Dexamethasone confirmation

In patients in whom the diagnosis of Cushing s syndrome has been established clinically and confirmed by a finding of elevated free cortisol in the urine, suppression with large doses of dexamethasone will help to distinguish patients with Cushing s disease from those with steroid-... 

How corticosteroids prevent vomiting is unclear, but many studies have confirmed the effectiveness of a single dose of dexamethasone against a variety of anticancer agents. A randomized trial found... 

Iontophoresis in the ear to relieve pain was reported by Albrecht in 1911 [47]. He used cocaine in high concentrations (20%-40%), copper electrodes, and uncontrolled high current (1.5-2 mA) on perforated tympanic membranes. Despite excellent anesthesia, many of his patients were vertiginous during and after treatment, with some patients suffering permanent loss of hearing. However, relatively recent studies have demonstrated that the use of lidocaine [48], A-acetylcysteine [49], or dexamethasone and fosfomycin [50] in iontophoresis to the ear has no adverse effects in either animal or clinical trials. Echols et al. [51] confirmed that lidocaine could be iontophoresed in the middle ear for at least 30 minutes at 1 mA without any adverse effects. 

In a report on the use of albendazole 15 mg/kg/day in two divided doses for 14 days in the treatment of persistent neurocysticercosis (10), adverse reactions were monitored in 43 patients with seizures and a sohtary cysticercal cyst, who had not been treated before. In aU patients CT scans confirmed the presence of a solitary cyst less than 2 cm in diameter. Antiepileptic treatment was continued. In seven patients dexamethasone 8 mg/day in four divided doses was given for the first 5-7 days after the start of treatment. Follow-up CT scans at 4-10 weeks after the start of treatment showed responses in 20 patients, with complete disappearance in seven patients and a reduction to 50% of the pretreatment size in the other 13. There were adverse effects in 15 patients, with a maximum on the fifth day after the start of treatment. Six patients had severe headaches, 11 had partial seizures, and 2 had epileptic seizures and severe postictal hemiparesis that persisted for a week or more. Because of these serious adverse effects treatment was discontinued in seven patients and dexamethasone was added in those patients who were not already taking it, although its use proved questionable. Adverse effects were seen in three of seven patients who took prophylactic steroid therapy and in 12 of 36 patients who did not. 

The incidence of deep venous thrombosis is increased by the co-administration of doxorubicin, as suggested by a study in 232 patients with multiple myeloma who received a combination of thahdomide and chemotherapy in two protocols that differed only by the inclusion of doxorubicin in one DT-PACE (dexamethasone -I- thahdomide -I-cisplatin -I- doxorubicin + cyclophosphamide -I- etoposide) and DCEP-T (dexamethasone + cyclophosphamide -I-etoposide -I- cisplatin + thalidomide) (25). There was an increased risk of deep venous thrombosis in those who received DT-PACE but not in those who received DCEP-T. Multivariate analysis confirmed that those who received thahdomide + doxorubicin had an increased risk of deep venous thrombosis. In two separate trials in patients taking thahdomide for multiple myeloma, deep venous thrombosis occurred in four of 15 patients who received concomitant treatment with doxorubicin -I- dexamethasone compared with three of 45 who received dexamethasone only (26). 

A 36-year-old white woman with relapsing acute myeloid leukemia took ceftazidime (2 g tds) and aciclovir for febrile neutropenia and Herpes labialis. She developed an itchy rash and treatment was changed to imi-penem (500 mg qds for 5 days), vancomycin (1 g bd for 3 days), and gentamicin (2 mg/kg for 3 days) chemotherapy included idambicin, cytarabine, etoposide, ondansetron, and dexamethasone for 3 days. Within a few days the rash developed into blisters and erosions, affecting more than 80% of the skin. The diagnosis was confirmed histologically, and she subsequently died from shock (70). 

For the analysis of corticosteroids, some of the methods described are the determination of corticosteroids in feed and mine [77], the analysis of dexamethasone and betamethasone in bovine hver [78], a multiresidne method for the quantification and confirmation of five corticosteroids in urine [79], and the analysis of seven corticosteroids in bovine mine [80], The LOQ for corticosteroids in urine are generally around 1 pg/1. 

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. 

To confirm the diagnosis, the infant was reinvestigated at the age of 14 months when, after stimulation with corticotropin for 14 days while on maintenance therapy with dexamethasone and fluorocortisol, the... 

To confirm hypercortisolism, early morning urinary corlisohcreatinine ratios will be elevated, diurnal rhythm of serum cortisol will be absent, there will be no cortisol rise during an insulin-tolerance test, and serum cortisol will not suppress with a low dose of dexamethasone. 

Friedrich, A. Schulz, R. Meyer, H.H. Use of enzyme immunoassay and reverse-phase high-performance liquid chromatography to detect and confirm identity of dexamethasone in equine blood. Am.J.Vet.Res., 1992, 53, 2213-2220... 

Nine patients treated with carmustine 80 mg/m daily for 3 days, cimetidine 300 mg four times daily for 1 to 4 weeks, steroids, and cranial irradiation over 6 weeks, demonstrated marked leucopenia during the first cycle. Bone marrow aspirates confirmed the marked decrease in granulocytic elements in 2 patients. In comparison, 31 patients treated similarly, but without cimetidine, had no significant white cell depression. Neutropenia was found in a man taking regular cimetidine, phenytoin, phenobarbital, and dexamethasone, 53 days after he was given lomustine 120 mg, and 16 days after he was given lomustine 160 mg. The cimetidine was discontinued and the neutropenia rapidly reversed within 14 days. The neutrophil nadir from the lomustine 160 mg dose occurred after a further 16 to 19 days and was much less severe. ... 

Information is limited but the interaction between dexamethasone and aminoglutethimide is established. The reduction in the serum corticosteroid levels can be enough to reduce or even abolish the effects of corticosteroid replacement therapy or to cause loss of control of a disease condition. This has been successfully accommodated by increasing the dosage of the dexamethasone. Hydrocortisone is routinely used with aminoglutethimide as replacement therapy, and would seem to be a suitable alternative to dexamethasone, where clinically appropriate. Other synthetic corticosteroids are predicted to interact in the same way as dexamethasone, but this needs confirmation. 

Information seems to be limited to these studies. The indication is that large doses of some antacids can reduce the bioavailability of corticosteroids, but small doses do not, although this needs confirmation. One manufacturer of dexamethasone suggests that the doses of antacid should be spaced as far as possible from the dexamethasone, while another suggests an interval of at least 2 hours. In other similar antacid interactions 2 to 3 hours is usually sufficient. The manufacturers of deflazacort also suggest an interval of at least 2 hours between administration of deflazacort and antacids. " Concurrent use should be monitored to confirm that the therapeutic response is adequate. Information about the interaction of other corticosteroids and antacids is lacking. 

Information is limited but the interaction appears to be established. Patients taking carbamazepine are likely to need increased doses of dexamethasone, methylprednisolone or prednisolone. Prednisolone is less affected than methylprednisolone and is probably preferred. The same interaction seems likely with other corticosteroids but more study is needed to confirm this. Note that hydrocortisone and prednisone are affected by another potent enzyme inducer, phenobarbital , (p.l052), and would therefore also be expected to interact with carbamazepine. 

Nine asthmatic patients had a 40% increase in the clearance and a similar reduction in the half-life of dexamethasone when they were given ephedrine 100 mg daily for 3 weeks. This would be expected to reduce the overall effects of dexamethasone, hut this requires confirmation. Be alert... 

A study in 7 patients found that phenytoin 300 to 400 mg daily reduced the plasma cortisol levels in response to dexamethasone from 22 to 19 microgram%, compared with a reduction from 18 to 4 microgram% in the absence of phenytoin. Other studies confirm that plasma cortisol and urinary 17-hydroxycorticosteroid levels are suppressed far less than might be expected with small doses of dexamethasone (500 micrograms every 6 hours for 8 doses), but with larger doses (2 mg every 6 hours for 8 doses) suppression was normal. However, one case describes a patient in whom even 16 mg of dexamethasone failed to cause cortisol depression while she was taking phenytoin, but when she was re-tested in the absence of phenytoin only 1 mg of dexamethasone was needed to elicit a response. ... 

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