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Cushing syndrome

Suppression tests For Cushing syndrome, give 1 mg at 11 pm. Draw blood for plasma cortisol determination the following day at 8 am. For greater accuracy, give 0.5 mg every 6 hours for 48 hours. Collect 24-hour urine to determine 17-hydroxycorticosteroid excretion. [Pg.257]

Speciai risk Use with caution in the following situations Nonspecific ulcerative colitis if there is a probability of impending perforation, abscess, or other pyogenic infection diverticulitis fresh intestinal anastomoses hypertension CHF thromboembolitic tendencies thrombophlebitis osteoporosis exanthema Cushing syndrome antibiotic-resistant infections convulsive disorders metastatic carcinoma myasthenia gravis vaccinia varicella diabetes mellitus hypothyroidism, cirrhosis (enhanced effect of corticosteroids). [Pg.264]

Children Children may be more susceptible to topical corticosteroid-induced hypothalamic-pituitary-adrenal (HPA) axis suppression and Cushing syndrome than adults because of a larger skin surface area to body weight ratio. [Pg.2050]

Systemic effects Systemic absorption of topical corticosteroids has produced reversible HPA axis suppression, Cushing syndrome, hyperglycemia, and glycosuria. As a general rule, little effect on the HPA axis will occur with a potent topical corticosteroid in amounts of less than 50 g weekly for an adult and 15 g weekly for a... [Pg.2050]

Quest Diagnostics use an LC-MS/MS panel for diagnosing cortisol-related disorders by urine analysis. This panel was designed to diagnose Cushings syndrome and the hypertensive conditions AME and GRA. The panel quantifies cortisone, cortisol, 6/j-hydroxycorlisol and 18-hydroxycortisol (18-OHF). The Quest analysis uses 2H4 cortisol as an internal standard and HTLC for on-line extraction. This panel has replaced the RIA and HPLC methods previously used by this commercial laboratory. Another recent publication describes MS/MS of cortisone and cortisol in serum using APPI and similar conditions and MRM transformations to those listed above [43]. [Pg.561]

Tsuruoka S, Sugimoto K, Fujimura A. Drug-induced Cushing syndrome in a patient with ulcerative colitis after betamethasone enema evaluation of plasma drug concentration. Ther Drug Monit 1998 20(4) 387-9. [Pg.68]

Cushing s syndrome occurred in a 44-year-old HIVpositive patient who used inhaled fluticasone (500 micrograms qds) for severe asthma for 2 years (153). Stavudine and nevirapine were replaced by abacavir and ritonavir + lopinavir and 2 months later he developed the typical features of Cushing syndrome. [Pg.87]

De Wachter E, Vanbesien J, De Schutter I, Malfroot A, De Schepper J. Rapidly developing Cushing syndrome in a 4-year-old patient during combined treatment with itraconazole and inhaled budesonide. Eur J Pediatr 2003 162 488-9. [Pg.92]

Dhein S. Cushing-Syndrom nach externer Glukokortikoid-Applikation bei psoriasis. [Cushing syndrome following external glucocorticoid administration in psoriasis.] Z Hautkr 1986 61(3) 161-6. [Pg.93]

Aminoglutethimide is normally prescribed for patients with breast cancer or Cushings Syndrome. In both cases patients suffer from catastrophic physiological decline. To a profound degree this is notably due to severe over production of endogenous glucocorticoids. The one glucocorticoid most readers would be familiar with is cortisol. [Pg.95]

In drug-induced Cushing syndrome, patients begin to exhibit many of the symptoms associated with the... [Pg.423]

Measures for attenuating or preventing drug-Induced Cushing syndrome, (a) Use... [Pg.244]

Obesity is a condition that is influenced by genetic and environmental factors (such as energy intake and expenditure, fetal nutrition, culture). There are four major physiological causes of obesity endocrine disorders (growth hormone deficiency, Cushing syndrome), genetic syndromes (Prader-Willi syndrome or Alstrom syndrome), disorders of the central nervous system (tumor, trauma) or the most common cause, multifactorial or primary obesity (caused by an interaction of multiple genes). [Pg.630]

A2. Albright, F., Cushings syndrome and its connection with the problem of the reaction of the body to injury. Harvey Led. 38, 123-130 (1943). [Pg.280]

Simard M. The biochemical investigation of Cushing syndrome. Neurosurg Focus 2004 16 E4. [Pg.2002]

Contreras P, Araya V Cushings syndrome Review of a national caseload. Rev Med Chh 1995 123 350-62. [Pg.2044]

Gai cia C, BiUer BM, Klibanski A. The role of the clinical laboratory in the diagnosis of Cushing syndrome. Am J Clin Pathol 2003 120 Suppl S38-45. [Pg.2051]

Sonino.N, Boscaro M, Fallo F. Pharmacologic management of Cushing syndrome New targets for therapy. Treat Endocrinol 2005 4 87-94. [Pg.2052]

D. Prednisone acts as a glncocorticoid hormone analog, giving rise to Cushing syndrome symptoms after prolonged administration. [Pg.440]

This patient presents with many of the classic findings of Cushing syndrome. Adrenal hyperplasia can be caused by excessive stimulation from ACTH (pituitary or ectopic production) or from a primary adrenal problem such as adenomas/ carcinomas. In addition to above symptoms, patients with Cushing syndrome are also at risk for osteoporosis and diabetes mellitus (DM). The diagnosis is confirmed with elevated cortisol levels after a dexamethasone suppression test. Treatment depends on the underlying etiology and is often surgical. [Pg.444]

Explain from a biochemical standpoint why hypertension is a common consequence of Cushing syndrome. [Pg.444]

Cushing disease A specific form of Cushing syndrome, which is caused by an ACTH-secreting pituitary adenoma represents approximately 66 percent of all cases of Cushing syndrome. Because of structural similarities with melanocyte-stimulating hormone (MSH), excess ACTH from pituitary adenomas can induce dermal hyperpigmentation. [Pg.444]

Dexamethasone suppression test An overnight test used to screen patients for Cushing syndrome by administering dexamethasone to a patient. Positive results for this test are indicated by a patient s inability to reduce cortisol levels after dexamethasone treatment—usually because the patient s feedback loop mechanism is ineffective at inhibiting cortisol release. [Pg.445]

Ectopic ACTH syndrome Form of Cushing syndrome in which benign or malignant tumors arise in places other than the pituitary, leading to excessive release of ACTH and subsequently, cortisol into the bloodstream represents approximately 10 to 15 percent of Cushing syndrome cases. [Pg.445]


See other pages where Cushing syndrome is mentioned: [Pg.189]    [Pg.883]    [Pg.587]    [Pg.58]    [Pg.421]    [Pg.423]    [Pg.425]    [Pg.426]    [Pg.916]    [Pg.91]    [Pg.304]    [Pg.11]    [Pg.949]    [Pg.2363]    [Pg.2025]    [Pg.2029]    [Pg.1404]    [Pg.444]    [Pg.444]    [Pg.444]   
See also in sourсe #XX -- [ Pg.244 , Pg.304 ]

See also in sourсe #XX -- [ Pg.439 , Pg.443 , Pg.444 , Pg.445 , Pg.446 , Pg.447 , Pg.448 ]




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Adrenal Disorders — Cushings Syndrome

Aminoglutethimide in Cushing’s syndrome

Cushing

Cushing syndrome, drug-induced

Cushing-like syndrome

Cushing’s syndrome

Cushing’s syndrome and

Cushing’s syndrome treatment

Hypercortisolism Cushing syndrome

Iatrogenic Cushing syndrome

Induced Cushing Syndrome

Pseudo-Cushing syndrome

Pseudo-Cushing’s syndrome

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