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PubMed2005

[Adrenal tuberculosis as a cause of primary adrenal insufficiency--case report].

Adrenal tuberculosis is relatively infrequent cause of primary adrenocortical insufficiency in developed countries. Adrenal involvement is most often the result of hematogenous spread of the pulmonary tuberculosis. Isolated adrenal tuberculosis, especially with enlargement of adrenal glands can cause diagnostic problems and requires differentiation from primary or secondary neoplastic disease. In this paper we present a case of 61-year-old man with several months history of adrenocortical insufficiency without signs of pulmonary tuberculosis. Computed tomography scan revealed asymmetrical mass-like enlargement in adrenal glands. Despite of consecutive investigations, the diagnosis remained uncertain. Because of the possibility of neoplastic process of unknown origin, the patient was qualified for surgical exploration during which both enlarged glands were removed. The diagnosis of tuberculosis was made on microscopic examination.

Addison Disease↗
PubMed1993

Plasma membrane cholesterol is utilized as steroidogenic substrate in Y-1 mouse adrenal tumor cells and normal sheep adrenal cells.

Previous studies from this laboratory indicate that plasma membrane cholesterol acts as an important source of steroidogenic substrate for MA-10 Leydig tumor cells. The present studies were designed to generalize these findings to other steroidogenic cells and to another species. Studies were performed using the Y-1 murine adrenal tumor cell line and primary cultures of sheep adrenocortical cells. Treating Y-1 cells with the acyl coenzyme A:cholesterol acyltransferase inhibitor, 58-035, caused cellular cholesteryl ester depletion and rendered more apparent the effect of dibutyryl-cAMP to cause cellular free cholesterol depletion. Radioactive 20 alpha-dihydroprogesterone was synthesized by Y-1 cells that had been plasma membrane-labeled with [3H]-cholesterol. Primary sheep adrenal cultures that had been cholesteryl ester-depleted also demonstrated cellular free cholesterol depletion after stimulation with dibutyryl cAMP. Plasma membrane label was converted to steroid hormones in these cells as well. Taken together, these data indicate that the use of plasma cholesterol is not restricted to the MA-10 cells. The present data indicate that both neoplastic mouse adrenal tumor cells and normal sheep adrenal cells utilize plasma membrane cholesterol.

Adrenal Gland Neoplasms↗
PubMed1979

Adrenal scintigraphy with 131I-19-iodochlesterol in the diagnosis of Cushing's syndrome associated with adrenal tumor.

Seven patients with Cushing's syndrome secondary to adrenocortical tumors were studied using 131I-19-iodocholesterol. The diagnosis of all cases were verified histologically. In three cases with adenoma the uptake of the tracer was in the tumor only, while the two patients with adrenocortical carcinoma failed to show adrenal accumulation of the labelled compound. In two patients there was a hyperplasia-like scintigraphic pattern, while the stimulation and suppression biochemical tests suggested adrenal tumor. One of these cases was verified as a mixed form (adenoma plus hyperplasia), and the tumor bearing gland was significantly larger on the scan which helped the preoperative localization. In the other case, verified as bilateral multiple adrenocortical adenomas, the autonomus function of both adrenals was proved by dexamethasone suppression scanning. It seens reasonable to use the latter as an adunctive diagnostic procedure in patients where there is a discrepancy between the standart scintiscan and the biochemical indexes of adrenal hyperfunction.

19-Iodocholesterol↗
PubMed1987

Early adrenal infection by herpes simplex virus type-1 (Miyama + GC strain): special reference to inoculation dose and spread from the adrenal to the central nervous system.

Male C3H/HeN mice, aged 5 weeks, were inoculated intraperitoneally (i.p.) with different doses (1 x 10(3), 1 x 10(5), 5 x 10(5), 1 x 10(6) pfu) of the herpes simplex virus type-1 (HSV-1) (Miyama + GC strain). The LD50 of this virus was 10(2) pfu (i.p.) per mouse. All the mice in each group died 12 days after inoculation. Adrenal necrosis was found to be dose-dependent, the threshold dose being 5 x 10(5) pfu. In addition, encephalitis and inflammatory cell infiltration in abdominal ganglia appeared in 3-4 days after inoculation. By the plaque method, HSV-1 was detected first in the adrenal glands, then in neurons in the spinal cord and the brain. These findings suggest that in mice inoculated with doses of virus sufficient to infect the adrenal gland, HSV-1 spreads to the central nervous system through peripheral nerves after replication in the adrenal.

Adrenal Gland Diseases↗
PubMed2005

An 88-year-old woman diagnosed with adrenal tumor and congenital adrenal hyperplasia: connection or coincidence?

An 88-yr-old woman presented with a 3x4x5 cm adrenal incidentaloma. Apart from partial cortisol deficiency there were no clinical or laboratory signs of abnormal hormone production. Because of suspicion of carcinoma, a urinary steroid profile was carried out which indicated 21-hydroxylase deficiency with elevated pregnantriol. Biopsy of the tumor showed benign adenoma tissue. The genetic analysis showed two mutations in the CYP21-gene, V281L and 1172N consistent with mild non-classic congenital adrenal hyperplasia (CAH). The patient showed a general improvement with a low prednisolone dose. Previous reports have shown increased prevalence of CAH in patients with adrenal tumors although, to our knowledge, no one has reported the combination in a patient as old as in ours. Thus, clinical signs and symptoms of CAH should be looked for in patients with adrenal incidentalomas, even in the very old ones, and if suspicion further diagnostic work-up should be carried out to provide adequate treatment and follow-up.

Adenoma↗
PubMed1977

Cholesterol side-chain cleavage enzyme activity and cytochrome P-450 content in adrenal mitochondria of a patient with congenital lipoid adrenal hyperplasia (Prader disease).

An autopsied case with congenital lipoid adrenal hyperplasia (Prader disease) was presented. The cholesterol side-chain cleavage (SCC) enzyme activity in adrenal mitochondria of this case was assayed with [3H]cholesterol as substrate, combined with purified bovine adrenodoxin and adrenodoxin reductase, by measuring the amount of [3H]pregnenolone formed. The cytochrome P-450 content was also measured by recording the difference absorption spectra of carbon monoxide-complexed P-450. The cholesterol SCC enzyme activity in adrenal mitochondria of Prader disease was 0.81 nmol pregnenolone/nmol P-450 per min, which was approximately 10% of that in normal tissue. The content of cytochrome P-450 was 0.074 nmol/mg protein, which was about half of that in controls. These results indicate that there is a cholesterol SCC enzyme deficiency in adrenal mitochondria in this disease.

Adrenal Glands↗
PubMed2005

Adrenal cortex autoantibodies in subjects with normal adrenal function.

The recent advances in our understanding of immunology have greatly improved our knowledge about the natural history of autoimmune diseases and, in particular, of autoimmune Addison's disease (Autoimmune AD). Autoimmune AD is a chronic disorder with a long preclinical period marked by the presence of adrenal cortex autoantibodies (ACAs). In this chapter the main data on this will be analyzed. The populations with the highest risk of Autoimmune AD are first relatives of patients with AAD and patients with autoimmune diseases, particularly those with chronic hypoparathyroidism or with premature ovarian failure. The best markers to identify the subjects at risk are ACAs detected by the immunofluorescence test on human or animal tissues, or 21-hydroxylase autoantibodies (21-OHAbs) detected by radioimmunoassay (RIA). The evaluation of adrenal cortex function in these individuals includes the basal determination of adrenocorticotropic hormone (ACTH), cortisol, aldosterone, plasma renin activity and cortisol after intravenous stimulation with synthetic ACTH. The multivariate analysis of the main factors (genetics, age, gender, titers of antibodies, pre-existing disease, status of the adrenal function) revealed that the risk of future AAD depends only on the presence of high antibody titers, chronic hypoparathyroidism or chronic candidiasis and adrenal dysfunction. On the basis of these parameters the risk of future Autoimmune AD can be calculated with an equation model. Patients with different risk scores need to be monitored at different time intervals, and those at high risk need to be strictly monitored and are the ideal subjects for future prevention trials.

Addison Disease↗
PubMed2005

Fetal adrenal development: insight gained from adrenal tumors.

Precise and coordinated mechanisms control the growth and functional differentiation of fetal organ systems. Conversely, tumor progression and the development of cancer probably occur through a process of dysregulation and dedifferentiation. Similarities exist between normal human fetal adrenal cortex and adrenal cancers, such as high expression of growth factors, including insulin-like growth factor II. Therefore, we might gain insight into factors involved in adrenocortical development through better understanding the development and progression of adrenocortical tumors. This review is prompted by recent gene profiling studies that have identified genes differentially expressed between normal and abnormal adrenal glands. Several of these genes are specific growth factors or key cell cycle regulators, in addition to genes not previously associated with adrenal growth or function.

Adrenal Gland Neoplasms↗
PubMed1990

Inappropriate adrenal androgen secretion with once-a-day corticosteroid therapy for congenital adrenal hyperplasia.

To determine whether cortisone acetate given as a single daily dose would be as effective as the same amount divided into three doses in suppressing adrenal androgen secretion in congenital adrenal hyperplasia, we studied three patients with the salt-losing variety, who were judged to have been adequately treated during the previous year. Each patient was receiving cortisone acetate, 20.6 to 22.6 mg/m2 body surface area per day, divided into three doses, and 9 alpha-fluorohydrocortisone, 0.05 to 0.1 mg/day. Their spontaneous and adrenocorticotropic hormone-stimulated blood concentrations of 17 alpha-hydroxyprogesterone, androstenedione, and testosterone were measured initially and were normal. Cortisone acetate was then given once a day in the same total daily dose. After 3 months, plasma adrenocorticotropic hormone concentration was increased in all three patients, and in two of them the plasma levels of 17 alpha-hydroxyprogesterone and androstenedione were also increased. In the third patient, after 7 months of once-daily therapy, plasma levels of 17 alpha-hydroxyprogesterone and androstenedione were increased. We conclude that a physiologic replacement dosage of cortisone acetate given once daily is not effective in controlling excessive adrenal androgen secretion in congenital adrenal hyperplasia.

17-alpha-Hydroxyprogesterone↗
PubMed1993

Bilateral testicular adrenal rests in a patient with 11-hydroxylase deficient congenital adrenal hyperplasia.

A 13-year-old boy was referred for investigation of hypertension, precocious puberty and giant testicles. Hormonal studies established the diagnosis of congenital adrenal hyperplasia due to 11-hydroxylase deficiency. Testicular biopsy revealed that the scrotal masses were adrenal rest tumors entirely composed of adrenocortical tissue. Primary testicular tissue was absent. The size of the tumors regressed following replacement steroid therapy together with restoration of normal blood pressure. This observation of a testicular adrenal rest tumor in a patient with 11-hydroxylase deficient congenital adrenal hyperplasia is unique.

Adolescent↗
PubMed1979

Usefulness of adrenal venography and iodocholesterol scan in adrenal surgery.

Adrenal scintiscanning and venography with sampling of adrenal venous blood are valuable methods to localize adrenal cortical lesions of Cushing's syndrome and primary aldosteronism. Adrenal scintiscanning with dexamethasone suppression is most useful in differentiating adenoma from hyperplasia of primary aldosteronism.

19-Iodocholesterol↗
PubMed1984

A comparison of the low-density-lipoprotein receptor from bovine adrenal cortex, rabbit and rat liver and adrenal glands by lipoprotein blotting.

This paper describes the use of lipoprotein blotting to detect low-density-lipoprotein (LDL) receptors in rat and rabbit liver and adrenal glands and in bovine adrenal glands. Using this technique we show that the rabbit and rat liver LDL receptors have Mr values of 128000 and 145000 respectively. Mr values for the rabbit, rat and bovine adrenal receptors are 131000, 142000 and 132000 respectively. Differences between the bovine adrenal and rat liver receptors are not due to differences in the degree of sialylation. Lipoprotein blotting can be used to detect dietary- and drug-induced changes in the concentrations of LDL receptors. When rabbits are fed on a cholesterol-rich diet, liver LDL receptors cannot be detected, consistent with the suppression of hepatic LDL receptors by cholesterol feeding. Pharmacological doses of 17 alpha-ethinyloestradiol cause a marked increase in hepatic LDL-receptor activity in the rat. This is accompanied by a corresponding increase in the number of LDL receptors detected by lipoprotein blotting. The Mr of the induced receptor is identical with that of the receptor from control rats, which suggests that the induced receptors are produced by the same gene as LDL receptors normally present in the liver.

Adrenal Cortex↗
PubMed1999

Effect of carbenoxolone on the plasma renin activity and hypothalamic-pituitary-adrenal axis in congenital adrenal hyperplasia due to 21-hydroxylase deficiency.

OBJECTIVE: To test the hypothesis that carbenoxolone, an inhibitor of 11beta-hydroxysteroid dehydrogenase, might augment the ACTH-suppressing and mineralocorticoid activities of hydrocortisone without a corresponding increase in peripheral hydrocortisone effects, we assessed the effects of carbenoxolone in patients with congenital adrenal hyperplasia. DESIGN AND PATIENTS: Six patients with classic 21-hydroxylase deficiency (5 salt-losing, 1 nonsalt-losing) were enrolled in this study. The study protocol involved 3 treatment periods (except for patient 3): phase 1, hydrocortisone and fludrocortisone; phase 2, hydrocortisone, fludrocortisone and carbenoxolone; phase 3, hydrocortisone and carbenoxolone. Patient 3 was not treated with fludrocortisone at baseline, so she participated only in phase 1 (hydrocortisone only) and phase 2 (hydrocortisone and carbenoxolone). Hydrocortisone and fludrocortisone dosages were kept the same during the study except for the discontinuation of fludrocortisone during phase 3. MEASUREMENTS: Plasma adrenal androgens or their precursors (androstenedione, 17-hydroxyprogesterone, and testosterone, and urine pregnanetriol); plasma cortisol, cortisol-binding globulin, ACTH, apparent cortisol metabolic clearance, 24-h urine 17-hydroxysteroids, and urine free cortisol; mineralocorticoid activity, as measured by plasma renin activity, body weight, plasma potassium, and mean blood pressure; fasting insulin/glucose ratio, protein balance, % eosinophils in peripheral blood, and total urine pyridinoline and deoxypyridinoline; TRH stimulation of TSH and pyridostigmine/GHRH stimulation of growth hormone. RESULTS: Compared to phase 1, the addition of carbenoxolone (with or without concurrent fludrocortisone administration) produced statistically significant decreases of 20-50% in mean plasma 17-hydroxyprogesterone, androstenedione, and renin activity. Since carbenoxolone also decreased the apparent metabolic clearance rate of cortisol by 20%, other measures of systemic glucocorticoid activity were examined. Carbenoxolone did not produce a cushingoid appearance or increase body weight, blood pressure, blood glucose or plasma insulin levels. Carbenoxolone also did not suppress stimulated GH levels, but did decrease TRH-stimulated TSH levels by approximately 20% (P < 0.05). CONCLUSION: Carbenoxolone can augment the adrenal androgen-suppressing activity of hydrocortisone in patients with 21-hydroxylase deficiency. These observations support the hypothesis that selective inhibition of enzymes that metabolize cortisol may lead to new approaches to improve the treatment of congenital adrenal hyperplasia.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed2005

Ectopic expression of vasopressin V1b and V2 receptors in the adrenal glands of familial ACTH-independent macronodular adrenal hyperplasia.

OBJECTIVE: ACTH-independent macronodular adrenal hyperplasia (AIMAH) is a rare and unusual cause of Cushing's syndrome, characterized by bilateral nodular adrenocortical hyperplasia and hypersecretion of cortisol. Familial AIMAH has rarely been reported. Recently, the aberrant expression of adrenal receptors for various ligands in AIMAH patients has become important in explaining the pathogenesis of AIMAH. In this study, we present the cases of two sisters who were affected with AIMAH. PATIENTS AND MEASUREMENTS: Two sisters, aged 46 and 58, respectively, at the time of diagnosis, were found to have Cushing's syndrome due to AIMAH. We performed provocation tests with various materials and reverse transcription polymerase chain reaction (RT-PCR) with their resected adrenal tissues to examine the hyper-responsiveness to steroidogenesis and the overexpression of related receptors, respectively. RESULTS: Provocation tests in vivo indicated that arginine vasopressin (AVP) promoted cortisol secretion through vasopressin V1a as well as V1b and V2 receptors. RT-PCR analysis revealed an abnormal cDNA expression of vasopressin V1b and V2 receptors, none of which is known to be normally expressed in the adrenal glands. CONCLUSION: The expression of ectopic vasopressin V1b and V2 receptors may be involved in the aetiology of AIMAH, at least in the case of the sibling patients presented here.

Adrenal Glands↗
PubMed1985

Adrenal insufficiency and bilateral adrenal enlargement: demonstration by computed tomography.

A patient presented with fever, malaise and a staphylococcal wound infection occurring 3 weeks after severe haemorrhage from a lacerated brachial artery. There were no clinical features to suggest Addison's disease but abdominal computed tomography to exclude abdominal sepsis showed bilateral adrenal gland enlargement with preservation of adrenal shape. This was consistent with resolving adrenal haemorrhage or infarction and endocrinological investigations confirmed primary adrenal failure.

Adrenal Glands↗
PubMed2005

Hypothalamic-pituitary disconnection in fetal sheep blocks the peripartum increases in adrenal responsiveness and adrenal ACTH receptor expression.

Although it has been recognized for over a decade that hypothalamic-pituitary disconnection (HPD) in fetal sheep prevents the late gestation rise in plasma cortisol concentrations, the underlying mechanisms remain unclear. We hypothesized that reductions in adrenal responsiveness and ACTH receptor (ACTH-R) expression may be mediating factors. HPD or sham surgery was performed at 120 days of gestation, and catheters were placed for blood sampling. At approximately 138 days of gestation, fetuses were killed, and adrenals were removed for cell culture and analyses of ACTH-R mRNA and protein. After 48 h, adrenocortical cells were stimulated with ACTH for 2 h, and the medium was collected for cortisol measurement. The same cells were incubated overnight with medium or medium containing ACTH or forskolin (FSK), followed by ACTH stimulation (as above) and cortisol and cellular ACTH-R mRNA analyses. HPD prevented the late gestation increase in plasma cortisol and bioactive ACTH and reduced adrenal ACTH-R mRNA and protein levels by over 35%. HPD cells secreted significantly less cortisol than sham cells (3.2 +/- 1.2 vs. 47.3 +/- 11.1 ng.ml(-1).2 h(-1)) after the initial ACTH stimulation. Overnight incubation of HPD cells with ACTH or FSK restored cortisol responses to acute stimulation to levels seen in sham cells initially. ACTH-R mRNA levels in cells isolated from HPD fetuses were decreased by over 60%, whereas overnight incubation with ACTH or FSK increased levels by approximately twofold. Our findings indicate that the absence of the cortisol surge in HPD fetuses is a consequence, at least in part, of decreased ACTH-R expression and adrenal responsiveness.

Adrenal Cortex↗
PubMed2001

Surgical management of isolated bilateral adrenal metastases from colon carcinoma causing adrenal insufficiency.

Adrenal insufficiency due to histologically proven bilateral metastatic adrenal involvement from colon cancer has been clinically reported only twice. Surgical treatment of bilateral adrenal metastases is seldom performed, since other metastatic localizations are usually concomitant. To the best of our knowledge, we report the first case of relatively long-term disease-free survival after bilateral adrenalectomy in a patient with adrenal insufficiency due to bilateral metastases from colon carcinoma.

Adenocarcinoma↗
PubMed2002

New diagnostic procedure for primary aldosteronism: adrenal venous sampling under adrenocorticotropic hormone and angiotensin II receptor blocker--application to a case of bilateral multiple adrenal microadenomas.

Formerly, the incidence of primary aldosteronism (PA) among patients with hypertension was believed to be less than 1%. However, recent studies have suggested a much higher incidence of 6.59%-14.4% among such patients. These findings suggest that many cases of PA caused by small aldosterone-producing adenoma (APA) or idiopathic hyperaldosteronism (IHA) have not been properly diagnosed. To make a more accurate diagnosis in such cases, we developed a new diagnostic procedure for localization of PA, namely, adrenal venous sampling under continuous infusion of adrenocorticotropic hormone (ACTH) and administration of angiotensin II receptor blocker (AVS with ACTH and ARB). Here, we confirm the efficacy of this procedure in the case of a 37-year-old male suspected of having PA. The anticipated diagnosis of PA was based on the presence of hypokalemia, low plasma renin activity (PRA), elevated plasma aldosterone concentration (PAC) and left adrenal mass. However, AVS with ACTH and ARB revealed the presence of bilateral multiple adrenal microadenomas. In the new AVS method, neither ACTH nor the renin-angiotensin system (RAS) exert any influence on the plasma aldosterone level, and a more accurate aldosterone secretary state and a more accurate assessment of the aldosterone secretion of both adrenal glands can be recognized than by conventional AVS. Use of this new method should enable identification of additional cases of APA among patients diagnosed with essential hypertension.

Adenoma↗