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At least 721 records · Page 40Linked to original sources
PubMed1983

Aldosterone metabolites and possible aldosterone precursors in hypertension.

The value of the urine tests: free aldosterone, aldosterone-18-glucuronide, tetrahydroaldosterone 18-hydroxycorticosterone and 18-hydroxydeoxycorticosterone in distinguishing primary aldosteronism from essential hypertension was studied in patients with typical and atypical primary aldosteronism and in patients with essential hypertension. The discriminating function of the tetrahydroaldosterone determination was the best, followed by 18-hydroxycorticosterone, free aldosterone and aldosterone-18-glucuronide. The measurement of 18-hydroxydeoxycorticosterone was without distinguishing value. Three cases with hypertension, adrenal adenoma, elevated 18-hydroxycorticosterone but normal aldosterone values were observed. In longitudinal studies the excretions of aldosterone, aldosterone metabolites and possible precursors periodically varied independently of each other. Determinations of urine aldosterone, aldosterone metabolites, 18-hydroxycorticosterone and 18-hydroxydeoxycorticosterone were not applicable for differential diagnosis of the adenoma and hyperplasia forms of primary aldosteronism.

Adenoma↗
PubMed1978

[Phaeochromocytoma with hypokalaemia (two cases) (author's transl)].

Two cases of phaeochromocytoma with hypokalaemia are reported. In the first, a carcinoma, hypokalaemia was potentially secondary to hyperreninaemia and hyperaldosteronism in association with probably paraneoplastic hypercorticism. The other was benign and the origin of isotopically demonstrated potassium deficiency was less clear, because hyperreninaemia, hyperaldosteronism and hypercortisolism were moderate.

Adrenal Gland Neoplasms↗
PubMed1981

[Difficulty in diagnosis of pheochromocytomas: ten cases (author's transl)].

Ten cases of atypical pheochromocytomas are reported, and physiopathologic mechanisms of the multiple clinical manifestations of these tumors are discussed. The embryologic origin of pheochromocyte, derived from neural crest, and common metabolic properties of endocrine cells coming from this germ layer, elucidate the coupling of pheochromocytoma with neuroectodermic diseases (neurocristopathic syndromes), and the biosynthetic capacity of these tumors (synthesis of corticotropic activity and thyrocalcitonin are reported). Atypical peripheral effects of pheochromocytoma are discussed: catecholamines are responsible for an unstable hemodynamic state, always threatened by a spontaneous or induced release of amines: then, misleading clinical features occur, which are analysed. A screening and detecting procedure of pheochromocytoma is proposed for these particular forms, which are explained by the common multiple properties of the tumors derived from chromaffin cells.

Adrenal Gland Neoplasms↗
PubMed1995

Pheochromocytoma and hyperadrenocorticism in dogs: six cases (1982-1992).

Pheochromocytoma was diagnosed in 4 dogs with pituitary-dependent hyperadrenocorticism and 2 dogs with hyperadrenocorticism caused by adrenocortical tumor. All dogs were examined initially because of clinical signs associated with hyperadrenocorticism. Pheochromocytoma was suspected in 2 dogs with pituitary-dependent hyperadrenocorticism that had ultrasonographic evidence of an adrenal gland mass, and in 1 dog suspected to have hyperadrenocorticism associated with an adrenocortical tumor after complications (systemic hypertension, cardiac arrhythmias) developed during induction of anesthesia. Pheochromocytoma was an unexpected finding at necropsy in the remaining 3 dogs. Two dogs collapsed suddenly and died before diagnostic tests could be performed; the other dog died during anesthesia for cobalt teletherapy of a pituitary macroadenoma. Hypertension, most notable during digital manipulation of the affected adrenal gland, developed during anesthesia and surgery in 3 dogs that underwent exploratory celiotomy.

Adrenal Gland Neoplasms↗
PubMed1995

Evaluation of urinary cortisol:creatinine ratios for the diagnosis of hyperadrenocorticism associated with adrenal gland tumors in ferrets.

Assays were validated for the measurement of urinary concentrations of cortisol and creatinine in domestic ferrets (Mustela putorius furo). Urinary concentrations of cortisol and creatinine and the calculated urinary cortisol:creatinine ratio (UCCR) values were determined for 29 clinically normal female ferrets, 22 clinically normal male ferrets, and 12 ferrets with adrenal gland tumors. The UCCR values for the 51 clinically normal ferrets ranged from 0.04 x 10(-6) to 1.66 x 10(-6), with a median value of 0.22 x 10(-6). The UCCR values were significantly (P < or = 0.01) higher in the 12 ferrets with adrenal tumors, with a range of 0.5 x 10(-6) to 60.13 x 10(-6) and a median of 5.98 x 10(-6). We concluded that determination of UCCR values was useful in the diagnosis of hyperadrenocorticism associated with adrenal neoplasia in domestic ferrets.

Adenocarcinoma↗
PubMed1993

[Nuclear medicine diagnosis of adrenal gland diseases].

Localization procedures are required in adrenal diseases after biochemical confirmation of hormonal excess. Whereas computed tomography, ultrasound and--in rare cases--also magnetic resonance are needed to image the morphological abnormalities and the anatomy of neighbouring structures, adrenocortical and adrenomedullary scintigraphy is dependent on a functioning adrenal gland. Adrenocortical scintigraphy has the advantage of being able to differentiate between unilateral adenoma and bilateral hyperplasia in patients with primary hyperaldosteronism. It is of minor significance in patients with Cushing's syndrome or hyperandrogenism. In patients with catecholamine-producing tumours scintigraphy with radioiodine-labelled meta-iodobenzylguanidine (MIBG) may detect intra- and extra-adrenal, uni- and bilateral or multilocular, benign and malignant lesions. In patients with malignant but inoperable phaeochromocytoma, therapy with high doses of MIBG may improve clinical symptoms and reduce tumour volume.

Adrenal Gland Diseases↗
PubMed1994

[Atypical overgrowth of the left suprarenal gland imitating pheochromocytoma].

In the work a case of an excessive functional activity of core of hyper suprarenal gland is presented. It is caused by atypical overgrowth of the left suprarenal gland. The cyst observed on the left kidney covering pathologically the changed suprarenal gland was an additional diagnostic difficulty.

Adrenal Gland Diseases↗
PubMed1996

Evaluation of plasma androgen and estrogen concentrations in ferrets with hyperadrenocorticism.

OBJECTIVE: To determine plasma concentrations of steroid hormones in ferrets with hyperadrenocorticism associated with adrenocortical neoplasia or nodular hyperplasia of the adrenal gland, the effect of surgical removal of the affected adrenal gland on concentrations of these hormones, and whether any hormone concentrations could be used as a marker for the disease. DESIGN: Prospective case series. ANIMALS: 32 ferrets with hyperadrenocorticism associated with adrenocortical neoplasia or nodular hyperplasia of the adrenal gland. PROCEDURE: A blood sample was obtained from each ferret before adrenalectomy. In 26 of the 32 ferrets, a second blood sample was collected 24 to 48 hours after adrenalectomy. Plasma concentrations of 7 hormones were measured (cortisol, estradiol, testosterone, progesterone, 17-hydroxyprogesterone, androstenedione, and dehydroepiandrosterone sulfate). RESULTS: Median plasma concentrations of 17-hydroxyprogesterone, androstenedione, and dehydroepiandrosterone sulfate were significantly higher in ferrets with adrenal gland disease, compared with concentrations in clinically normal ferrets. After adrenalectomy, median concentrations of estradiol, 17-hydroxyprogesterone, and androstenedione decreased significantly. Of 23 ferrets in which concentrations of estradiol, 17-hydroxyprogesterone, and androstenedione all were measured, 22 (96%) had high concentrations of at least 1 of these 3 hormones, but only 5 (22%) ferrets had high concentrations of all 3 hormones. CLINICAL IMPLICATIONS: The condition that develops in ferrets with adrenal gland disease apparently is caused by excessive secretion of 1 or more steroids other than cortisol. Because concentration of a particular hormone was not high in all ferrets, we recommend determining plasma concentrations of several sex steroids, including androstenedione, 17-hydroxyprogesterone, and estradiol.

17-alpha-Hydroxyprogesterone↗
PubMedDate not supplied

Adrenal gland photoscanning by means of 131I-iodinated cholesterol.

Photoscanning by means of 131I-19-iodinated cholesterol was performed on 10 patients with various diseases of the adrenal glands. The authors confirmed that the method was suitable for study of the morphology and function of the adrenal glands in disease, especially when combined with stimulation by ACTH or suppression by dexamethasone. The radiation dose absorbed by the thyroid and by the gonads can be controlled during the examination by blocking the iodine trapping and suppression of the gonado-stimulating action, respectively.

Adrenal Gland Diseases↗
PubMed1988

[Surgical diseases of the adrenal glands in childhood--pediatric aspects].

Detailed discussion of diseases of the adrenals in children where surgery may be indicated, seen from the paediatric point of view. Following differentiation between adrenal insufficiency and adrenal hyperfunction, as well as adrenal haemorrhage--where differential diagnosis is often rather difficult--the tumours of the zona glomerulosa, fasciculata and reticularis as well as of the adrenal medulla are presented and their signs and symptoms, their clinical hormonal diagnosis, localisation diagnosis and therapy are described.

Adrenal Gland Diseases↗
PubMed1990

[Unilateral adrenalectomy for cortisol producing adenoma: prolonged suppression of the hypothalamus-pituitary-adrenal axis].

Hypercortisolism induces a functional suppression of the hypothalamus-pituitary-adrenal axis which is expected to subside within a year following either the removal of the cortisol producing adrenal adenoma or the withdrawal of glucocorticoid therapy. We report 3 women (35, 40 and 43 years old) with Cushing's syndrome due to cortisol producing adrenal adenoma. All had typical clinical and biochemical features of the syndrome dating from up to 4 years before surgery. Cortisol supplementation was given during the postoperative period (20 mg/day po at 9 AM, reduced to 10 mg/day after 6 months). Cortisol was withdrawn 16, 20 and 39 months after surgery, when 9 AM plasma concentration raised over 10 ug/dl [corrected]. An ACTH stimulatory test was performed until a normal response was obtained. Patients showed and abnormal response up to 16, 17 and 30 months after surgery, respectively. Complete recovery took place at 21, 36, and 55 months after the operation. We concluded that risk of hypocortisolism may persist up to 30 months after surgery for cortisol producing adenomas, due to complete or partial suppression of the hypothalamus-pituitary-adrenal axis.

Adenoma↗