United States - English - NLM (National Library of Medicine)

dr. reddy's laboratories limited - oxaprozin (unii: mhj80w9lrb) (oxaprozin - unii:mhj80w9lrb) - oxaprozin 600 mg - oxaprozin tablets are indicated: - for relief of the signs and symptoms of osteoarthritis - for relief of the signs and symptoms of rheumatoid arthritis - for relief of the signs and symptoms of juvenile rheumatoid arthritis oxaprozin tablets are contraindicated in the following patients: - known hypersensitivity (e.g., anaphylactic reactions and serious skin reactions) to oxaprozin or any components of the drug product [see warnings and precautions (5.7, 5.9) ]   - history of asthma, urticaria, or other allergic-type reactions after taking aspirin or other nsaids. severe, sometimes fatal, anaphylactic reactions to nsaids have been reported in such patients [see warnings and precautions (5.7, 5.8 )]   - in the setting of cabg surgery [see warnings and precautions (5.1)]   risk summary use of nsaids, including oxaprozin, can cause premature closure of the fetal ductus arteriosus and fetal renal dysfunction leading to oligohydramnios and, in some cases, neonatal renal impairment. because of these risks, limit dose and duration of oxaprozin use between about 20 and 30 weeks of gestation, and avoid oxaprozin use at about 30 weeks of gestation and later in pregnancy (see clinical considerations, data ). premature closure of fetal ductus arteriosus use of nsaids, including oxaprozin, at about 30 weeks gestation or later in pregnancy increases the risk of premature closure of the fetal ductus arteriosus. oligohydramnios/neonatal renal impairment use of nsaids at about 20 weeks gestation or later in pregnancy has been associated with cases of fetal renal dysfunction leading to oligohydramnios, and in some cases, neonatal renal impairment. data from observational studies regarding other potential embryofetal risks of nsaid use in women in the first or second trimesters of pregnancy are inconclusive. in animal reproduction studies, oral administration of oxaprozin to pregnant rabbits at doses 0.1-times the maximum daily human dose (based on body surface area) resulted in evidence of teratogenicity; however, oral administration of oxaprozin to pregnant mice and rats during organogenesis at doses equivalent to the maximum recommended human dose revealed no evidence of teratogenicity or embryotoxicity. in rat reproduction studies in which oxaprozin was administered through late gestation failure to deliver and a reduction in live birth index was observed at doses equivalent to the maximum recommended human dose. based on animal data, prostaglandins have been shown to have an important role in endometrial vascular permeability, blastocyst implantation, and decidualization. in animal studies, administration of prostaglandin synthesis inhibitors such as oxaprozin, resulted in increased pre-and post-implantation loss. prostaglandins also have been shown to have an important role in fetal kidney development. in published animal studies, prostaglandin synthesis inhibitors have been reported to impair kidney development when administered at clinically relevant doses. the estimated background risk of major birth defects and miscarriage for the indicated population(s) is unknown. all pregnancies have a background risk of birth defect, loss, or other adverse outcomes. in the u.s. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively. clinical considerations fetal/neonatal adverse reactions premature closure of fetal ductus arteriosus:avoid use of nsaids in women at about 30 weeks gestation and later in pregnancy, because nsaids, including oxaprozin, can cause premature closure of the fetal ductus arteriosus (see data ). oligohydramnios/neonatal renal impairment:if an nsaid is necessary at about 20 weeks gestation or later in pregnancy, limit the use to the lowest effective dose and shortest duration possible. if oxaprozin treatment extends beyond 48 hours, consider monitoring with ultrasound for oligohydramnios. if oligohydramnios occurs, discontinue oxaprozin and follow up according to clinical practice (see data ). labor or delivery there are no studies on the effects of oxaprozin during labor or delivery. in animal studies, nsaids, including oxaprozin, inhibit prostaglandin synthesis, cause delayed parturition, and increase the incidence of stillbirth. data human data premature closure of fetal ductus arteriosus: published literature reports that the use of nsaids at about 30 weeks of gestation and later in pregnancy may cause premature closure of the fetal ductus arteriosus. oligohydramnios/neonatal renal impairment: published studies and postmarketing reports describe maternal nsaid use at about 20 weeks gestation or later in pregnancy associated with fetal renal dysfunction leading to oligohydramnios, and in some cases, neonatal renal impairment. these adverse outcomes are seen, on average, after days to weeks of treatment, although oligohydramnios has been infrequently reported as soon as 48 hours after nsaid initiation. in many cases, but not all, the decrease in amniotic fluid was transient and reversible with cessation of the drug. there have been a limited number of case reports of maternal nsaid use and neonatal renal dysfunction without oligohydramnios, some of which were irreversible. some cases of neonatal renal dysfunction required treatment with invasive procedures, such as exchange transfusion or dialysis. methodological limitations of these postmarketing studies and reports include lack of a control group; limited information regarding dose, duration, and timing of drug exposure; and concomitant use of other medications. these limitations preclude establishing a reliable estimate of the risk of adverse fetal and neonatal outcomes with maternal nsaid use. because the published safety data on neonatal outcomes involved mostly preterm infants, the generalizability of certain reported risks to the full-term infant exposed to nsaids through maternal use is uncertain. animal data teratology studies with oxaprozin were performed in mice, rats, and rabbits in pregnant animals administered oral doses up to 200 mg/kg/day, 200 mg/kg/day, and 30 mg/kg/day, respectively, during the period of organogenesis. in rabbits, malformations were observed at doses greater than or equal to 7.5 mg/kg/day of oxaprozin (0.1 times the maximum recommended human dailydose [mrhd] of 1,800 mg based on body surface area). however, in mice and rats, no drug-related developmental abnormalities or embryo-fetal toxicity were observed at doses up to 50 and 200 mg/kg/day of oxaprozin, respectively (0.1 times and 1.1 times the maximum recommended human daily dose of 1,800 mg based on a body surface area comparison, respectively).in fertility/reproductive studies in rats, 200 mg/kg/day oxaprozin was orally administered to female rats for 14 days prior to mating through lactation day (ld) 2, or from gestation day (gd) 15 through ld 2 and the females were mated with males treated with 200 mg/kg/day oxaprozin for 60 days prior to mating. oxaprozin administration resulted in failure to deliver and a reduction in live birth index at 200 mg/kg/day (1.1 times the maximum recommended human daily dose of 1,800 mg based on a body surface area comparison). risk summary lactation studies have not been conducted with oxaprozin. it is not known whether oxaprozin is excreted in human milk. oxaprozin should be administered to lactating women only if clearly indicated. the developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for oxaprozin and any potential adverse effects on the breastfed infant from the oxaprozin or from the underlying maternal condition. infertility females based on the mechanism of action, the use of prostaglandin-mediated nsaids, including oxaprozin, may delay or prevent rupture of ovarian follicles, which has been associated with reversible infertility in some women. published animal studies have shown that administration of prostaglandin synthesis inhibitors has the potential to disrupt prostaglandin-mediated follicular rupture required for ovulation. small studies in women treated with nsaids have also shown a reversible delay in ovulation. consider withdrawal of nsaids, including oxaprozin, in women who have difficulties conceiving or who are undergoing investigation of infertility.   males testicular degeneration was observed in beagle dogs treated with 37.5 mg/kg/day (0.7 times the maximum recommended human daily dose based on body surface area) of oxaprozin for 42 days or 6 months [see nonclinical toxicology (13.1 )] safety and effectiveness of oxaprozin in pediatric patients below the age of 6 years of age have not been established. the effectiveness of oxaprozin for the treatment of the signs and symptoms of juvenile rheumatoid arthritis (jra) in pediatric patients aged 6 to 16 years is supported by evidence from adequate and well controlled studies in adult rheumatoid arthritis patients, and is based on an extrapolation of the demonstrated efficacy of oxaprozin in adults with rheumatoid arthritis and the similarity in the course of the disease and the drug’s mechanism of effect between these two patient populations. use of oxaprozin in jra patients 6 to16 years of age is also supported by the following pediatric studies. the pharmacokinetic profile and tolerability of oxaprozin were assessed in jra patients relative to adult rheumatoid arthritis patients in a 14 day multiple dose pharmacokinetic study. apparent clearance of unbound oxaprozin in jra patients was reduced compared to adult rheumatoid arthritis patients, but this reduction could be accounted for by differences in body weight [see clinical pharmacology (12.3)]. no pharmacokinetic data are available for pediatric patients under 6 years. adverse events were reported by approximately 45% of jra patients versus an approximate 30% incidence of adverse events in the adult rheumatoid arthritis patient cohort. most of the adverse events were related to the gastrointestinal tract and were mild to moderate. in a 3 month open label study, 10 to 20 mg/kg/day of oxaprozin were administered to 59 jra patients. adverse events were reported by 58% of jra patients. most of those reported were generally mild to moderate, tolerated by the patients, and did not interfere with continuing treatment. gastrointestinal symptoms were the most frequently reported adverse effects and occurred at a higher incidence than those historically seen in controlled studies in adults. fifty-two patients completed 3 months of treatment with a mean daily dose of 20 mg/kg. of 30 patients who continued treatment (19 to 48 week range total treatment duration), nine (30%) experienced rash on sun-exposed areas of the skin and 5 of those discontinued treatment. controlled clinical trials with oxaprozin in pediatric patients have not been conducted. elderly patients, compared to younger patients, are at greater risk for nsaid-associated serious cardiovascular, gastrointestinal, and/or renal adverse reactions. if the anticipated benefit for the elderly patient outweighs these potential risks, start dosing at the low end of the dosing range, and monitor patients for adverse effects [see warnings and precautions (5.1, 5.2, 5.3, 5.6, 5.14)].   no adjustment of the dose of oxaprozin is necessary in the elderly, although many elderly may need to receive a reduced dose because of low body weight or disorders associated with aging [see clinical pharmacology (12.3) ].    of the total number of subjects evaluated in four placebo controlled clinical studies of oxaprozin, 39% were 65 and over, and 11% were 75 and over. no overall differences in safety or effectiveness were observed between these subjects and younger subjects, and other reported clinical experience has not identified differences in responses between the elderly and younger patients, but greater sensitivity of some older individuals cannot be ruled out. although selected elderly patients in controlled clinical trials tolerated oxaprozin as well as younger patients, caution should be exercised in treating the elderly.   oxaprozin is substantially excreted by the kidney, and the risk of toxic reactions to oxaprozin may be greater in patients with impaired renal function. because elderly patients are more likely to have decreased renal function, care should be taken in dose selection, and it may be useful to monitor renal function [see warnings and precautions (5.6)].  

United States - English - NLM (National Library of Medicine)

teva pharmaceuticals usa, inc. - oxaprozin (unii: mhj80w9lrb) (oxaprozin - unii:mhj80w9lrb) - oxaprozin 600 mg - oxaprozin tablets are indicated: - for relief of the signs and symptoms of osteoarthritis - for relief of the signs and symptoms of rheumatoid arthritis - for relief of the signs and symptoms of juvenile rheumatoid arthritis oxaprozin tablets are contraindicated in the following patients: - known hypersensitivity (e.g., anaphylactic reactions and serious skin reactions) to oxaprozin or any components of the drug product [see warnings and precautions (5.7, 5.9) ] - history of asthma, urticaria, or other allergic-type reactions after taking aspirin or other nsaids. severe, sometimes fatal, anaphylactic reactions to nsaids have been reported in such patients [see warnings and precautions (5.7, 5.8) ] - in the setting of cabg surgery [see warnings and precautions (5.1) ] risk summary   use of nsaids, including oxaprozin, can cause premature closure of the fetal ductus arteriosus and fetal renal dysfunction leading to oligohydramnios and, in some cases, neonatal renal impairment. because of these risks, limit dose

United States - English - NLM (National Library of Medicine)

pd-rx pharmaceuticals, inc. - oxaprozin (unii: mhj80w9lrb) (oxaprozin - unii:mhj80w9lrb) - oxaprozin 600 mg - oxaprozin tablets are indicated: - for relief of the signs and symptoms of osteoarthritis - for relief of the signs and symptoms of rheumatoid arthritis - for relief of the signs and symptoms of juvenile rheumatoid arthritis oxaprozin tablets are contraindicated in the following patients: - known hypersensitivity (e.g., anaphylactic reactions and serious skin reactions) to oxaprozin or any components of the drug product [ see warnings and precautions ( 5.7, 5.9) ] - history of asthma, urticaria, or other allergic-type reactions after taking aspirin or other nsaids. severe, sometimes fatal, anaphylactic reactions to nsaids have been reported in such patients [ see warnings and precautions ( 5.7, 5.8) ] - in the setting of cabg surgery [ see warnings and precautions ( 5.1) ] risk summary   use of nsaids, including oxaprozin, can

United States - English - NLM (National Library of Medicine)

pfizer laboratories div pfizer inc - oxaprozin (unii: mhj80w9lrb) (oxaprozin - unii:mhj80w9lrb) - oxaprozin 600 mg - daypro is indicated: - for relief of the signs and symptoms of osteoarthritis - for relief of the signs and symptoms of rheumatoid arthritis - for relief of the signs and symptoms of juvenile rheumatoid arthritis daypro is contraindicated in the following patients: - known hypersensitivity (e.g., anaphylactic reactions and serious skin reactions) to oxaprozin or any components of the drug product [see warnings and precautions (5.7, 5.9) ] - history of asthma, urticaria, or other allergic-type reactions after taking aspirin or other nsaids. severe, sometimes fatal, anaphylactic reactions to nsaids have been reported in such patients [see warnings and precautions (5.7, 5.8) ] - in the setting of cabg surgery [see warnings and precautions (5.1) ] risk summary use of nsaids, including daypro, can cause premature closure of the fetal ductus arteriosus and fetal renal dysfunction leading to oligohydramnios and, in some cases, neonatal renal impairment. because of these risks, limit dose and duration of daypro use b

United States - English - NLM (National Library of Medicine)

greenstone llc - oxaprozin (unii: mhj80w9lrb) (oxaprozin - unii:mhj80w9lrb) - oxaprozin 600 mg - oxaprozin is indicated: oxaprozin is contraindicated in the following patients: risk summary use of nsaids, including oxaprozin, can cause premature closure of the fetal ductus arteriosus and fetal renal dysfunction leading to oligohydramnios and, in some cases, neonatal renal impairment. because of these risks, limit dose and duration of oxaprozin use between about 20 and 30 weeks of gestation, and avoid oxaprozin use at about 30 weeks of gestation and later in pregnancy (see clinical considerations, data) . premature closure of fetal ductus arteriosus use of nsaids, including oxaprozin, at about 30 weeks gestation or later in pregnancy increases the risk of premature closure of the fetal ductus arteriosus. oligohydramnios/neonatal renal impairment use of nsaids at about 20 weeks gestation or later in pregnancy has been associated with cases of fetal renal dysfunction leading to oligohydramnios, and in some cases, neonatal renal impairment. data from observational studies regarding other potential embryofeta

United States - English - NLM (National Library of Medicine)

teva pharmaceuticals usa, inc. - flurbiprofen (unii: 5gro578klp) (flurbiprofen - unii:5gro578klp) - flurbiprofen 100 mg - flurbiprofen tablets are indicated: - for relief of the signs and symptoms of rheumatoid arthritis. - for relief of the signs and symptoms of osteoarthritis. flurbiprofen tablets are contraindicated in the following patients: - known hypersensitivity (e.g., anaphylactic reactions and serious skin reactions) to flurbiprofen or any components of the drug product [see warnings and precautions (5.7, 5.9) ] - history of asthma, urticaria, or other allergic-type reactions after taking aspirin or other nsaids. severe, sometimes fatal, anaphylactic reactions to nonsteroidal anti-inflammatory drugs have been reported in such patients [see warnings and precautions (5.7, 5.8) ]. - in the setting of coronary artery bypass graft (cabg) surgery [see warnings and precautions (5.1) ]. risk summary use of nsaids, including flurbiprofen tablets, can cause premature closure of the fetal ductus arteriosus and fetal renal dysfunction leading to oligohydramnios and, in some cases, neonatal renal impairment. because of these risks,

United States - English - NLM (National Library of Medicine)

northstar rxllc - celecoxib (unii: jcx84q7j1l) (celecoxib - unii:jcx84q7j1l) - celecoxib 50 mg - celecoxib capsules are indicated for the management of the signs and symptoms of oa [see clinical studies (14.1) ]. for the management of the signs and symptoms of ra [see clinical studies (14.2) ]. for the management of the signs and symptoms of jra in patients 2 years and older [see clinical studies (14.3) ]. for the management of the signs and symptoms of as [see clinical studies (14.4) ]. for the management of acute pain in adults [see clinical studies (14.5) ]. for the management of primary dysmenorrhea [see clinical studies (14.5) ]. celecoxib capsules are contraindicated in the following patients: - known hypersensitivity (e.g., anaphylactic reactions and serious skin reactions) to celecoxib, any components of the drug product [see warnings and precautions (5.7, 5.9) ]. - history of asthma, urticaria, or other allergic-type reactions after taking aspirin or other nsaids. severe, sometimes fatal, anaphylactic reactions to nsaids, have been reported in such patients [see warnings and precautions (5.7, 5.8)]. - in the setting of cabg surgery [see warnings and precautions (5.1)]. - in patients who have demonstrated allergic-type reactions to sulfonamides [see warnings and precautions (5.7) ]. risk summary use of nsaids, including celecoxib capsules, can cause premature closure of the fetal ductus arteriosus and fetal renal dysfunction leading to oligohydramnios and, in some cases, neonatal renal impairment. because of these risks, limit dose and duration of celecoxib use between about 20 and 30 weeks of gestation and avoid celecoxib use at about 30 weeks of gestation and later in pregnancy (see clinical considerations, data). premature closure of fetal ductus arteriosus use of nsaids, including celecoxib, at about 30 weeks gestation or later in pregnancy increases the risk of premature closure of the fetal ductus arteriosus. oligohydramnios/neonatal renal impairment use of nsaids at about 20 weeks gestation or later in pregnancy has been associated with cases of fetal renal dysfunction leading to oligohydramnios, and in some cases, neonatal renal impairment. data from observational studies regarding other potential embryofetal risks of nsaid use in women in the first or second trimesters of pregnancy are inconclusive. in animal reproduction studies, embryo-fetal deaths and an increase in diaphragmatic hernias were observed in rats administered celecoxib daily during the period of organogenesis at oral doses approximately 6 times the maximum recommended human dose (mrhd) of 200 mg twice daily. in addition, structural abnormalities (e.g., septal defects, ribs fused, sternebrae fused and sternebrae misshapen) were observed in rabbits given daily oral doses of celecoxib during the period of organogenesis at approximately 2 times the mrhd (see data). based on animal data, prostaglandins have been shown to have an important role in endometrial vascular permeability, blastocyst implantation, and decidualization. in animal studies, administration of prostaglandin synthesis inhibitors such as celecoxib, resulted in increased pre- and post-implantation loss. prostaglandins also have been shown to have an important role in fetal kidney development. in published animal studies, prostaglandin synthesis inhibitors have been reported to impair kidney development when administered at clinically relevant doses. the estimated background risk of major birth defects and miscarriage for the indicated population is unknown. all pregnancies have a background risk of birth defect, loss, or other adverse outcomes. in the the u.s. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively. clinical considerations fetal/neonatal adverse reactions premature closure of fetal ductus arteriosus: avoid use of nsaids in women at about 30 weeks gestation and later in pregnancy, because nsaids, including celecoxib capsules, can cause premature closure of the fetal ductus arteriosus (see data). oligohydramnios/neonatal renal impairment: if an nsaid is necessary at about 20 weeks gestation or later in pregnancy, limit the use to the lowest effective dose and shortest duration possible. if celecoxib capsules treatment extends beyond 48 hours, consider monitoring with ultrasound for oligohydramnios. if oligohydramnios occurs, discontinue celecoxib capsules and follow up according to clinical practice (see data ). labor or delivery there are no studies on the effects of celecoxib capsules during labor or delivery. in animal studies, nsaids, including celecoxib, inhibit prostaglandin synthesis, cause delayed parturition, and increase the incidence of stillbirth. data human data the available data do not establish the presence or absence of developmental toxicity related to the use of celecoxib capsules. premature closure of fetal ductus arteriosus: published literature reports that the use of nsaids at about 30 weeks of gestation and later in pregnancy may cause premature closure of the fetal ductus arteriosus. oligohydramnios/neonatal renal impairment: published studies and postmarketing reports describe maternal nsaid use at about 20 weeks gestation or later in pregnancy associated with fetal renal dysfunction leading to oligohydramnios, and in some cases, neonatal renal impairment. these adverse outcomes are seen, on average, after days to weeks of treatment, although oligohydramnios has been infrequently reported as soon as 48 hours after nsaid initiation. in many cases, but not all, the decrease in amniotic fluid was transient and reversible with cessation of the drug. there have been a limited number of case reports of maternal nsaid use and neonatal renal dysfunction without oligohydramnios, some of which were irreversible. some cases of neonatal renal dysfunction required treatment with invasive procedures, such as exchange transfusion or dialysis. methodological limitations of these postmarketing studies and reports include lack of a control group; limited information regarding dose, duration, and timing of drug exposure; and concomitant use of other medications. these limitations preclude establishing a reliable estimate of the risk of adverse fetal and neonatal outcomes with maternal nsaid use. because the published safety data on neonatal outcomes involved mostly preterm infants, the generalizability of certain reported risks to the full-term infant exposed to nsaids through maternal use is uncertain. animal data celecoxib at oral doses ≥150 mg/kg/day (approximately 2 times the human exposure at 200 mg twice daily as measured by auc0-24 ), caused an increased incidence of ventricular septal defects, a rare event, and fetal alterations, such as ribs fused, sternebrae fused and sternebrae misshapen when rabbits were treated throughout organogenesis. a dose-dependent increase in diaphragmatic hernias was observed when rats were given celecoxib at oral doses ≥30 mg/kg/day (approximately 6 times human exposure based on the auc0-24 at 200 mg twice daily for ra) throughout organogenesis. in rats, exposure to celecoxib during early embryonic development resulted in pre-implantation and post-implantation losses at oral doses ≥50 mg/kg/day (approximately 6 times human exposure based on the auc0-24 at 200 mg twice daily for ra). celecoxib produced no evidence of delayed labor or parturition at oral doses up to 100 mg/kg in rats (approximately 7-fold human exposure as measured by the auc0-24 at 200 mg twice daily). the effects of celecoxib capsules on labor and delivery in pregnant women are unknown. risk summary limited data from 3 published reports that included a total of 12 breastfeeding women showed low levels of celecoxib in breast milk. the calculated average daily infant dose was 10 to 40 mcg/kg/day, less than 1% of the weight-based therapeutic dose for a two-year old-child. a report of two breastfed infants 17 and 22 months of age did not show any adverse events. caution should be exercised when celecoxib capsules are administered to a nursing woman. the developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for celecoxib capsules and any potential adverse effects on the breastfed infant from the celecoxib capsules or from the underlying maternal condition. infertility females based on the mechanism of action, the use of prostaglandin-mediated nsaids, including celecoxib capsules, may delay or prevent rupture of ovarian follicles, which has been associated with reversible infertility in some women. published animal studies have shown that administration of prostaglandin synthesis inhibitors has the potential to disrupt prostaglandin mediated follicular rupture required for ovulation. small studies in women treated with nsaids have also shown a reversible delay in ovulation. consider withdrawal of nsaids, including celecoxib capsules, in women who have difficulties conceiving or who are undergoing investigation of infertility. celecoxib capsules are approved for relief of the signs and symptoms of juvenile rheumatoid arthritis in patients 2 years and older. safety and efficacy have not been studied beyond six months in children. the long-term cardiovascular toxicity in children exposed to celecoxib capsules has not been evaluated and it is unknown if long-term risks may be similar to that seen in adults exposed to celecoxib capsules or other cox-2 selective and non-selective nsaids [see boxed warning, warnings and precautions (5.5), and clinical studies (14.3)]. the use of celecoxib in patients 2 years to 17 years of age with pauciarticular, polyarticular course jra or in patients with systemic onset jra was studied in a 12-week, double-blind, active controlled, pharmacokinetic, safety and efficacy study, with a 12-week open-label extension. celecoxib has not been studied in patients under the age of 2 years, in patients with body weight less than 10 kg (22 lbs), and in patients with active systemic features. patients with systemic onset jra (without active systemic features) appear to be at risk for the development of abnormal coagulation laboratory tests. in some patients with systemic onset jra, both celecoxib and naproxen were associated with mild prolongation of activated partial thromboplastin time (aptt) but not prothrombin time (pt). when nsaids including celecoxib are used in patients with systemic onset jra, monitor patients for signs and symptoms of abnormal clotting or bleeding, due to the risk of disseminated intravascular coagulation. patients with systemic onset jra should be monitored for the development of abnormal coagulation tests [see dosage and administration (2.4), warnings and precautions (5.15), adverse reactions (6.1), animal toxicology (13.2), clinical studies (14.3)]. alternative therapies for treatment of jra should be considered in pediatric patients identified to be cyp2c9 poor metabolizers [see poor metabolizers of cyp2c9 substrates (8.8)]. elderly patients, compared to younger patients, are at greater risk for nsaid-associated serious cardiovascular, gastrointestinal, and/or renal adverse reactions. if the anticipated benefit for the elderly patient outweighs these potential risks, start dosing at the low end of the dosing range, and monitor patients for adverse effects [see warnings and precautions (5.1, 5.2, 5.3, 5.6, 5.14 )]. of the total number of patients who received celecoxib capsules in pre-approval clinical trials, more than 3,300 were 65-74 years of age, while approximately 1,300 additional patients were 75 years and over. no substantial differences in effectiveness were observed between these subjects and younger subjects. in clinical studies comparing renal function as measured by the gfr, bun and creatinine, and platelet function as measured by bleeding time and platelet aggregation, the results were not different between elderly and young volunteers. however, as with other nsaids, including those that selectively inhibit cox-2, there have been more spontaneous post-marketing reports of fatal gi events and acute renal failure in the elderly than in younger patients [see warnings and precautions (5.2, 5.6) ]. the daily recommended dose of celecoxib capsules in patients with moderate hepatic impairment (child-pugh class b) should be reduced by 50%. the use of celecoxib capsules in patients with severe hepatic impairment is not recommended [see dosage and administration (2.7) and clinical pharmacology (12.3)]. celecoxib capsules are not recommended in patients with severe renal insufficiency [see warnings and precautions  (5.6)  and clinical pharmacology (12.3 )].  in patients who are known or suspected to be poor cyp2c9 metabolizers (i.e., cyp2c9*3/*3), based on genotype or previous history/experience with other cyp2c9 substrates (such as warfarin, phenytoin) administer celecoxib capsules starting with half the lowest recommended dose. alternative management should be considered in jra patients identified to be cyp2c9 poor metabolizers [see dosage and administration (2.7) and clinical pharmacology (12.5)].  

United States - English - NLM (National Library of Medicine)

bryant ranch prepack - celecoxib (unii: jcx84q7j1l) (celecoxib - unii:jcx84q7j1l) - celecoxib 100 mg - celecoxib capsules are indicated for the management of the signs and symptoms of oa [see clinical studies (14.1) ]. for the management of the signs and symptoms of ra [see clinical studies (14.2) ]. for the management of the signs and symptoms of jra in patients 2 years and older [see clinical studies (14.3) ]. for the management of the signs and symptoms of as [see clinical studies (14.4) ]. for the management of acute pain in adults [see clinical studies (14.5) ]. for the management of primary dysmenorrhea [see clinical studies (14.5) ]. celecoxib capsules are contraindicated in the following patients: - known hypersensitivity (e.g., anaphylactic reactions and serious skin reactions) to celecoxib, any components of the drug product [see warnings and precautions (5.7, 5.9) ]. - history of asthma, urticaria, or other allergic-type reactions after taking aspirin or other nsaids. severe, sometimes fatal, anaphylactic reactions to nsaids, have been reported in such patients [see warnings and precautions (5.7, 5.8) ]. - in the setting of cabg surgery [see warnings and precautions (5.1) ]. - in patients who have demonstrated allergic-type reactions to sulfonamides [see warnings and precautions (5.7)]. risk summary use of nsaids, including celecoxib capsules, can cause premature closure of the fetal ductus arteriosus and fetal renal dysfunction leading to oligohydramnios and, in some cases, neonatal renal impairment. because of these risks, limit dose and duration of celecoxib capsules use between about 20 and 30 weeks of gestation and avoid celecoxib capsules use at about 30 weeks of gestation and later in pregnancy (see clinical considerations, data).   premature closure of fetal ductus arteriosus use of nsaids, including celecoxib capsules, at about 30 weeks gestation or later in pregnancy increases the risk of premature closure of the fetal ductus arteriosus.  oligohydramnios/neonatal renal impairment use of nsaids at about 20 weeks gestation or later in pregnancy has been associated with cases of fetal renal dysfunction leading to oligohydramnios, and in some cases, neonatal renal impairment. data from observational studies regarding other potential embryofetal risks of nsaid use in women in the first or second trimesters of pregnancy are inconclusive. in animal reproduction studies, embryo-fetal deaths and an increase in diaphragmatic hernias were observed in rats administered celecoxib daily during the period of organogenesis at oral doses approximately 6 times the maximum recommended human dose (mrhd) of 200 mg twice daily. in addition, structural abnormalities (e.g., septal defects, ribs fused, sternebrae fused and sternebrae misshapen) were observed in rabbits given daily oral doses of celecoxib during the period of organogenesis at approximately 2 times the mrhd (see data). based on animal data, prostaglandins have been shown to have an important role in endometrial vascular permeability, blastocyst implantation, and decidualization. in animal studies, administration of prostaglandin synthesis inhibitors such as celecoxib, resulted in increased pre- and post- implantation loss. prostaglandins also have been shown to have an important role in fetal kidney development. in published animal studies, prostaglandin synthesis inhibitors have been reported to impair kidney development when administered at clinically relevant doses. the estimated background risk of major birth defects and miscarriage for the indicated population is unknown. all pregnancies have a background risk of birth defect, loss, or other adverse outcomes. in the u.s. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively. clinical considerations fetal/neonatal adverse reactions premature closure of fetal ductus arteriosus: avoid use of nsaids in women at about 30 weeks gestation and later in pregnancy, because nsaids, including celecoxib capsules, can cause premature closure of the fetal ductus arteriosus (see data).   oligohydramnios/neonatal renal impairment: if an nsaid is necessary at about 20 weeks gestation or later in pregnancy, limit the use to the lowest effective dose and shortest duration possible. if celecoxib capsules treatment extends beyond 48 hours, consider monitoring with ultrasound for oligohydramnios. if oligohydramnios occurs, discontinue celecoxib capsules and follow up according to clinical practice (see data). labor or delivery there are no studies on the effects of celecoxib capsules during labor or delivery. in animal studies, nsaids, including celecoxib, inhibit prostaglandin synthesis, cause delayed parturition, and increase the incidence of stillbirth. data human data the available data do not establish the presence or absence of developmental toxicity related to the use of celecoxib capsules. premature closure of fetal ductus arteriosus: published literature reports that the use of nsaids at about 30 weeks of gestation and later in pregnancy may cause premature closure of the fetal ductus arteriosus. oligohydramnios/neonatal renal impairment: published studies and postmarketing reports describe maternal nsaid use at about 20 weeks gestation or later in pregnancy associated with fetal renal dysfunction leading to oligohydramnios, and in some cases, neonatal renal impairment. these adverse outcomes are seen, on average, after days to weeks of treatment, although oligohydramnios has been infrequently reported as soon as 48 hours after nsaid initiation. in many cases, but not all, the decrease in amniotic fluid was transient and reversible with cessation of the drug. there have been a limited number of case reports of maternal nsaid use and neonatal renal dysfunction without oligohydramnios, some of which were irreversible. some cases of neonatal renal dysfunction required treatment with invasive procedures, such as exchange transfusion or dialysis.   methodological limitations of these postmarketing studies and reports include lack of a control group; limited information regarding dose, duration, and timing of drug exposure; and concomitant use of other medications. these limitations preclude establishing a reliable estimate of the risk of adverse fetal and neonatal outcomes with maternal nsaid use. because the published safety data on neonatal outcomes involved mostly preterm infants, the generalizability of certain reported risks to the full-term infant exposed to nsaids through maternal use is uncertain. animal data celecoxib at oral doses ≥150 mg/kg/day (approximately 2 times the human exposure at 200 mg twice daily as measured by auc0-24 ), caused an increased incidence of ventricular septal defects, a rare event, and fetal alterations, such as ribs fused, sternebrae fused and sternebrae misshapen when rabbits were treated throughout organogenesis. a dose-dependent increase in diaphragmatic hernias was observed when rats were given celecoxib at oral doses ≥30 mg/kg/day (approximately 6 times human exposure based on the auc0-24 at 200 mg twice daily for ra) throughout organogenesis. in rats, exposure to celecoxib during early embryonic development resulted in pre-implantation and post-implantation losses at oral doses ≥50 mg/kg/day (approximately 6 times human exposure based on the auc0-24 at 200 mg twice daily for ra). celecoxib produced no evidence of delayed labor or parturition at oral doses up to 100 mg/kg in rats (approximately 7-fold human exposure as measured by the auc0-24 at 200 mg twice daily). the effects of celecoxib on labor and delivery in pregnant women are unknown. risk summary limited data from 3 published reports that included a total of 12 breastfeeding women showed low levels of celecoxib in breast milk. the calculated average daily infant dose was 10 to 40 mcg/kg/day, less than 1% of the weight-based therapeutic dose for a two-year old-child. a report of two breastfed infants 17 and 22 months of age did not show any adverse events. caution should be exercised when celecoxib is administered to a nursing woman. the developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for celecoxib capsules and any potential adverse effects on the breastfed infant from the celecoxib capsules or from the underlying maternal condition. infertility females based on the mechanism of action, the use of prostaglandin-mediated nsaids, including celecoxib capsules, may delay or prevent rupture of ovarian follicles, which has been associated with reversible infertility in some women. published animal studies have shown that administration of prostaglandin synthesis inhibitors has the potential to disrupt prostaglandin mediated follicular rupture required for ovulation. small studies in women treated with nsaids have also shown a reversible delay in ovulation. consider withdrawal of nsaids, including celecoxib capsules, in women who have difficulties conceiving or who are undergoing investigation of infertility. celecoxib is approved for relief of the signs and symptoms of juvenile rheumatoid arthritis in patients 2 years and older. safety and efficacy have not been studied beyond six months in children. the long-term cardiovascular toxicity in children exposed to celecoxib has not been evaluated and it is unknown if long-term risks may be similar to that seen in adults exposed to celecoxib or other cox-2 selective and non-selective nsaids [see boxed warning, warnings and precautions (5.5) , and clinical studies (14.3) ]. the use of celecoxib in patients 2 years to 17 years of age with pauciarticular, polyarticular course jra or in patients with systemic onset jra was studied in a 12-week, double-blind, active controlled, pharmacokinetic, safety and efficacy study, with a 12-week open-label extension. celecoxib has not been studied in patients under the age of 2 years, in patients with body weight less than 10 kg (22 lbs), and in patients with active systemic features. patients with systemic onset jra (without active systemic features) appear to be at risk for the development of abnormal coagulation laboratory tests. in some patients with systemic onset jra, both celecoxib and naproxen were associated with mild prolongation of activated partial thromboplastin time (aptt) but not prothrombin time (pt). when nsaids including celecoxib are used in patients with systemic onset jra, monitor patients for signs and symptoms of abnormal clotting or bleeding, due to the risk of disseminated intravascular coagulation. patients with systemic onset jra should be monitored for the development of abnormal coagulation tests [see dosage and administration (2.4), warnings and precautions (5.15), adverse reactions (6.1), animal toxicology (13.2), clinical studies (14.3)] .   alternative therapies for treatment of jra should be considered in pediatric patients identified to be cyp2c9 poor metabolizers [see poor metabolizers of cyp2c9 substrates (8.8) ]. elderly patients, compared to younger patients, are at greater risk for nsaid-associated serious cardiovascular, gastrointestinal, and/or renal adverse reactions. if the anticipated benefit for the elderly patient outweighs these potential risks, start dosing at the low end of the dosing range, and monitor patients for adverse effects [see warnings and precautions (5.1, 5.2, 5.3, 5.6, 5.14) ]. of the total number of patients who received celecoxib in pre-approval clinical trials, more than 3,300 were 65 to 74 years of age, while approximately 1,300 additional patients were 75 years and over. no substantial differences in effectiveness were observed between these subjects and younger subjects. in clinical studies comparing renal function as measured by the gfr, bun and creatinine, and platelet function as measured by bleeding time and platelet aggregation, the results were not different between elderly and young volunteers. however, as with other nsaids, including those that selectively inhibit cox-2, there have been more spontaneous post-marketing reports of fatal gi events and acute renal failure in the elderly than in younger patients [see warnings and precautions (5.2, 5.6) ]. the daily recommended dose of celecoxib capsules in patients with moderate hepatic impairment (child-pugh class b) should be reduced by 50%. the use of celecoxib capsules in patients with severe hepatic impairment is not recommended [see dosage and administration (2.7) and clinical pharmacology (12.3) ]. celecoxib is not recommended in patients with severe renal insufficiency [see warnings and precautions (5.6) and clinical pharmacology (12.3) ]. in patients who are known or suspected to be poor cyp2c9 metabolizers (i.e., cyp2c9*3/*3), based on genotype or previous history/experience with other cyp2c9 substrates (such as warfarin, phenytoin) administer celecoxib capsules starting with half the lowest recommended dose. alternative management should be considered in jra patients identified to be cyp2c9 poor metabolizers [see dosage and administration (2.7) and clinical pharmacology (12.5) ].

United States - English - NLM (National Library of Medicine)

pd-rx pharmaceuticals, inc. - celecoxib (unii: jcx84q7j1l) (celecoxib - unii:jcx84q7j1l) - celecoxib 200 mg - celecoxib capsules are indicated for the management of the signs and symptoms of oa [ see clinical studies (14.1) ]. for the management of the signs and symptoms of ra [ see clinical studies (14.2) ]. for the management of the signs and symptoms of jra in patients 2 years and older [ see clinical studies (14.3) ]. for the management of the signs and symptoms of as [ see clinical studies (14.4) ]. for the management of acute pain in adults [ see clinical studies (14.5) ]. for the management of primary dysmenorrhea [ see clinical studies (14.5) ]. celecoxib capsules are contraindicated in the following patients : - known hypersensitivity (e.g., anaphylactic reactions and serious skin reactions) to celecoxib, any components of the drug product [see warnings and precautions (5.7, 5.9) ]. - history of asthma, urticaria, or other allergic-type reactions after taking aspirin or other nsaids. severe, sometimes fatal, anaphylactic reactions to nsaid

United States - English - NLM (National Library of Medicine)

st. mary's medical park pharmacy - celecoxib (unii: jcx84q7j1l) (celecoxib - unii:jcx84q7j1l) - celecoxib 200 mg - celecoxib capsules are indicated for the management of the signs and symptoms of oa [ see clinical studies (14.1) ] for the management of the signs and symptoms of ra [ see clinical studies (14.2) ] for the management of the signs and symptoms of jra in patients 2 years and older [ see clinical studies (14.3) ] for the management of the signs and symptoms of as [ see clinical studies (14.4) ] for the management of acute pain in adults [ see clinical studies (14.5) ] for the management of primary dysmenorrhea [ see clinical studies (14.5) ] celecoxib capsules are contraindicated in the following patients : - known hypersensitivity (e.g., anaphylactic reactions and serious skin reactions) to celecoxib, any components of the drug product [see warnings and precautions (5.7, 5.9) ]. - history of asthma,