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At least 811 records · Page 45Linked to original sources
PubMed1989

Adrenal imaging.

CT provides exquisite anatomic detail of normal and pathologic adrenal glands but little specificity as to the nature of adrenal masses. MR reliably distinguishes non-functioning and hyperfunctioning adenomas (adrenal mass/liver ratio less than 1.2) and pheochromocytomas (adrenal mass liver ratio greater than 2.5). Metastases to the adrenal gland and primary adrenocortical carcinomas lie in the intermediate range (adrenal mass/liver ratio 1.4-2.5). Particularly problematic are masses with ratios in the 1.2-1.4 range since some non-functioning adenomas and some metastases will have similar signal intensities and cannot be distinguished.

Adenoma↗
PubMed1977

[Morphofunctional reaction of the cortical lamina of the adrenal gland to reparative osteogenesis and administration of thyrocalcitonin].

A complex of morphofunctional changes of the adrenal cortex was studied on 150 albino male rats in case of thyrocalcitonin (TCT) administration and experimental fracture. There proved to be an increase of functional activity of the gland under conditions of reparative osteogenesis. The state of hyperfunction developed the first five days of TCT administration in a dose of 5 Units daily. The following saturation of the organism with TCT caused depression of the adrenal gland, particularly of its glucocorticoid function. It is supposed that the inhibitory effect of TCT on the adrenal cortex served as one of the mechanisms accelerating the repair processes in the bone tissue.

Adrenal Cortex↗
PubMed1979

Evaluation of steroid laboratory tests and adrenal gland imaging with radiocholesterol in the aetiological diagnosis of Cushing's syndrome.

Basal values of the urinary excretion of 17-oxogenic steroids and serum levels of cortisol were not satisfactory in the differentiation of 'suspected' subjects from patients with true Cushing's syndrome. With an RIA method for serum cortisol determination, the overnight dexamethasone suppression test provided the most reliable single test in establishing adrenocortical hyperfunction. Thirty-five normal subjects, fifty-nine obese patients, thirteen 'suspected' patients, and thirteen patients with disease states other than Cushing's syndrome had suppressed values below 4.0 microgram/100 ml. None of the ten patients with Cushing's syndrome had a cortisol concentration less than 16.3 microgram/100 ml. Adrenal gland scintigraphy after radiocholesterol injection is a more valuable tool than the metyrapone test and the high-dose dexamethasone suppression test in the localization and differential diagnosis of adrenocortical lesions causing Cushing's syndrome. It obviates the need for angiographic procedure in the localization of adenomas. It is a reliable technique for identifying functioning adrenal remnants. We therefore propose a schedule for studying patients with suspected adrenocortical hyperfunction.

17-Ketosteroids↗
PubMed2002

Growth in disorders of adrenal hyperfunction.

Growth is disturbed by adrenal hypersecretion of androgens or cortisol. Androgen excess in virilizing adrenal tumours causes advanced growth and bone age. In 9 girls with virilizing tumours, mean heights at diagnosis and final heights were 1.23 +/- 0.42 and 1.3 +/- 0.37 SDS respectively. In poorly controlled CAH, excess androgens cause early epiphyseal fusion and adult short stature. Increased growth occurs only after 18 months of age, even in untreated CAH, i.e. hydrocortisone >10 mg/m(2)/day is not generally required and may suppress infantile growth, affecting childhood and adult height. Growth was studied in 19 patients, aged 6.4-17.8 years, with Cushing's disease (CD). At diagnosis, mean height SDS was -1.81 (1.2 to -4.17), 53% < -1.8 SDS, height velocity in 6 was 0.9-3.8 cm/year and mean BMI SDS 2.29 (0.7-5.06). From 1983 to 2001, CD was cured in 18 patients (61%) by transsphenoidal surgery (TSS) alone and 39% by TSS plus pituitary irradiation (RT). In 13 patients, growth hormone (GH) was assessed by ITT/glucagons at 1-108 months after cure. Four had severe GH deficiency (<9 mU/l), 7 subnormal (10-29 mU/l) and 2 normal (>30 mU/l) GH status. Subnormal GH was present in 7 subjects >2 years after TSS or RT cure. In 10 subjects, aged 12.9 +/- 3.4 years, growth after cure was studied for 9.1 +/- 5.0 years. Nine had no catch-up growth in the interval of 0.3-1.1 years after cure (mean HV 5.3 +/- 2.4 cm/year). All these had GH deficiency peak GH 0.5-20.9 mU/l, and received hGH 2.7 mg/m(2)/week, 3 with GnRHa. All 10 showed long-term catch-up growth with mean delta SDS at diagnosis (Ht SDS-target Ht SDS) -1.72 +/- 1.26 improving to -0.83 +/- 1.08 (p = 0.0005) at latest of final Ht. At diagnosis, virilization was present in 82% of 17 patients with CD. Mean SDS values of serum androstenedione, DHEA-S and testosterone were normal, i.e. 0.72 (-2.9 to 3.0), -0.8 (6.0 to 2.2), 0.7 (-7.9 to 9.5) respectively, whereas SHBG was reduced at -2.1 (-5.3 to 1.2), increasing free androgen levels. Bone age (BA) was delayed (mean 1.46 years) in 14/16 patients, suggesting cortisol excess contributed more then androgen effect to skeletal maturation. In conclusion, most paediatric patients with CD had subnormal linear growth with delayed BA. After cure by TSS or pituitary irradiation, GH deficiency was frequent and persisted for many years. Treatment with hGH induced significant long-term catch-up growth leading to reasonable final height.

Adolescent↗
PubMed2006

The role of adrenal venous sampling in the surgical management of primary aldosteronism.

OBJECTIVE: Primary aldosteronism is the most common endocrine form of secondary hypertension, but no single test or imaging method always identifies it. Identification of a unilateral overproduction of aldosterone due to Conn's adenoma or unilateral hyperplasia is of utmost importance to the surgeon. MATERIALS AND METHODS: We reviewed our experience with primary aldosteronism in 46 consecutive patients who had undergone adrenalectomy at the Surgical Pathology Institute, University of Padua since 1993. All the patients underwent a CT scan. Adrenal venous sampling was performed in those patients with negative or equivocal findings on imaging studies. RESULTS: Computed tomography was non-contributory in 12 patients and frankly misleading in 2 patients, demonstrating a probable mass lesion in the contralateral but not in the ipsilateral adrenal. Eighteen patients had selective venous sampling that was successful in altering the management of 14 cases. Eleven patients who biochemically had an adrenal adenoma, had normal/equivocal CT, while the remaining 3 had bilateral or contralateral adrenal masses. Venous sampling localized aldosterone secretion and an adenoma, less than 1 cm in diameter, was removed, curing their hypertension. Eleven patients were treated by open adrenalectomy and 35 by the lateral transperitoneal laparoscopic approach. Histological examination revealed 45 Conn's adenomas, of which 13 had a diameter of less than 1 cm (range 0.3-0.8), and 1 case of nodular hyperplasia. CONCLUSIONS: Patients who have equivocal or unexpected CT findings should proceed to hormonal localization. Adrenal venous sampling is essential in patients with equivocal CT scans to avoid unnecessary and inappropriate adrenalectomy.

Adrenal Cortex Neoplasms↗
PubMed1978

Failure to suppress adrenal function in congenital adrenal hyperplasia (21-hydroxylase deficiency). Three case reports.

Three patients, aged 14, 16, and 32 years respectively, with congenital adrenal hyperplasia (21-hydroxylase deficiency) are described. Excessive adrenal activity and ACTH secretion could not be suppressed with doses of corticosteroids sufficient to cause iatrogenic Cushing's syndrome, even though part of the steroid dosage was administered in the late evening. The resistance to feed-back suppression was of the same order as that seen in Cushing's syndrome. Adrenalectomy was performed in the 16-year-old girl, and was followed by a menarche. Adrenalectomy was considered inadvisable in the other two patients.

Adolescent↗
PubMed1980

Physiological effects of exogenous adrenocorticotropin injections in Japanese quail.

Administration of exogenous adrenocorticotropin (ACTH) into young Japanese quail resulted in certain physiological changes consistent with those which have been reported in chickens. These include reduced body weight gains and bursa weights. Also adrenal cholesterol values were decreased, and serum cholesterol and plasma refractive indices were increased. However, spleen weights, right adrenal weights, and packed cell volumes were not consistently altered at 24 hr post-ACTH administration. Collectively, these findings suggest that Japanese quail are less responsive to ACTH-induced adrenal hyperfunction than chickens.

Adrenal Glands↗