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PubMed1988

Hypercortisolism and the resistance to dexamethasone suppression during gestation.

Maternal adrenocortical function was studied by measuring plasma cortisol and urinary free cortisol during gestation. Changes in suppressibility of pituitary-adrenocortical function were determined by dexamethasone administration. Urinary free cortisol as well as plasma cortisol increased during the course of gestation. The suppressibility by dexamethasone became less effective as pregnancy advanced. These results suggest that pregnant women have pituitary-adrenocortical hyperfunction and tissue refractoriness to glucocorticoid which increases during the course of gestation.

Adrenal Cortex↗
PubMed1986

Primary pigmented nodular adrenocortical disease: diagnosis and management.

A rare cause of Cushing's syndrome appearing to originate in the adrenal glands is primary pigmented nodular adrenocortical disease (PPNAD). It may be variably associated with a complex of other pathologic characteristics that include cardiac myxomas, cutaneous myxomas, and lentigines, mammary myxoid lesions, testicular tumors, pituitary adenomas, and neuroectodermal tumors. We have reviewed the clinical, biochemical, radiographic, operative, and pathologic details of seven patients with PPNAD who have been evaluated at Mayo Clinic. Biochemical testing supported autonomous adrenal hyperfunction. This was based on the failure of cortisol suppression by high-dose dexamethasone, failure of pituitary stimulation by metyrapone administration, either normal or suppressed basal adrenocorticotropic hormone (ACTH) levels, normal radiographic studies of the sella turcica, and normal abdominal and thoracic computerized tomography in search of an ectopic ACTH-producing tumor. Six patients underwent bilateral total adrenalectomy without postoperative complications. Nelson's syndrome has not occurred, but acute adrenocortical insufficiency may have contributed to the death of one patient. To recognize the possible diagnosis of PPNAD preoperatively is important to proceed directly with adrenalectomy, avoiding unnecessary pituitary surgery. Moreover, if PPNAD is part of the broader pathologic complex, the possible presence of cardiac myxomas that may be multiple, recurrent, in atypical locations, and familial must be borne in mind.

Adolescent↗
PubMed1981

[Circadian rhythm of free catecholamine excretion in disturbed adrenal function (author's transl)].

The daily time course of urinary catecholamine excretion was determined for hyperactivity of the sympathoadrenal system (3 phaeochromocytomas, 1 neuroblastoma), disturbed adrenal function (M. Addison and partial adrenal insufficiency), bilateral adrenalectomy (one patient), in 8 healthy patients receiving dexamethasone, and in a control group. All groups showed a circadian rhythm of catecholamine excretion. In the patients with phaeochromocytoma, the excretion of catecholamines and vanilmandelic acid showed a shift of phase compared with the control group. In patients with hyperfunction of the sympathoadrenal system, catecholamines and vanilmandelic acid fluctuated with similar amplitudes, whereas in healthy patients vanilmandelic acid and dopamine showed much smaller fluctuations of concentration than adrenaline and noradrenaline.

Adrenal Gland Diseases↗
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↗
PubMed1988

Perianal adenomas and hypertestosteronemia in a spayed bitch with pituitary-dependent hyperadrenocorticism.

Hypertestosteronemia was diagnosed in a spayed bitch with pituitary-dependent hyperadrenocorticism and perianal adenomas. Serum concentrations of cortisol and testosterone decreased after treatment with mitotane was instituted. Excessive testosterone in this dog was thought to have been produced by the adrenal cortex, possibly in response to excessive ACTH concentrations. Development of androgen- or estrogen-responsive tumors in castrated dogs may be an early indication of adrenocortical hyperfunction.

Adenoma↗
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↗
PubMed1985

The utility of adrenal scintigraphy in Cushing's syndrome and hyperaldosteronism.

Thirty-three adrenal scintigrams in 30 patients were reviewed to determine the utility of this noninvasive imaging technique. It was found to be very accurate in distinguishing bilateral from unilateral hyperfunction in patients who have clinical and biochemical evidence of adrenal cortical hyperfunction. The technique proved correct in 12 of 12 cases of Cushing's syndrome and 14 of 19 cases of hyperaldosteronism. Specific clinical questions were also answered in three miscellaneous cases.

19-Iodocholesterol↗
PubMed1993

[The effect of adrenal-regeneration hypertension on protein-nucleic acid metabolism in rat atrial cardiomyocytes].

A study was made on cardiomyocytes of the left atrium of rats with experimental arterial hypertension due to adrenal regeneration. The nuclear DNA and the total protein in the cytoplasm were revealed using two consecutive tests: the Feulgen reaction, and Naphthol yellow S staining. The two-wavelength scanning cytophotometry was used for measuring DNA and protein contents. It has been ascertained that the polyploidy level in the nuclei of the left atrium myocytes, measured 6 and 9 weeks after nephradrenalectomy, remained the same as in the intact animals. The increase in the share of tetra- and octaploid nuclei occurred by 12 weeks. The mean nuclear volume decreased gradually throughout 9 weeks and subsequently was seen to increase, but by 12 weeks it did not yet reach the control level. The cytoplasm volume decreased by 6 weeks, then started to increase by 9 weeks to reach almost the standard level. The common protein content in the atrial myocytes decreases also by 6 weeks, but restores more rapidly than the volume, and reaches the standard level by 9 weeks, exceeding the same by 12 weeks. Thus, the prolonged hyperfunction of the atrial cardiomyocytes, associated with arterial hypertension, results in their hypertrophy which becomes apparent both in the increased polyploidy and in the augmented protein mass of the cells.

Adrenal Glands↗
PubMed1976

The influence of streptozotocin diabetes on adrenal function in male rats.

Male Wistar rats were treated with an i.v. dose of 100 mg/kg of Streptozotocin (STZ). Either 5 days or 1, 2 or 3 months after induction of diabetes, the adrenal function of these animals was studied. Short course diabetes (5 days) was accompanied by adrenal hypertrophy and high plasma corticosterone levels; during later periods the diabetic rats consistenly showed signs of adrenal hyperactivity, yet both adrenal weight and plasma corticosterone tended to be lower than in the 5 day-treated animals. Adrenal incubations with 14C-progesterone showed that 5 days and one month diabetic animals synthesized more deoxycorticosterone than controls; production of corticosterone and 18-hydroxydeoxycorticosterone was normal at all time periods studied. Synthesis of 18-hydroxycorticosterone, a compound which affects sodium metabolism, was increased in 5 day-treated rats; thereafter, the function of the zona glomerulosa seemed to be impaired in diabetic rats. These results suggest that early after induction of diabetes there is adrenal hyperfunction of the mixed type (i.e. gluco and mineralcorticoid), and that in the later periods (2-3 months), the deranged metabolism of the diabetic rat acts as a chronic stress.

Adrenal Glands↗
PubMed1980

Primary aldosteronism due to unilateral adrenal hyperplasia.

A 45-yr-old man with hypertension, hypokalemia, low plasma renin, and hyperaldosteronism was studied. Plasma and urine aldosterone were consistently above normal, remaining abnormally high even on a 300-meq sodium intake. Plasma aldosterone had a marked circadian rhythm, which was correlated with plasma cortisol. Aldosterone secretion was temporarily suppressed after dexamethasone administration and was stimulated by exogenous ACTH. The effect of posture was variable in the eight studies performed, possible due to episodic secretion of aldosterone observed near the sampling times of 0800 and 1200 h. Blood from the right adrenal vein contained 50--100 times more aldosterone than the left adrenal venous samples. The right adrenal gland was excised and found to contain many microscopic subcapsular nests of clear cells. Plasma aldosterone, renin, and potassium returned to normal after surgery, and blood pressure fell to 120/75 over the next 8 months. Three years later, the patient is normotensive without drugs.

Adrenalectomy↗
PubMed1982

Scintigraphy in pheochromocytoma.

In four patients with pheochromocytoma, scintigraphy with 131I-meta-iodobenzylguanidine was performed to localize hyperfunctioning adrenergic tissue. In three patients unilateral adrenal pheochromocytoma was found, whereas one patient with a malignant pheochromocytoma showed multilocular dissemination. The results document that scintigraphy with 131I-meta-iodobenzylguanidine seems to be a safe and reliable method of detecting adrenal and extra-adrenal pheochromocytomas, both benign and malignant.

3-Iodobenzylguanidine↗
PubMed1996

Magnetic resonance imaging of adrenocortical adenomas in childhood: correlation with computed tomography and ultrasound.

There are few descriptions of the magnetic resonance (MR) appearance of hyperfunctioning adrenocortical tumours, particularly those occurring in childhood. We studied five patients, two girls and three boys, aged 6-14.3 years, presenting with clinical syndromes of adrenocortical hyperfunction. The diagnoses were Cushing's syndrome (n = 2), virilisation (n = 2), and Conn's syndrome (n = 1). Biochemical features suggested an adrenal lesion in each case. MR and ultrasound were performed in all five cases, with CT in four. Each patient had a functional adrenal tumour secreting either cortisol, androgens or aldosterone alone, or a combination of cortisol, androgens and oestradiol. The histological diagnosis was adenoma in four cases and tumour of indeterminate nature in one case. MR clearly showed the tumours (diameter 1.0-7.5 cm), all the lesions being of high signal intensity relative to liver on T2-weighted sequences. CT revealed an adrenal mass in each of the four patients scanned, three of which enhanced after intravenous contrast medium injection. The multiplanar imaging of MR allowed better distinction from adjacent structures and also demonstrated an unenlarged contralateral adrenal gland. In the patient with a 1-cm Conn's adenoma the lesion was more easily seen on MR than CT. Ultrasound showed the four larger tumours but was unable to visualise the contralateral adrenal or the Conn's adenoma. In conclusion, the MR appearances of four adrenocortical adenomas and one indeterminate tumour in children are described. MR has been found to be at least equal to CT in the detection of these tumours, with some possible advantages. Both techniques are superior to ultrasound.

Adenoma↗
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↗
PubMed1976

Endocrinopathy in thalassaemia major.

Pituitary, adrenal, and pancreatic functions were investigated in 9 patients with thalassaemia major. 9 a.m. plasma ACTH values were 148-480 pg/ml (normal range 15-70 pg/ml). Cortisol and growth hormone response to insulin-induced hypoglycaemia was normal in all. 24-hour urinary excretions of 17-ketosteroids and 17-hydroxycorticosteroids were normal. There was normal cortisol response to intramuscular injection of ACTH. In a physiological adrenal stimulation test there was a significantly smaller response to each physiological dose of tetracosactrin. 4 patients had diabetic glucose tolerance tests--none are clinically diabetic. The mean plasma glucose utilization constant (Kgl=2-02) is significantly smaller than normal. Plasma insulin response both in the oral and the intravenous glucose tolerance test was significantly smaller than normal. The data were consistent with severe and widespread impairment of endocrine function and a plausible explanation would be iron deposition in endocrine organs. It is suggested that pituitary hyperfunction of ACTH secretion is due to target organ unresponsiveness which can be shown in its early stages only by a physiological test of the adrenal cortex. Skin pigmentation in thalassaemia seems to be due to the melanophore-stimulating effect of this raised plasma ACTH.

17-Hydroxycorticosteroids↗
PubMed2005

Clinical study of adrenal incidentaloma in Korea.

BACKGROUND: This study was designed to evaluate the clinical, endocrinological and histological characteristics of adrenal incidentalomas. METHODS: Eighty patients (41, males; 38, females; age range 17-80 years) who were diagnosed with adrenal incidentaloma at Korea University Hospital from 1992 to 2003 were studied retrospectively. RESULTS: Endocrinological investigation revealed 16 pheochromocytomas (20%), nine Cushing's syndromes (11%), eight primary aldosteronism (10%) and 46 non-functioning tumors (58%). Forty-four patients received operations, and biopsies were performed on two patients. Pathologic examination revealed 16 adrenocortical adenomas (20%), five carcinomas (6%), 13 pheochromocytomas (16%), three metastatic cancers (4%), and other tumors (10%). The diameter of the carcinomas (mean: 10.8 cm, range: 5-19 cm) were significantly larger than the diameter of benign adenomas (mean: 2.84 cm, range: 1-6 cm) (p=0.002). According to the receiver operating charactenstic (ROC) curve analysis, the cut-off value of tumor size for discriminate malignant tumor was 4.75 cm (sensitivity 90%, specificity 58%). Twenty-four patients with non-functioning tumors were followed up for a period of 3 to 72 months. During the follow up period, two patients showed an increase in tumor size of more than 1 cm, and one patient developed Cushing's syndrome. Changes in mass size and function were observed only between 10 and 26 months after the initial diagnosis. CONCLUSIONS: These data show that an endocrine evaluation should be performed in all adrenal incidentalomas, and an adrenalectomy is recommended for tumors 5 cm or greater or tumors with adrenocortical hyperfunction. In addition, these tumors should be monitored for changes in mass size and function for a follow up period of approximately 26 months.

Adolescent↗
PubMed1991

Routine inferior petrosal sinus sampling in the differential diagnosis of adrenocorticotropin (ACTH)-dependent Cushing's syndrome: early recognition of the occult ectopic ACTH syndrome.

The clinical, biochemical, and radiographic features of ectopic ACTH-dependent Cushing's syndrome are often indistinguishable from those of pituitary ACTH-dependent hypercortisolism (Cushing's disease). We prospectively evaluated 29 patients with ACTH-dependent hypercortisolism by means of bilateral inferior petrosal sinus ACTH sampling with ovine CRH (oCRH) stimulation. Patients with Cushing's disease (n = 20), had a maximal basal inferior petrosal sinus to peripheral ACTH ratio (IPS:P-ACTH) of 11.7 +/- 4.4 (+/- SE) from the dominant IPS, which increased to 50.8 +/- 18.3 after oCRH administration. Bilateral IPS sampling was necessary to correctly identify patients with Cushing's disease, since the maximal basal nondominant IPS:P-ACTH was less than 2.0 in over 50% of the patients and remained less than 2.0 after oCRH administration in one third. In contrast, patients with occult ectopic ACTH-secreting neoplasms (n = 9) had maximal basal IPS:P-ACTH of 1.2 +/- 0.1 that did not change after oCRH administration. Occult ectopic ACTH-secreting neoplasms were found in 7 of 9 patients from 0.4-14 yr after the recognition of Cushing's syndrome, and 4 of these patients had intermittent hypercortisolism with prolonged periods of remission. Selective endobronchial lavage for ACTH correctly localized a radiologically occult ACTH-secreting bronchial carcinoid in 1 patient, and magnetic resonance imaging identified a similar neoplasm in a patient with a normal chest computed tomographic scan. Basal ACTH and urinary free cortisol excretion were significantly higher in patients with ectopic ACTH than in those with Cushing's disease, but overlap existed between groups. High dose dexamethasone suppression testing inaccurately classified 24% of patients, and radiological imaging of the pituitary and adrenal glands was misleading. The occult ectopic ACTH syndrome is a common form of ACTH-dependent hypercortisolism that cannot be distinguished from Cushing's disease with routine clinical studies. The accurate differential diagnosis of ACTH-dependent Cushing's syndrome requires bilateral inferior petrosal sinus ACTH sampling with oCRH stimulation.

Adrenocortical Hyperfunction↗
PubMed1978

Adrenal scanning and uptake with 131I-6beta-iodomethyl-nor-cholesterol.

Adrenal scans were obtained in 50 patients with suspected adrenal disease; 131I-19-iodocholesterol was used in 12 and 131I-6-beta-iodomethyl cholesterol (NP-59) in 38 cases (42 scans). The scan diagnosis was correct in 48 patients. Successful images were obtained with 0.5 mCi, or less, of NP-59 instead of the standard dose of 2 mCi, thus reducing radiation dose to the patient and cost of the agent. Satisfactory scans were obtained in 2--3 days in patients with hyperfunctioning adrenals, and in 3--7 days in other groups of patients, when NP-59 was used. With 131I-19-iodocholesterol, however, 5--10 days were required for optimal results in all patients including those with Cushing disease. Adrenal uptake studies were very useful in the evaluation of adrenal function, particularly in differentiating bilateral hyperplasia from normal adrenals.

Adrenal Gland Diseases↗
PubMed1989

Scintigraphic studies in adrenal hypertension.

Endocrine hypertension secondary to disorders of the adrenal glands is uncommon, but by no means rare. The importance of correct biochemical diagnosis and subsequent localization of the responsible lesion(s) lie in the fact that many of these syndromes occur in younger patients, may exhibit familial patterns of inheritance and are frequently amenable to surgical cure. The radiopharmaceuticals (131)1-6 beta-iodomethyl-19-norcholesterol (NP-59), a marker of adrenocortical cholesterol uptake, and (131)1- and (123)1-metaiodobenzylguanidine (MIBG), a norepinephrine (NE) analog and marker of energy-dependent NE storage vesicle accumulation, can be shown to accurately localize adrenal cortex and sympathoadrenal dysfunction, respectively. In Cushing's syndrome (CS) not only does the pattern of NP-59 uptake depict the adrenal dysfunction and its pathophysiologic basis, but the level of NP-59 accumulation reflects the degree of adrenocortical hyperfunction. Adrenocorticotrophin-independent CS is uniformly and accurately localized, especially in bilateral cortical nodular hyperplasia where even high resolution computed tomography (CT) may fail to depict the often subtle, asymmetric anatomic abnormalities. Dexamethasone suppression NP-59 adrenal scintigraphy has been shown to be highly sensitive and specific, and exceeds the efficacy of CT in the differentiation of adenoma and bilateral hyperplasia in primary aldosteronism. MIBG is useful as a sympathoadrenal imaging agent whose clinical utility has been demonstrated in the localization of pheochromocytoma, especially as a modality to screen the body for multiple and extraadrenal, recurrent, or metastatic lesions. Moreover, the extent of metastatic involvement from neuroblastoma can also be accurately depicted using MIBG. In this review we will examine the role of adrenal scintigraphy in the characterization of hypersecretory disorders of the adrenal cortex, medulla, and related conditions that produce hypertension as part of their symptom(s) complex. This approach, which is complementary to other anatomical modalities of imaging, can be used to advantage in the localization of functioning cortical and medulla adrenal diseases and other neoplasms of adrenergic origin.

3-Iodobenzylguanidine↗