Disease relevance of Cushing Syndrome

• To investigate the pathogenetic mechanisms of Cushing's syndrome, we studied variations in plasma cortisol levels (episodic variations, or pulses) over 24 hours in 51 normal subjects, 14 patients with adrenal adenoma, and 46 patients with Cushing's disease [1].
• We studied a 48-year-old woman with Cushing's syndrome, nodular adrenal hyperplasia, and undetectable plasma corticotropin concentrations in whom food stimulated cortisol secretion [2].
• Remission was defined as the regression of symptoms and signs of Cushing's syndrome, normal urinary cortisol excretion, and a low plasma cortisol concentration in the morning after the administration of 1 mg of dexamethasone at midnight [3].
• Three of 59 patients (5 percent) with the sporadic form of the Zollinger-Ellison syndrome had Cushing's syndrome, with severe symptoms due to ectopic production of ACTH [4].
• Before their weight loss was corrected, the anorexic patients had marked hypercortisolism but normal basal plasma ACTH [5].

Psychiatry related information on Cushing Syndrome

• To study the pathophysiology of hypercortisolism in patients with anorexia nervosa, we examined plasma ACTH and cortisol responses to ovine corticotropin-releasing hormone before and after correction of weight loss [5].
• We undertook this study because alprazolam is the only benzodiazepine effective in treating both major depressive and anxiety disorders, and recent data suggest that the hypercortisolism of major depression reflects hypersecretion of CRH [6].
• Our findings in untreated patients with seasonal affective disorder are similar to those in patients with Cushing's disease 2 weeks after transsphenoidal hypophysectomy, who uniformly show sustained suppression of their CRH neuron because of long-standing hypercortisolism [7].
• Region-specific CORT-induced inhibition of DAergic activity may help to explain depressive symptoms in patients with chronic hypercortisolemia and normalization after medical or surgical correction of hypercortisolism [8].
• Conversely, estrogen directly stimulates the CRH gene, which may explain the slight hypercortisolism of females and the preponderance of depressive, anxiety, and eating disorders, as well as Cushing's disease in women [9].

High impact information on Cushing Syndrome

• They die before 9 weeks of severe Cushing's syndrome arising from pituitary intermediate lobe ACTH hypersecretion [10].
• Leuprolide acetate therapy in luteinizing hormone--dependent Cushing's syndrome [11].
• Propranolol therapy for ectopic beta-adrenergic receptors in adrenal Cushing's syndrome [12].
• It is possible to determine the specific abnormality in most patients, but it can sometimes be difficult to decide whether the patient has hypercortisolism and whether it is primary or due to major depressive disorder or to the stress of other diseases [13].
• The cause of hypercortisolism was identified by low- and high-dose dexamethasone suppression tests, the ovine corticotropin-releasing hormone (CRH) stimulation test, imaging studies, and bilateral sampling of the inferior petrosal sinuses combined with administration of CRH [14].

Chemical compound and disease context of Cushing Syndrome

• Cushing's syndrome is usually caused by the secretion of corticotropin or cortisol by a pituitary or adrenal tumor, respectively, or by ectopic secretion of corticotropin [13].
• Treatment with octreotide decreased urinary cortisol excretion and ameliorated the clinical manifestations of Cushing's syndrome [15].
• CS comprises a group of disorders characterized by hypercortisolism [16].
• A second patient without clinical findings of Cushing's syndrome also had normal basal steroid levels [17].
• Mitotane. Spironolactone antagonism in Cushing's syndrome [18].
• ACTH-dependent Cushing's syndrome is a heterogeneous disorder requiring a multidisciplinary and individualized approach to patient management [19].

Biological context of Cushing Syndrome

• Cushing syndrome from percutaneous absorption of triamcinolone cream [20].
• Of a total of 26 reported patients with adrenal autotransplants surveyed, 22 exhibited evidence of graft survival, 16 were able to discontinue steroid replacement therapy and three eventually developed recurrent Cushing's syndrome from the transplants [21].
• In summary, patients with Cushing's syndrome have moderately elevated leptin levels that maintain an intact circadian rhythm but do not respond to acute or subacute alterations of cortisol [22].
• In Cushing's syndrome, cortisol causes fat accumulation in specific sites most likely to be associated with insulin resistance, notably in omental adipose and also perhaps in the liver [23].
• Gene expression of angiotensin II receptor in blood cells of Cushing's syndrome [24].

Anatomical context of Cushing Syndrome

• It is concluded that trilostane is an effective inhibitor of 3 beta-hydroxysteroid dehydrogenase enzyme system in human adrenal gland; it inhibits biosynthesis of cortisol and it is useful in the treatment of Cushing's syndrome [25].
• Two 8-yr-old children, a boy and girl, are described with Cushing's syndrome secondary to ectopic ACTH-secreting pancreatic islet cell carcinomas [26].
• A patient with Cushing's syndrome is described who had a metastatic medullary carcinoma of the thyroid which contained corticotropin-releasing factor [27].
• In patients with Cushing's syndrome, both mononuclear leukocyte and platelet AT1A mRNA levels, which were elevated, were reduced after removal of the adrenal tumors, whereas AT1B receptor mRNA levels of both types of blood cells did not significantly change after adrenalectomy [24].
• Femoral and abdominal adipose tissue cellularity and metabolism as well as muscle morphology and metabolism were examined in women with Cushing's syndrome and compared with those in nonobese women and obese women with the android and gynoid types of fat distribution [28].

Gene context of Cushing Syndrome

• CONCLUSIONS: Suppressed ACTH secretion in patients with Cushing syndrome results in reduction of the ACTH-R mRNA expression in nonneoplastic adrenocortical cells [29].
• OBJECTIVE: To examine whether inhibition of endogenous adrenocorticotropin (ACTH) secretion in patients with Cushing syndrome affects the expression of the ACTH receptor (ACTH-R) gene in adrenocortical adenoma and attached atrophic normal gland [29].
• Somatostatin receptor scintigraphy: its value in tumor localization in patients with Cushing's syndrome caused by ectopic corticotropin or corticotropin-releasing hormone secretion [30].
• However, hCRH-induced acute hypercortisolism does not alter gonadotropin secretion in agonadal women [31].
• However, whereas the potentiating effect of PRO on GHRH-elicited GH release was still observed under hypercortisolism, it was lacking for both CLO and PD when these drugs were given in this situation [32].

Analytical, diagnostic and therapeutic context of Cushing Syndrome

• Petrosal sinus sampling with and without corticotropin-releasing hormone for the differential diagnosis of Cushing's syndrome [33].
• Cortisol secretion in Nelson syndrome: Persistence after "total" adrenalectomy for Cushing syndrome [34].
• New modalities including the ovine CRH test, MRI, and petrosal sinus sampling have improved the evaluation of certain patients with Cushing's syndrome [35].
• In order to investigate the effect of glucocorticoids on gastrin secretion, plasma gastrin levels were measured by radioimmunoassay in patients with Cushing's syndrome and those treated with glucocorticoids [36].
• EEG sleep in Cushing's disease and Cushing's syndrome: comparison with patients with major depressive disorder [37].

References