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At least 109 records · Page 6Linked to original sources
PubMed1989

Immunohistochemical study of cytochrome P-45017 alpha in human adrenocortical disorders.

Cytochrome P-450 specific for steroid 17 alpha-hydroxylation (P-45017 alpha) was immunolocalized in normal and hyperfunctioning adrenal glands of pigs, bovines, and humans, using a specific IgG fraction raised against the enzyme. P-45017 alpha was present in the zona fasciculata (ZF) and zona reticularis (ZR), but not in the zona glomerulosa (ZG), in pig, bovine, and human adrenal glands. In the adrenal glands of patients with Cushing's disease, the positive immunoreactivity to P-45017 alpha was intense in ZF and ZR, particularly in cortical micronodules, corresponding to the sites of active steroidogenesis. Cells of hyperplastic ZG and outer ZF in the adrenal glands of idiopathic hyperaldosteronism were negative for P-45017 alpha. In aldosteronoma, positive immunoreactivity was observed in some tumor cells, which is consistent with cortisol production and its responsiveness to ACTH in aldosteronoma. In the attached adrenal glands of aldosteronoma, the immunoreactive P-45017 alpha was clearly present in the inner ZF and ZR, suggesting persistent androgen production. In Cushing's adenoma, the positive immunoreactivity was intense in tumor cells, and the ZR of the attached adrenal glands was weakly immunoreactive.

Adenoma↗
PubMed1993

Roles of adrenal and gonadal steroids and season in uropygial gland function in male pigeons, Columba livia.

To gauge the relative regulative roles of adrenal, gonadal, and thyroid hormones on uropygial gland of male adult pigeons, morphometric, histological, and histochemical observations have been made on a seasonal basis in normal as well as experimentally manipulated birds. Normal birds showed a parallel adrenal-gonadal-uropygial relationship and inverse adrenal-thyroid, thyroid-gonadal, and thyroid-uropygial relationships. Induced hypocorticalism by dexamethasone in the breeding season and hypercorticalism by ACTH or corticosterone treatment in the nonbreeding season were marked by inhibitory and stimulatory changes respectively in the uropygial gland and testis and by inverse thyroid activity. Further, cyproterone acetate treatment in the breeding season completely suppressed testicular functions and increased thyroid activity without affecting either adrenal or uropygial weight, structure, and functions. Based on the observations it is concluded that adrenal steroids are principally involved in regulating the uropygial gland while the gonadal steroids are involved in qualitative aspects of secretion during the breeding phase and thyroid hormones in maintaining the general metabolic profile.

17-Hydroxysteroid Dehydrogenases↗
PubMed1993

Nuclear DNA patterns in adrenal cortex proliferative lesions.

In cortical adrenal gland tumours there are discrepancies between morphological criteria for malignancy and biological behaviour. This makes it difficult to select the appropriate treatment. We have studied morphometric and DNA densitometric features of 24 adrenal proliferative lesions (hyperplasia, adenoma, and carcinoma) by means of slide cytometry. All variables have been correlated with pathological diagnosis. The samples were selected from paraffin-embedded tissue, and representative lesions were Feulgen stained. Densitometric study showed aneuploid cell lines in every carcinoma, 5 of 8 adenomas, and 5 of 10 hyperplastic lesions. Both DNA nuclear content (mean ploidy of 2.11 c, 2.41 c, and 3.05 c) mean nuclear area (average of 31.26 microns 2, 35.92 microns 2, and 42.39 microns 2) showed progressive increase from hyperplasia to adenoma, and carcinoma. Mean shape factors were lowest in adenomas (1.69) and highest in carcinomas (1.82). Those karyometric variables which showed statistically significant differences (p < 0.05) among diagnostic groups were included in a stepwise three-way discriminant analysis. Only three parameters, shape factor (p = 0.0008), mean ploidy (p = 0.0012), and adrenal weight (p = 0.0055) persisted as independent predictive factors. Using the three variables selected by discriminant analysis on our cases, 100% of the adenomas were correctly classified, 83% of the carcinomas, and 80% of the hyperplasias. Tumour weight and nuclear shape factor differentiated adrenal cortex adenoma from carcinoma, while mean ploidy distinguished adrenal cortical hyperplasia from carcinoma. Nuclear pleomorphism (shape factor) and DNA-ploidy are the most important nuclear features in predicting the biological course of proliferative adrenal cortex lesions, although by themselves they are not bona-fide discriminators.

Adenoma↗
PubMed1975

A comparison of canine normal hepatic alkaline phosphatase and variant alkaline phosphatase of serum and liver.

The isoenzyme of alkaline phosphatase from normal liver, the corticosteroid induced isoenzyme of alkaline phosphatase from serum and liver and a hepatocellular variant isoenzyme of alkaline phosphatase induced by lymphosarcoma have been partially purified and their the present modification incorporates Polybrene into buffer to eliminate this heparin interference. The proposed method shown excellent agreement with a reference procedure based on clottable protein, and excellent day-to-day precision (C.V.3.5%). The present method is easily adaptable to semi-automated measurements.

Adrenal Cortex Diseases↗
PubMed1987

Physiological and pathological effects of steroids on the function of the adrenal cortex.

The adrenal cortex is the site of the synthesis of steroid hormones such as the glucocorticoid cortisol and the mineralocorticoid aldosterone. The pathway of biosynthesis of these steroids from cholesterol involves a sequence of transformations using cytochrome P-450 enzymes which varies within the adrenal cortex as a result of the differential localization of enzymes within the zones. The hypothesis presented here is that as a result of the arrangement of the vasculature in the adrenal gland, high concentrations of steroids may be expected to accumulate and may have autoregulating effects. These may include the following: (1) the normal morphological and functional zonation of the adrenal cortex may be regulated by gradients of steroids in the adrenal cortex; (2) destruction of cytochrome P-450 enzymes on interaction with certain steroids which act as pseudosubstrates may form part of the pathogenesis of some steroidogenic enzyme deficiencies. Under normal conditions, the individual cytochrome P-450s are not rate-limiting for steroidogenesis. Under some pathological conditions, individual cytochrome P-450 enzyme activities may become rate-limiting, with consequent overproduction of precursor steroids, leading to mineralocorticoid or androgen excess.

Adrenal Cortex↗
PubMed1995

Corticosteroids in human blood: IX. Evidence for adrenal secretion of sulfate-conjugated cortisol, 11 beta,17 alpha-dihydroxy-4-pregnene-3,20-dione-21-yl-sulfate.

A method was developed for the estimation of levels of cortisol-21-sulfate (F KS), cortisone-21-sulfate (ES), and 20(alpha + beta)-reduced cortisol-21-sulfates in blood plasma. Levels of these conjugates were determined in peripheral vein plasma of 42 normal subjects, 21 men, and 21 women (age range 20-64 years) and in adrenal vein plasma of patients with various adrenocortical disorders, six patients with primary hyperaldosteronism, five patients with Cushing's syndrome, and in two obese patients, suspected to have Cushing's syndrome, but with inconclusive laboratory findings. Adrenal vein blood was obtained by percutaneous, trans-femoral adrenal vein catheterization. Levels of non-conjugated (free) cortisol were determined in all plasma samples along with those of the sulfated steroids. F kappa S was found in all plasma samples, both in men and women. The variation in F kappa S levels paralleled that in the free cortisol levels, thus the ratio of F kappa/F kappa S was the same in the blood samples drawn at 8 AM as in those drawn at 4 PM or 5 PM (ranges: 17.5-36.3 in men, 23.6-45.8 in women). The levels of F kappa S were relatively lower in women than in men (women 610-880 ng/100 mL at AM, 300-510 ng/100 mL at PM; men: 760-1,220 ng/100 mL at AM, 380-760 ng/100 mL at PM). Plasma levels of total sulfate-conjugated delta 4-3-keto-C-21 steroids (F kappa S + E kappa S + 20(alpha+beta)-dihydrocortisol-21-sulfates) were 30-40% higher than those of the levels of cortisol-21-sulfate alone (separated by thin-layer chromatography). In the adrenal vein plasma, levels of delta 4-3-keto-C-21-steroid-21-yl sulfates were 20 to 40 times higher than levels of these steroids in the peripheral blood. The bulk of the steroid sulfate measured in the adrenal vein plasma consisted of cortisol-21-sulfate. The ratio of F kappa/F kappa S in the adrenal vein plasma was markedly smaller than in the peripheral vein plasma; it was 6.9-12.3 in males and 4.9-6.7 in females, whereas in the peripheral vein of the same subjects it was 19.2-43.7 in males and 21.4-48.3 in females. Cortisol-21-sulfate isolated from adrenal vein plasma was identified by mass spectrometry. The data presented provide evidence for the secretion of this conjugate by the adrenal cortex. Its secretion appears to be markedly elevated in patients with Cushing's syndrome, both due to hyperplasia and due to adrenal adenoma, as compared with normal subjects and patients with primary aldosteronism, both males and females. However, the F kappa/F kappa S ratio was markedly lower in Cushing's patients due to adrenal adenoma than due to adrenal hyperplasia, this suggesting that ACTH is stimulating intra-adrenal hydrolysis of cortisol sulfate.

Adrenal Cortex Diseases↗
PubMed1987

In vitro adrenal cortex lesions characterization by NMR spectroscopy.

Percentage of lipid content of 22 adrenal cortex lesions and their water proton longitudinal relaxation time were measured in vitro at 60 MHz. Although water relaxation times obtained on benign and malignant samples overlap each other, measurements of the percentage of lipids performed on the same tissues allow us to distinguish the two pathologies. The specific tool of characterization should be possible to obtain through in vivo spectroscopic imaging techniques.

Adenoma↗
PubMed2004

Plasma cortisol and cortisone concentrations in normal subjects and patients with adrenocortical disorders.

Two isozymes of the 11beta-hydroxysteroid dehydrogenase (11-HSD) are responsible for the interconversion of cortisol (F) and cortisone (E). The type 1 isozyme, 11-HSD1, acts mainly as a reductase in vivo, activating E to F, whereas the type 2, 11-HSD2, acts as a dehydrogenase, inactivating F to E. 11-HSD1 is the most abundant in the liver and 11-HSD2 in the kidney. In this study, we attempted to determine which isozyme and organs primarily contribute to equilibrium of plasma F and E concentrations in the peripheral circulation and to clarify differences in 11-HSD activities among adrenocortical disorders. Upon selective catheterizations for adrenocortical and renovascular disorders, plasma F and E concentrations in the femoral vein were closer to those in the renal vein than those in the hepatic vein. Values for mean plasma F/E ratios in the peripheral vein were in-between those of the adrenal and renal veins. A double reciprocal plot between peripheral plasma F and E concentrations in patients with various adrenocortical tumors was almost identical to that in normal subjects. Mean plasma F/E ratio in peripheral blood was higher in patients with Cushing's syndrome and was lower in patients with primary aldosteronism and nonfunctioning adrenocortical adenoma than that in normal subjects. These results suggest that renal 11-HSD2 is a main factor controlling the equilibrium of plasma F and E concentrations in the periphery and that cortisol and aldosterone excess do not change the equilibrium of plasma F and E concentrations in the peripheral circulation, but may alter expression of 11-HSD2. Alternation of 11-HSD2 activities as well as corticosteroid levels may be important in the pathophysiology of adrenocortical disorders.

11-beta-Hydroxysteroid Dehydrogenase Type 1↗
PubMed1985

Hyperprolactinemia in primary adrenocortical insufficiency.

A patient with primary adrenocortical deficiency presented with galactorrhea and hyperprolactinemia, in addition to the usual characteristic symptoms of adrenal insufficiency. With steroid replacement therapy, PRL levels returned to normal, with resumption of normal ovulatory cycles; and the patient became pregnant. Primary adrenocortical deficiency should be considered as one of the very rare causes in the differential diagnosis of hyperprolactinemia.

Abdomen↗