Flurbiprofen (flurbiprofen)

Dosage of flurbiprofen must be carefully adjusted according to individual requirements and response, using the lowest possible effective dosage.

The usual dosage of flurbiprofen for the management of osteoarthritis or rheumatoid arthritis in adults is 200-300 mg daily given in 2-4 divided doses. Single doses of flurbiprofen should not exceed 100 mg. Limited evidence suggests similar efficacy whether the total daily dosage of flurbiprofen is administered in 2, 3, or 4 divided doses.

Flurbiprofen is administered orally. Administration with food or antacids may alter the rate but not the extent of absorption. Flurbiprofen tablets should be stored at room temperature (20-25degreesC).

No dosing information is available for this tab.

No dosing information is available for this tab.

There is no enhanced messaging for this drug.

There are no contraindication interactions for this drug.

There are no severe interactions for this drug.

There are no moderate interactions for this drug.

*Known hypersensitivity to flurbiprofen or any ingredient in the formulation.

*History of asthma, urticaria, or other sensitivity reactions precipitated by aspirin or other NSAIAs.

*In the setting of CABG surgery.

There are no contraindication contraindications for this drug.

There are no severe contraindications for this drug.

There are no moderate contraindications for this drug.

The most common adverse effects (>3%) from clinical trials include abdominal pain, dyspepsia, nausea, diarrhea, constipation, headache, edema, and signs and symptoms suggesting urinary tract infection.

There are no severe adverse reactions for this drug.

There are no less severe adverse reactions for this drug.

No enhanced messaging available.

Safety and efficacy of flurbiprofen have not been established in pediatric patients.

Use of NSAIAs during pregnancy at about 30 weeks of gestation or later can cause premature closure of the fetal ductus arteriosus, and use at about 20 weeks of gestation or later has been associated with fetal renal dysfunction resulting in oligohydramnios and, in some cases, neonatal renal impairment. Because of these risks, use of NSAIAs should be avoided in pregnant women at about 30 weeks of gestation or later; if NSAIA therapy is necessary between about 20 and 30 weeks of gestation, the lowest effective dosage and shortest possible duration of treatment should be used. Monitoring of amniotic fluid volume via ultrasound examination should be considered if the duration of NSAIA treatment exceeds 48 hours; if oligohydramnios occurs, the drug should be discontinued and follow-up instituted according to clinical practice.

Fetal renal dysfunction resulting in oligohydramnios and, in some cases, neonatal renal impairment has been observed, on average, following days to weeks of maternal NSAIA use, although oligohydramnios has been observed infrequently as early as 48 hours after initiation of NSAIA therapy. Oligohydramnios is often, but not always, reversible (generally within 3-6 days) following discontinuance of NSAIA therapy. Some cases of neonatal renal dysfunction have required treatment with invasive procedures such as exchange transfusion or dialysis. Deaths associated with neonatal renal failure have been reported. Methodologic limitations of these postmarketing studies and case reports include lack of a control group; limited information regarding dosage, duration, and timing of drug exposure; and concomitant use of other drugs. These limitations preclude establishing a reliable estimate of the risk of adverse fetal and neonatal outcomes with maternal NSAIA use. Available data on neonatal outcomes generally involved preterm infants, and the extent to which certain reported risks can be generalized to full-term infants is uncertain.

Animal data indicate that prostaglandins have an important role in endometrial vascular permeability, blastocyst implantation, and decidualization. In animal studies, inhibitors of prostaglandin synthesis, such as flurbiprofen, were associated with increased pre- and post-implantation losses. Prostaglandins also have an important role in fetal kidney development. In animal studies, inhibitors of prostaglandin synthesis impaired kidney development at clinically relevant doses.

There are no adequate and well-controlled studies of flurbiprofen in pregnant women. In animal studies, embryofetal lethality was observed in pregnant rats and rabbits receiving flurbiprofen during the period of organogenesis at exposure levels of 0.03 and 0.5 times, respectively, the exposure at the maximum recommended human dose (MRHD) of 300 mg; no evidence of malformations was observed in rats, rabbits, or mice receiving flurbiprofen at dosages of 0.8, 0.5, or 0.2 times, respectively, the MRHD. Reproduction studies revealed delayed parturition, prolonged labor, stillborn fetuses, and the presence of retained fetuses at necropsy in rats at flurbiprofen dosages that were lower than the MRHD.

The effects of flurbiprofen on labor and delivery are unknown. In studies in rats, drugs that inhibit prostaglandin synthesis, including NSAIAs, delayed parturition and increased the incidence of stillbirth.

Flurbiprofen is distributed into human milk in very small amounts (estimated to be 0.1 mg daily based on a daily maternal dosage of 200 mg). The developmental and health benefits of breast-feeding should be considered along with the mother's clinical need for flurbiprofen and any potential adverse effects on the breast-fed infant from the drug or from the underlying maternal condition.

Use flurbiprofen with caution at the lowest effective dosage for the shortest possible duration.

Geriatric patients may experience a higher incidence of adverse GI effects (e.g., ulceration, bleeding, flatulence, bloating, abdominal pain) than younger patients and are at greater risk of developing renal decompensation with NSAIAs. Use flurbiprofen with caution and at the lowest effective dosage for the shortest possible duration.