Pharmacotherapy
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Physicians and pharmacists routinely advise patients receiving warfarin to take acetaminophen for pain or fever because of its relative safety; however, a recent study questioned the safety of such practice. A comprehensive search of MEDLINE and IPA for human studies and case reports from 1966-1999 revealed evidence that acetaminophen may potentiate the effect of warfarin by a mechanism that has yet to be elucidated. Due to lack of a safer alternative, acetaminophen still should be the analgesic and antipyretic of choice in patients taking warfarin, as long as excessive amounts and prolonged administration (> 1.3 g acetaminophen/day for > 2 wks) are avoided. With the high degree of interpatient variability and the unpredictability of various drug-drug interactions with warfarin, close and frequent monitoring of international normalized ratios is the key for safe oral anticoagulation therapy.
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Crohn's disease is a chronic inflammatory disorder that can present with symptoms throughout the gastrointestinal system. Though the etiology of Crohn's disease is unknown, genetic and environmental factors seem to play a role. ⋯ Several treatment modalities for Crohn's disease exist, recently including antitumor necrosis factor chimeric monoclonal antibody (cA2). Treatment for Crohn's disease, including data on the safety and efficacy of cA2, will be reviewed.
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Review
Clinical pharmacology of rapacuronium bromide, a new short-acting neuromuscular blocking agent.
Rapacuronium is a new steroidal, nondepolarizing, neuromuscular blocking agent. It appears to be the least potent of all available nondepolarizing muscle relaxants. ⋯ The clinical duration of rapacuronium can be shortened significantly with early (2 min) administration of neostigmine, which may be beneficial in patients with difficult airway or failed intubation. Rapacuronium appears to be free of significant cardiovascular complications.
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Case Reports
Peripheral neuropathy in healthy men volunteers anesthetized with 1.25 MAC sevoflurane for 8 hours.
Two men volunteers developed peripheral neuropathy after prolonged anesthesia with 1.25 minimum alveolar concentration sevoflurane at an inflow rate of 2 L/minute of fresh gas that caused concurrent administration of relatively large doses (ppm-hrs) of the degradation product of sevoflurane, compound A. Other similarly treated volunteers had lesser degrees of transient neuropathy. This result does not prove but raises the question of whether compound A or other factors associated with sevoflurane anesthesia can predispose patients to peripheral neuropathy.