An anticonvulsant and antineuralgic agent whose exact mechanism unknown. May increase the synthesis or accumulation of gamma-aminobutyric acid (GABA) by binding to as-yet-undefined receptor sites in brain tissue.
Adjunctive therapy in patients 12 yr or older with partial seizures with or without secondary generalization and as adjunctive therapy for partial seizures in children 3–12 yr; postherpetic neuralgia in adults
Well absorbed from the GI tract (not affected by food). Protein binding: less than 5%. Widely distributed. Crosses the blood-brain barrier. Primarily excreted unchanged in urine. Removed by hemodialysis. Half-life: 5–7 hr (increased in impaired renal function and the elderly).
|60 ml/min or higher||400 mg q8h|
|30–59 ml/min||300 mg q12h|
|16–29 ml/min||300 mg daily|
|Less than 16 ml/min||300 mg every other day|
|Hemodialysis||200–300 mg after each 4-hr hemodialysis session|
Initially, 4 mg twice a day (8 mg/day). After a minimum of 4 wk (if well tolerated), may increase to 8 mg twice a day (16 mg/day). After another 4 wk, may increase to 12 mg twice daily (24 mg/day). Range: 16–24 mg/day in 2 divided doses.
Potentiation of succinylcholine-like neuromuscular blocking drugs, obstructive GI disease, Parkinson’s disease, epilepsy, cardiac conduction disorders, AV block, bradycardia, history of GI ulcer, hypersecretory disorders (gastric), bladder outflow obstruction, COPD, asthma, moderate hepatic impairment, moderate renal impairment, lactation, pediatric use
! Overdose may cause cholinergic crisis, characterized by increased salivation, lacrimation, severe nausea and vomiting, bradycardia, respiratory depression, hypotension, and increased muscle weakness. Treatment usually consists of supportive measures and an anticholinergic such as atropine.
A recombinant normal variant form of a polymorphic enzyme (N-acetylgalactosamine 4-sulfatase), produced in Chinese hamster cells, that is taken up into lysosomes and increases the catabolism of glycosaminoglycans.
Antibody development, abdominal pain, ear pain, headache, fever, arthralgia, vomiting, upper respiratory infections, diarrhea, cough, otitis media, infusion-related reactions, pain, rigors, conjunctivitis, dyspnea, chest pain, pharyngitis, facial edema, hypertension, malaise, gastroenteritis, areflexia, corneal opacification, nasal congestion, umbilical hernia
Treatment of acute bacterial exacerbation of chronic bronchitis caused by S. pneumoniae, H. influenzae, H. parainfluenzae, M. catarrhalis, or S. aureus; acute sinusitis (S. pneumoniae, H. influenzae); community-acquired pneumonia (S. pneumoniae, H. influenzae, H. para-influenzae, M. catarrhalis, M. pneumoniae, C. pneumoniae, L. pneumoniae, or S. aureus); complicated or uncomplicated UTI (E. coli, K. pneumoniae, P. mirabilis); pyelonephritis (E. coli), acute uncomplicated rectal infections in women or uncomplicated urethral or cervical gonorrhea (N. gonorrhoeae); uncomplicated skin and skin-structure infections
Reduce dose with creatinine clearance less than 40 ml/min; probenecid increases half-life; children younger than 18 yr, lactation, seizure history, avoid use with class IA and III antiarrhythmics; many prolong QT interval; cross resistance with other fluoroquinolones, monitor blood glucose in diabetes
• Ruptures of the shoulder, hand, and Achilles tendons requiring surgical repair or resulting in prolonged disability have been reported with use of fluoroquinolones. Question patient about history of side effects associated with fluoroquinolone use.
Blocks the signaling pathway that binds to the epidermal growth factor receptor (EGFR) on the surface of normal and cancer cells. EGFR activates the enzyme tyrosine kinase, which sends signals instructing the cells to grow.
Not extensively distributed after IV infusion (increased with length of infusion). Protein binding: less than 10%. Excreted primarily in urine as metabolite. Half-life: 42–94 min (influenced by gender of patient and duration of infusion).
1000 mg/m2 once weekly for up to 7 wk or until toxicity necessitates decreasing dosage or withholding the dose, followed by 1 wk of rest. Subsequent cycles should consist of once-weekly dose for 3 consecutive wk out of every 4 wk. For patients completing cycles at 1000 mg/m2, increase dose to 1250 mg/m2 as tolerated. Dose for next cycle may be increased to 1500 mg/m2.
• Patient on chronic drug therapy may rarely present with symptoms of blood dyscrasias, which can include infection, bleeding, and poor healing. If dyscrasia is present, caution patient to prevent oral tissue trauma when using oral hygiene aids.
A fibric acid derivative that inhibits lipolysis of fat in adipose tissue; decreases liver uptake of free fatty acids and reduces hepatic triglyceride production. Inhibits synthesis of very low-density lipoproteins (VLDLs) carrier apolipoprotein B.