Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ADRENALS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 271 records · Page 15Linked to original sources
PubMed1983

Adrenal and sex steroid hormone production by a virilizing adrenal adenoma and its diagnosis with computerized tomography.

The presence of an androgen-secreting tumor in a 29-year-old woman was confirmed and its location was determined by computerized axial tomographic (CAT) scanning. The hormone production from this virilizing adrenal adenoma was studied in vivo and in vitro. The major secretory products of the tumor (as compared to normal adrenal tissue) were testosterone (24-fold) and 17 beta-estradiol (five-fold). Although the adenoma produced lesser amounts of dehydroepiandrosterone sulfate (DHEAS), the demonstration of elevated serum testosterone and DHEAS in serial samples was a better marker for an androgen-secreting adrenal tumor than were the urinary 17-ketosteroids, which remained in the upper limit of normal. The hormone production from the tumor depended neither on adrenocorticotropic hormone nor on human chorionic gonadotropin. The conclusions were that: (1) on the basis of serial measurements of serum testosterone and DHEAS, virilizing adrenal adenomas may be suspected when the concentrations of these hormones reach or exceed 200 ng/dl and 6,600 ng/ml, respectively; (2) the high-resolution CAT scanner can accurately localize these tumors; (3) cosmetic and menstrual dysfunction regressed after resection of the tumor; and (4) virilizing adrenal adenomas may produce both androgens and estrogens.

17-Ketosteroids↗
PubMed2003

Ghrelin and growth hormone secretagogue receptor are expressed in the rat adrenal cortex: Evidence that ghrelin stimulates the growth, but not the secretory activity of adrenal cells.

Ghrelin is an endogenous ligand of the growth hormone secretagogue receptor (GHS-R), which has been originally isolated from rat stomach. Evidence has been previously provided that adrenal gland possesses abundant ghrelin-displaceable GHS-Rs, but nothing is known about the possible role of ghrelin in the regulation of adrenocortical function. Reverse transcription-polymerase chain reaction demonstrated the expression of ghrelin and GHS-R in the rat adrenal cortex, and high adrenal concentrations of immunoreactive ghrelin were detected by radioimmune assay (RIA). Autoradiography localized abundant [(125)I]ghrelin binding sites in the adrenal zona glomerulosa (ZG) and outer zona fasciculata (ZF). Ghrelin (from 10(-10) to 10(-8) M) did not affect either basal steroid hormone (pregnenolone, progesterone, 11-deoxycorticosterone, corticosterone, 18-hydroxycorticosterone and aldosterone) secretion from dispersed ZG and zona fasciculata/reticularis (ZF/R) cells (as evaluated by quantitative high pressure liquid chromatography), or basal and agonist-stimulated aldosterone and corticosterone production from cultured ZG and ZF/R cells, respectively (as measured by RIA). Ghrelin (10(-8) and 10(-6) M) raised basal, but not agonist-stimulated, proliferation rate of cultured ZG cells (percent of cells able to incorporate 5-bromo-2'-deoxyuridine), without affecting apoptotic deletion rate (percent of cells able to incorporate biotinylated nucleosides into apoptotic DNA fragments). The tyrosine kinase (TK) inhibitor tyrphostin-23 and the p42/p44 mitogen-activated protein kinase (MAPK) inhibitor PD-98059 abolished the proliferogenic effect of 10(-8) M ghrelin, while the protein kinase A and C inhibitors H-89 and calphostin-C were ineffective. Ghrelin (10(-8) M) stimulated TK and MAPK activity of dispersed ZG cells, and the effect was abolished by preincubation with tyrphostin-23 and PD-98059, respectively. Tyrphostin-23 annulled ghrelin-induced activation of MAPK activity. Taken together, the present findings indicate that (i) ghrelin and GHS-R are both expressed in the rat adrenal cortex, ghrelin binding sites being very abundant in the ZG; (ii) ghrelin does not affect the secretory activity of rat adrenocortical cells, but significantly enhances the proliferation rate of cultured ZG cells, without affecting apoptotic deletion rate; and (iii) the ZG proliferogenic action of ghrelin involves the TK-dependent activation of the p42/p44 MAPK cascade.

Adrenal Cortex↗
PubMed2002

Inherited adrenocorticotropin-independent macronodular adrenal hyperplasia with abnormal cortisol secretion by vasopressin and catecholamines: detection of the aberrant hormone receptors on adrenal gland.

ACTH-independent macronodular adrenal hyperplasia (AIMAH) is a rare disorder and an unusual cause of Cushing s syndrome, of which familial transmission has rarely been reported. In this study, a mother and her son, the former affected with definite AIMAH and the latter with possible AIMAH, are described. Although the mother manifested overt Cushing s syndrome, her son remained with no stigmata of Cushing s syndrome except for bilateral adrenal tumor and mild hypertension, and a full suppression of plasma cortisol by lowdose dexamethasone was observed in him. Recently, aberrant expression of adrenal receptors for various ligands has been noted in AIMAH patients. In our cases, provocation tests in vivo suggested that AVP and catecholamines promoted cortisol production through V1a and/or V1b receptors and via beta-adrenergic receptor, respectively. Reverse transcriptional-PCR analysis of the operated adrenal tissues of mother revealed the abnormal expression of mRNA of receptors for V1b, V2, and LH/hCG, none of which was observed in a normal control. Inherited AIMAH is very rare, and the son might be at the earliest developmental stage of AIMAH among the cases reported so far. An intervention could be tried to prevent the development of overt Cushing s syndrome by suppression of the possible endogenous ligands or by blockade of the receptors that may be aberrantly expressed in his adrenal glands.

Adrenal Gland Diseases↗
PubMed1978

Adrenal hyperandrogenism: detection by adrenal scintigraphy.

Hyperandrogenism is a common endocrinopathy in women. Localization of the source of excess androgen production is mandatory for proper management. Ovarian hyperandrogenism has been implicated in the majority of patients studied, though the true prevalence of adrenal hyperandrogenism is not yet known. Adrenal scintigraphy is a simple non-invasive technique which detects adrenal functional abnormalities. The detection of adrenal hyperandrogenism by adrenal scintigraphy in three women with mild hirsutism is discussed.

Adenoma↗
PubMed2003

[Adrenal crisis. Diagnostic and therapeutic management of acute adrenal cortex insufficiency].

Acute adrenal insufficiency is a rare but life-threatening disorder that develops as a result of inadequate adrenal steroid production. Early diagnosis is key for effective and life-saving treatment of the affected patients. The main clinical features are non-specific, thus often leading to misdiagnosis and invasive diagnostic work up, in particular in patients with previously unknown disease. Adrenal crisis in patients with known chronic adrenal insufficiency is nowadays rare, but can only be prevented by structured patient education on stress-related glucocorticoid dose adjustment. Outcome of adrenal crisis is crucially determined by the physician's clinical competence and immediate initiation of specific treatment.

Acute Disease↗
PubMed1985

Non-Hodgkin's lymphoma limited to the adrenal gland with adrenal insufficiency.

A 81-year-old man presented with bilateral adrenal masses found pathologically to be a large cell, non-follicular center, non-Hodgkin's lymphoma. His clinical course was remarkable for the lack of macroscopic extra-adrenal tumor and for adrenal insufficiency in response to stress and cosyntropin stimulation. This is believed to be the first reported case of a non-Hodgkin's lymphoma limited to the adrenal glands with associated adrenal insufficiency.

Adrenal Gland Neoplasms↗
PubMed1988

Lymphoma presenting with adrenal insufficiency. Adrenal enlargement on computed tomographic scanning as a clue to diagnosis.

A 73-year-old woman who presented with primary adrenal insufficiency and enlarged adrenal glands on computed tomographic scanning was ultimately found to have a large-cell lymphoma that had initially involved the adrenals and the stomach. A search of the English language medical literature revealed only seven other cases of lymphoma presenting with hypoadrenalism, none of which involved the stomach. As in this case, in most of those cases adrenal enlargement was documented on computed tomographic scanning. Despite its rare occurrence, lymphoma should be searched for in patients presenting with Addison's disease and enlarged adrenal glands.

Adrenal Glands↗
PubMed1980

Differences between adrenal adenoma causing primary aldosteronism and other adrenal tissues in the incorporation of labeled steroid precursors into their products.

The incorporation and conversion of several labeled steroid precursors into their products were examined in slices of adrenal tissue from two patients with primary aldosteronism and compared with that in "normal" adrenal tissue and adrenal tissues from a patient with Cushing's syndrome. The products of the incorporation were separated by Sephadex LH-20 column chromatography. The major products of conversion in the adenomatous tissue of primary aldosteronism were 18-hydroxycorticosterone and lesser amounts of aldosterone. Smaller amounts of 18-hydroxycorticosterone were isolated from all other adrenal tissues studied. No aldosterone could be recovered after incubating any of the adrenal tissue studied with labeled 18-hydroxy-11-deoxycorticosterone or 18-hydroxycorticosterone as precursor steroid. These in vitro results seem to suggest that there is increased 18-hydroxylation in the adenoma of primary aldosteronism compared with other tissues and that relatively more 18-hydroxycorticosterone is produced in such tissue than aldosterone.

Adenoma↗
PubMed1979

Effects of morphine upon the pituitary-adrenal system and adrenal catecholamines: a comparative study in cats and rats.

The aim of the present study was to investigate the effects of acute and chronic administration of morphine upon the pituitary-adrenal activity and adrenal catecholamines in rats and cats, two animal species with very different behavioural patterns of response to the opiate. Acute administration of the drug induced in both animal species an activation of the pituitary-adrenal system. Chronic administration of morphine to cats and rats induced a depression in the pituitary-adrenal function. No significant changes in the adrenal levels of catecholamines were observed in rats treated chronically with the drug. However, in the cat, the effects of morphine on adrenomedullary function seemed to depend on the stage of morphine treatment. The behavioural patterns of response in both animal species during chronic administration of the opiate, as well as the effects of induced withdrawal with nalorphine (an antagonist of morphine), indicated that dependence on morphine had developed, not only in the rats, but also in the cats. Acute morphine administration had a sedative effect, while in the cats the opiate produced a species-specific manic response characterized by hyperexcitement and aggressive behavior.

Adrenal Glands↗
PubMed2004

Atrial natriuretic factor: localization in the adrenal gland of the lizard Podarcis sicula and effects on pituitary-adrenal axis activity.

The occurrence of atrial natriuretic factor (ANF) immunoreactivity was investigated in the adrenal gland of the lizard Podarcis sicula by avidin-biotinylated peroxidase complex (ABC) immunocytochemical technique: ANF immunoreactivity was present in the chromaffin tissue, and was absent in the steroidogenic tissue. The role of ANF in the modulation of the pituitary-adrenal axis activity was investigated in vivo by intraperitoneal administration of ANF. The effects were evaluated by examination of the morphological and morphometrical features of the tissues, as well as the plasma levels of adrenocorticotropic hormone (ACTH), corticosterone, aldosterone, norepinephrine, and epinephrine. ANF (28 microg/100 g body wt) did not affect ACTH plasma levels, that remained almost unchanged; in contrast, corticosterone plasma levels increased from 6.45 +/- 0.070 ng/ml in carrier-injected lizards to 9.69 +/- 0.080 ng/ml 24 h after the injection; aldosterone levels decreased from 2.19 +/- 0.010 ng/ml in carrier-injected specimens to 0.58 +/- 0.003 ng/ml 24 h after the experimental treatment. In the chromaffin tissue, an increase in the number of epinephrine cells and a decrease in the number of norepinephrine cells were observed, decreasing the numeric norepinephrine/epinephrine cell ratio, from 1.4/1 of control specimens to 0.3/1 24 h after ANF administration. Moreover, norepinephrine plasma levels decreased from 998 +/- 4.600 pg/ml in carrier-injected specimens to 321 +/- 2.230 pg/ml 24 h after ANF administration; epinephrine plasma levels were elevated from 614 +/- 3.410 pg/ml in carrier-injected specimens to 1672 +/- 10.800 pg/ml 24 h after the experimental treatment. The presence of ANF in the adrenal gland suggests that, also in reptiles as in other vertebrates, this peptide, locally released from the chromaffin cells, may modulate the activity of the adrenal gland, probably in a paracrine manner. The effects of ANF on the adrenal gland suggest that this peptide may affect reptilian salt and fluid homeostasis.

Adrenal Glands↗
PubMed1985

Effect of hydrocortisone dose schedule on adrenal steroid secretion in congenital adrenal hyperplasia.

To explore the potential effect of dose schedule on the adrenal suppressive action of hydrocortisone in congenital adrenal hyperplasia, eight patients (six with 21-hydroxylase deficiency and two with 11-hydroxylase deficiency) were given five different dose schedules. Two of the schedules used single daily doses (morning or evening), two twice daily doses (two-thirds dose in the morning or evening), one and three equal doses at morning, noon, and night. Each dose schedule used the same total daily hydrocortisone dose (12.5 mg/m2/day), which is within the normal range of hydrocortisone production rate. Each schedule was given for 4 to 6 weeks. The different dose schedules caused the predicted alterations in the temporal pattern of adrenal steroid levels, with the greatest apparent suppression during the 2 to 4 hours after each dose. None of the schedules, however, caused significant differences in the mean 24-hour plasma concentration of 17-hydroxyprogesterone (21-hydroxylase deficiency) or 11-deoxycortisol (11-hydroxylase deficiency) or in the 24-hour urine pregnanetriol or 17-ketosteroid concentrations, either in the six patients undertreated at the dose of 12.5 mg/m2/day or in the two patients adequately treated. Nocturnal administration of all or a part of the daily dose did not improve adrenal suppression. These observations suggest that treatment of congenital adrenal hyperplasia with a once-a-day hydrocortisone dose schedule may be as effective as conventional multiple-dose schedules. Until this hypothesis has been tested by more extended clinical studies, however, we do not recommend a once-a-day schedule. Regardless of the dose schedule, the total daily hydrocortisone dose must be adjusted to achieve a normal rate of growth and bone age advancement.

17-Ketosteroids↗
PubMed1997

Adrenal insufficiency from bilateral adrenal hemorrhage after total knee replacement surgery.

Adrenal hemorrhage is a rare cause of adrenal insufficiency in adults. We examine the incidence, etiology, diagnosis, and therapy of adrenal insufficiency secondary to adrenal hemorrhage. This case illustrates the nonspecific presentation of adrenal insufficiency and the necessity of maintaining a high index of suspicion in a clinically confusing scenario.

Adrenal Gland Diseases↗
PubMed1999

Restoration of adrenal steroidogenesis by adenovirus-mediated transfer of human cytochromeP450 21-hydroxylase into the adrenal gland of21-hydroxylase-deficient mice.

21-Hydroxylase deficiency, a potentially fatal disease due to deletions or mutations of the cytochrome P450 21-hydroxylase gene (CYP21), causes congenital adrenal hyperplasia (CAH) with low or absent glucocorticoid and mineralocorticoid production. The feasibility of gene therapy for CAH was studied using 21OH-deficient mice (21OH-) and a replication-deficient adenovirus containing the genomic sequence of human CYP21 (hAdCYP21). Intra-adrenal injection of hAdCYP21 in 21OH- mice induced hCYP21 mRNA with the highest expression from 2 to 7 days before a gradual decline. 21OH activity measured in adrenal tissue increased from undetectable to levels found in wild-type mice 2 to 7 days after AdhCYP21 injection. Adrenal morphology of 21OH- mice showed lack of zonation, and hypertrophy and hyperplasia of adrenocortical mitochondria with few tubulovesicular christae. These morphological abnormalities were markedly improved 7 days after hAdCYP21 gene therapy. Plasma corticosterone increased from undetectable levels to values similar in wild-type mice by 7 and 14 days, declining over the next 40 days. This is the first demonstration that a single intra-adrenal injection of an adenoviral vector encoding CYP21 can compensate for the biochemical, endocrine and histological alterations in 21OH-deficient mice, and shows that gene therapy could be a feasible option for treatment of CAH.

Adenoviridae↗
PubMed1996

[Computerized tomography findings score in the differentiation of adrenal tumors in patients with extra-adrenal malignomas].

PURPOSE: In a retrospective study the diagnostic accuracy of computed tomography for the differentiation of benign from malignant adrenal masses in patients with extra-adrenal malignancies was evaluated. For this differentiation a new score system was tested. PATIENTS AND METHODS: Size, density, structure, and borders of adrenal masses in 60 patients with extra-adrenal tumours were analysed and scored. The single criteria and the total score values were correlated with the final diagnosis achieved either by histology or by follow-up CT examinations. RESULTS: Score values above 4 indicated always metastases and score values below 2 were benign lesions. An overlap occurred at score values between 2 and 3 resulting in an overall accuracy of 83.3%. CONCLUSION: Single CT criteria are not reliable enough to differentiate benign from malignant adrenal lesions: better results are achieved by using our scoring system.

Adenoma↗
PubMed1998

Cytokeratin expression in adrenal phaeochromocytomas and extra-adrenal paragangliomas.

AIM: To examine whether adrenal phaeochromocytomas and extra-adrenal paragangliomas are immunoreactive for commercially available and routinely used cytokeratin antibodies. METHODS: 18 extra-adrenal paragangliomas and seven adrenal phaeochromocytomas were stained with CAM 5.2, AE1/3, and 34 beta E12 following microwave antigen retrieval of formalin fixed tissue. RESULTS: A single case from the cauda equina was positive for both CAM 5.2 and AE1/3. In addition, two other cases--an intravagal and an orbital paraganglioma--also showed strong immunopositivity with CAM 5.2 and AE1/3. All phaeochromocytomas were negative with all epithelial markers. CONCLUSIONS: Cauda equina paragangliomas are known to stain with cytokeratins; however, occasional paragangliomas from other sites may also be immunoreactive with cytokeratins. If the results of immunohistochemistry are not interpreted in the clinical and morphological context, the failure to recognise that extra-adrenal paragangliomas may on occasion react with anticytokeratin antibodies may lead to their being confused with metastatic carcinomas.

Adolescent↗
PubMed1992

Pseudo-adrenal incidentaloma: magnetic resonance imaging in a patient with para-adrenal Castleman's disease.

We report a case of para-adrenal angiofollicular lymph node hyperplasia (Castleman's disease) of the hyaline-vascular type. The mass could not be differentiated from an adrenal tumor by ultrasonography and computed axial tomography (CT). However, magnetic resonance imaging (MRI) suggested the possibility of an extra-adrenal origin of the mass. The intensity of the mass by MRI was homogeneous and of a higher intensity in the T2-weighted image than in the T1-weighted image, a finding similar to lymphadenopathy, lymphatic tumorous mass or metastatic tumor of the lymph node. Ultrasonography, CT and MRI may not be useful in characterizing Castleman's disease, but MRI was useful to distinguish asymptomatic para-adrenal masses from those of adrenal origin.

Adrenal Gland Neoplasms↗
PubMed2005

Analysis of unilateral adrenal hyperplasia with primary aldosteronism from the aspect of messenger ribonucleic acid expression for steroidogenic enzymes: a comparative study with adrenal cortices adhering to aldosterone-producing adenoma.

Unilateral adrenal hyperplasia with primary aldosteronism is very rare and shows similar endocrine features to aldosterone-producing adenoma and bilateral adrenal hyperplasia. In this study, the mRNA expression of steroidogenic enzymes in unilateral adrenal hyperplasia was examined by in situ hybridization. We found subcapsular micronodules composed of spironolactone body-containing cells, which showed intense expression for 3beta-hydroxysteroid dehydrogenase, 11beta-hydroxylase, 18-hydroxylase, and 21-hydroxylase but not 17alpha-hydroxylase, indicating aldosterone production. This expression pattern was the same as that in unilateral multiple adrenocortical micronodules, reported recently. Additionally, it was noted that a nodule with active aldosterone production was closely adjacent to one showing intense 17alpha-hydroxylase expression. In the adrenal cortices adhering to aldosterone-producing adenoma, the majority of hyperplastic zona glomerulosa and hyperplastic nodules demonstrated a decreased steroidogenic activity. However, minute nodules indicative of active aldosterone production were found at high frequency. These results suggest that the subcapsular micronodules observed might be the root of aldosterone-producing adenoma. Furthermore, we emphasize the need for long-term follow-up after unilateral adrenalectomy or enucleation of the adenoma because of the possibility that buds with autonomous aldosterone production may still be present in the contralateral or remaining adrenal tissue.

3-Hydroxysteroid Dehydrogenases↗
PubMed1979

Dissociation of cortisol and adrenal androgen secretion in patients with secondary adrenal insufficiency.

Plasma cortisol, dehydroepiandrosterone (DHA), dehydroepiandrosterone sulfate (DHAS), and androstenedione (delta4-A) were measured by RIA during ACTH infusion in preadrenarchal children with constitutional short stature, normal adults, and patients with secondary adrenal insufficiency resulting from hypothalamic-pituitary disease or corticosteroid therapy. The plasma levels of all four steroids were decreased in patients with secondary adrenal insufficiency compared to normal adults, but the decrease in DHA and DHAS was considerably greater than that in cortisol and delta4-A, resulting in significant decreases in the plasma ratios of DHA to cortisol, DHAS to cortisol, DHA to delta4-A, and DHAS to delta4-A (P less than 0.00001). The decreased DHA and DHAS responses to ACTH persisted in one glucocorticoid-treated patient after glucocorticoid therapy was terminated and the cortisol response to ACTH had normalized. The data suggest that adrenal atrophy due to hypothalamic-pituitary disease or corticosteroid therapy is associated with a greater impairment in the secretion of the delta5 adrenal androgens DHA and DHAS than in the secretion of cortisol and delta4-A, and that the capacity to secrete cortisol and delta4-A recovers more rapidly than the capacity to secrete the delta5 adrenal androgens when corticosteroid therapy is withdrawn.

Adolescent↗