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Cushing Cortisol levels

Close monitoring of 24-hour urinary free cortisol levels and serum cortisol levels are essential to identify adrenal insufficiency in patients with Cushing s syndrome. Steroid secretion should be monitored with all drug therapy and corticosteroid replacement given if needed. [Pg.220]

Most importantly, the determination of cortisol levels is considered useful in the diagnosis and treatment of various ailments, namely Addison s Disease i.e., pernicious anaemia—a condition whereby the maturation of the red cells may not proceed beyond the stage of megaloblasts Cushing s Syndrome. [Pg.64]

The steroid-inhibiting properties of metyrapone have also been used in the treatment of Cushing s syndrome, and it remains one of the more effective drugs used to treat this syndrome. However, the compensatory rise in corticotrophin levels in response to falling cortisol levels tends to maintain adrenal activity. This requires that glucocorticoids be administered concomitantly to suppress hypothalamic-pituitary activity. Although metyrapone interferes with lip- and 18-hydroxylation reactions and thereby inhibits aldosterone synthesis, it may not cause mineralocorticoid deficiency because of the compensatory increased production of 11-desoxycorticosterone. [Pg.699]

Medical illness or medication side effects may directly affect cognition virtually all classes of medication have been implicated. In adult patients, glucocorticoids can impair memory at relatively low doses (Keenan et ah, 1995 Newcomer et ah, 1999), as there are postulated effects on hippocampal neurons. Newcomer et ah, (1999) have reviewed the literature on illnesses in adults in which memory inversely correlates with cortisol levels, such as in Cushing s disease, Alzheimer s dementia, schizophrenia, and depression. There is no similar literature on the pediatric population. The risk of memory impairment puts chronic steroid treatment, such as that seen in certain pediatric rheumatologic disorders and severe asthmatics, for example, into a different perspective, however. Documentation of memory both before and during chronic steroid treatment might help determine detrimental effects in the pediatric population. [Pg.632]

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]

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]

Pseudo-Cushing syndrome Condition in which alcohol induces symptoms of Cushing syndrome without the tumor that leads to increased cortisol levels. [Pg.445]

Also, because cortisol is a stress hormone, people who suffer a great deal of stress, such as athletes, alcoholics, and pregnant women may have high blood cortisol levels and exhibit symptoms of Cushing syndrome (also known as pseudo-Cushing syndrome). [Pg.449]

Treatment of Cushing syndrome is intended to return cortisol levels back to normal and usually occurs through surgery. In some cases medications, such as mitotane, which lower blood and urine cortisol levels, can be used alone or in combination with radiation therapy. [Pg.449]

A 45-year-old female patient presents with hirsutism, striae, bruising, acne, and hyperpigmentation of the skin. After a thorough physical examination the physician notes that she also suffers from hypertension and shows signs of a buffalo hump on her back between the shoulders. Cushing syndrome is snspected and after laboratory tests show elevated blood cortisol levels she is given a dexamethasone suppression test. Her resnlts are positive. [Pg.449]

Failure of 1 mg of dexamethasone taken at 23 00 to suppress the serum cortisol level at 08 00 the following morning, or failure to suppress urinary cortisol secretion oveniight (as measured by an early morning urine cortisol creatinine ratio) is another pointer towards the presence of Cushing s syndrome. [Pg.154]

Dexamethasone (Decadron) PO/IV/iM. In addition to uses listed in text, it is used to reduce elevated intracranial pressure. Few mineralocorticoid effects. Dexamethasone suppreslon test examines whether the hypothalamus/pituitary can be suppressed by glucocorticoids. If the plasma cortisol level is < 5 ug/dl eight hours after receiving Igm of dexamethasone, Cushing s syndrome is ruled out. [Pg.151]

A report describes two patients suspected of having Cushing s syndrome because the overnight suppression test with dexamethasone 1 mg had not suppressed their cortisol levels. Further investigation found no clinical evidence of Cushing s syndrome and the false-positive test results were attributed to the fact that both patients were taking carbamazepine 400 mg three times daily at the time of the test. The test was repeated in one patient 3 weeks after carbamazepine was stopped and it indicated normal cortisol suppression. A study in 8 healthy subjects found that, in the presence of carbamazepine 800 mg daily, the dosage of dexamethasone needed to suppress cortisol secretion (as part of the dexamethasone adrenal suppression test) was increased two to fourfold. A further study found that it took 2 to 13 days for false-positive results to occur after carbamazepine was started, and 3 to 12 days to recover when the carbamazepine was stopped. ... [Pg.1054]

A 40-year-old woman with cystic fibrosis given clarithromycin 500 mg twice daily for 4 years for a Mycobacterium abscessus infection developed Cushing s syndrome with adrenal suppression 6 weeks after starting to use inhaled budesonide 400 micrograms daily. A slow rise in morning free cortisol levels was found 4 weeks after stopping budesonide, but she died 8 weeks later of severe respiratory failure. ... [Pg.1056]

Starkman, M.N., Gebarski, S.S., Berent, S., and Schteingart, D.E. 1992. Hippocampal formation volume, memory dysfunction, and cortisol levels in patients with Cushing s syndrome. Biol. Psychiatry 32 756-765. [Pg.368]

In all forms of Cushing s disease, cortisol levels in the plasma are raised and there is loss of the diurnal rhythm. This is accompanied by increased urinary excretion of cortisol. Another feature common to all forms of Cushing s disease is the failure to reduce cortisol secretion with a small dose of dexamethasone. [Pg.108]

The majority of the plasma cortisol is protein bound, only a small proportion being in the free state. This free cortisol is filtered at the glomerulus and passes into the urine where it can be measured, for example by radioimmunoassay. Urinary free cortisol determinations therefore correlate with the plasma free cortisol and the cortisol secretion rate. Increased urinary free cortisol levels are found in cases of Cushing s syndrome. [Pg.141]

The low dose dexamethasone suppression test (qv) is an example of such a test. Dexamethasone is a powerful cortisol analogue which is capable of suppressing ACTH production and therefore cortisol secretion. In Cushing s syndrome, however, the cortisol levels do not fall, e.g. due to pituitary disease (when the feedback mechanism is insensitive) or due to adrenal carcinoma or adenoma when cortisol secretion is auto-nonomous. [Pg.332]

In view of its effects on adrenal steroidogenesis, ketoconazole has also been examined in the treatment of Cushing s syndrome. The drug was efficacious in the management of this condition and led to normalisation of urinary cortisol levels, while other symptoms such as hypertension and hypokalaemia reduced. " Fluconazole has also proved effective in the treatment of Cushing s syndrome. ... [Pg.94]

If ACTH or cortisol is given to healthy subjects, it will cause a rise in the electrophoretic a2-fraction, which is mainly secondary to an increased Hp level in plasma this also holds for dogs (VI). In Cushing s disease slight hyperhaptoglobinemia is demonstrable (B3). [Pg.178]

Starkman MN, Schteingart DE, Schurtt AM Cushing s syndrome after treatment changes in cortisol and ACTH levels and amelioration of the depressive syndrome. Psychiatry Res 19 177-188, 1985... [Pg.750]


See other pages where Cushing Cortisol levels is mentioned: [Pg.693]    [Pg.279]    [Pg.242]    [Pg.885]    [Pg.920]    [Pg.65]    [Pg.1396]    [Pg.450]    [Pg.793]    [Pg.363]    [Pg.655]    [Pg.356]    [Pg.107]    [Pg.192]    [Pg.600]    [Pg.192]    [Pg.243]    [Pg.538]    [Pg.545]    [Pg.545]    [Pg.301]    [Pg.301]    [Pg.700]    [Pg.703]    [Pg.883]    [Pg.883]    [Pg.884]    [Pg.889]   
See also in sourсe #XX -- [ Pg.478 ]




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