortisol, DHEAS) at baseline in patients with active and untreated PMR. The defect seems mainly related to altered adrenal responsiveness to the ACTH stimulation (i.e., increased 17-OHP), at least in untreated patients. The 12 month glucocorticoid treatment of patients reduced the production of inflammatory mediators (i.e., IL-6) in a stable manner that persisted after glucocorticoids were tapered.

17-alpha-Hydroxyprogesterone↗