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Antiemetics glucocorticoids

In 15 men with osteonecrosis of the femoral head after short-term therapy the mean duration of therapy was 21 (range 7-39) days and the mean dose in milligram equivalents of prednisone was 850 (range 290-3300) mg (269). The time from administration of glucocorticoids to hip pain was 17 (range 6-33) months. A new case of bilateral avascular necrosis of the femoral heads after high-dose short-term dexamethasone therapy as an antiemetic in cancer chemotherapy has been reported (270). [Pg.33]

Virik K, Karapetis C, Droufakou S, Harper P. Avascular necrosis of bone the hidden risk of glucocorticoids used as antiemetics in cancer chemotherapy. Int J Clin Pract 2001 55(5) 344-5. [Pg.63]

Successful rechallenge has been reported after a reaction to etoposide in a 19-year-old man, who was successfully re-treated with etoposide phosphate with only antiemetic doses of glucocorticoids as cover (134). This case tends to support the old assumption that etoposide hypersensitivity is due to the excipients in the formulation. [Pg.3461]

Nephrotoxicity is the principal dose-limiting side effect of intravenous cidofovir. Proximal tubular dysfunction includes proteinuria, azotemia, glycosuria, and metabolic acidosis. Concomitant oral probenecid and saline prehydration reduce the risk of renal toxicity. On maintenance doses of 5 mg/kg every 2 weeks, up to 5Wo of patients develop proteinuria, 10-15% show an elevated serum creatinine, and 15-20% develop neutropenia. Anterior uveitis that is responsive to topical glucocorticoids and cycloplegia occur commonly and ocular hypotony occurs infrequently with intravenous cidofovir. Administration with food and pretreatment with antiemetics, antihistamines, and/or acetaminophen may improve tolerance. [Pg.819]

Antihistamines, dronabinol, glucocorticoids, and metoclopramide have antiemetic actions that are useful in the management of vomiting caused by anticancer drugs. Levodopa causes nausea because it is converted to dopamine, which activates dopamine receptors in the emetic center. The answer is (C). [Pg.530]

The well-known clinical effects of glucocorticoids include anti-inflammation, anti-edema, anti-allergic jgj and antipyrexia. Also, analgesia and antiemetic effects... [Pg.383]

The optimal dose for glucocorticoid analgesic effect is not established, as controlled dose-finding studies have not been performed. For the antiemetic effect, a dexamethasone dose of 3-4 mg seems to be optimal, whereas for analgesia 8-16 mg seems to be necessary in adults. [Pg.385]

Metallothionein is also induced by a variety of nonmetals, and exposure to these agents often can cause tesistance to anticancer drugs such as cisplatin (Basu and Lazo 1991). Expression of v mos can attenuate the glucocorticoid-induced metallothionein expression and cisplatin resistance. Transcriptional activation of c-Ha-ras oncogene expression in murine NIH 3T3 cells with dexamethasone produces an increase in metallothionein content and a decrease in cisplatin accumulation (Isonishi et al. 1991). The ability of dexamethasone to affect the sensitivity of cells to electrophilic antineoplastic agents could be of some clinical interest because of its frequent usage as an antiemetic. [Pg.272]

A premedication regime consisting of an opioid, an antiemetic as well as a glucocorticoid should be administered intravenously before the TACE treatment to reduce the acute side-effects of TACE. [Pg.49]


See other pages where Antiemetics glucocorticoids is mentioned: [Pg.315]    [Pg.43]    [Pg.46]    [Pg.567]    [Pg.56]    [Pg.937]    [Pg.939]    [Pg.1367]    [Pg.2912]    [Pg.2912]    [Pg.104]    [Pg.123]    [Pg.233]    [Pg.589]    [Pg.2533]   
See also in sourсe #XX -- [ Pg.334 ]




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