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

ibsa pharma inc. - diclofenac epolamine (unii: x5f8ekl9zg) (diclofenac - unii:144o8ql0l1) - licart is indicated for the topical treatment of acute pain due to minor strains, sprains, and contusions. licart is contraindicated in the following patients: - known hypersensitivity (e.g., anaphylactic reactions and serious skin reactions) to diclofenac 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 coronary artery bypass graft (cabg) surgery [see warnings and precautions (5.1)]. - on non-intact or damaged skin resulting from any etiology, including exudative dermatitis, eczema, infected lesions, burns or wounds. risk summary use of nsaids, including licart, 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 licart use between about 20 and 30 weeks of gestation, and avoid licart use at about 30 weeks of gestation and later in pregnancy (see clinical considerations and data ). premature closure of fetal ductus arteriosus use of nsaids, including licart, 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, diclofenac epolamine administered orally to pregnant rats and rabbits during the period of organogenesis produced embryotoxicity at approximately 3 and 7 times, respectively, the topical exposure from the maximum recommended human dose (mrhd) of licart. in rats, increased incidences of skeletal anomalies and maternal toxicity were also observed at this dose. diclofenac epolamine administered orally to both male and female rats prior to mating and throughout the mating period, and during gestation and lactation in females produced embryotoxicity at doses approximately 3 and 7 times, respectively, the topical exposure from 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 diclofenac, 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 licart, 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 licart treatment extends beyond 48 hours, consider monitoring with ultrasound for oligohydramnios. if oligohydramnios occurs, discontinue licart and follow up according to clinical practice ( see data ). 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 pregnant sprague dawley rats were administered 1, 3, or 6 mg/kg diclofenac epolamine via oral gavage daily from gestation days 6 to15. maternal toxicity, embryotoxicity, and increased incidence of skeletal anomalies were noted with 6 mg/kg/day diclofenac epolamine, which corresponds to 3-times the maximum recommended daily exposure in humans based on a body surface area comparison. pregnant new zealand white rabbits were administered 1, 3, or 6 mg/kg diclofenac epolamine via oral gavage daily from gestation days 6 to18. no maternal toxicity was noted; however, embryotoxicity was evident at 6 mg/kg/day group which corresponds to 7-times the maximum recommended daily exposure in humans based on a body surface area comparison. male rats were orally administered diclofenac epolamine (1, 3, 6 mg/kg) for 60 days prior to mating and throughout the mating period, and females were given the same doses 14 days prior to mating and through mating, gestation, and lactation. embryotoxicity was observed at 6 mg/kg diclofenac epolamine (3-times the maximum recommended daily exposure in humans based on a body surface area comparison), and was manifested as an increase in early resorptions, post-implantation losses, and a decrease in live fetuses. the number of live born and total born were also reduced as was f1 postnatal survival, but the physical and behavioral development of surviving f1 pups in all groups was the same as the deionized water control, nor was reproductive performance adversely affected despite a slight treatment-related reduction in body weight. risk summary data from published literature reports with oral preparations of diclofenac indicate the presence of small amounts of diclofenac in human milk (see data ). there are no data on the effects on the breastfed infant or the effects on milk production. the developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for licart and any potential adverse effects on the breastfed infant from licart or from the underlying maternal condition. data one woman treated orally with a diclofenac salt, 150 mg/day, had a milk diclofenac level of 100 mcg/l, equivalent to an infant dose of about 0.03 mg/kg/day. diclofenac was not detectable in breast milk in 12 women using diclofenac (after either 100 mg/day orally for 7 days or a single 50 mg intramuscular dose administered in the immediate postpartum period). the relative bioavailability for licart is < 1% of a single 50 mg diclofenac tablet. infertility females based on the mechanism of action, the use of prostaglandin-mediated nsaids, including licart may delay or prevent rupture of ovarian follicles, which has been associated with reversible infertility in some women [see clinical pharmacology (12.1)]. 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 licart, in women who have difficulties conceiving or who are undergoing investigation of infertility. the safety and effectiveness of licart in pediatric patients have not been established. 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)]. clinical studies of licart did not include sufficient numbers of subjects aged 65 and over to determine whether they respond differently from younger subjects. other reported clinical experience has not identified differences in responses between the elderly and younger patients.

Belgium - English - AFMPS (Agence Fédérale des Médicaments et des Produits de Santé)

ibsa farmaceutici italia s.r.l. - diclofenac epolamine 180 mg - eq. diclofenac sodium 140 mg - medicated plaster - 140 mg - diclofenac epolamine 180 mg - diclofenac

Belgium - English - AFMPS (Agence Fédérale des Médicaments et des Produits de Santé)

ibsa farmaceutici italia s.r.l. - diclofenac epolamine 180 mg - eq. diclofenac sodium 140 mg - medicated plaster - 140 mg - diclofenac epolamine 180 mg - diclofenac

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

ipg pharmaceuticals, inc. - diclofenac sodium (unii: qtg126297q) (diclofenac - unii:144o8ql0l1) - diclofenac sodium 30 mg in 1 g - diclofenac sodium gel is indicated for the topical treatment of actinic keratoses (ak). sun avoidance is indicated during therapy. diclofenac sodium gel is contraindicated in patients with a known hypersensitivity to diclofenac, benzyl alcohol, polyethylene glycol monomethyl ether 350 and/or hyaluronate sodium. diclofenac sodium gel is contraindicated in the following patients: - in the setting of coronary artery bypass graft (cabg) surgery.

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

actavis pharma, inc. - diclofenac sodium (unii: qtg126297q) (diclofenac - unii:144o8ql0l1) - diclofenac sodium 30 mg in 1 g - diclofenac sodium topical gel is indicated for the topical treatment of actinic keratosis (ak). diclofenac sodium topical gel is contraindicated in the following patients: - with known hypersensitivity (e.g., anaphylactic reactions and serious skin reactions) to diclofenac or any components of the drug product [see warnings and precautions (5.1, 5.3, 5.10) and description (11)] - with the 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 (5.1, 5.2)] - application on damaged skin resulting from any etiology, including exudative dermatitis, eczema, infected lesions, burns or wounds [see warnings and precautions (5.3)] - in the setting of coronary bypass graft (cabg) surgery [see warnings and precautions (5.4)] risk summary use of nsaids, including diclofenac sodium can cause premature closure of the fetal ductus arteriosus and fetal ren

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

pharmaceutica north america, inc - diclofenac sodium (unii: qtg126297q) (diclofenac - unii:144o8ql0l1) - diclofenac sodium 30 mg in 1 g - diclofenac sodium gel is indicated for the topical treatment of actinic keratoses (ak). sun avoidance is indicated during therapy. diclofenac sodium gel is contraindicated in patients with a known hypersensitivity to diclofenac, benzyl alcohol, polyethylene glycol monomethyl ether 350 and/or hyaluronate sodium.

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

taro pharmaceuticals u.s.a., inc. - diclofenac sodium (unii: qtg126297q) (diclofenac - unii:144o8ql0l1) - diclofenac sodium 30 mg in 1 g - diclofenac sodium topical gel is indicated for the topical treatment of actinic keratoses (ak). diclofenac sodium topical gel is contraindicated in the following patients: - with known hypersensitivity (e.g., anaphylactic reactions and serious skin reactions) to diclofenac or any components of the drug product [see warnings and precautions (5.1, 5.3, 5.10) and description (11) ]. - with the 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 (5.1, 5.2) ]. - application on damaged skin resulting from any etiology, including exudative dermatitis, eczema, infected lesions, burns or wounds [see warnings and precautions (5.3) ]. - in the setting of coronary bypass graft (cabg) surgery [see warnings and precautions (5.4) ]. risk summary use of nsaids, including diclofenac sodium topical gel, can cause premature closure of the fetal ductus arteri

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

lupin pharmaceuticals, inc. - diclofenac sodium (unii: qtg126297q) (diclofenac - unii:144o8ql0l1) - diclofenac sodium 16.05 mg in 1 ml - diclofenac sodium is indicated for the treatment of signs and symptoms of osteoarthritis of the knee(s) (1). diclofenac sodium is contraindicated in the following patients: - known hypersensitivity (e.g., anaphylactic reactions and serious skin reactions) to diclofenac 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 coronary artery bypass graft (cabg) surgery [see warnings and precautions (5.1)]. risk summary use of nsaids, including diclofenac sodium, 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 diclofenac sodium use between about 20 and 30 weeks of gestation, and avoid diclofenac sodium 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 diclofenac sodium, 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 , no evidence of teratogenicity was observed in mice, rats, or rabbits given diclofenac daily during the period of organogenesis at doses up to approximately 0.6, 0.6, and 1.3 times, respectively, the maximum recommended human dose (mrhd) of diclofenac sodium, despite the presence of maternal and fetal toxicity at these doses [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 [active moiety], 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 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 diclofenac sodium, 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 diclofenac sodium treatment extends beyond 48 hours, consider monitoring with ultrasound for oligohydramnios. if oligohydramnios occurs, discontinue diclofenac sodium and follow up according to clinical practice (see data ). 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 reproductive and developmental studies in animals demonstrated that diclofenac sodium administration during organogenesis did not produce teratogenicity despite the induction of maternal toxicity and fetal toxicity in mice at oral doses up to 20 mg/kg/day (approximately 0.6 times the maximum recommended human dose [mrhd] of diclofenac sodium, 154 mg/day, based on body surface area (bsa) comparison), and in rats and rabbits at oral doses up to 10 mg/kg/day (approximately 0.6 and 1.3 times, respectively, the mrhd based on bsa comparison). published reproductive and developmental studies of dimethyl sulfoxide (dmso, the solvent used in diclofenac sodium topical solution) are equivocal as to potential teratogenicity. in rats, maternally toxic doses of diclofenac were associated with dystocia, prolonged gestation, reduced fetal weights and growth, and reduced fetal survival. labor or delivery: there are no studies on the effects of diclofenac sodium during labor or delivery. in animal studies, nsaids, including diclofenac, inhibit prostaglandin synthesis, cause delayed parturition, and increase the incidence of stillbirth. risk summary based on available data, diclofenac may be present in human milk. the developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for cataflam and any potential adverse effects on the breastfed infant from the cataflam or from the underlying maternal condition. data one woman treated orally with a diclofenac salt, 150 mg/day, had a milk diclofenac level of 100 mcg/l, equivalent to an infant dose of about 0.03 mg/kg/day. diclofenac was not detectable in breast milk in 12 women using diclofenac (after either 100 mg/day orally for 7 days or a single 50 mg intramuscular dose administered in the immediate postpartum period). infertility females: based on the mechanism of action, the use of prostaglandin-mediated nsaids, including diclofenac sodium, 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 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 diclofenac sodium, in women who have difficulties conceiving or who are undergoing investigation of infertility. safety and effectiveness in pediatric patients have not been established. elderly patients, compared to younger patients, are a 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, 5.13)]. of the 911 patients treated with diclofenac sodium in seven controlled, phase 3 clinical trials, 444 subjects were 65 years of age and over. there was no age-related difference in the incidence of adverse events. of the 793 patients treated with diclofenac sodium in one open-labeled safety trial, 334 subjects were 65 years of age and over including 107 subjects 75 and over. there was no difference in the incidence of adverse events with long-term exposure to diclofenac sodium for this elderly population.

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

avkare - diclofenac sodium (unii: qtg126297q) (diclofenac - unii:144o8ql0l1) - diclofenac sodium 10 mg in 1 g - diclofenac sodium topical gel, 1% is indicated for the relief of the pain of osteoarthritis of joints amenable to topical treatment, such as the knees and those of the hands. - diclofenac sodium topical gel, 1% has not been evaluated for use on the spine, hip, or shoulder. diclofenac sodium topical gel is contraindicated in the following patients: - known hypersensitivity (e.g., anaphylactic reactions and serious skin reactions) to diclofenac 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 coronary artery bypass graft (cabg) surgery [see warnings and precautions ( 5.1)] pregnancy category c prior to 30 weeks gestation; category d starting 30 weeks gestation risk summary use of nsaids, inc

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

proficient rx lp - diclofenac sodium (unii: qtg126297q) (diclofenac - unii:144o8ql0l1) - diclofenac sodium 10 mg in 1 g - diclofenac sodium topical gel, 1% is indicated for the relief of the pain of osteoarthritis of joints amenable to topical treatment, such as the knees and those of the hands. diclofenac sodium topical gel is contraindicated in the following patients: pregnancy category c prior to 30 weeks gestation; category d starting 30 weeks gestation risk summary use of nsaids, including diclofenac sodium topical gel, during the third trimester of pregnancy increases the risk of premature closure of the fetal ductus arteriosus. avoid use of nsaids, including diclofenac sodium topical gel, in pregnant women starting at 30 weeks of gestation (third trimester). there are no adequate and well-controlled studies of diclofenac sodium topical gel in pregnant women. human and animal studies indicate that diclofenac crosses the placenta. data from observational studies regarding potential embryofetal risks of nsaid use in women in the first or second trimesters of pregnancy are inconclusive. in the general u.s. population, all cli