SEARCH · Search PubMed
Results for “Adrenal Cortex Function Tests”
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
[Indications and limitations of the use of ACTH in clinical practice].
Explore the source record for details and available documents.
[The diagnosis of adrenal cortical function in animals using hormone analysis].
This paper describes the use of hormone analysis in the diagnosis of adrenal cortex dysfunction in the dog, cat and horse. Analytical problems concerning the determination of corticosteroid levels are discussed and the pathology of adrenal dysfunction is briefly presented. The paper focuses on the problems in establishing physiological norms for adrenal function based on the established assays. Own experiences and other reported data are referred to.
Primary adrenal insufficiency: a new cause of reversible gastric stasis.
Primary adrenal insufficiency is known to cause a wide spectrum of sometimes severe upper gastrointestinal symptoms; however, it has not previously been shown to be the cause of reversible gastric stasis. We have documented such a case in which the symptoms and physiologic abnormalities associated with gastric stasis were reversed by steroid replacement. A follow-up radionuclide gastric-emptying study after physiologic steroid replacement showed complete normalization of gastric emptying. Although gastric stasis has long been suspected of being present with primary adrenal insufficiency, this represents the first case in which it has been documented, and so should be included in the differential diagnosis of patients presenting with chronic nausea and vomiting.
Assessment of survey radiography and comparison with x-ray computed tomography for detection of hyperfunctioning adrenocortical tumors in dogs.
Results of abdominal survey radiography and x-ray computed tomography (CT) were compared in 13 dogs with hyperadrenocorticism histologically attributed to adrenocortical tumors. X-ray computed tomography enabled accurate localization of the tumor in all 13 dogs. Apart from 2 poorly demarcated irregular-shaped and mineralized carcinomas, there were no differences between adenoma (n = 3) and carcinoma (n = 10) on CT images. In 1 dog, invasion of the caudal vena cava by the tumor was suggested on CT images and was confirmed during surgery. Suspicion of adhesions between tumors of the right adrenal gland and the caudal vena cava on the basis of CT images was confirmed during surgery in only 2 of 6 dogs. Survey radiography allowed accurate localization of the tumor in 7 dogs (4 on the right side and 3 on the left). In 6 of these dogs, the tumor was visible as a well-demarcated soft tissue mass and, in the other dog, as a poorly demarcated mineralized mass. The smallest tumor visualized on survey radiographs had a diameter of 20 mm on CT images. Six tumors with diameter less than or equal to 20 mm were not visualized on survey radiographs. In 1 of these dogs, a mineralized nodule was found in the left adrenal region, without evidence of a mass. In a considerable number of cases, survey radiography can provide presurgical localization of adrenocortical tumors in dogs with hyperadrenocorticism; CT is redundant in these instances. In the absence of positive radiographic findings, CT is valuable for localization of adrenocortical tumors.
[Pathogenesis of respiratory insufficiency in pulmonary diseases].
Explore the source record for details and available documents.
[Normal and pathologic endocrinology of the adrenal glands].
The adrenal glands produce glucocorticoids (approximately 25 mg cortisol/day), mineralocorticoids (approximately 100 micrograms aldosterone/day) and androgens (e.g. dehydroepiandrosterone = DHEA approximately 10 mg/day) in their cortex and catecholamines in their medulla. Excessive cortisol production leads to Cushing's syndrome. In approximately 2/3 of the cases this is due to ACTH oversecretion most often from a pituitary adenoma and can be cured by removal of this adenoma. Cushing's syndrome caused by an adrenal adenoma, carcinoma or bilateral nodular adrenal hyperplasia is treated by adrenal surgery. Nelson's syndrome consists of hyperpigmentation of the skin and an often aggressively growing pituitary adenoma which secretes excessive amounts of ACTH. Treatment is surgical. Conn's syndrome (primary hyperaldosteronism) is due to aldosterone hypersecretion most often from an adrenal adenoma (therapy: unilateral adrenalectomy), more seldom from bilaterally hyperplastic adrenals (therapy: spironolactone). Excessive adrenal androgen secretion is found in the adrenogenital syndrome in which defective cortisol biosynthesis leads to ACTH oversecretion and ACTH-stimulated overproduction of cortisol precursors, some of which are androgens. Treatment consists of glucocorticoids which suppress the ACTH oversecretion. Pheochromocytomas produce excessive amounts of catecholamines and cause hypertension which can be persistent as well as episodic. Therapy consists of adrenalectomy. Malignant tumors of the adrenals have a poor prognosis. Incidentally found adrenal masses ("incidentalomas") are observed at regular intervals if they are small and should be surgically removed if they have a tendency to grow or are large (greater than or equal to 5 cm phi).
Adrenocortical suppression by topically applied corticosteroids in healthy dogs.
Three corticosteroid products (triamcinolone acetonide, fluocinonide, betamethasone valerate) and a control product composed of water, petrolatum, mineral oil, cetyl alcohol, steryl alcohol, sodium lauryl sulfate, cholesterol, and methylparaben each were applied topically to healthy dogs (5 dogs/product) once daily for 5 consecutive days. Plasma concentrations of immunoreactive adrenocorticotropic hormone (iACTH) and cortisol were determined before 1 microgram of ACTH/kg of body weight was given intravenously (pre-ACTH values) and cortisol was again measured 60 minutes after ACTH was given (post-ACTH values). Cortisol and iACTH concentrations were determined in each dog before, during, and after administration of the corticosteroid products. All 3 corticosteroids caused prompt and sustained pituitary-adrenocortical suppression. Compared with control applications, the application of corticosteroids resulted in significant reduction of plasma cortisol and iACTH concentrations by day 2 of treatment, and the lower concentrations continued to day 5. One week after the last application of the corticosteroids, plasma iACTH concentrations in the corticosteroid-treated dogs had returned to the range of values for the control dogs; however, pre- and post-ACTH cortisol concentrations remained suppressed in all corticosteroid-treated dogs. Two weeks after the last treatment, the pre-ACTH plasma cortisol concentrations of corticosteroid-treated dogs returned to those of the control dogs, but the post-ACTH plasma cortisol concentrations remained suppressed. By 3 weeks after the last treatment, post-ACTH plasma cortisol concentrations of dogs treated with triamcinolone acetonide had returned to the range of values for the control dogs, but remained suppressed in the other 2 groups of dogs. All indices of pituitary-adrenocortical activity were within the control range by 4 weeks after the last treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
Adrenocortical function in the acquired immunodeficiency syndrome (AIDS)
These discussions are selected from the weekly staff conferences in the Department of Medicine, University of California, San Francisco. Taken from transcriptions, they are prepared by Drs Homer A. Boushey, Professor of Medicine, and David G. Warnock, Associate Professor of Medicine, under the direction of Dr Lloyd H. Smith, Jr, Professor of Medicine and Associate Dean in the School of Medicine. Requests for reprints should be sent to the Department of Medicine, University of California, San Francisco, School of Medicine, San Francisco, CA 94143.
[Cushing's Syndrome classification and endocrinological diagnosis].
Explore the source record for details and available documents.
[Endocrinological diagnosis of hypercorticism].
Explore the source record for details and available documents.
[Clinical and experimental observations in Cushing's syndrome based on an autonomous adrenal cortex tumor].
Explore the source record for details and available documents.
[Adrenomyeloneuropathy: an adult form of adrenoleukodystrophy spastic paraparesis, and chronic adrenal insufficiency (concerning 3 cases) (author's transl)].
Three cases of adult males with spastic paraparesis and adrenal insufficiency are reported. The adrenal insufficiency is primary and in one case associated with Leydig cell insufficiency. Ultrastructural examination of peripheral nerve revealed abnormal cytoplasmic inclusions in Schwann cells. A decrease in the percentage of linoleate to total fatty acids was found in the sera. A child with adrenoleucodystrophy and an adult with adreno myeloneuropathy were observed in the same family. It allows adrenomyeloneuropathy to be considered as an adult form of adrenoleucodystrophy.
[Adrenal cortex cancer in childhood with endocrine activity].
Explore the source record for details and available documents.
[Use of mitotane (o,p'-DDD) in adrenal cortex hyperfunction].
Explore the source record for details and available documents.
[Combination of a hormonally active adrenal tumor with hypertensive disease of the kidneys].
The author observed 230 patients with hormone-active tumor of the adrenal attended with arterial hypertension. In 90 patients there were concomitant hypertensive diseases of the kidneys. The diagnosis of the concomitant disease was verified during roentgenography, aortography included. In 66 of 90 patients (73.3%) arterial hypertension followed a malignant course. The presence of adrenal tumor was verified morphologically after the operation in 208 patients and during autopsy in 22. The concomitant renal disease was confirmed histologically on autopsy in 7 fatal cases and by kidney biopsy in 36. The clinical characteristics of the variants of combined lesions of the kidneys and adrenals and the methods of their diagnosis are discussed. The author recommends examining the adrenals in all patients suffering from malignant arterial hypertension.
[Adrenal cortex hormones in acute myocardial infarct complicated by pulmonary edema].
The results of the study of adrenal cortical function in 94 patients (including 20 patients with acute myocardial infarction and pulmonary edema) and in 20 practically healthy persons are discussed. Marked activation of adrenal cortical hormones was noted in patients with acute myocardial infarction and edema of the lungs.