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At least 523 records · Page 29Linked to original sources
PubMed1984

Stages of hyperadrenocorticism: response of hyperadrenocorticoid dogs to the combined dexamethasone suppression/ACTH stimulation test.

A study was designed to evaluate the response of blood cortisol content in dogs tentatively diagnosed as having hyperadrenocorticism by using the combined dexamethasone suppression/ACTH stimulation test procedure. Four groups of abnormal responses were identified in 54 dogs. In group I (14.8% of the dogs with abnormal responses), the only abnormality was partial suppression with dexamethasone (clinically normal dogs suppressed to less than 10 ng/ml). In group II (29.6%), 2 abnormalities were found: partial suppression with dexamethasone and hyperreactivity to the ACTH stimulation test. In group III (typical pituitary-dependent hypercortisolism, 48.1%), 3 abnormalities were found: base-line hypercortisolemia, partial suppression with dexamethasone, and hyperreactivity to the ACTH stimulation test. In group IV (7.4%), 2 abnormalities were found: base-line hypercortisolemia and partial suppression with dexamethasone. Base-line blood cortisol content was normal in 44.4% of the adrenopathic dogs. A normal response to ACTH stimulation was seen in 25.9% of the dogs, and 74.1% of the dogs hyperreacted to the ACTH stimulation test. All of the adrenopathic dogs were found to suppress partially with dexamethasone. Failure to suppress the adrenal gland completely (less than 10 ng/ml) with dexamethasone was the most consistent finding in adrenopathic dogs when using the combined dexamethasone suppression/ACTH stimulation test procedure. It was concluded that the test procedure is feasible, flexible, and convenient for clinical situations. Also, these results suggested that there may be several stages in the negative feedback failure associated with hyperadrenocorticism in dogs.

Adrenal Cortex Function Tests↗
PubMed1999

Risk factors and long-term follow-up of adrenal incidentalomas.

The natural course of adrenal incidentalomas and the risk that such lesions evolve toward hormonal hypersecretion or malignancy are still under evaluation. Of 246 consecutive patients with adrenal incidentaloma studied at our institution in the last 15 yr, 91 underwent surgery. Of the remaining patients, a group of 75 (52 females and 23 males; median age, 56 yr; range, 19-77 yr) with incidentally discovered asymptomatic adrenal masses (60 unilateral and 15 bilateral; median diameter, 2.5 cm; range, 1.0-5.6) was enrolled in an endocrine and morphological follow-up of at least 2 yr after diagnosis (median, 4 yr; range, 2-10). During follow-up, no patients developed malignancy; 9 showed mass enlargement, with appearance of a new mass in the contralateral gland in 2; 3 developed adrenal hyperfunction (overt Cushing's syndrome in 2, nonclinical hypercortisolism in 1); and 3 showed adrenal mass enlargement associated with adrenal hyperfunction (nonclinical hypercortisolism in 2, pheochromocytoma in 1). The estimated cumulative risks to develop mass enlargement and hyperfunction were 8% and 4%, respectively, after 1 yr, 18% and 9.5% after 5 yr, and 22.8% and 9.5% after 10 yr. Nine risk factors for adrenal mass enlargement or hyperfunction were arbitrarily selected and evaluated: sex, age, presence of obesity, hypertension, diabetes, abnormal endocrine tests, mass size, mass location, and scintigraphic uptake pattern. Three of them attained statistical significance: mass size of 3 cm or more at diagnosis and exclusive radiocholesterol uptake by the mass at scintigraphy had relevance for the occurrence of adrenal hyperfunction, whereas the presence of endocrine test abnormalities at diagnosis had predictive value for mass enlargement. It is concluded that subtle hormonal abnormalities are risk factors for mass size increase, which is not a sign of malignant transformation. Both mass size of 3 cm or more at diagnosis and exclusive radiocholesterol uptake, indicating higher risks of hyperfunction, should be considered to plan a more thorough endocrine follow-up.

Adolescent↗
PubMed1989

[Crisis of arterial hypertension in patients with primary aldosteronism].

A clinical picture of the disease was analyzed in 55 patients with primary aldosteronism due to adrenal aldosteronoma. A crisis variant of the course in arterial hypertension was detected in 50% of the patients. Its comparison with morphological signs of the adrenals enabled the authors to reveal that the crisis of arterial hypertension was accompanied by adrenal medullary hyperplasia and hyperfunction.

Adrenal Cortex Neoplasms↗
PubMedDate not supplied

[Effect of ethanolamine on corticosterone concentration in experimental myocardial hyperfunction in the white rat].

An initial step of experimental myocardium hyperfunction, caused by coarctation of the subphrenic part of abdominal aorta, was accompanied by a distinct increase in content of corticosterone in rat blood and adrenal glands. Administration of ethanolamine at a dose of 10 mg/kg decreased the hormone content under conditions of heart hyperfunction. The data obtained suggest that adrenal gland cortex was activated in response to the myocardium pathology as well as that content of corticosterone in blood and adrenal glands might be regulated by administration of ethanolamine.

Adrenal Cortex↗
PubMed1995

[Sudden death from hypoglycemia].

The sudden death by hypoglycemia is an aspect of the forensic pathology frequently neglected. Authors initially described the pathogenesis of different hypoglycemia forms, distinguishing the primary ones due to hyperinsulinism and the secondary ones due to functional insufficiency of other organs (hypophysis, thyroid, adrenal gland, liver); after that Authors described three cases of sudden death induced hypoglycemia by hyperinsulinism: two were unweaned with nesidioblastosis and one adolescent. In any form of hypoglycemia the central nervous system damage is present with evident neuronal degenerative-necrotic phenomena, widespread edema with microhemorrhage, swollen and dissociation of myelin sheath, glial cells hyperplasia. Death caused by primary hypoglycemia is histopathologically different from the secondary one because of the maintenance of hepatic glycogen content in the former, that increase in striated muscles, including the heart, in spite of the constant secretion of catecholamine from the adrenal medulla. Glycogen is depleted in secondary hypoglycemia. In the primary form, behind the adrenal medulla hyperfunction, the increased functional activity of the adrenal cortex is moderate, contrasting with the seriousness of the syndrome, due prevalently to inhibit the gluconeogenesis response conditioned by the persistence of stored glycogen in the liver, heart and striated muscles. The rare anoxic processes coming with resynthesis of hepatic glycogen have to be considered in the differential diagnosis. The primary hypoglycemic death, especially in unweaned, is frequently promoted by other processes inducing hypoxia (fetal asphyxia outcome, pneumonia, etc.) or worsening the hypoglycemia (hypothyroidism, etc.). The secondary hypoglycemias are characterized by the normality of exocrine pancreas and by organic alterations that cause glycogen depletion from the liver.

Adolescent↗
PubMed1985

Precocious breast development: a case of unilateral hyperplasia of the adrenal cortex.

The case of a 14-month-old girl presenting with precocious breast development due to adrenal hyperplasia is reported. The endocrine studies revealed a slight elevation of the plasma progesterone, 17 alpha-hydroxyprogesterone, testosterone and oestrone levels, and an increased urinary oestrogen excretion. The findings of the ultrasound examination and the evidence that the oestradiol concentration in the left adrenal vein was higher than in the right adrenal vein confirmed the diagnosis of left adrenal hyperfunction. Surgical exploration revealed unilateral hyperplasia of the adrenal cortex. After adrenalectomy the plasma hormone levels and urinary oestrogen excretion fell to normal, with concomitant regression of breast tissue. The girl shows no signs of recurrence of the disorder in a 2 year follow-up. This adrenal hyperplasia might be a benign adrenal disorder causing precocious breast development.

17-alpha-Hydroxyprogesterone↗
PubMed1992

Endocrinopathies of hyperfunction: Cushing's syndrome and aldosteronism.

Increased function of the adrenal cortex is a normal response in times of physiologic and psychologic stress. Adrenal cortical secretions (e.g., glucocorticoids, aldosterone) orchestrate a multitude of internal processes aimed at maintaining homeostasis and psychologic integrity. Many patients admitted to a critical care unit will manifest some increase, even minor, in adrenal function. However, excessive secretions of these hormones can have a lethal effect of fluid and electrolyte balance, energy metabolism, and immune function. Cushing's syndrome denotes a disorder characterized by increased circulating levels of glucocorticoids (primarily cortisol). An easily recognizable disorder, it may arise from pathology of the adrenal cortex or the anterior pituitary glands, ectopic secretions from a nonendocrine tumor, or from excessive doses of exogenously administered glucocorticoids. Cushing's syndrome is rarely an admitting diagnosis to critical care but is a disorder that can seriously affect recovery from coexisting illnesses if not treated. Aldosteronism, although rare, will often be diagnosed after admission to a critical care unit for management of troublesome hypertension, hypokalemia, congestive heart failure, and various dysrhythmias. Suspicion of the diagnosis should always arise when these manifestations occur, particularly when hypokalemia is refractory to potassium supplementation. Without timely diagnosis and treatment, these patients will succumb to lethal dysrhythmias.

Adrenocortical Hyperfunction↗
PubMed1982

The effect of alpha-melanocyte-stimulating hormone on the adrenal cortex of the fetal rat.

The effect of alpha-melanocyte-stimulating hormone (alpha-MSH) on the fetal adrenal cortex in rat was studied in vivo and in vitro. In vivo, an injection of alpha-MSH stimulated the adrenal cortex slightly. Treatment of the adrenal cortex with alpha-MSH in organ culture caused hyperfunctional change in the innermost layer of the cortex, the detection of which was done by electron microscope. This treatment caused at the same time an increase in corticosterone in the culture medium. Furthermore, comparison was made between alpha-MSH and ACTH with respect to their effect on the fetal adrenal cortex.

Adrenal Cortex↗
PubMed1981

[Associated role of surgery and antimitotic o, p'-DDD treatment in hyperfunctioning adrenal cancers with diffuse metastases].

The observation of two cases of hyperworking corticosuprarenal carcinomata with diffuse metastases, has induced the authors to examine this problem on the base of the most actual bibliography of the last years. They explain in detail the 2 cases, that are a feminizing tumor in a 55 years old man and a Cushing syndrome with hypertension in a 18 years old women. The peculiar characteristic are in the first case the clinical rareness of feminizing syndrome from suprarenal carcinoma and in the second case the histopathological particularity of splenic metastases. In regard to therapy for this particular tumor, the AA. incline for the surgical removal of tumor, that can induce, in the most favourable cases, a partial or total reduction of endocrine symptomatology and for the giving in great doses of o,p'-DDD from the immediate post-operating period.

Adolescent↗