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At least 199 records · Page 11Linked to original sources
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↗
PubMed1989

[Methods of suppression of adrenal hyperfunction].

Evolution of the methods for suppression of adrenal hyperfunction has now made it possible to give up bilateral adrenalectomy in favour of portalization of the adrenal blood flow from the left adrenal by its autotransplantation with maintained blood supply into the transverse mesocolon and cryodestruction of the right adrenal. Analysis of the mortality showed two-stage suppression of adrenal hyperfunction to be advisable.

Adrenal Glands↗
PubMedDate not supplied

[Effect of vibration on gamma-aminobutyric acid metabolism in the brain in various functional conditions of the adrenal cortex].

The low-frequency vibration during 30 min (20 Hz, A = 0.4 mm) has been studied for its influence on the level of components of the GABA system and dicarbonic ++amino acids in male rats at hypo- and hyperfunction of the adrenal cortex. It is shown that under these conditions of the experiment the GABA level and glutamate-decarboxylase activity increase. Hyperfunction of the adrenal cortex against the background of vibration causes a relatively less pronounced increase in the GABA content, than the vibration alone or against the background of inhibition of adrenocortical function in the organism.

4-Aminobutyrate Transaminase↗
PubMed1981

Suppression of growth hormone secretion in spontaneous canine hyperadrenocorticism and its reversal after treatment.

The plasma growth hormone response to the provocative agent, xylazine, was assessed in 4 dogs with spontaneous hyperadrenocorticism, before and after therapy. Before treatment of the hyperadrenocorticism, no significant increase in growth hormone concentration occurred in any of the dogs following the administration of xylazine. A significant increase in growth hormone concentrations following xylazine administration occurred in 2 of the 3 dogs with hypophysis (pituitary)-dependent hyperadrenocorticism after treatment with mitotane (o,p'-DDD) and in 1 dog after surgical removal of a hyperfunctional adrenal adenoma. Although the impaired growth hormone response persisted in 1 dog, the administration of xylazine was repeated in this animal after only 3 weeks of mitotane therapy; it is likely that growth hormone unresponsiveness would reverse if the hyperadrenocorticism were controlled for a longer period. These findings demonstrate that in dogs, as in persons, the excessive production of endogenous corticosteroids associated with either hypophysis-dependent hyperadrenocorticism or hyperfunctional adrenal tumor can induce suppression of growth hormone release which is reversible following treatment.

Adenoma↗
PubMed1979

The normal dexamethasone-suppression adrenal scintiscan.

To establish the parameters of adrenal imaging under dexamethasone suppression (DS), 18 normotensive, normal male volunteers underwent dexamethasone-suppression adrenal scintiscanning. Five control groups were established and given dexamethasone, either 8 mg for 2 days or 4 mg for 7 days before 6 beta-[131I]iodomethyl-norcholesterol (NP-59) administration. NP-59 was given in doses of 2, 1, or 0.5 mCi. Early visualization (3--5 days) of the adrenals was noted in the groups on the 8 mg DS regimen with either 1 or 2 mCi of NP-59. Late visualization (5--7 days) was noted in the groups that received 4 mg DS and either 2, 1, or 0.5 mCi of NP-59, respectively. The normal adrenal will demonstrate uptake of NP-59 under DS, and the duration of DS before imaging is the critical factor as to when discernible adrenal visualization will occur. The documentation of the noraml suppression interval on these DS regimens provides a basis for the correct diagnostic interpretation of adrenal hyperfunction as seen on the dexamethasone-suppression NP-59 adrenal scan.

Adosterol↗
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↗