Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ADRENAL GLAND HYPERFUNCTION”

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.

At least 991 records · Page 55Linked to original sources
PubMedDate not supplied

[Differences in the mechanisms of thermoregulation in rats in separate and combined adaptation to cold and heat].

Combined adaptation of rats to heat and cold increasing mechanisms of thermogenesis enhances resistance to both factors and heat dissipation. Adaptive changes in thermogenesis are mainly a result of activation of adrenergic mechanisms, while the separate cold adaptation is accompanied by hyperfunction of thyroid glands. Mechanisms of heat dissipation in rats of the "combined" group increase even more than those of "heat" group.

Acclimatization↗
PubMedDate not supplied

[Thiamine prevention of the corticosteroid reaction afer surgery].

Thiamine effect on the blood 11-HOCS, hydrocortisone and corticosterone levels were studied in patients subjected to herniotomy and/or appendectomy under local anaesthesia. Intramuscular injections of thiamine in a dose of 0.12 g one day and 1.5 to 2 hours before surgery reduced the corticosteroid reaction prior to the operation (psychogenic factor effect) and at the height of the surgery (operation trauma effect). The subsequent administration of the vitamin averted a decrease in the blood corticosteroid level within the postoperative period. Positive results of experimental and clinical studies allow recommending thiamine as an effective remedy for adrenal gland protection from functional exhaustion at surgical stress.

Adrenal Cortex↗
PubMed1976

Plasma cortisol level is an index for functional state of adrenal cortex during pregnancy.

Measurement of plasma cortisol is necessary in assessing the functional state of the adrenal cortex and the availability of other active steroids to the tissues during pregnancy. Coupled with clinical endocrine tests, these determinations can give the physician a good indication of the type of disorder present e.g. Addison's diseases, panhypopituitarism and adrenal hyperfunction. The method used for estimation of venous plasma cortisol when adequately controlled, is very sensitive and accurate.

Addison Disease↗
PubMed1997

Use of urine cortisol:creatinine ratio versus adrenocorticotropic hormone stimulation testing for monitoring mitotane treatment of pituitary-dependent hyperadrenocorticism in dogs.

OBJECTIVE: To evaluate use of urine cortisol-to-creatinine ratio (UC:C) as a means of monitoring response to long-term mitotane treatment in dogs with pituitary-dependent hyperadrenocorticism. DESIGN: Prospective uncontrolled study. ANIMALS: 101 dogs with pituitary-dependent hyperadrenocorticism. PROCEDURE: Urine samples were obtained from dogs on the morning an ACTH stimulation test was performed, and owners were asked their opinion on the health of their dog to monitor response to mitotane treatment. Urine was assayed for cortisol and creatinine concentrations, and UC:C was calculated. The UC:C was compared with post-ACTH plasma cortisol concentration. RESULTS: Post-ACTH plasma cortisol concentration was used to categorize each dog's response to mitotane treatment. The UC:C did not correlate satisfactorily with results of ACTH stimulation testing. Twenty-seven of 85 (32%) dogs would have been incorrectly considered as having received appropriate doses using UC:C. In addition, 16 dogs that received overdoses could not be distinguished from 29 dogs that received appropriate doses. CLINICAL IMPLICATIONS: UC:C does not provide a consistent, correct assessment of mitotane-induced adrenocortical destruction. The ACTH stimulation test, although more time-consuming and expensive, is recommended for monitoring response to mitotane treatment.

Adrenal Cortex↗
PubMed1986

Pheochromocytoma associated with adrenocortical adenoma: case report and literature review.

The case of a 60-year-old woman with pheochromocytoma and concomitant adrenocortical adenoma in the same gland is presented. She complained of episodic headache, palpitation, nausea, vomiting and sweating. Physical examination revealed that the patient has generalized obesity, wet skin and paroxysmal hypertension, but no signs of Cushing's syndrome. Elevated levels of urinary noradrenaline, adrenaline and total metanephrine were sequentially observed. In addition, urinary 17-OHCS was also slightly elevated, but plasma cortisol was normal and suppressed after oral administration of 0.5 mg of dexamethasone. Abdominal echography and CT scanning demonstrated a left adrenal tumor, which took up both 131I-meta-iodobenzylguanidine and 75Se-scintadoren in the same region. A left adrenalectomy was performed and the tumor was found to consist of two parts, pheochromocytoma (2.5 X 2.5 X 2.5 cm) and cortical adenoma (2.5 X 3 X 5 cm). A total of 23 reported cases showing evidence of hyperfunction of the adrenal cortex and the medulla were noted. So far as we know, this patient was the second case of pheochromocytoma with adrenocortical adenoma in Japan.

Adenoma↗
PubMed1975

The pituitary-adrenal system of the genetically obese (ob/ob) mouse.

Adult genetically obese (ob/ob) mice which are characterized by adrenal hypertrophy and increased secretion of corticosteroids have considerably increased levels of ACTH in the pituitary gland. At 5 weeks of age there is no difference in the pituitary ACTH content of lean and obese animals and dietary restriction, sufficient to maintain body weight at normal values, reduces the pituitary ACTH content of adult obese mice from 14 times the level found in lean litter-mate controls to almost normal values. Using an in-vitro perifusion system, the release of ACTH from isolated pituitary glands was studied. Pituitaries from lean and obese mice responded similarly to stimulation with a crude extract of hypothalamic tissue containing coticotrophin releasing factor (CRF). The CRF content of the hypothalamus in both groups appears to be similar. In contrast with the high pituitary content, plasma values for ACTH in unstressed obese mice are not increased. The results are discussed in relation to other evidence for a hypothalamic disorder in ob/ob mice.

Adrenocortical Hyperfunction↗
PubMed1982

Plasma cortisol response to exogenous ACTH in 22 dogs with hyperadrenocorticism caused by adrenocortical neoplasia.

The plasma cortisol response to exogenous ACTH (ACTH stimulation test) was evaluated in 22 dogs with hyperadrenocorticism caused by adrenocortical neoplasia. The mean basal cortisol concentration (6.3 microgram/dl) was high, but 7 dogs had basal cortisol concentrations that were within normal range. Administration of exogenous ACTH increased the plasma cortisol concentrations in each dog. Normal post-ACTH cortisol concentrations were found in 9 (41%) of the 22 dogs; 13 (59%) had an exaggerated increase in cortisol concentrations after ACTH administration. In 9 of 13 dogs with carcinoma and in 4 of 9 with adenoma, the cortisol response was exaggerated. The mean post-ACTH cortisol concentration in the dogs with carcinoma was approximately 4 times that of the dogs with adenoma; the 7 dogs with the highest concentrations had carcinoma. Repeat studies were performed in 6 dogs 2 to 8 weeks after initial testing. In 5 of the 6 dogs, repeat testing yielded data of similar diagnostic significance. One dog, however, had an abnormally high post-ACTH cortisol concentration at initial evaluation, but had only a minimal response to ACTH administration, with a normal post-ACTH cortisol concentration, at time of resting. Although ACTH stimulation testing is useful in diagnosing hyperadrenocorticism, it can not reliably separate dogs with hyperfunction adrenocortical tumors from clinically normal dogs or from dogs with pituitary-dependent hyperadrenocorticism (bilateral adrenocortical hyperplasia).

Adenoma↗
PubMed1989

Radiochemical diagnosis of adrenal disease.

The adrenal gland consists of cortical and medullary components, both of which may be functionally imaged using radiopharmaceuticals designed to take advantage of the specialized physiology of each tissue. Radiolabeled cholesterol derivatives are taken up by normal and abnormal adrenal cortex and provide an in vitro map of adrenocortical function in Cushing's Syndrome, hyperaldosteronism, and hyperadrenogenism. Quantification of uptake shows strong correlation with biochemical parameters of adrenocortical hyperfunction. In the case of incidentally discovered euadrenal masses scintigraphy may help to distinguish between benign, nonfunctional cortical adenomas, and destructive, potentially malignant lesions. Radiolabeled metaiodobenzylguanidine (MIBG) is a tracer of type I uptake and intracellular storage capacity for catecholamines in sympathomedullary tissues and tumors derived from this system. This permits the location of pheochromocytomas of all types (benign and malignant, intra- and extra-adrenal, sporadic and familial) as well as neuroblastomas in all stages. Other neuroendocrine tumors with type I uptake capacity may also be imaged. In suitable cases preliminary data suggests the administration of large doses of MIBG may permit internal radiotherapy of otherwise untreatable neuroendocrine tumors.

Adrenal Gland Diseases↗
PubMed1993

Adrenal masses: differentiation with chemical shift, fast low-angle shot MR imaging.

The purpose of this study was to investigate the efficacy of chemical shift, fast low-angle shot (FLASH) imaging at 1.5 T to differentiate adrenal masses. The materials included patients with adrenocortical adenomas (n = 32), metastatic tumors (n = 17), and pheochromocytomas (n = 4). FLASH images were obtained with breath holding at 100/11 (repetition time msec/echo time msec) (out-of-phase images) and 100/13 (in-phase images) and a flip angle of 20 degrees to differentiate the lipid contents in the adrenal tumors. The signal-intensity (SI) indexes of adrenal masses ([SI on IP - SI on OP]/[SI on IP x 100]), where IP = in-phase image and OP = out-of-phase image, were calculated. All adenomas had SI indexes of more than 5%, while SI indexes of metastatic tumors and pheochromocytomas were less than 5%, with accuracy of 100% in the differentiation between adenoma and nonadenoma. Hyperfunctioning adenoma, however, could not be differentiated from nonhyperfunctioning adenoma. Chemical shift FLASH imaging was superior to the calculated T2 in the characterization of adrenal masses.

Adenoma↗
PubMedDate not supplied

Ultrastructural pathology of the adrenal gland in Cushing's syndrome.

Authors studied the ultrastructural pathology of Cushing's syndrome. Some specific features correlated with the pathological aspects of the adrenals could be found. In the hyperplastic adrenal cortex the cytoplasm contains a rich smooth endoplasmic reticulum and numerous mitochondria. Increased lipid-pigment complexes were also found. The clear cell adenomas showed large lipid vacuoles. In the compact cell adenomas the mitochondria are of variable size and the smooth endoplasmic reticulum is well developed; the pigment bodies are frequent. The nuclei and especially the nucleoli are increased in size. In the adrenal carcinoma the nuclear and nucleolar alterations are still more evident. A marked pleomorphism of mitochondria was noticed. The behaviour of the steroidogenic activity in both tumoral and hyperplastic adrenal glands can be assessed using the ultrastructural picture of the agranular endoplasmic reticulum and of the mitochondria as functional parameters.

Adrenal Cortex↗
PubMed1986

Difficulties in the prospective diagnosis of functional adrenal diseases by CT.

The accuracy of prospective diagnosis of functional adrenal disorders by computed tomography (CT) was evaluated in 65 patients strongly suspected of having such disorders. Thirty-seven patients also underwent adrenal venography and selective adrenal venous sampling. Of the 65 patients, 21 had a hyperfunctioning cortical adenoma, 25 had cortical or medullary hyperplasia, and 11 pheochromocytoma, while 10 had no functional adrenal disease. Diagnosis by CT alone was correct in 66%; diagnosis by CT and venous sampling was correct in 89%. Incorrect prospective CT diagnosis resulted most often from a normal appearance of functionally hyperplastic glands (9 cases), nodular hyperplasia simulating a focal adenoma (8 cases), or an incidental nonfunctioning mass (3 cases). This study emphasizes the need to correlate CT findings with biochemical evaluation and the usefulness of venous sampling in selected cases to avoid inappropriate surgery. When CT is interpreted in correlation with complete biochemical analysis, correct diagnosis can usually be made. A small number of cases may still require adrenal venous sampling.

Adenoma↗
PubMed2006

[Diabetes mellitus and frequently associated endocrine diseases].

The simultaneous occurrence of type 1 or type 2 diabetes with various hormonal diseases (e.g. thyroid, adrenal, pituitary disease) is a frequent observation. A chronically poorly controlled metabolism can alter the hormone parameters of the diabetic. In contrast, an acute loss of metabolic control may be a sign of a newly manifesting hormonal disease, and needs always prompt an appropriate diagnostic work-up and treatment. In view of the frequency both of diabetes mellitus and thyroid disease, a regular check--at least yearly and always in case of unclear worsening of diabetic control--of thyroid gland function is mandatory. The aim is to provide appropriate treatment, and thus to stabilize the patient's metabolic status, as early as possible.

Adrenal Insufficiency↗
PubMed1988

Diseases of the adrenal cortex.

The adrenal cortex is functionally a three-dimensional gland that secretes glucocorticoids, mineralocorticoids, and sex steroids. Of these three classes of steroids only the gluco- and mineralocorticoid hormones are necessary to sustain life. The availability of sensitive and specific radioimmunoassays has permitted accurate measurement of practically every steroid hormone secreted by the adrenal cortex. As in other endocrinopathies, suppression studies are employed when hyperfunction is suspected, while provocative tests are used to detect hypofunction. These dynamic studies enable the clinician to evaluate the functional status of the adrenal cortex. The anatomic configuration of the adrenal cortices is delineated by high-resolution computed tomography (and magnetic resonance imaging), obviating the need for invasive procedures such as venography or arteriography. The disorders of the adrenal cortex can be viewed from the dual perspectives of hyperfunction and hypofunction. Clinical expressions of hyperfunctional adrenocortical syndromes include Cushing's syndrome, primary hyperaldosteronism, and the adrenogenital syndrome. The expressions of hypofunctional syndromes include Addison's disease and selective hypoaldosteronism. The diagnosis and treatment of these disorders are outlined in this issue.

Addison Disease↗
PubMed1995

Corticotropin-releasing hormone induces an exaggerated response of adrenocorticotropic hormone and cortisol in polycystic ovary syndrome.

OBJECTIVE: To evaluate pituitary-adrenal responsive to corticotropin-releasing hormone (CRH) stimulus in polycystic ovary syndrome (PCOS). DESIGN: Controlled clinical study. PATIENTS: Twelve women aged 17 to 32 years, who had been diagnosed as having PCOS, were studied. Fifteen appropriately age- and weight-matched ovulatory patients served as the control. INTERVENTION: In the early follicular phase or after progestin-induced menses, human CRH was injected at 8:00 A.M. and blood samples were collected at 0, 15, 30, 60, and 90 minutes after stimulus. Plasma levels of ACTH and cortisol were measured. RESULTS: Baseline levels of ACTH and cortisol were similar in PCOS and control patients. Both ACTH and cortisol response to CRH were markedly greater in the PCOS population as compared with controls. Moreover, ACTH- and cortisol-stimulated secretion was prolonged for the whole period of the study in hyperandrogenic patients with respect to controls, where baseline levels were attained 60 minutes after the stimulus. CONCLUSIONS: Our results are consistent with the hypothesis that women with PCOS may demonstrate hyperfunction of the hypothalamic-pituitary-adrenal axis, which may be involved in the physiopathologic events leading to the complexity of the syndrome.

Adolescent↗
PubMed2004

Macronodular adrenocortical hyperplasia in a postmenopausal woman.

This case report describes the diagnosis of Cushing's syndrome due to macronodular adrenal hyperplasia in an elderly woman who presented with fatigue, muscle weakness and oedema, and recent excessive bruising. Long-standing disease and comorbidity precluded adrenalectomy. Despite treatment with metyrapone and diuretics, the patient died after two months hospitalisation. Postmortal examination revealed overexpression of luteinising hormone (LH) receptors in the adrenal glands, suggesting that the postmenopausal rise in LH may have a role in adrenal hyperplasia and hypercortisolism.

Adrenal Cortex↗
PubMed2003

Computerized tomography guided percutaneous ethanol injection for the treatment of hyperfunctioning pheochromocytoma.

PURPOSE: We validated the therapeutic efficacy of computerized tomography (CT) guided percutaneous ethanol injection (PEI) for hyperfunctioning pheochromocytoma. MATERIALS AND METHODS: Pheochromocytoma was treated with CT guided PEI in 41 patients, including 19 men and 22 women with a mean age of 42 years (range 31 to 59). Of the 41 patients 40 had a solitary adrenal benign pheochromocytoma (18 on the left and 22 on the right side), which was diagnosed by biopsy in 36 and by typical clinical manifestations, laboratory and CT findings in 4. The remaining patient with malignant pheochromocytoma, who underwent surgical resection 2 years ago, had 2 recurrent lesions along the right sympathetic chain. RESULTS: CT or magnetic resonance imaging followup 7 to 20 days after treatment showed that adrenal benign pheochromocytoma disappeared in 27 patients and became completely necrotic or shrank in 13. The 2 malignant recurrent lesions also disappeared completely. During the followup of 23 to 54 months the foci disappeared completely in 31 patients, and shrank and completely necrotized in 10. All patients showed normal blood pressure without intermittent vertigo, complexion pallor or numbness of the 4 extremities. Blood and urine catecholamine was also within the normal range. CONCLUSIONS: The therapeutic efficacy of CT guided PEI for hyperfunctioning pheochromocytoma is definite and worth widespread application because the procedure is safe, microtraumatic and less costly, and has low morbidity.

Adrenal Gland Neoplasms↗
PubMed2000

Influence of morphine treatment in pregnant rats on the mineralocorticoid activity of the adrenals in their neonates.

Exposure of pregnant rats to morphine, from day 11 to day 18 of gestation, was previously reported to induce both an adrenal atrophy and hypoactivity of the glucocorticoid function in newborns at term, but did not affect, in vitro, the responsiveness of those glands to adrenocorticotrophin hormone (ACTH) concerning corticosterone release. Moreover, these effects were mediated by maternal hormones from the adrenal glands. In the present work, we investigated the effects of a prenatal morphine exposure on the mineralocorticoid activity of the adrenals in neonates. The first aim of the present study was to determine in these newborns 1) the adrenal and plasma aldosterone concentrations at birth time and during the early postnatal period 2) the plasma levels of Na+ and K+ at birth time, 3) the in vitro responsiveness of the newborn adrenals to angiotensin II (A(II)) and ACTH. The second aim of our study was to investigate the mineralocorticoid activity of the adrenals in newborns from adrenalectomized mothers treated with morphine during gestation. According to present data morphine given to intact mothers induced in newborns a severe adrenal atrophy but increased adrenal aldosterone content and plasma aldosterone level. However, prenatal morphine was unable to affect significantly Na+/K+ ratio in both mothers and newborns. In vitro, the adrenals of neonates from morphine-treated mothers were unresponsive to An and ACTH for promoting aldosterone release; in contrast, aldosterone secretion was significantly stimulated by high potassium levels (55 mEq). Maternal adrenalectomy performed one day before the beginning of morphine treatment prevented morphine-induced adrenal atrophy but was unable to affect significantly the adrenal mineralocorticoid function of the offspring. Such data suggest that a prenatal morphine exposure stimulated both aldosterone synthesis and release in neonates. However, this basal hyperfunction did not appear to be coupled with an enhanced adrenal responsivity to AII or ACTH. Prenatal morphine-induced hyperactivity of the mineralocorticoid function of the newborn adrenals, which drastically contrast with hypoactivity of the glucocorticoid one, was independent of adrenal factors from maternal origin.

Adrenal Glands↗