Clinical therapeutics
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Clinical therapeutics · Jul 2008
ReviewTopiramate monotherapy in the treatment of newly or recently diagnosed epilepsy.
The efficacy of topiramate (TPM) as an adjunctive treatment for epilepsy has been established in placebo-controlled clinical trials. Clinical trials of antiepileptic monotherapy usually evaluate low and high doses of study drug or compare study drug with another active agent. ⋯ In the 3 studies reviewed, TPM monotherapy was effective and generally well tolerated in patients with newly diagnosed epilepsy.
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Clinical therapeutics · Jul 2008
ReviewAcetylsalicylic acid + extended-release dipyridamole combination therapy for secondary stroke prevention.
Approximately 25% of strokes are recurrent. Antiplatelet therapy is indicated for the prevention of recurrent stroke in patients with a history of noncardioembolic minor stroke or transient ischemic attack (TIA). Although clinicians may choose acetylsalicylic acid (ASA) as first-line therapy for secondary prevention, clinical guidelines and evidence from trials suggest that ASA may not be the most effective strategy. ⋯ Based on the results from these 2 large, randomized trials, ASA + dipyridamole was more effective than ASA monotherapy as first-line therapy for secondary stroke prevention in these patients with a history of minor stroke or TIA of noncardioembolic etiology.
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Clinical therapeutics · Jul 2008
ReviewClinically relevant pharmacokinetic drug interactions with second-generation antidepressants: an update.
The second-generation antidepressants include selective serotonin reuptake inhibitors (SSRIs), serotonin and norepinephrine reuptake inhibitors (SNRIs), and other compounds with different mechanisms of action. All second-generation antidepressants are metabolized in the liver by the cytochrome P450 (CYP) enzyme system. Concomitant intake of inhibitors or inducers of the CYP isozymes involved in the biotransformation of specific antidepressants may alter plasma concentrations of these agents, although this effect is unlikely to be associated with clinically relevant interactions. Rather, concern about drug interactions with second-generation antidepressants is based on their in vitro potential to inhibit > or = 1 CYP isozyme. ⋯ Second-generation antidepressants are not equivalent in their potential for pharmacokinetic drug interactions. Although interactions may be predictable in specific circumstances, use of an antidepressant with a more favorable drug-interaction profile may be justified.