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PubMed1977

[Experimental hypertension in rats and their adrenal activity].

The authors examined dynamically the arterial pressure and plasma activity of 11-hydroxycorticosteroids in two groups of rats with pure hypertension and with hypertension on the background of beta-adrenergic activity. There was an elevation of arterial pressure in both groups, less manifested in the rats, treated with beta blocker. The values after six months were equally high in both groups. The content of 11-hydroxycorticosteroids was increased with a maximum at the sixth month. The authors make an inference that beta blocker-obsidan lowers blood pressure, but does not affect the level of 11-hydroxycorticosteroidids in plasma.

11-Hydroxycorticosteroids↗
PubMed1984

[Bioelectric activity of the brain and glucocorticoid production in patients with hematologic malignancies].

A parallel study of bioelectrical activity of the brain and urine excretion of 17-hydroxycorticosteroids was carried out in 107 patients with various malignant tumors of hemopoietic tissue before, during and after treatment. In all of them, electroencephalography showed excitation of the hypothalamus, the central component of the hypothalamo-pituitary-adrenal system. Moreover, the patients revealed a significant increase in the excretion of 17-hydroxycorticosteroids that pointed to the activation of the peripheral component--the adrenal cortex. Activation of both central and peripheral components suggests that its intermediate component--the pituitary--is activated in patients with hemopoietic system neoplasms, too.

17-Hydroxycorticosteroids↗
PubMedDate not supplied

[Pathophysiological significance of the determination ofthe glucocorticoid concentration in bronchial secretions in children with bronchopulmonary diseases].

Simultaneous estimation of glucocorticoid content was carried out in bronchial secretion products and in blood plasma of 95 children with chronic bronchopulmonary pathology. 11-hydroxycorticosteroids were found in bronchial secretion product; its concentration depended on the type, phase of the disease and the character of bronchial mucose impairment. The highest content of 11-hydroxycorticosteroids was observed in purulent endo-bronchitis.

11-Hydroxycorticosteroids↗
PubMed1983

Cortisol in diabetic retinopathy.

Plasma cortisol levels and its metabolite-17-hydroxycorticosteroids from the urine of 53 patients were evaluated. These 53 patients had early and late stages of diabetic retinopathy. Values were compared with 30 cases of a control group. Plasma cortisol was found to be raised significantly in early as well as in advanced stages of retinopathy, while 17-hydroxycorticosteroid was significantly raised in earlier stages of diabetic retinopathy only. The findings suggest that increased plasma cortisol levels may take some part in the production of diabetic retinopathy.

17-Hydroxycorticosteroids↗
PubMedDate not supplied

[Changes in the concentration of various collagen fractions after electric stimulation and electrocoagulation of the rabbit amygdaloid body].

Content of catecholamines, 11-hydroxycorticosteroids, free and bound hydroxyproline in blood as well as metabolism of collagen in rabbit aorta wall were studied after electrostimulation and bilateral electrocoagulation of brain amygdaloid complex. The stimulation was shown to alter the content of adrenal gland hormones and activated the collagen metabolism in aorta wall. After electrocoagulation within the first month content of noradrenaline, 11-hydroxycorticosteroids and accumulation of collagen in aorta tissue were decreased.

11-Hydroxycorticosteroids↗
PubMedDate not supplied

[Different effects of kynurenines on rat liver tryptophan pyrrolase activity].

3-Hydroxyanthranilic, quinolinic and nicotinic acids/50 mg/kg, intraperitoneally/increased the content of rat blood plasma 11-hydroxycorticosteroids as well as the activity of liver tryptophane pyrrolase. After administration of anthranili and picolinic acids, elevation in 11-hydroxycorticosteroid content was not followed by an increase in the tryptophane pyrrolase activity. Picolinic acid diminished induction of tryptophane pyrrolase activity by hydroxycortisone and anthranilic acid dicc not affect the induction. Adrenalectomy prevented the increase in tryptophane pyrrolase activity after treatment with nicotinic, quinolinic and 3-hydroxyanthranilic acids. Prolonged augmentation of kynurenines in the organism might be a result of a mediated through corticosteroids increase in the tryptophane pyrrolase activity caused by elevation in the level of 3-hydroxyanthranilic, quinolinic and nicotinic acids.

11-Hydroxycorticosteroids↗
PubMedDate not supplied

[Biologically active substances during treatment of pulmonary hypertension with ATP infusions immediately after general anesthesia and surgery of hypervolemic congenital heart defects].

In 95 patients with hypervolemic congenital heart valve defects (42 with interventricular and interatrial septal defects, and 53 with patent ductus arteriosus) mixed venous blood levels of serotonin, histamine, adrenalin, noradrenaline, total 11-hydroxycorticosteroids were studied using spectrofluorimetry, cyclic adenosine- and guanosine monophosphate (cAMP and cGMP), prostaglandins E + A and F2 alpha and their interaction were assessed using radioimmunoassay and correlation analysis, respectively. Immediately after general anesthesia and surgical correction of septal defects using cardiopulmonary bypass adrenalin level was increased, while noradrenaline, cAMP, cGMP, prostaglandin E + A levels remained high. Similar pattern was observed in patients after arterial duct ligation. Mean pulmonary artery pressure was elevated in both groups of patients (above 4 kPa). Effective therapy of pulmonary hypertension with intravenous ATP infusions immediately after general anesthesia and elimination of septal defects (20 patients) was accompanied by a decline in noradrenaline, cGMP and total 11-hydroxycorticosteroid level (with adrenalin level increased), while after open arterial duct ligation (20 patients) it was followed by a drop in noradrenaline and prostaglandin F2 alpha level (with adrenalin level increased) and the activation of the interaction of biologically active substances aimed predominantly at attenuation of vasoconstrictor reactions in the lungs.

11-Hydroxycorticosteroids↗
PubMed1993

Corticotropin-releasing hormone stimulation following low-dose dexamethasone administration. A new test to distinguish Cushing's syndrome from pseudo-Cushing's states.

OBJECTIVE: The biochemical and phenotypic presentation of mild hypercortisolism in Cushing's syndrome is often indistinguishable from that seen in pseudo-Cushing's states such as depression. Both dexamethasone suppression and corticotropin-releasing hormone (CRH) stimulation tests have been used individually to distinguish these conditions, but neither approach has achieved a diagnostic accuracy greater than 85%. Therefore, we sought to develop a combined dexamethasone-CRH test that would take advantage of the altered sensitivity of patients with Cushing's syndrome to both dexamethasone and CRH and would achieve greater accuracy in the diagnosis of Cushing's syndrome. DESIGN: Prospective cohort study. SETTING: Tertiary care research hospital. PATIENTS: A total of 58 adults referred for evaluation of mild hypercortisolism (urine free cortisol level < 1000 nmol/d). The diagnosis of Cushing's syndrome was confirmed at surgery in 39 patients. The diagnosis of a pseudo-Cushing's state was made in 19 patients on the basis of extended follow-up (mean, 28 months) without progression of cushingoid features. INTERVENTION: The low-dose dexamethasone suppression test, the CRH stimulation test, and the CRH stimulation test started 2 hours after completion of low-dose dexamethasone suppression (the dexamethasone-CRH test) were performed in all patients. MAIN OUTCOME MEASURES: Sensitivity, specificity, and accuracy of the three procedures for diagnosis of Cushing's syndrome were calculated from plasma corticotropin, plasma cortisol, urine free cortisol, and urine 17-hydroxycorticosteroid values. RESULTS: The low-dose dexamethasone suppression test had 74% specificity, 69% sensitivity, and 71% diagnostic accuracy, using the standard criterion (17-hydroxycorticosteroid excretion level > 11.0 mumol/d on the second day of dexamethasone administration). With a urine free cortisol criterion for Cushing's syndrome of greater than 100 nmol/d, the low-dose dexamethasone suppression test had 100% specificity, 56% sensitivity, and 71% diagnostic accuracy. The CRH stimulation test without dexamethasone pretreatment had 100% specificity, 64% sensitivity, and 76% diagnostic accuracy. The diagnostic accuracy of the dexamethasone-CRH test for Cushing's syndrome was significantly greater than the accuracy of either the low-dose dexamethasone test or the CRH test alone (P < .01). A plasma cortisol concentration greater than 38 nmol/L measured 15 minutes after the administration of CRH correctly identified all cases of Cushing's syndrome and all cases of pseudo-Cushing's states (100% specificity, sensitivity, and diagnostic accuracy). CONCLUSION: The dexamethasone-CRH test is a more accurate test to distinguish Cushing's syndrome from pseudo-Cushing's states in patients with mild hypercortisolism.

17-Hydroxycorticosteroids↗
PubMed1977

[Urinary excretion of adrenaline, noradrenaline and 11-hydroxycorticoids under job stress (author's transl)].

The role of the sympathoadrenomedullary and adrenocortical systems has been assessed by measuring serially the urinary excretion of free adrenaline, noradrenaline and 11-hydroxycorticosteroids in 32 healthy men under two conditions of job stress: piece-work and assembly line. The urinary levels of two catecholamines and 11-hydroxycorticosteroids rose significantly in piece work and assembly line workers, compared with the values observed respectively during salaried and "ordinary" work. Identical results were obtained in the same workers after six months of stressor exposure to piece-work and assembly line conditions. The results support the assumption that long-term exposure of conditions of work stress significant effects on the function under study, this being in the same direction and of the same order of magnitude as that described during short-term exposure in other types of every-day stress and distress. The methodological and clinical implication of these results are discussed.

11-Hydroxycorticosteroids↗
PubMed1988

Studies of transformer repair workers exposed to PCBs: II. Results of clinical laboratory investigations.

Thirty-eight transformer repairmen currently exposed to polychlorinated biphenyls (PCBs), 17 former transformer repairmen, and 56 comparison workers not known to be exposed to PCBs were studied. Measurements were made of serum liver function tests, gamma-glutamyl transpeptidase (GGT), lipid profile, thyroid function tests, and other serum biochemistry; hemoglobin; white cell count; 24-hour excretion of delta-aminolevulinic acid, porphyrins, 17-hydroxycorticosteriods and 17-ketosteroids; sperm count; spirometry; and antipyrine half-life to evaluate microsomal mixed function oxidase induction. The total exposed group differed significantly from the comparison group in albumin, LDH, T4, T4-RT3 index, and actual/predicted FEV1. Significant differences among all three exposure groups were seen for albumin, T4, T4-RT3 index, and 17-hydroxycorticosteroid excretion. Differences in FEV1 were attributable to smoking. Significant correlations between serum PCBs and serum lipids were removed by adjustment for confounding variables. After adjustment for confounding variables, there was a statistically significant positive correlation between serum PCBs and GGT and a negative correlation between adipose PCBs and 17-hydroxycorticosteroid excretion. These may reflect subtle metabolic effects of PCBs.

Analysis of Variance↗
PubMed1996

Phenobarbital minimally alters plasma concentrations of losartan and its active metabolite E-3174.

Losartan, a selective angiotensin II (AT1) receptor antagonist for hypertension, is metabolized to an active carboxylic acid metabolite, E-3174, which has a longer half-life. To investigate the effects of induction of cytochrome P450 on the metabolism of losartan, we evaluated the effects of phenobarbital on the plasma profiles of losartan and E-3174 in 15 healthy male subjects. Ten subjects received a single 100 mg oral dose of losartan before and during phenobarbital administration (100 mg/day for 16 days), and five subjects received losartan before and during placebo. Urinary excretion of 6-beta-hydroxycortisol (relative to 17-hydroxycorticosteroids) was measured as an endogenous marker of cytochrome P450 induction. The geometric mean area under the plasma concentration-time curve ratios (with/without phenobarbital and 90% confidence intervals) for losartan and its metabolite (E-3174) were 0.795 (0.723, 0.875) and 0.799 (0.778, 0.820), respectively, indicating that phenobarbital treatment significantly but to a clinically minor extent reduced plasma concentrations of losartan and E-3174 (p<0.01). Half-life values of losartan and E-3174 were unchanged. The ratio of 6-beta-hydroxycortisol to 17-hydroxycorticosteroids doubled in the phenobarbital group (p < 0.001) and did not change appreciably in the placebo group.

Adult↗
PubMed1998

Secondary adrenal insufficiency associated with autoimmune disorders: a report of twenty-five cases.

OBJECTIVE: Addison's disease is frequently a component of autoimmune polyendocrinopathies while secondary adrenal insufficiency associated with autoimmune disorders is believed to be a rare event. We present a series of patients with secondary adrenal insufficiency coexisting with autoimmune diseases and/or antithyroid autoantibodies. DESIGN AND PATIENTS: Among a group of 102 patients with secondary adrenal failure of unknown origin diagnosed at the Department of Endocrinology of the Centre for Postgraduate Medical Education (Warsaw, Poland) we have identified a group with associated autoimmune disorders. Thyroid abnormalities occurred most frequently. Other diseases included insulin-dependent diabetes mellitus, pernicious anaemia, vitiligo, premature ovarian failure and autoimmune thrombocytopaenia. There were 23 women and one man aged 17-72 years at the time of investigation. Additionally, we included a woman with Addison's disease in whom the ACTH deficiency appeared 18 years after the onset of primary adrenal hypofunction. MEASUREMENTS: Pituitary-adrenal function tests comprised urinary excretion of 17-hydroxycorticosteroids in basal conditions and during a 2-day tetracosactrin test, plasma concentrations of ACTH and cortisol, and a 2-day metyrapone test (in eight cases). Thyroid function and immunity tests were: TSH, thyroxine, the antithyroglobulin, antimicrosomal and anti-peroxidase autoantibodies. Other endocrine studies included: serum LH, FSH and PRL. RESULTS: The 17-hydroxycorticosteroid values, both basally and during stimulation tests were consistent with a diagnosis of secondary adrenal insufficiency. Serum cortisol and plasma ACTH concentrations were low. In 14 patients primary hypothyroidism was confirmed by low T4 levels. In three patients subclinical primary hypothyroidism was revealed (elevated TSH levels). Three patients who had a past history of Graves' disease were euthyroid at the time of investigation. Twenty-three patients had antibodies against peroxidase. Most patients had gonadotrophins and PRL values within normal limits. CONCLUSIONS: The co-existence of autoimmune disorders with secondary adrenal insufficiency suggests an autoimmune aetiology for the ACTH deficiency.

Adolescent↗
PubMed2000

Metabolic and anthropometric consequences of interruption of highly active antiretroviral therapy.

BACKGROUND: HAART has been associated with metabolic abnormalities (hyperlipidemia, insulin resistance, alterations in cortisol metabolism) and fat redistribution. SETTING: A prospective study of 26 Caucasian men (median age 43.5 years) with HIV-1 viral loads < 500 copies/ml for 12 months while on highly active antiretroviral therapy (HAART) who interrupted treatment for a median of 7.0 weeks (range 4.9-10.3 weeks). Seventeen (65.4%) patients reported at least one fat redistribution symptom at baseline. METHOD: Serum lipids, glucose and insulin levels during an oral glucose tolerance test, 24-h urinary free cortisol and 17-hydroxycorticosteroids, and anthropometric parameters were measured before HAART cessation and prior to its reinstitution. RESULTS: When baseline values were compared with those obtained after HAART interruption (means +/- SD), there was a significant decrease in total cholesterol (194+/-47.3 versus 159+/-29.3 mg/dl; P < 0.0001), low density lipoprotein (LDL) cholesterol (114+/-32.6 versus 96+/-24.7 mg/dl; P = 0.0013), triglycerides (261+/-244.3 versus 185+/-165.4 mg/dl; P = 0.008), and 24-hour urinary 17-hydroxycorticosteroids (15+/-7.9 versus 5+/-2.5 mg/24 h, P < 0.0001) and a significant increase in 24-hour urinary free cortisol (45+/-34.1 versus 62+/-32.2 microg/24 h; P = 0.016). There were no significant changes in glucose or insulin levels or in anthropometric measurements. CONCLUSIONS: A relatively brief interruption of HAART resulted in significant improvements in total cholesterol, LDL cholesterol, and triglyceride levels. No changes were observed in insulin resistance profiles or anthropometric measurements, perhaps because of the brief duration of HAART interruption. These results suggest that hyperlipidemia and alterations in corticosteroid metabolism in the setting of HAART are a direct drug effect that reverses with drug withdrawal. However, glucose metabolism and fat redistribution do not change over the short term.

Adult↗
PubMed1977

Some metabolic effects of maximal exercise in the horse and adaptations with training.

The effects of intermittent maximal exercise (galloping) before and after a 10 week training programme were studied in 6 horses. Determinations were carried out on venous blood for packed cell volume, total plasma protein, glucose, glycerol, free fatty acids, lactate, 11-hydroxycorticosteroids, blood gases and pH. There were marked changes associated with galloping and some of these could be modified with training. The major findings included (i) an elevated blood glucose, (ii) a large increase in glycerol, which was greatest at 30 min post-exercise and was higher following training, (iii) smaller increases in free fatty acids following training, (iv) higher levels of lactate after training, (v) a marked fall in pH which was less after training, (vi) an increase in 11-hydroxycorticosteroids with possibly a more rapid return to resting levels following training. It was concluded that with maximal exercise in the horse both glycogen and free fatty acids served as important substrates for working muscle, and following training greater utilisation of both these substrates occurred.

Animals↗
PubMed1969

Comparison of depot tetracosactrin and corticotrophin gel.

Depot tetracosactrin has been compared with corticotrophin gel in 12 inpatients of a rheumatic diseases unit Every patient received one subcutaneous infection each of the synthetic and the animal preparation, with serial measurements of plasma 11-hydroxycorticosteroids, 12-hourly urinary 11-hydroxycorticosteroids, and 17-oxogenic steroids. The duration of action of the depot tetracosactrin was virtually twice that of corticotrophin gel, the dose relationship being about 0.25 mg. of depot tetracosactrin to 50 units of gel. Local reaction to the injection of depot tetracosactrin was relatively frequent.

17-Ketosteroids↗
PubMed1989

Adrenocorticotropin-independent bilateral macronodular adrenal hyperplasia: an unusual cause of Cushing's syndrome.

Inappropriate ACTH secretion with bilateral diffuse or macronodular adrenal hyperplasia is the most common cause of Cushing's syndrome. This report describes a patient with Cushing's syndrome and feminization due to ACTH-independent bilateral macronodular adrenal hyperplasia. A 47-yr-old black man presented with Cushingoid features, diabetes mellitus, hypertension, impotence, and gynecomastia. Urinary cortisol and 17-hydroxycorticosteroid excretion were 94 nmol/mmol creatinine (normal, less than 32) and 5.8 mumol/mmol creatinine (normal, 0.6-3.6), respectively. Both decreased by less than 30% after administration of dexamethasone (8 and 16 mg/day), and urinary 17-hydroxycorticosteroid excretion did not increase after metyrapone (750 mg, orally, every 4 h for six doses). Plasma ACTH was undetectable (less than 1 pmol/L) and was not stimulated by administration of metyrapone or ovine CRH. Serum testosterone was 5.2 nmol/L (normal, 7-30), FSH was 5 U/L (normal, 3-18), LH was 2.8 U/L (normal, 1.5-9.2), and estrone was 767 pmol/L (normal, 55-240). Both adrenal glands were enlarged, with a total weight of 86 g (normal, 8-10), and contained multiple nodules (diameter, greater than 0.5 cm) composed of two active cell types, one of which was also observed between the nodules. Cushing's syndrome with feminization due to ACTH-independent bilateral macronodular adrenal hyperplasia is an unusual process of unknown etiology that should be included with the other known causes of Cushing's syndrome.

Adrenal Glands↗
PubMed1990

A patient with hypocortisolism and Cushing's syndrome-like manifestations: cortisol hyperreactive syndrome.

One patient is reported who has the manifestations of Cushing's syndrome in spite of persistent hypocortisolemia. His serum levels of cortisol and free cortisol were below normal, and 24-h urinary excretion of 17-hydroxycorticosteroids and cortisol were decreased. There was a rapid and substantial increase in serum cortisol in response to synthetic ACTH-(1-24). Plasma levels of ACTH were marginally increased by successive administration of CRH and vasopressin, which were followed by substantial increases in serum cortisol. Glucocorticoid activity of the patient's serum, as measured by a RRA was low. There were no responses of urinary 17-hydroxycorticosteroids after metyrapone treatment. These laboratory examinations ruled out any known clinical conditions resulting in hypocortisolemia. The clinical condition could also be explained by cortisol hyperreactivity of the patient's cells. In vitro hyperreactivity to glucocorticoids was demonstrated in cultured skin fibroblasts whose aromatase activity was increased 1.5- to 1.8-fold above that of normal cells, and [3H]thymidine incorporation was inhibited more effectively by the addition of cortisol or dexamethasone. The mechanism by which the patient is hyperreactive to glucocorticoids remains unexplained.

Adrenocorticotropic Hormone↗
PubMed1990

Corticotropin-releasing hormone- and adrenocorticotropin-producing pituitary carcinoma with metastases to the liver and lung in a patient with Cushing's disease.

A 53-yr-old man with Cushing's disease was found to have a pituitary carcinoma with metastases to the liver and lung which produced both CRH and ACTH simultaneously. Despite removal of the pituitary tumor, his Cushing's disease worsened. Endocrinological examination then demonstrated elevated plasma CRH and markedly elevated plasma ACTH, beta-lipotropin, and cortisol concentrations, increased urinary 17-hydroxycorticosteroid and 17-ketosteroid excretion, and no suppression of serum cortisol after low or high dose dexamethasone administration. Urinary 17-hydroxycorticosteroid excretion increased in response to metyrapone, and lysine vasopressin elicited a striking increase in plasma ACTH. A computed tomographic scan of abdomen revealed multiple hypodense areas in the liver and bilateral adrenal hyperplasia. Postmortem histological examination revealed a necrotic hemorrhagic pituitary carcinoma with metastases to the liver, lung, and olfactory bulb. Immunohistochemical staining, gel filtration, and Northern blot analysis of liver and lung metastases revealed evidence of the production of both CRH and ACTH in these metastases. We concluded that the patient's pituitary carcinoma produced both CRH and ACTH.

Adrenocorticotropic Hormone↗