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PubMed1993

Primary adrenocortical nodular dysplasia presented as adrenal adenoma by functional scintigraphy.

This is a report of a case of a 12-year-old boy with Cushing's syndrome in which high doses of dexamethasone failed to suppress glucocorticoid secretion. Neither CT nor MRI (morphologic studies) revealed any adrenal abnormality. Functional images with NP-59 (I-131 beta-iodomethyl-norcholesterol) clearly revealed intense unilateral uptake in the right adrenal gland. A right adrenalectomy was performed, and the pathologic diagnosis was primary adrenocortical nodular dysplasia. One year later, the cushingoid signs had virtually disappeared and urinary steroid excretion and serum cortisol levels were within the normal range. Nevertheless, primary adrenocortical nodular dysplasia is essentially a bilateral disease. In this case, a remission in the adrenocortical hyperfunction was observed. Although there was confusion in the etiological diagnosis, functional scintigraphy correctly indicated the status of adrenal function.

Adenoma↗

PubMed2000

MR imaging of the adrenal neoplasms.

The most commonly encountered adrenal mass is the non-hyperfunctioning adrenal adenoma. Chemical-shift MR imaging can detect and characterize these adrenal masses as benign but cannot distinguish between hypersecreting and nonhypersecreting adrenal adenomas. Because of its direct multiplanar capability and superb soft tissue contrast, MR imaging can detect and potentially characterize other adrenal neoplasms.

Adrenal Cortex Neoplasms↗

PubMed1991

Inappropriate elevation of the aldosterone/plasma renin activity ratio in hypertensive patients with increases of 11-deoxycorticosterone and 18-hydroxy-11-deoxycorticosterone: a subtype of essential hypertension?

Among 436 patients with hypertension unrelated to any renal lesion, renovascular damage, pheochromocytoma, Cushing's syndrome or hyperthyroidism, 15 patients had low plasma renin activity (PRA) and elevated plasma aldosterone concentrations in the upright position and resultant high aldosterone/PRA ratios: 8 with aldosterone-producing adenoma (APA; group 1) and 7 with idiopathic hyperaldosteronism (IHA; group 2). Thirty-nine patients had suppressed PRA in the presence of normal plasma aldosterone levels and moderately elevated aldosterone/PRA ratios (group 3). Thirty of them had elevated plasma 11-deoxycorticosterone (DOC) and 18-hydroxy-11-deoxycorticosterone (18-OH-DOC) concentrations (group 3a) and 9 of them had normal levels of those mineralocorticoids (group 3b). The rest of them (382 patients) had low aldosterone/PRA ratios (group 4). Adrenal scintigraphy with dexamethasone pretreatment revealed [13I]-cholesterol accumulation not only in patients with APA (unilateral) or IHA (bilateral), but also in patients of group 3a (bilateral). In patients in groups 3a and 3b adrenal size (especially thickness), as measured by computed tomography (CT scan), was enlarged, as in patients with IHA (group 2), and was significantly greater than in patients of group 4 (p less than 0.001). Spironolactone reduced blood pressure in all tested patients of group 3a, and the removal of adrenal tumor or hyperplastic tissue normalized blood pressure in patients of groups 1, 2 and 3a. Excised adrenal glands exhibited cortical hyperplasia with or without nodular hyperplasia in patients of group 3a. Good agreement was found between the actual size of the excised tissue and the measurement obtained by CT scan. Since beta-endorphin and beta-lipotropin were depressed in patients of group 3a, it is suggested that an unknown pituitary substance stimulates the adrenal cortex to release too large amounts of DOC and 18-OH-DOC and inappropriate secretion of aldosterone.

18-Hydroxydesoxycorticosterone↗

PubMed1985

Glucocorticoid-suppressible hyperaldosteronism. Ultrastructural observation of a case.

A 56-year-old woman presented with intracranial hemorrhage. Laboratory examinations revealed severe hypertension, hypokalemia, elevated aldosterone excretion, and suppressed plasma renin activity. Left adrenocortical tumor was suspected and adrenalectomy was performed. The laboratory data after operation, however, showed no significant difference from the preoperative data. On the basis of further examinations, dexamethasone was administered and returned blood pressure to normal, and also normalized serum potassium, plasma aldosterone, and renin activity. The patient's illness was diagnosed as glucocorticoid-suppressible hyperaldosteronism. Light microscopically, the zona glomerulosa was hypertrophic and the outer zona fasciculata decreased in lipid droplets and was centrifugally arranged in small alveoli. Electronmicroscopically, the cells of the outer zona fasciculata had several lipid droplets and well-developed sER. Mitochondria were round to oval with lamellar or lamellovesicular cristae. These findings were evidence of hyperfunction. The cytoplasm of the cells also contained spironolactone bodies. Therefore, it is assumed that the aldosterone, which induced the disorder, was produced mainly in the outer zona fasciculata.

Adrenal Cortex↗

PubMed1978

Adrenal function testing.

Glucocorticoid stimulation and suppression tests are essential to the definitive diagnosis of diseases of the hypothalamic-pituitary-adrenal axis, because they document abnormal physiologic control of hormonal secretion. Similarly, diseases of the renin-angiotensin-aldosterone axis are diagnosed by mineralocorticoid stimulation and suppression testing. [Ed. Note: See Moore TJ, Williams GH: Adrenal causes of hypertension, in this issue.] Unlike tests of glucocorticoid function, testing of the renin-angiotension-aldosterone system is more complicated, because knowledge of posture and dietary sodium are necessary to interpret the results. However, measurement of the tropic hormone renin and plasma levels of aldosterone can be accurately made, allowing precise definition of this system. Errors are most commonly encountered when dynamic tests of cortisol output are performed in patients taking medications that may interfere with the assays or with the metabolism of the administered compounds, such as dexamethasone or metyrapone. Abnormal, spurious values may also be obtained in some individuals who do not have adrenocortical hyperfunction if they are very obese or if testing is performed in a setting of clinical stress. Careful attention to these pitfalls will avoid errors and allow the clinician to arrive at the correct diagnosis.

17-Hydroxycorticosteroids↗

PubMed1993

Estradiol stimulates cortisol production by adrenal cells in estrogen-dependent primary adrenocortical nodular dysplasia.

Adrenal glands from a patient with ACTH-independent Cushing's syndrome, whose symptoms worsened during pregnancy and oral contraceptive use, were cultured in different concentrations of estradiol. Estradiol stimulated cortisol secretion in a dose-response manner in the absence of ACTH. Since immunoglobulins G from this patient did not stimulate corticosterone production in a mouse adrenal bioassay, an adrenal-stimulating immunoglobulin is unlikely to be the cause of adrenal hyperfunction in this case. This is the first description of estradiol stimulation of cortisol production by cultured adrenal cells in ACTH-independent Cushing's syndrome.

Adrenal Cortex↗

PubMed1983

Familial Cushing's syndrome due to pigmented multinodular adrenocortical dysplasia.

Cushing's syndrome was diagnosed in a 14 year old girl and, 5 years later, in her nephew (sister's son) also when he was 14 years of age. Administration of tetracosactid (Synacthen) did not stimulate adrenocortical function in either patient, nor did dexamethasone suppress the elevated urinary steroids in the girl, and only partially suppressed them in the boy. Both patients were adrenalectomized and made an uneventful recovery. The surgical specimens were identical both on gross inspection and histologically, showing the typ ical morphological features of pigmented multinodular adrenocortical dysplasia. We believe that this lesion represents an inherited adrenocortical maldevelopment (rather than true neoplasia) leading to an autonomous adrenocortical hyperfunction which typically manifests itself clinically during adrenarche (i.e. functional adrenocortical maturation) at the beginning of puberty. Family Cushing's syndrome, caused by pigmented multinodular adrenocortical dysplasia, represents a disease entity.

17-Ketosteroids↗

PubMed1977

Radioisotopic study of the adrenal glands using 131I-19-iodocholesterol.

Scintigraphy of the adrenal gland with 131I-19-iodocholesterol has recently been added to radiological techniques in adrenal imaging and has been used successfully to demonstrate anatomical and functional disorders of the adrenals in a variety of clinical situations. A review of the authors' experience stresses the diagnostic value of this method. Radiological findings and results of scintillation imaging are complementary: their comparison improves and clarifes indications for scintigraphy. Hyperadrenal cortical diseases always gave satisfactory scintigrams, the most interesting results being obtained in adrenal cortical hyperplasia and unilateral hyperfunctioning adenomas. In these cases the evaluation of the response to stimulation or suppression tests was very useful. On the other hand scintigraphy was less valuable in demonstrating malignant and non malignant tumours.

Adenoma↗

PubMed1993

Adrenomedullary hyperplasia associated with cortisol producing adenoma.

We report a case of a 58-year-old man with adrenal medullary hyperplasia associated with cortisol producing adenoma. Preoperative examination showed both adrenocortical and adrenomedullary hyperfunction. No Cushingoid sign was present and pheochromocytoma-like symptoms were predominant. Abdominal computerized tomography revealed a left adrenal tumor stained by contrast medium. Histologically, the adrenal tumor was found to be a cortical adenoma, and medullary hyperplasia was observed in the remaining parenchyma.

Adenoma↗

PubMed2003

Computed tomography-guided percutaneous acetic acid injection therapy for functioning adrenocortical adenoma.

We reported the outcomes of computed tomography (CT)-guided percutaneous acetic acid injection therapy for functioning adrenocortical adenomas. With the patient in a prone position, the puncture needle was inserted vertically downward into the adenoma with frequent CT scanning. After confirmation by pilot injection with contrast medium, a small aliquot of 40-50% acetic acid was injected and repeated. Between 1997 and 2002, 18 sessions of CT-guided injection therapy, including one session of ethanol injection, were performed on 10 patients (five patients with primary aldosteronism and five patients with Cushing's or subclinical Cushing's syndrome) without any complications except transient upper abdominal pain during the acetic acid injection. The follow-up period ranged from 5-69 months. The treatment resulted in almost an extirpation of the adrenocortical hyperfunction in seven patients after one or two sessions. CT-guided percutaneous acetic acid injection might be a simple, cost-effective, and far less invasive treatment for small functioning adrenocortical adenomas.

Acetic Acid↗

PubMed1997

Plasma dehydroepiandrosterone sulfate levels in patients with hyperfunctioning and non-hyperfunctioning adrenal tumors before and after adrenal surgery.

To investigate the clinical significance of plasma dehydroepiandrosterone sulfate (DHEAS) measurements, 175 patients with histologically confirmed adrenal tumors, 10 cortisol-producing adenomas, 59 aldosterone-producing adenomas, 56 non-hyperfunctioning adenomas, 13 adrenocortical carcinomas, 13 adrenal cysts, and 24 adrenomedullary tumors were studied. Plasma DHEAS levels were expressed as percentage of the mean of sex- and age-matched groups of healthy, normal subjects (DHEAS %). We found that before adrenal surgery, DHEAS % values were significantly reduced in patients with cortisol-producing (mean, 15.2% of control; 95% confidence interval (CI), 9.4-24.7%), non-hyperfunctioning (28.4%; 22.4-36.0%) as well as aldosterone-producing adrenocortical adenomas (55.4%; 47.1-65.1%) compared with controls, while values were normal in patients with adrenal cysts and in those with adrenomedullary tumors. Plasma DHEAS % values exhibited a great variability in adrenocortical carcinomas (mean, 84.0%; 95% CI, 33.2-212.5%). Death from adrenocortical carcinoma was more frequent in patients with high plasma DHEAS % values compared with those with low DHEAS %. During long-term postoperative monitoring, we found that plasma DHEAS levels of patients with aldosterone-producing and non-hyperfunctioning adenomas returned to normal in the second and fourth postoperative year respectively. In patients with cortisol-producing adenomas, plasma DHEAS remained suppressed for as long as 8 years after the operation. These findings show that except in adrenocortical carcinomas and cysts, plasma DHEAS levels are significantly decreased in all groups of adrenocortical tumors, including non-hyperfunctioning and aldosterone-producing tumors. The extent of this decrease and the postoperative persistence of suppressed plasma DHEAS levels may be related to the glucocorticoid production of adrenocortical tumors.

Adenoma↗

PubMed2005

Tomographic evaluation of [131I] 6beta-iodomethyl-norcholesterol standardised uptake trend in clinically silent monolateral and bilateral adrenocortical incidentalomas.

AIM: The aim of this study was three-fold: 1) to quantify [131I]-6beta-iodomethyl-norcholesterol ([131I]-NP-59) adrenal uptake trend in patients with incidentalomas, 2) to identify a specific uptake trend (TREND) capable of characterising pre-clinical Cushing syndrome (PC-CS) patients, 3) to assess the clinical availability of TREND as a prognostic factor of late clinical outcome in a cohort of patients with bilateral adrenal adenomas. METHODS: Fifty-seven consecutive patients were examined using three-head SPECT at 24, 48, 72 hours following intravenous injection of [131I ]-NP-59. On the basis of the absence or presence of hormonal abnormalities, the selected population was classified as GR1 or GR2, respectively. Adrenal glands were classified into 4 groups taking into account both the patient group (GR1, GR2) and the presence (+) or absence (-) of the adenoma (AD) on CT scan. Using ROI technique, adrenal-liver uptake ratio (A/L) was estimated bilaterally at 24, 48 and 72 hours. For each adrenal group, mean [131I]-NP-59 uptake trends were derived. RESULTS: TREND was significantly different between GR1/AD+ and GR2/AD+. Among GR2/AD+ patients, TREND correctly identified PC-CS with a global accuracy of 74%. Two patients with bilateral incidentaloma developed an overt CS. In both patients, TREND correctly identified the hyperfunctioning adrenal, thus permitting an effective sparing adrenalectomy. CONCLUSIONS: TREND seems to be a parameter which closely reflects adrenal physiological behaviour, especially in the case of bilateral adrenal involving. The possibility to quantify even contralateral adrenal uptake as standardised index provides additional useful information about normal adrenal parenchyma and, indirectly, about adenoma functional autonomy.

19-Iodocholesterol↗

PubMed2006

[Subclinical Cushing's syndrome in adrenal incidentalomas].

In the heyday of high-tech medicine, the incidental discovery of an adrenal mass is a frequent event owing to the routine use of sophisticated radiological techniques. The potential harm to health associated with incidentally discovered cortical adenoma, the most frequent tumor among adrenal incidentalomas, is unclear at present. Incidentally discovered adrenal adenoma may secrete cortisol autonomously, in a way that is no longer under close control by pituitary feedback, in 5 to 20% of cases. At present, data are insufficient to estimate the outcome of patients with subclinical Cushing's syndrome. However, evidence is gathering that subclinical Cushing's syndrome may contribute to develop the phenotype of insulin resistance thus portending to atherosclerosis and relevant cardiovascular complications. It is tempting to speculate that subclinical Cushing's syndrome represents a very mild variant of endogenous glucocorticoid excess syndrome. Even if progression to overt glucocorticoid excess is rare, subclinical Cushing's syndrome has the potential to carry an adverse prognosis. At present, data are insufficient to indicate the superiority of a surgical or nonsurgical approach to manage patients with subclinical hyperfunctioning adrenal cortical adenoma. It is of the utmost importance to establish collaborative prospective studies with clearly defined entry criteria and standardized evaluation protocols and treatment modalities to appraise the natural history and long-term morbidity of clinically inapparent adrenal adenoma and subclinical Cushing's syndrome.

Adrenal Cortex Neoplasms↗

PubMed1995

Adrenal cortical and medullary imaging.

Adrenal disease can be manifested by endocrine dysfunction or anatomic abnormalities detected by cross-sectional imaging modalities. With the advent of newer and more reliable in vitro assays and a better understanding of the spectrum of adrenal pathology, the physician can now adopt a more accurate and cost-effective approach to the diagnosis of adrenal disease. Both functional and anatomic imaging modalities can play an important role in the evaluation of the incidental adrenal mass, the early detection of adrenal metastases, differentiation of the various causes of Cushings's syndrome, selection of patients for potentially curative surgery in primary aldosteronism and adrenal hyperandrogenism, and localization of pheochromocytomas and neuroblastomas. The usefulness of the adrenal cortical radiopharmaceutical, 131I-6-beta-iodomethylnorcholesterol (NP-59), and the adrenal medullary radiopharmaceuticals, 131I and 123I-metaiodobenzylguanidine (MIBG), is detailed for these various clinical settings and the role of NP-59 and MIBG is contrasted to that of the cross-sectional modalities, computed tomography and magnetic resonance imaging (MRI). Incidental adrenal masses are common, but malignancies are few. Imaging studies select those patients who require a further evaluation by biopsy examination or adrenalectomy. In the hyperfunctioning endocrine states, such as Cushing's syndrome, primary aldosteronism, adrenal androgenism, and pheochromocytoma, correlation of biochemical findings with both functional and anatomic imaging is necessary to avoid inappropriate and ineffective surgical intervention, yet not miss an opportunity for curative resection. Lastly, MIBG and MRI are complementary in the detection and staging of neuroblastoma.

3-Iodobenzylguanidine↗

PubMed2004

Morphology of the pituitary gland in ferrets (Mustela putorius furo) with hyperadrenocorticism.

Pituitary tumours are the cause of hyperadrenocorticism in a variety of species, but the role of the pituitary gland in hyperadrenocorticism in ferrets is not known. In this species, the disease is mediated by the action of excess gonadotrophins on the adrenal cortex and is characterized by an excessive secretion of sex steroids. In this study, the pituitary gland of four healthy control ferrets, intact or neutered, and 10 neutered ferrets with hyperadrenocorticism was examined histologically following immunohistochemical labelling for adrenocorticotrophic hormone, alpha-melanocyte-stimulating hormone, growth hormone, thyroid-stimulating hormone, luteinizing hormone, follicle-stimulating hormone, and prolactin. Immunohistochemistry revealed that somatotrophs, thyrotrophs and lactotrophs were the most abundant cell types of the pars distalis of the pituitary gland in the healthy ferrets. The distribution of corticotrophs was similar to that in the dog and man. In ferrets, as in dogs, the melanotrophic cell was almost the only cell type of the pars intermedia. Gonadotrophs were found in the pars distalis of neutered, but not intact ferrets. All the ferrets with hyperadrenocorticism had unilateral or bilateral alterations of the adrenal gland. In addition, in the pituitary gland of two of these ferrets a tumour was detected. These tumours were not immunolabelled by antibodies against any of the pituitary hormones, and had characteristics of the clinically non-functional gonadotroph tumours seen in man. In some of the other ferrets low pituitary immunoreactivity for gonadotrophic hormones was detected, which may have been due to the feedback of autonomous steroid secretion by the neoplastic transformation of the adrenal cortex. It is concluded that initially high concentrations of gonadotrophins resulting from castration may initiate hyperactivity of the adrenal cortex. The low incidence of pituitary tumours and the low density of gonadotrophin-positive cells in non-affected pituitary tissue in this study suggest that persistent hyperadrenocorticism is not dependent on persistent gonadotrophic stimulation.

Adenoma↗

PubMed1976

[Ways of correcting certain metabolic processes in the myocardium in myocardial insufficiency].

The article deals with the following trends along which according to the author, investigations aimed at search for ways of correcting disturbed metabolic processes in the cardiac muscle in its incompetence should develop: 1) restoration of properties of contractile proteins and creation of a basis for successful formation of the processes of compensatory hyperfunction and hypertrophy of the myocardium; 2) correction of the electrolytic balance with regulation of the skin mechanisms of the process of contraction of myofibrils; 3) restoration of the energy potential of cells; 4) withdrawal of the damaging effect upon the myocardium of some products of its disturbed metabolism.

Acidosis↗

PubMed1978

Preadolescent and adolescent endocrinology: physiology and physiopathology. II. Hormonal changes during abnormal pubertal development.

Based on the knowledge of the physiology of regulation of gonadotropins and gonadal steroids, basal levels of these hormones might be indicative of the etiologic factors of abnormal pubertal development. In addition, stimulatory tests may help in the diagnosis of such conditions. It is interesting that the pubertal maturation of the adrenal cortex is independent of the hypothalamic-pituitary-gonadal axis. The role of the adrenal cortex for the pubertal development remains questionable: adrenal androgens are low in isosexual precocious puberty, low in delayed adolescence, and normal in hyper- or hypogonadotropic hypogonadism. The importance of this role is doubled in congenital virilizing adrenal hyperplasia. When the disease is untreated, although adrenal androgens in excess advance bone age and hypothalamic maturation, girls remain prepubertal. When the therapeutic control is good, normal puberty occurs. The action of the adrenal androgens on growth and puberty remains to be determined.

Adolescent↗

PubMed1969

Plasma progesterone and 17-hydroxyprogesterone in normal men and children with congenital adrenal hyperplasia.

Plasma 17-hydroxyprogesterone (17-OHP) concentrations in normal men averaged 0.094 mug/100 ml. Studies using suppressive doses of androgens and glucocorticoids showed that 90% of the 17-OHP originated from the Leydig cell. The 17-OHP production rate was 1.8 mg/24 hr. Plasma 17-OHP has a marked circadian variation, the 8 p.m. values being only 40% of the 8 a.m. values. Plasma luteinizing hormone measured in the same samples did not vary. The adrenal cortex has the capacity to synthesize and secrete 17-OHP and progesterone since adrenocorticotrophic hormone (ACTH) caused a fourfold increase in these plasma steroids. In children with congenital adrenal hyperplasia, plasma 17-OHP levels were 50-200 times those of normal men and plasma progesterone was increased 6- to 10-fold over normal men.

Adolescent↗