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At least 19 recordsLinked to original sources
PubMed1979

Adrenal gland function in the horse: effects of cosyntropin (synthetic) and corticotropin (natural) stimulation.

The plasma concentration of hydrocortisone was determined in mares given either cosyntropin (100 IU, given IV) or corticotropin (200 IU, given IM). Plasma hydrocortisone concentrations of the mares treated with cosyntropin increased by 46%, 57% and 80% at 30, 60, and 120 minutes, respectively, when compared with base-line values; these values returned to base line at 240 minutes. In mares treated with corticotropin, mean plasma hydrocortisone concentrations increased by 42%, 143%, 101% and 155% at 30, 60, 120, and 240 minutes, respectively, when compared with base-line values. Differences in total leukocyte count, total eosinophil count, and plasma concentrations of electrolytes (calcium, sodium, magnesium, potassium) of cosyntropin- and corticotropin-treated mares, and these values in control animals were not significant. Results of the present study indicated that the horse responds to small dosages of cosyntropin (IV) in a prompt and reproducible manner as determined by plasma hydrocortisone values. Response to corticotropin was slow and less consistent. Thus, administration of cosyntropin to the horse, according to test results with paired samples collected (before administration and again at 2 hours after injection), was found to be a prompt and meaningful test of adrenal gland function.

Adrenal Glands↗
PubMed1979

17-Hydroxyprogesterone in the cosyntropin test: results in normal and hirsute women and in mild congenital adrenal hyperplasia.

The variations in plasma cortisol, testosterone and 17-hydroxyprogesterone (17-OHP) induced by an im injection of 0.25 mg cosyntrophin were studied in three groups of subjects: 16 healthy women, 16 hirsute women (HW) and 10 mild cases of congenital adrenal hyperplasia (CAH). The basal values of cortisol and testosterone were comparable between the three groups. In the patients with mild CAH, the mean 17-OHP concentration was increased: 483.9 ng/100 ml (113-1200 ng), but it should be noted that the individual values could overlap with the normal concentrations found in the controls and the HW during the luteal phase of the cycle. One hour after the injection of cosyntropin, a massive response of 17-OHP was observed in the mild cases of CAH, the mean basal concentration was multiplied by ten: 4843 ng/100 ml. The minimum concentration reached was 1740 ng/100 ml which is still 3-fold the highest level seen either in normal women (400 ng/ml) or in hirsute women (550 ng/100 ml). Determination of 17-OHP following a short-term ACTH stimulation, therefore provides evidence of partial 21-hydroxylase deficiency.

Adrenal Hyperplasia, Congenital↗
PubMed1977

Partial 11- and 21-hydroylase deficiencies in hirsute women.

Thirty-one women with idiopathic hirsutism were evaluated for partial 11- and 21-hydroxylase adrenocortical enzyme deficencies. Twenty-four hour urine collections for 17-ketosteroids, 17-hydroxycorticoids, tetrahydro compound S (THS), and -pregnanetriol were obtained basally and following a continuous 24 hours infusion of alpha 1-24 ACTH (cosyntropin). The results were compared to those in eight normal, nonhirsute women studied under identical conditions. Normal control subjects and 18 of 31 hirsute female patients (Group I) showed similar small increments in the excretion of THS and pregnanetriol following the infusion of cosyntropin. Thirteen hirsute women (Group II) showed cosyntropin-stimulated increments in either THS and/or pregnanetriol that were significantly greater than the mean response of the control group. The cosyntropin-stimulated increments in 17-ketosteroid excertion and basal sebum production rates were also significantly greater in Group II. The results are consistent with partial II - and/or 21-adrenocortical hydroxylase deficiencies in some hirsute women whose condition would have previously been designated as "idiopathic." Thus, prolonged ACTH stimulation testing may identify patients who might benefit from glucocorticoid suppression therapy.

17-Hydroxycorticosteroids↗
PubMed1977

Simplified assessment of pituitary-adrenal axis in a stable group of chronic hemodialysis patients.

1) A stable group of hemodialysis patients in our study do not have a normal response to the cosyntropin test; 2) although one would expect chronic renal failure patients to accommodate to hemodialysis, our study demonstrates that hemodialysis may still serve as a useful stress test; 3) the reduced response to the metyrapone suppression test in our stable group of hemodialysis patients suggests impairment of the feedback mechanism of the pituitary-adrenal axis.

Adrenal Cortex↗
PubMed1979

Reversible adrenocorticol insufficiency in fulminant meningococcemia.

A 13-year-old girl who had been well previously was admitted with fulminant meningococcemic purpura. Her plasma cortisol level was only 3 micrograms/dL and failed to rise after cosyntropin administration. Maintenance doses of corticosteroid were administered. As her infection cleared her adrenal glands were restimulated and shown to have near normal response. Replacement doses of corticosteroids should be given to patients with fulminant meningococcemia until adrenal cortical insufficiency can be excluded because of the high incidence of adrenal failure in these patients and the possibility that excessive adrenal stimulation might contribute to adrenal abnormality.

Adolescent↗
PubMed1976

Percutaneous adrenal suppression with topically applied corticosteroids.

Synthetic fluorinated derivatives of cortisone, when topically applied, are absorbed readily and may suppress adrenal function. In the case presented here, large quantities of topically applied triamcinolone acetonide were used in the treatment of atopic dermatitis. This caused a noticeable decrease in the plasma cortisol level. That this was the result of adrenal suppression rather than insufficiency was indicated by a satisfactory response of the plasma cortisol levels to a cosyntropin injection test. In patients with a history of recent and extensive use of topically applied corticosteroids, appropriate diagnostic and therapeutic measures are indicated to avoid postoperative adrenal insufficiency.

Adrenal Cortex Hormones↗
PubMed1978

Hyporeninemic hypoaldosteronism--case report and observation of dissociated renin and erythropoietin activity.

A case is reported of hyporeninemic hypoaldosteronism, diagnosed during an evaluation of hyperkalemia. Urine and plasma aldosterone concentrations were depressed despite hyperkalemia and were not responsive to ACTH, cosyntropin, and angiotensin 2. Adrenal glucocorticoid function was normal. Plasma renin activity also was low, and was hyporesponsive to stimulation, including intravascular volume contraction and potassium depletion. Autonomic nervous function was intact. Of the 32 previously reported cases of selective hypoaldosteronism, plasma renin activity was low in the majority of cases in which it was measured. A classification of the types of selective hypoaldosteronism is presented. It is of interest that the serum erythropoietin activity in this case was increased while plasma renin activity was markedly depressed.

Aged↗
PubMed1979

Effect of indomethacin and adrenocorticotrophic hormone on renal function in man: an experimental model of inappropriate antidiuresis.

The effect of prostaglandin synthesis inhibition on basal and ACTH-stimulated adrenal and renal function was investigated in normal volunteers. Data were collected during control and experimental study periods (13 days each). Adrenocorticotrophic hormone (Cosyntropin, 80 U/day) was administered i.v. on days 8 and 9 of each period. Indomethacin (150 mg/day) was given on days 5 through 13 of the experimental period. The subjects ate a constant diet containing 9 mEq of sodium, 100 mEq of potassium, and 2,500 ml of fluid daily. Indomethacin markedly inhibited urinary PGE excretion and plasma PGE concentration. The effect of ACTH alone as compared to the effect of ACTH and indomethacin showed: plasma sodium concentration, 139 +/- 1 vs. 131 +/ 3 mEg/liter (P less than 0.01, mean +/- SEM); plasma osmolality, 287 +/- 3 vs. 270 +/- 3 mOsm/liter (P less than 0.01); free water clearance, 97 +/- 66 vs. -1100 +/- 380 ml/24hr (P less than 0.01); urine volume, 2,000 +/- 60 vs. 950 +/- 200 ml/day (P less than 0.01); and urine osmolality 282 +/- 12 vs. 720 +/- 144 mOsm/liter (P less than 0.01). We conclude that the effects of ACTH and prostaglandin synthesis inhibition interact to result in inappropriate antidiuresis.

Adrenal Glands↗
PubMed1979

Therapy of adrenocortical hydroxylase deficiencies in acne vulgaris.

Twenty women with acne vulgaris who presented to a gynecologist's office with the complaints of hirsutism, infertility, menorrhagia, or oligomenorrhea were subjected to a 24-hour cosyntropin (ACTH) infusion to detect partial 11- or 21-adrenocortical hydroxylase deficiencies. All patients demonstrated enzymatic defects and were placed on prednisone therapy. The six patients with moderate acne either showed improvement of their acne or conceived. Of the 14 patients with mild acne, seven showed improvement of their acne or conceived; whereas, the remainder showed no improvement. Patients with acne and gynecologic signs and symptoms should be evaluated for the presence of 11- or 21-adrenocortical hydroxylase deficiencies.

Acne Vulgaris↗
PubMed1979

Hypothalamic-pituitary-adrenal function in extrinsic asthma.

Hypothalamic-pituitary-adrenal function in a well-defined, carefully selected group of 25 patients with extrinsic asthma was assessed by measuring plasma levels of adrenocorticotropic hormone (ACTH) and of 11-deoxycorticol after administration of metyrapone and by measuring the level of cortisol following stimulation with cosyntropin. No difference was demonstrated between asthmatic subjects and 20 normal age-matched controls. In addition, neither the response of the level of ACTH nor of 11-deoxycortisol correlated with the duration of asthma or the severity as assessed in 23 patients by tests of pulmonary function. We conclude that there is no abnormality in hypothalamic-pituitary-adrenal function in patients with extrinsic asthma, and we suggest that previous data suggesting such an abnormality may reflect heterogeneous groups of patients, inaccurate methods, and the variability of normal responses to ACTH and stimulation with metyrapone.

17-Hydroxycorticosteroids↗
PubMed1978

Adrenal status assessed by direct radioimmunoassay of cortisol in whole saliva or parotid saliva.

We describe a direct radioimmunoassay for cortisol in 10-microliter volumes of parotid saliva or whole saliva. Binding proteins are absent from these fluids, as demonstrated by the excellent correlation between results for samples assayed directly and by a comparison procedure involving extraction with 1,2-dichloroethane. The direct assay is specific, precise, and had a lower limit of sensitivity of 4 pg per assay tube. Comparison of cortisol concentrations in plasma, parotid saliva, and whole saliva in persons undergoing investigations for assessing adrenal function, including stimulation with cosyntropin (Synacthen) and suppression with dexamethasone, indicated that changes in plasma cortisol concentration were accurately and immediately reflected in saliva from either the parotidgland or whole saliva. A marked circadian rhythm has also been demonstrated for cortisol in parotid-gland saliva and whole saliva. We had to modify the 1,2-dichloroethane extraction procedure for accurate determination of cortisol in parotid saliva and whole saliva of patients undergoing treatment with metyrapone.

Adrenal Glands↗
PubMed1976

Beclomethasone dipropionate use in chronic asthmatic patients. Effect on adrenal function after substitution for oral glucocorticosteroids.

The clinical effectiveness of beclomethasone dipropionate (BDP) aerosol and adrenal function after withdrawal of oral corticosteroid therapy were evaluated in 32 severely steroid-dependent asthmatic patients. Twenty-four of 28 patients were able to discontinue oral glucocorticosteroid therapy, while four failed to do so. Ventilatory studies showed no substantial changes at the end of six months' BDP treatment. In 24 patients, adrenal insufficiency was present before BDP therapy was started. In 20 of those patients, the response of cosyntropin returned to normal two months after discontinuation of systemic steroid treatment and administration of BDP.

Administration, Oral↗
PubMed1975

[Eosinophil leucocytes in csf after myelography (author's transl)].

2 cases one of polyneuropathy and one of funicular myelosis, in which myelography was performed, are reported. After the insertion of the contrast medium an increase of eosinophil leucocytes was observed. In one case an additional increase of IgG and IgA, as well as a penetration of macromolecular proteins and an increase of the total protein, was detected. The second case showed an increase in haptoglobulin in addition to the cellular reaction described. After removal of the contrast medium, the CSF became normal in both cases. These changes were on one hand interpreted as a functional lesion of the barrier, and on the other hand as a special cellular and humoral immune reaction. This could be distinctly detected in the lumbar CSF while in the suboccipital CSF there was only an indication of it. This emphasizes the assumption of a pathological reaction in the section of the cerebrospinal region that was in contact with the contrast medium (allergen-hyperergic reaction of the vascular fibrous tissue of the leptomeninges). No marked changes were observed in the serum.

Adult↗
PubMed1976

Adrenal cortex adenylate cyclase. In vitro acitivity of ACTH fragments and analogues.

The ability of ACTH fragments and of an ACTH analogue [9-tryptophan(o-nitrophenylsulfenyl)] corticotropin-(1-24)-tetracosapeptide[Trp-(Nps)9 ACTH1-24] to stimulate adenylate cyclase in bovine adrenal cortex membranes and a crude membrane fraction from rat adrenals has been determined. Partial agonists like Trp (Nps)9 ACTH1-24 displayed intrinsic activity in the rat adrenal preparation only if tested in the presence of 5'-guanylylimidodiphosphate [Gpp(NH)p]. On the other hand, no addition of Gpp(NH)p was necessary to demonstrate intrinsic activity of Trp(Nps)9 ACTH1-24 for bovine adrenal cortex adenylate cyclase. A large decrease (15-fold) of the apparent Km values for ACTH1-24, ACTH1-23 and ACTH1-17 was observed with the rat adrenal preparation when Gpp(NH)p was added. The shift in apparent Km values for ACTH1-24 and ACTH1-23 for the bovine adrenal cortex adenylate cyclase system was small or insignificant when Gpp(NH)p was added. The observations suggest that the hormone receptor facilitates the action of guanylnucleotide sites in the membrane. When guanylnucleotide sites are occupied by Gpp(NH)p even weak interactions of the hormone receptor with e.g. partial agonists are propagated to the catalytic subunits of the adenylate cyclase complex resulting in enhanced activity. The differences in adenylate cyclase activation with hormone fragments or analogues and different target tissues may rather reflect the state of the coupling process involving guanylnucleotide binding sites of the isolated membrane fraction than differences in the receptor itself.

Adenylyl Cyclases↗
PubMed1978

Behavioural effects of naloxone in rats.

Naloxone in rats induces a behavioural syndrome closely resembling that induced by intraliquorally injected ACTH peptides. This effect is probably due to a displacement of the ACTH peptides from other receptors (e.g. opiate receptors).

Animals↗
PubMed1979

The pathogenesis of hyperadrenergic postural hypotension in diabetic patients.

Patients with diabetes generally exhibit normal plasma catecholamine responses to standing. Some have blunted norepinephrine responses and postural hypotension-hypoadrenergic postural hypotension due to classic diabetic adrenergic neuropathy. Others, including some with postural hypotension, have exaggerated norepinephrine responses to standing. In order to clarify the pathogenesis of this hyperadrenergic state which occurs in a subset of diabetic patients, we studied aldosterone secretion, vascular and metabolic responsiveness to the administration of norepinephrine, and intravascular volumes in four diabetic patients who were selected for their exaggerated plasma norepinephrine responses to standing. Three of the four patients also exhibited (hyperadrenergic) postural hypotension. None of the hyperadrenergic diabetic patients had evidence of hypoaldosteronism or vascular resistance to norepinephrine, but all four patients had subnormal red blood cell masses and the mean (+/-SE) red blood cell mass (13.1 +/- 1.0 ml/kg) was approximately half of that of age- and sex-matched diabetic controls (26.5 +/- 2.7 ml/kg, p less than 0.01). Thus, intravascular volume contraction, specifically a reduction in the red blood cell mass, may play an important role in the pathogenesis of hyperadrenergic state observed in a subset of diabetic patients and in the pathogenesis of hyperadrenergic postural hypotension in affected diabetic patients.

Acetoacetates↗