[Notes on clinical syndromes of adrenal cortex hyperfunction and their differential diagnosis].
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Adrenal Cortex↗
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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↗
Atypical adrenal hyperfunction: in vivo studies and incubations of adrenal tissue with 4-14C progestrone.
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17-Hydroxycorticosteroids↗
[Adrenal cortex hyperfunction in a bronchial carcinoma patient with a high ACTH level. Regression following antimitotic combination therapy].
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Adrenal Gland Neoplasms↗
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↗
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↗
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↗
Nocardia lung infection with hematogenous spread in a woman with adrenal cortical hyperfunction.
An increased prevalence of nocardiosis has been reported in patients receiving immunosuppressive therapy, or affected by immunodeficiency disorders and autoimmune diseases. A case of severe Nocardia lung infection with pleurisy and hematogenous spread to the
Adenoma↗
[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↗
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↗
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↗
Recognition of ectopic hormone syndromes produced by tumors.
Ectopic production of polypeptide hormones by tumors of nonendocrine tissues can serve as a clue to diagnosis of the tumor and as a focus for management of the patient with cancer. In the differential diagnosis of syndromes of endocrine hyperfunction, the ectopic hormone syndromes have achieved an increasingly prominent position. Available evidence on the properties of ectopic ACTH, MSH, parathyroid hormone, erythropoietin, gonadotropins, and thyrotropin is consistent with the unifying hypothesis of genetic derepression.
Abdominal Neoplasms↗
Ruder syndrome. Clinical and pathologic correlation.
Ruder syndrome is an unusual varient of adrenal hyperfunction characterized clinically by debilitating osteopenia, and pathologically by bilateral micronodular adrenal hyperplasia. A unique case resembling Ruder syndrome is described in which the dominant pathologic feature was unilateral adrenal adenomatosis.
Adenoma↗
Non-tumorous adrenal hyperfunction: problems in angiographic-clinical correlation.
Hyperfunctioning non-neoplastic adrenal glands may be associated with Cushing's syndrome, congenital adrenal hyperplasia, and aldosteronism. The problems in radiographic diagnosis may be resolved by correlation of the angiogram with the clinical and laboratory findings.
Adrenal Glands↗
Steroid contents and cortical steroidogenic enzymes in non-hyperfunctioning adrenal adenoma.
The recent increasing use of ultrasound and computed tomography has revealed numbers of incidentally discovered adrenal tumors. Many studies have focused on their surgical management, but the biological characteristics of these adrenal tumors have remained unclear. Adrenal tumors were resected from 10 patients who underwent gastrectomy or cholecystectomy. No signs or symptoms of adrenal hormone excess or deficiency were evident either before or after the operation. Moreover, after surgery, no major differences in signs and symptoms including blood pressure levels were observed. Before surgery, neurogenic tumors and cysts were excluded by enhanced magnetic resonance imaging. Steroid contents and both the activities and amounts of steroidogenic cytochrome P-450s in the adrenocortical adenomas of these patients were examined. Microscopic examination revealed that the tumors were surrounded by a thin, non-intact capsule; the surrounding cortex was not atrophic and apparently normal; and the cells of both the tumor and adjacent portions were arranged in nests and cords. Measurements of all steroid content (pregnenolone, progesterone, corticosterone, 11-deoxycorticosterone, 18-hydroxydeoxycorticosterone, cortisol, and dehydroepiandrosterone) except aldosterone in 5 resected adrenal tumors were within the normal ranges for the adrenals of 5 patients with renal cell carcinoma. Aldosterone content in tumor portions was significantly lower than in the apparently normal adrenals. Although in both tumor and adjacent portions of another 5 resected adrenal tumors the activities and amounts of cytochrome P-450s (P-450scc, P-450(11 beta), P-450aldo, P-450(17 alpha), and P-450c21) were also within the normal ranges, the activities of P-450scc and P-450(17 alpha) in the tumor portion were greater than those in the adjacent portion.(ABSTRACT TRUNCATED AT 250 WORDS)
Adrenal Cortex Neoplasms↗
Imaging of medullary thyroid carcinoma and hyperfunctioning adrenal medulla using iodine-131 metaiodobenzylguanidine.
Scintigraphy with radiolabeled metaiodobenzylguanidine was performed in a patient with MEN Type IIa having a pheochromocytoma of the right adrenal gland, adrenomedullary hyperplasia of the left adrenal gland and a primary medullary thyroid carcinoma. The scintigraphic findings demonstrate visualization of all the above mentioned pathologies.
3-Iodobenzylguanidine↗
[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↗
[A method for suppressing adrenal hyperfunction under computed tomography control in the combined treatment of Itsenko-Cushing disease].
Method of dermal adrenal hyperfunctional suppression under CT-control in Itsenko-Cushing disease has been offered. Studies in the laboratory and in the clinic have revealed that this method is a method of choice in treatment of mild and middle forms of Itsenko-Cushing disease.
Adrenal Glands↗