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At least 559 records · Page 31Linked to original sources
PubMed1996

[Subclinical hypercortisolism in incidentally detected adrenal adenoma].

AIM OF STUDY: To define in a prospective study the prevalence and manifestations of subclinical hypercortisolism in a sizeable group of patients with incidentally detected adrenal adenoma. Such tumour - although usually clinically silent - may cause discrete endocrine dysfunctions. PATIENTS AND METHODS: Between 1990 and 1994, 85 consecutive patients with incidentally discovered adrenal adenoma were investigated (54 women, 31 men; mean age 54.1 +/- 13 [24-81] years). In addition to history and clinical examination all patients had a low-dose dexamethasone suppression test (2mg) and their morning basal plasma ACTH concentration was measured. The diagnosis of subclinical hypercortisolism was made if there was inadequate suppression of cortisol after dexamethasone administration, plasma ACTH level was decreased and there were no clinical signs of Cushing's syndrome. RESULTS: Five of the patients fulfilled the criteria of subclinical hypercortisolism (prevalence of 6%). One of them had oligomenorrhoea, another arterial hypertension, and three had mild histological proof of adrenal adenoma. Postoperatively the patient with oligomenorrhoea had normal menstrual cycles, while in all others with subclinical hypercortisolism excision of the tumour had no influence of their clinical state. CONCLUSIONS: Subclinical hypercortisolism is rare, but is one of the most common endocrine disorders in patients with incidental adrenal adenoma. It can be diagnosed only by hormonal analysis. Once the latent cortisol excess has been eliminated, those symptoms which are due to hormonal abnormality may regress, but nonspecific signs, such as obesity or hypertension, may not necessarily improve.

Adenoma↗
PubMed1994

[Bilateral massive macronodular adrenal gland hyperplasia. A rare cause of Cushing's syndrome].

A 46-year-old man with known arterial hypertension for 10 years had, over the last two years, developed increasing obesity, particularly of the trunk, with other symptoms typical of Cushing's syndrome. Hormone analysis demonstrated hypercortisolism and decreased plasma ACTH concentration. The dexamethasone inhibition test failed to show any significant suppression of serum cortisol. Plasma ACTH was not increased in the corticotrophin-releasing hormone and the metyrapone tests. In the short ACTH test there was an excessive cortisol increase. Abdominal computed tomography revealed both adrenals to be enlarged (6 x 4 cm) and coarsely nodular. Adrenolytic treatment with ketoconazole (400 mg daily) caused symptoms of adrenal insufficiency, but a reduced dosage of 200 mg daily lowered the cortisol level to between 5 and 11 micrograms/dl and normalized the blood pressure and clinical signs of Cushing's syndrome disappeared. Subsequent bilateral adrenalectomy confirmed the diagnosis of massive macronodular adrenal hyperplasia. Substitution treatment with twice daily 25 mg cortisone acetate and 0.05 mg fludrocortisone was started postoperatively.

Adrenal Gland Diseases↗
PubMed1997

Urinary corticoid/creatinine ratios in the differentiation between pituitary-dependent hyperadrenocorticism and hyperadrenocorticism due to adrenocortical tumour in the dog.

In a study on the differentiation between pituitary-dependent hyperadrenocorticism (PDH) and hyperadrenocorticism due to adrenocortical tumour (AT), two questions were addressed: 1. Do basal urinary corticoid/creatinine (c/c) ratios have any value in this respect, and 2. what is the reference percentage suppression of the urinary c/c ratios in the high-dose dexamethasone suppression test? Data obtained from 160 dogs with hyperadrenocorticism were analysed. In 49 dogs the diagnosis AT was confirmed by the finding of plasma ACTH concentrations < 40 ng/l, by visualisation of the tumour by ultrasonography and/or computed tomography, and by histological examination of the adrenal tissue obtained at surgery or autopsy. Among the 111 dogs with PDH, there were 31 animals with resistance to dexamethasone suppression, i.e., suppression < 50%. The basal urinary c/c ratios of dogs with PDH and AT did not differ significantly, although urinary c/c ratios > 100 x 10(-6) almost exclusively occurred in association with PDH. Among the dogs with hyperadrenocorticism, the positive predictive value of a basal urinary c/c ratio > 100 x 10(-6) for the diagnosis of PDH was 0.90 (95% CI: 0.74-0.98). Of the 49 dogs with AT, 34 had a urinary c/c ratio after dexamethasone administration higher than the basal urinary c/c ratio. The maximum suppression of the basal urinary c/c ratio in dogs with AT was 43.7%. It is concluded that in dogs with hyperadrenocorticism basal urinary c/c ratios only have predictive value in the differentiation between AT and PDH when the ratio exceeds 100 x 10(-6). The generally accepted criterion of 50% suppression by dexamethasone in the differentiation between PDH and AT is also applicable to the urinary c/c ratio.

Adrenal Gland Neoplasms↗
PubMed1984

Hyperadrenalism in childhood and adolescence.

Hyperadrenalism in childhood and adolescence has unique features that influence diagnosis and management. We reviewed our experience with 18 patients, ranging in age from 18 months to 18 years. Nine had bilateral adrenal hyperplasia, eight had adrenal neoplasms, and one had micronodular hyperplasia. Patients with congenital adrenal hyperplasia and hyperaldosteronism were excluded. Six patients with Cushing's disease diagnosed in earlier years were treated by total adrenalectomy and recently two patients underwent transsphenoidal removal of pituitary tumors. Bilateral adrenalectomy was carried out in one patient with micronodular hyperplasia and in a second because of elevated adrenocorticotrophic hormone (ACTH) levels from an undefined source. Eight patients had adrenal neoplasms, including five adenomas and three carcinomas. We found no reliable criteria to differentiate before surgery between adrenal adenomas and adrenal carcinomas. The most recognizable characteristic of malignancy was tumor size, specifically weight greater than 75 gms. Of the three patients with adrenal carcinoma, one expired 20 months after adrenalectomy and 8 months after receiving palliative partial hepatectomy for liver metastasis. Two patients are well with normal growth and development at 11 and 20 years following adrenalectomy. With the exception of one patient who died 6 years after surgery from a glioblastoma multiforme, all patients with adrenal adenomas are well. Eight patients underwent bilateral adrenalectomy for hypercortisolism. Five of the six who have reached their adult stature are significantly stunted. Four of six patients with Cushing's disease, treated by total adrenalectomy, have developed Nelson's syndrome at 2, 6, 10, and 12 years after surgery. Of the two patients undergoing transsphenoidal surgery, one had recurrent disease at 2 years and was treated by pituitary irradiation with recovery. The patients undergoing adrenalectomy for micronodular hyperplasia and ectopic ACTH are well at 2 and 4 years, respectively. Cushing's disease in children and adolescents is best treated by transsphenoidal removal of the pituitary adenoma. Adrenalectomy, once the most accepted approach, plays a secondary role and is indicated primarily in micronodular adrenal hyperplasia, in patients with ectopic ACTH production of an undefined source, and in recurrent Cushing's disease following prior pituitary irradiation. The high incidence of Nelson's syndrome in children treated by adrenalectomy mandates that patients at risk be monitored lifelong for the progression of a pituitary tumor.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenoma↗
PubMedDate not supplied

CT and MR imaging of massive macronodular adrenocortical disease: a rare cause of autonomous primary adrenal hypercortisolism.

We studied four patients with adrenocorticotropic hormone (ACTH)-independent hypercortisolism due to bilateral massive enlargement of the adrenal glands. The combined weight of the adrenal glands ranged from 69 to 149 g and the adrenal cortex was replaced in three of four patients by multiple nodules ranging from microscopic to 4 cm in diameter. One patient had massive diffuse enlargement. All patients had low or undetectable levels of serum ACTH, absence of petrosal sinus to peripheral gradients of ACTH in bilateral samples from the inferior petrosal sinuses before and after stimulation by corticotropin releasing hormone, and absence of an adenoma on MR imaging of the pituitary gland. The marked degree of adrenocortical enlargement and absence of ACTH dependency separates this massive macronodular disease from the more common ACTH-dependent macronodular hyperplasia encountered in older patients with pituitary-dependent Cushing disease. All patients required bilateral adrenalectomy to control hypercortisolism. We present the spectrum of nodular adrenal disease associated with hypercortisolism and a differential diagnosis based on morphologic criteria.

Adrenal Cortex Diseases↗
PubMed1985

Hypercortisolism, diarrhea with steatorrhea, and massive proteinuria due to pheochromocytoma.

Amelioration or cure of hypertension, hypercortisolism, diarrhea with steatorrhea, and massive proteinuria resulted from excision of a pheochromocytoma that contained immunoreactive ACTH, VIP, and somatostatin. Ectopic ACTH production by the tumor was clearly the cause of the hypercortisolism, and the possible involvement of VIP and somatostatin in the diarrhea and steatorrhea was considered. The response to tumor removal suggested that the mesangioproliferative glomerulonephritis shown on renal biopsy was also a paraneoplastic phenomenon.

Adrenal Gland Neoplasms↗
PubMed1979

In vitro biosynthesis of 18-hydroxy-11-deoxycorticosterone from deoxycorticosterone by human adrenal glands removed from patients with hypercorticism.

The biosynthesis of 18-hydroxy-11-deoxycorticosterone (18-OH-DOC) was studied by in vitro incubations of human adrenals resected from patients with Cushing's syndrome, using deoxycorticosterone as precursor. 18-OH-DOC synthesis was similar in adrenals from normal subjects and in those derived from patients with different types of Cushing's syndrome (hyperplasia, adenoma, carcinoma). The in vitro addition of o,p'-DDD (5 x 10(-3) M) to an adrenocortical carcinoma incubation did not alter 18-OH-DOC biosynthesis. By contrast, treatment of the patient with o,p'-DDD prior to adrenalectomy resulted in a low production of 18-OH-DOC in vitro but only when cortisol synthesis was drastically decreased.

18-Hydroxydesoxycorticosterone↗
PubMed1998

Hyperadrenocorticism in six cats.

The case records of six cats with hyperadrenocorticism presented to the Department of Clinical Veterinary Medicine, University of Cambridge, over an 11-year period were reviewed. Signalment and clinical signs were similar to previous reports but, in contrast to other reports, only three cats had diabetes mellitus on presentation. Abdominal radiographs revealed an adrenal mass in one case, obesity in all cases but no hepatomegaly. The adrenal glands were identified ultrasonographically in three out of six cases. Clinicopathological findings were non-specific. The diabetic cats had a significantly lower serum potassium concentration than the non-diabetic cats (P < 0.05). Results of adrenocorticotrophic hormone (ACTH) stimulation tests were supportive of a diagnosis of hyperadrenocorticism in the five cats in which they were performed. Five cats had pituitary-dependent hyperadrenocorticism (PDH) and one had an adrenal tumour. Differentiation between the two forms of hyperadrenocorticism was possible preoperatively in five out of six cats. Adrenal histopathology confirmed hyperplasia in four cats and adenocarcinoma in one cat. Three cats with PDH underwent bilateral adrenalectomy and two of these cats had low, flat ACTH stimulation tests postoperatively and survived for significant periods. The cat with an adrenal tumour underwent partial unilateral adrenalectomy, maintained a positive ACTH stimulation test postoperatively and was euthanased one week after surgery.

Adrenal Cortex Function Tests↗
PubMed2004

Adrenal necrosis in a dog receiving trilostane for the treatment of hyperadrenocorticism.

Clinical and biochemical changes suggestive of hypoadrenocorticism were observed in a 10-year-old male neutered Staffordshire bull terrier shortly after beginning therapy with trilostane for the treatment of hyperadrenocorticism. The dog's condition was stabilised with intravenous fluids, fludrocortisone and prednisolone. An exploratory laparotomy and excisional biopsy of the left adrenal gland were performed. Histopathological analysis showed adrenal cortical necrosis with reactive inflammation and fibrosis. Trilostane is a reversible inhibitor of steroid synthesis and this complication has not been reported previously. Clinicians should be aware that trilostane therapy may result in adrenal necrosis but that prompt treatment might correct a life-threatening situation.

3-Hydroxysteroid Dehydrogenases↗