Drug Interactions between Serpex and Thalomid

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: 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 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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MONITOR: Thalidomide can cause peripheral neuropathy, and concurrent use of other agents that are also associated with this adverse effect can potentiate the risk and/or severity of nerve damage. Peripheral neuropathy is a common, potentially severe side effect of thalidomide that may be irreversible. The condition generally occurs following chronic use over a period of months, although there have also been reported cases following relatively short-term use. The median time to first neuropathy event was 42.3 weeks in one phase 3 study. Occasionally, symptoms may occur some time after thalidomide treatment has been discontinued. The incidence of neuropathy requiring thalidomide discontinuation, dosage reduction, or interruption increases with cumulative dose and duration of therapy.

MANAGEMENT: Caution is advised if thalidomide is used in combination with other neurotoxic agents. All patients treated with thalidomide should be examined at monthly intervals for the first three months of therapy and periodically thereafter to detect early signs of neuropathy such as burning, tingling, pain, or numbness in the hands and feet. Electrophysiological testing may be performed at baseline and every six months during therapy to detect asymptomatic neuropathy. Consideration should be given to immediate discontinuation of thalidomide in patients who develop peripheral neuropathy to limit further damage. Symptoms may improve or return to baseline in some patients upon discontinuation of thalidomide, although the complete time course of this toxicity has not been fully characterized. If necessary, therapy should generally be reinstituted only after neuropathy returns to baseline status. A dosage reduction of thalidomide may be required as clinically indicated.

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MONITOR: Thalidomide can commonly cause drowsiness/sedation and may have additive effects with other drugs that cause central nervous system (CNS) depression.

MANAGEMENT: Caution is advised when thalidomide is used with other CNS depressants such as anticonvulsants, antihistamines, antidepressants, antipsychotics, anxiolytics, opioids, and sedatives/hypnotics. Patients should be advised to avoid hazardous activities requiring mental alertness and motor coordination until they know how these agents affect them, and to notify their physician if they experience excessive or prolonged CNS effects that interfere with their normal activities. Dosage reductions may be necessary. Thalidomide should preferably be administered at bedtime to reduce the impact of somnolence. Alcohol use is not recommended.

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