Drug Interactions between dexamethasone / lidocaine and Uni Serp

MONITOR: Corticosteroids may antagonize the effects of antihypertensive medications by inducing sodium and fluid retention. These effects may be more common with the natural corticosteroids (cortisone, hydrocortisone) because they have greater mineralocorticoid activity. Conversely, some calcium channel blockers such as diltiazem and verapamil may increase corticosteroid plasma levels and effects by inhibiting their clearance via CYP450 3A4 metabolism.

MANAGEMENT: Patients on prolonged (i.e., longer than about a week) or high-dose corticosteroid therapy should have blood pressure, electrolyte levels, and body weight monitored regularly, and be observed for the development of edema and congestive heart failure. The dosages of antihypertensive medications may require adjustment.

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MONITOR: Concomitant treatment with other antihypertensive agents or vasodilators, including alpha-adrenoreceptor antagonists, angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), beta-adrenergic blockers, calcium channel blockers, diuretics and nitrates, may potentiate the hypotensive effects of hydralazine and dihydralazine.

MANAGEMENT: Blood pressure and heart rate should be closely monitored when hydralazine or dihydralazine is used with other agents that can induce hypotension.

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MONITOR: The concomitant use of corticosteroids and agents that deplete potassium (e.g., potassium-wasting diuretics, amphotericin B, cation exchange resins) may result in increased risk of hypokalemia. Corticosteroids can produce hypokalemia and other electrolyte disturbances via mineralocorticoid effects, the degree of which varies with the agent (from most to least potent: fludrocortisone - cortisone/hydrocortisone - prednisolone/prednisone - other glucocorticoids) and route of administration (i.e. systemic vs. local). However, large systemic doses of any corticosteroid can demonstrate these effects, particularly if given for longer than brief periods. When used pharmacologically, adrenocorticotropic agents such as corticotropin have similar mineralocorticoid activities as cortisone and hydrocortisone.

MANAGEMENT: Patients receiving potassium-depleting agents with corticosteroids should be monitored closely for development of hypokalemia, particularly if fludrocortisone or large doses of another corticosteroid or adrenocorticotropic agent is given. Potassium supplementation may be necessary. Patients should be advised to notify their physician if they experience signs of electrolyte disturbances such as weakness, lethargy, and muscle pains or cramps.

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MONITOR: Concomitant treatment with other antihypertensive agents or vasodilators, including alpha-adrenoreceptor antagonists, angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), beta-adrenergic blockers, calcium channel blockers, diuretics and nitrates, may potentiate the hypotensive effects of hydralazine and dihydralazine.

MANAGEMENT: Blood pressure and heart rate should be closely monitored when hydralazine or dihydralazine is used with other agents that can induce hypotension.

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MONITOR: Corticosteroids may antagonize the effects of antihypertensive medications by inducing sodium and fluid retention. These effects may be more common with the natural corticosteroids (cortisone, hydrocortisone) because they have greater mineralocorticoid activity. Conversely, some calcium channel blockers such as diltiazem and verapamil may increase corticosteroid plasma levels and effects by inhibiting their clearance via CYP450 3A4 metabolism.

MANAGEMENT: Patients on prolonged (i.e., longer than about a week) or high-dose corticosteroid therapy should have blood pressure, electrolyte levels, and body weight monitored regularly, and be observed for the development of edema and congestive heart failure. The dosages of antihypertensive medications may require adjustment.

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MONITOR: The hypotensive effects of thiazide diuretics and alpha-adrenergic blockers may be additive. Postural hypotension may occur.

MANAGEMENT: Hemodynamic responses should be monitored during coadministration, especially during the first few weeks of therapy. Patients should be advised to take the alpha-blocker at bedtime and to notify their physician if they experience dizziness or syncope while awake.

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Coadministration with inducers of CYP450 1A2 and/or 3A4 may decrease the plasma concentrations of lidocaine, which is primarily metabolized by these isoenzymes. In four healthy volunteers (2 smokers and 2 nonsmokers), administration of a single 400 mg oral dose of lidocaine following pretreatment with the CYP450 inducer phenobarbital (15 mg/day for 4 weeks, followed by 30 mg/day for 4 weeks) decreased lidocaine systemic exposure (AUC) by 37% and increased its oral clearance by 56% compared to administration of lidocaine alone. In another study, the mean bioavailability of a single 750 mg oral dose of lidocaine in six patients receiving chronic antiepileptic drug therapy (consisting of one or more of the following enzyme-inducing anticonvulsants: phenobarbital, primidone, phenytoin, carbamazepine) was approximately 2.5-fold lower than that reported for six healthy control subjects, while intrinsic clearance was nearly threefold higher. By contrast, the interaction was modest for lidocaine administered intravenously, suggesting induction of primarily hepatic first-pass rather than systemic metabolism of lidocaine. When a single 100 mg dose of lidocaine was given intravenously, mean lidocaine AUC was reduced by less than 10% and serum clearance increased by just 17% in the epileptic patients compared to controls. These changes were not statistically significant. Likewise, mean lidocaine AUC decreased by approximately 11% and plasma clearance increased by 15% when a single 50 mg intravenous dose of lidocaine was administered following pretreatment with the potent CYP450 inducer rifampin (600 mg/day for six days) in ten healthy, nonsmoking male volunteers. Another pharmacokinetic study found that cigarette smoke, an inducer of CYP450 1A2, reduced the bioavailability of lidocaine when administered orally, but had only minor effects on lidocaine administered intravenously. When 4 smokers and 5 non-smokers received 2 doses of lidocaine (100 mg IV followed by 100 mg orally after a 2-day washout period), the smoker's systemic exposure (AUC) of oral lidocaine was 68% lower than non-smokers. The AUC of IV lidocaine was only 9% lower in smokers compared with non-smokers. The clinical impact of smoking on lidocaine has not been studied, however, a loss of efficacy may occur.

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