Dexamethasone oral steroid

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Potentiated by CYP3A4 inhibitors (eg, ketoconazole, macrolides), cyclosporine, estrogens. Antagonized by CYP3A4 inducers (eg, barbiturates, phenytoin, carbamazepine, rifampin), ephedrine. May potentiate cyclosporine. May anatgonize anticoagulants (monitor), isoniazid, other CYP3A4 substrates (eg, indinavir, erythromycin). Increased risk of arrhythmias with digitalis. May need to adjust dose of antidiabetic agents. Increased GI effects with aspirin. Monitor for hypokalemia with potassium-depleting drugs (eg, amphotericin B, diuretics). Toxic epidermal necrolysis possible with thalidomide. Concomitant indomethacin: may get false-negative on dexamethasone suppression test. May suppress reactions to skin tests.

Unneeded medications should be disposed of in special ways to ensure that pets, children, and other people cannot consume them. However, you should not flush this medication down the toilet. Instead, the best way to dispose of your medication is through a medicine take-back program. Talk to your pharmacist or contact your local garbage/recycling department to learn about take-back programs in your community. See the FDA's Safe Disposal of Medicines website ( http:///c4Rm4p ) for more information if you do not have access to a take-back program.

Several processes have been implicated in the breakdown of the blood-retinal barrier that leads to ME, including the production of inflammatory mediators (., prostaglandins and interleukin-6), increased amounts of vascular permeability factors (., vascular endothelial growth factor) and the loss of endothelial tight junction proteins.  Corticosteroids are thought to have beneficial effects on these processes, but delivering therapeutic concentrations of any medication to the retina while limiting systemic exposure presents a challenge.  Intra-vitreal injections of the corticosteroid triamcinolone have shown promise in the treatment of ME.  Dexamethasone, a more potent corticosteroid than triamcinolone, has been shown to produce high intra-vitreal levels of the drug, however, a short intra-ocular half-life after intra-vitreal injection (approximately 3 hours) has led to the investigation of other delivery methods.  

Dexamethasone has also been used during pregnancy as an off-label prenatal treatment for the symptoms of congenital adrenal hyperplasia (CAH) in female fetuses. CAH causes a variety of physical abnormalities, notably ambiguous genitalia in girls. Early prenatal CAH treatment has been shown to reduce some CAH symptoms, but it does not treat the underlying congenital disorder . This use is controversial: it is inadequately studied, only around one in ten of the foetuses of women treated are at risk of the condition, and serious adverse events have been documented. [21] Experimental use of dexamethasone in pregnancy for foetal CAH treatment was discontinued in Sweden when one in five cases suffered adverse events. [22]

The efficacy and safety of corticosteroids in the pediatric population are based on the well-established course of effect of corticosteroids, which is similar in pediatric and adult populations. Published studies provide evidence of efficacy and safety in pediatric patients for the treatment of nephrotic syndrome (patients > 2 years of age), and aggressive lymphomas and leukemias (patients > 1 month of age). Other indications for pediatric use of corticos-teroids, e. g. , severe asthma and wheezing , are based on adequate and well-controlled trials conducted in adults, on the premises that the course of the diseases and their pathophysiology are considered to be substantially similar in both populations.

Dexamethasone oral steroid

dexamethasone oral steroid

Several processes have been implicated in the breakdown of the blood-retinal barrier that leads to ME, including the production of inflammatory mediators (., prostaglandins and interleukin-6), increased amounts of vascular permeability factors (., vascular endothelial growth factor) and the loss of endothelial tight junction proteins.  Corticosteroids are thought to have beneficial effects on these processes, but delivering therapeutic concentrations of any medication to the retina while limiting systemic exposure presents a challenge.  Intra-vitreal injections of the corticosteroid triamcinolone have shown promise in the treatment of ME.  Dexamethasone, a more potent corticosteroid than triamcinolone, has been shown to produce high intra-vitreal levels of the drug, however, a short intra-ocular half-life after intra-vitreal injection (approximately 3 hours) has led to the investigation of other delivery methods.  

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