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Results for “Adrenocortical Hyperfunction”

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At least 55 records · Page 3Linked 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↗
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↗
PubMed1987

Acute, massive, haemorrhagic adrenal necrosis experimentally produced by the Shwartzman mechanism in rabbits.

Acute and severe haemorrhagic necrosis of the adrenal was produced experimentally in rabbits by means of intravenous injection of endotoxin after pretreatment by adrenocorticotropic hormone (ACTH) administration. The change occurred mainly in the zona fasciculata of the adrenal cortex, and its pathology was quite similar to that of the Shwartzman reaction. Numerous microthrombi were found in and around the lesion, but no marked changes were seen in other parts of the body. Heparin administration was very effective in preventing the necrosis. The pathogenesis of this lesion was postulated to be a univisceral Shwartzman mechanism in the adrenal. This seems to be a good experimental model for massive haemorrhagic necrosis of the adrenal in man, for example in the Waterhouse-Friderichsen syndrome, the pathogenesis of which has been assumed to involve intravascular clotting. It is suggested that hyperfunction of the adrenal cortex caused by ACTH administration could be a preparative condition for the Shwartzman reaction.

Acute Disease↗
PubMed1988

[Changes in the functional status of the adrenal glands in patients with chronic renal failure during the treatment by programmed hemodialysis].

A study was made of adrenal function in 2 groups of patients with chronic renal insufficiency on programmed hemodialytic therapy. Insufficiency of gluco- and mineralo-corticoid function of the adrenal glands and hyperfunction of their medulla developed in patients with normal BP and controlled hypertension. In patients with uncontrolled hypertension, insufficiency of adrenal glucocorticoid function was attended by hypercatecholaminemia and aldosteronism. Genesis of the revealed disorders was associated with the loss of hormones into the dialysing solution through the membrane, depletion of adrenocortical functional reserves and disturbance of pulmonary regulation of the level of biologically active substances as a result of microthromboembolization of the vessels of the lesser circulation attending hemodialysis.

Adrenal Glands↗
PubMed1989

Salivary corticosteroids in the study of adrenal function.

Salivary corticosteroids (SCC) and plasma corticosteroids (PCC) were studied under basal conditions, after dexamethasone (DXM) and in the ACTH stimulation test in a reference group (RG) of 33 adults, in three groups with non-adrenal pathology and in a group of 4 patients with hypercortisolaemia. SCC and PCC were measured using a non-extraction RIA method using [3H]cortisol. The results for SCC in the RG and in the groups with non-adrenal pathology were similar to those obtained for PCC in terms of percentage of decrease in the circadian rhythm or DXM suppression. However, the responsiveness to ACTH in saliva was twice that obtained in plasma. In patients with hypercortisolism, SCC were in closer agreement with the adrenal hyperfunction than PCC. From the previous results the following conclusions may be drawn: (a) SCC differentiate adrenal gland normal function from hyperfunction as clearly or even better than PCC does; (b) SCC were in a closer agreement with the symptomatology of adrenal hyperfunction than were PCC; and (c) the responses to ACTH obtained with SCC were clearly higher than those obtained with PCC.

Adenoma↗
PubMed1989

Hyperfunctioning and nonhyperfunctioning benign adrenal cortical lesions: characterization and comparison with MR imaging.

The authors evaluated the potential of magnetic resonance (MR) imaging at 0.35 T to permit differentiation of nine hyperfunctioning adrenal cortical lesions from 21 nonhyperfunctioning adrenal cortical adenomas. Both qualitative data (visual assessment) and quantitative data (signal intensity ratios, T1, and T2) were used for tissue characterization. With a 2,000/56-100 sequence (repetition time msec/echo time msec), the majority of lesions were visually isointense to liver. Of 34 quantitative measures, only lesion-liver and lesion-kidney intensity ratios at 2,000/150 showed statistically significant differences among nonhyperfunctioning adenomas, aldosterone-producing lesions, and corticosteroid-producing lesions; however, the authors question the significance of these differences because of the abundant noise associated with the 2,000/150 sequence. The results suggest that nonhyperfunctioning adrenal cortical adenomas cannot be distinguished from benign hyperfunctioning cortical lesions with use of MR imaging at 0.35 T.

Adenoma↗
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↗
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↗
PubMed1978

Involutive morphological modifications in the rat adrenal glomerular zone after a low-sodium diet.

We have studied glomerular zone involution in the rat's adrenal gland after a period of hyperfunction brought about by a low-sodium diet. The changes observed in this zone effect those organoids that are more directly involved in steroid genesis; mitochondria, smooth endoplasmic reticulum and liposomes. The Golgi complexes appear very developed, often, showing, a positive acid phosphatase activity. Lysosomes suffered a considerable increase in their number, and carried out their digestive function on liposomes. All those changes discussed here are seen as an accomodation of this zone to the new normofunctional situation.

Acid Phosphatase↗