Hoa Kỳ - Tiếng Anh - NLM (National Library of Medicine)

alembic pharmaceuticals inc. - diclofenac sodium (unii: qtg126297q) (diclofenac - unii:144o8ql0l1) - diclofenac sodium topical solution is indicated for the treatment of the pain of osteoarthritis of the knee(s). diclofenac sodium topical solution 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 topical solution, 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 topical solution use between about 20 and 30 weeks of gestation, and avoid diclofenac sodium topical solution 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 topical solution, 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 malformations were observed in mice, rats, or rabbits given diclofenac 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 162 mg diclofenac sodium via diclofenac sodium topical solution, 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 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 the fetal ductus arteriosus: avoid use of nsaids in women at about 30 weeks gestation and later in pregnancy, because nsaids, including diclofenac sodium topical solution, 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 topical solution treatment extends beyond 48 hours, consider monitoring with ultrasound for oligohydramnios. if oligohydramnios occurs, discontinue diclofenac sodium topical solution and follow up according to clinical practice (see data) . labor or delivery there are no studies on the effects of diclofenac sodium topical solution during labor or delivery. in animal studies, nsaids, including diclofenac 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 reproductive and developmental studies in animals demonstrated that diclofenac sodium administration during organogenesis did not produce malformations 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 topical solution, 162 mg diclofenac sodium/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 a study in which pregnant rats were orally administered 2 or 4 mg/kg diclofenac (0.12 and 0.24 times the mrhd, respectively, based on bsa comparison) from gestation day 15 through lactation day 21, significant maternal toxicity (peritonitis, mortality) was noted. these maternally toxic doses were associated with dystocia, prolonged gestation, reduced fetal weights and growth, and reduced fetal survival. diclofenac has been shown to cross the placental barrier in mice and rats. in published studies, diclofenac administration to pregnant rats prolonged gestation and produced liver toxicity and neuronal loss in offspring (1 mg/kg, ip; 0.06 times the mrhd based on bsa comparison), impaired nephrogenesis in the kidney (3.6 mg/kg, ip; 0.2 times the mrhd based on bsa comparison), and caused adverse effects on the developing testes (6.1 mg/kg, oral; 0.4 times the mrhd based on bsa comparison). 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 diclofenac sodium topical solution and any potential adverse effects on the breastfed infant from the diclofenac sodium topical solution 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 topical solution, 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 diclofenac sodium topical solution, in women who have difficulties conceiving or who are undergoing investigation of infertility. males published studies in adult male rodents report that diclofenac, at clinically relevant doses, can produce adverse effects on male reproductive tissues. the impact of these findings on male fertility is not clear [see nonclinical toxicology (13.1)] . safety and effectiveness 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) ]. of the 911 patients treated with diclofenac sodium topical solution 1.5% 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 topical solution 1.5% 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 topical solution 1.5% for this elderly population.

Hoa Kỳ - Tiếng Anh - NLM (National Library of Medicine)

allergan, inc. - botulinum toxin type a (unii: e211kpy694) (botulinum toxin type a - unii:e211kpy694) - botulinum toxin type a 100 [usp'u] - overactive bladder botox  for injection is indicated for the treatment of overactive bladder with symptoms of urge urinary incontinence, urgency, and frequency, in adults who have an inadequate response to or are intolerant of an anticholinergic medication. detrusor overactivity associated with a neurologic condition botox  is indicated for the treatment of urinary incontinence due to detrusor overactivity associated with a neurologic condition (e.g., sci, ms) in adults who have an inadequate response to or are intolerant of an anticholinergic medication. botox is indicated for the treatment of neurogenic detrusor overactivity (ndo) in pediatric patients 5 years of age and older who have an inadequate response to or are intolerant of anticholinergic medication. botox is indicated for the prophylaxis of headaches in adult patients with chronic migraine (≥15 days per month with headache lasting 4 hours a day or longer). limitations of use safety and effectiveness have not been established for the prophylaxis of episodic migraine (14 headache days or fewer per month) in seven placebo-controlled studies. botox is indicated for the treatment of spasticity in patients 2 years of age and older. limitations of use   botox has not been shown to improve upper extremity functional abilities, or range of motion at a joint affected by a fixed contracture. botox is indicated for the treatment of adults with cervical dystonia, to reduce the severity of abnormal head position and neck pain associated with cervical dystonia. botox is indicated for the treatment of severe primary axillary hyperhidrosis that is inadequately managed with topical agents. limitations of use the safety and effectiveness of botox for hyperhidrosis in other body areas have not been established. weakness of hand muscles and blepharoptosis may occur in patients who receive botox for palmar hyperhidrosis and facial hyperhidrosis, respectively. patients should be evaluated for potential causes of secondary hyperhidrosis (e.g., hyperthyroidism) to avoid symptomatic treatment of hyperhidrosis without the diagnosis and/or treatment of the underlying disease. safety and effectiveness of botox have not been established for the treatment of axillary hyperhidrosis in pediatric patients under age 18. botox is indicated for the treatment of strabismus and blepharospasm associated with dystonia, including benign essential blepharospasm or vii nerve disorders in patients 12 years of age and older. botox is contraindicated: - in patients who are hypersensitive to any botulinum toxin product or to any of the components in the formulation [see warnings and precautions ( 5.4 )] .  - in the presence of infection at the proposed injection site(s). - for intradetrusor injection in patients with a urinary tract infection; or in patients with urinary retention or post-void residual (pvr) urine volume >200 ml who are not routinely performing clean intermittent self-catheterization (cic) [see warnings and precautions ( 5.12 , 5.13 )] . risk summary there are no studies or adequate data from postmarketing surveillance on the developmental risk associated with use of botox in pregnant women. in animal studies, administration of botox during pregnancy resulted in adverse effects on fetal growth (decreased fetal weight and skeletal ossification) at clinically relevant doses, which were associated with maternal toxicity [see data ]. in the u.s. general population, the estimated background risk of major birth defects and miscarriages in clinically recognized pregnancies is 2-4% and 15-20%, respectively. the background risk of major birth defects and miscarriage for the indicated populations is unknown. data animal data when botox (4, 8, or 16 units/kg) was administered intramuscularly to pregnant mice or rats two times during the period of organogenesis (on gestation days 5 and 13), reductions in fetal body weight and decreased fetal skeletal ossification were observed at the two highest doses. the no-effect dose for developmental toxicity in these studies (4 units/kg) is approximately equal to the human dose of 400 units, on a body weight basis (units/kg). when botox was administered intramuscularly to pregnant rats (0.125, 0.25, 0.5, 1, 4, or 8 units/kg) or rabbits (0.063, 0.125, 0.25, or 0.5 units/kg) daily during the period of organogenesis (total of 12 doses in rats, 13 doses in rabbits), reduced fetal body weights and decreased fetal skeletal ossification were observed at the two highest doses in rats and at the highest dose in rabbits. these doses were also associated with significant maternal toxicity, including abortions, early deliveries, and maternal death. the developmental no-effect doses in these studies of 1 unit/kg in rats and 0.25 units/kg in rabbits are less than the human dose of 400 units, based on units/kg. when pregnant rats received single intramuscular injections (1, 4, or 16 units/kg) at three different periods of development (prior to implantation, implantation, or organogenesis), no adverse effects on fetal development were observed. the developmental no-effect level for a single maternal dose in rats (16 units/kg) is approximately 2 times the human dose of 400 units, based on units/kg. risk summary there are no data on the presence of botox in human or animal milk, 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 botox and any potential adverse effects on the breastfed infant from botox or from the underlying maternal conditions. detrusor overactivity associated with a neurologic condition the safety and effectiveness of botox for detrusor overactivity associated with a neurologic condition have been established in pediatric patients 5 years of age and older who have an inadequate response to or are intolerant of anticholinergic medication. use of botox in this patient population is based on the results of a randomized, double-blind, parallel group trial in 113 pediatric patients 5 to 17 years of age (inclusive) with detrusor overactivity associated with a neurologic condition (study 191622-120) and a long-term, multicenter, double-blind, long-term extension trial (study 191622-121) [see clinical studies ( 14.3 )]. the most common adverse reactions in this population were urinary tract infection, bacteriuria, hematuria, and leukocyturia [see adverse reactions   ( 6.1 ) ] . the safety and effectiveness of botox have not been established in patients with ndo younger than 5 years of age. overactive bladder the safety and effectiveness of botox for the treatment of overactive bladder have not been established in pediatric patients. efficacy was not demonstrated in a multicenter, randomized, double-blind, parallel-group, multiple-dose clinical study which was conducted to evaluate the efficacy and safety of botox in pediatric patients aged 12 to 17 years with overactive bladder. fifty-five patients who had an inadequate response to or were intolerant of at least one anticholinergic medication were treated with botox. there was not a statistically significant difference in the mean change from baseline in the daily average frequency of daytime urinary incontinence episodes (primary efficacy endpoint) at week 12 post-treatment when a medium and high dose were each compared to a low dose of botox. the adverse reactions in pediatric patients treated with botox were comparable with the known safety profile in adults with overactive bladder.  prophylaxis of headaches in chronic migraine safety and effectiveness in patients below the age of 18 years have not been established. in a 12-week, multicenter, double-blind, placebo-controlled clinical trial, 123 adolescent patients (ages 12 to below 18 years) with chronic migraine were randomized to receive botox 74 units, botox 155 units, or placebo, for one injection cycle. this trial did not establish the efficacy of botox, compared with placebo, for the prophylaxis of headaches in adolescents with chronic migraine. spasticity safety and effectiveness have been established in pediatric patients 2 to 17 years of age [see warnings and precautions ( 5.1 ), adverse reactions ( 6.1 ) , and clinical studies ( 14.6 )] . the safety and effectiveness of botox have been established by evidence from adequate and well-controlled studies of botox in patients 2 to 17 years of age with upper and lower limb spasticity. safety and effectiveness in pediatric patients below the age of 2 years have not been established [see boxed warning and warnings and precautions ( 5.1 )]. axillary hyperhidrosis safety and effectiveness in patients below the age of 18 years have not been established. cervical dystonia safety and effectiveness in pediatric patients below the age of 16 years have not been established. blepharospasm and strabismus safety and effectiveness in pediatric patients below the age of 12 years have not been established. juvenile animal data in a study in which juvenile rats received intramuscular injection of botox (0, 8, 16, or 24 units/kg) every other week from postnatal day 21 for 12 weeks, changes in bone size/geometry associated with decreased bone density and bone mass were observed at all doses, in association with limb disuse, decreased muscle contraction, and decreased body weight gain. impairment of fertility and male reproductive organ histopathology (degeneration of seminiferous tubules of the testis) were observed at the mid and high doses. bone and male reproductive organ effects showed evidence of reversibility after dosing cessation. the no-effect dose for adverse developmental effects in juvenile animals (8 units/kg) is similar to the human dose (400 units) on a body weight (kg) basis. of the 2145 adult patients in placebo-controlled clinical studies of botox for the treatment of spasticity, 33.5% were 65 or older, and 7.7% were 75 years of age or older. no overall differences in safety were observed between elderly patients and adult patients younger than 65 years of age.  in clinical studies of botox across other indications, no overall differences in safety were observed between elderly patients and younger adult patients, with the exception of overactive bladder (see below). other reported clinical experience has not identified differences in responses between the elderly and younger adult patients, but greater sensitivity of some older individuals cannot be ruled out. overactive bladder of 1242 overactive bladder patients in placebo-controlled clinical studies of botox, 41.4% were 65 years of age or older, and 14.7% were 75 years of age or older. adverse reactions of uti and urinary retention were more common in patients 65 years of age or older in both placebo and botox groups compared to younger patients (see table 24). otherwise, there were no overall differences in the safety profile following botox treatment between patients aged 65 years and older compared to adult patients younger than 65 years of age in these studies. observed effectiveness was comparable between these age groups in placebo-controlled clinical studies.

Hoa Kỳ - Tiếng Anh - NLM (National Library of Medicine)

preferred pharmaceuticals inc. - diclofenac sodium (unii: qtg126297q) (diclofenac - unii:144o8ql0l1) - diclofenac sodium topical solution is indicated for the treatment of the pain of osteoarthritis of the knee(s). diclofenac sodium topical solution  is contraindicated in the following patients: risk summary use of nsaids, including diclofenac sodium topical solution, 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 topical solution use between about 20 and 30 weeks of gestation, and avoid diclofenac sodium topical solution 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 topical solution, 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 malformations were observed in mice, rats, or rabbits given diclofenac 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 162 mg diclofenac sodium via diclofenac sodium topical solution, 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 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 the fetal ductus arteriosus: avoid use of nsaids in women at about 30 weeks gestation and later in pregnancy, because nsaids, including diclofenac sodium topical solution, 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 topical solution treatment extends beyond 48 hours, consider monitoring with ultrasound for oligohydramnios. if oligohydramnios occurs, discontinue diclofenac sodium topical solution and follow up according to clinical practice (see data) .  labor or delivery           there are no studies on the effects of diclofenac sodium topical solution during labor or delivery. in animal studies, nsaids, including diclofenac 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 reproductive and developmental studies in animals demonstrated that diclofenac sodium administration during organogenesis did not produce malformations 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 topical solution, 162 mg diclofenac sodium/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 a study in which pregnant rats were orally administered 2 or 4 mg/kg diclofenac (0.12 and 0.24 times the mrhd, respectively, based on bsa comparison) from gestation day 15 through lactation day 21, significant maternal toxicity (peritonitis, mortality) was noted. these maternally toxic doses were associated with dystocia, prolonged gestation, reduced fetal weights and growth, and reduced fetal survival. diclofenac has been shown to cross the placental barrier in mice and rats. in published studies, diclofenac administration to pregnant rats prolonged gestation and produced liver toxicity and neuronal loss in offspring (1 mg/kg, ip; 0.06 times the mrhd based on bsa comparison), impaired nephrogenesis in the kidney (3.6 mg/kg, ip; 0.2 times the mrhd based on bsa comparison), and caused adverse effects on the developing testes (6.1 mg/kg, oral; 0.4 times the mrhd based on bsa comparison). 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 diclofenac and any potential adverse effects on the breastfed infant from the diclofenac 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 topical solution, 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 diclofenac sodium topical solution, in women who have difficulties conceiving or who are undergoing investigation of infertility. males published studies in adult male rodents report that diclofenac, at clinically relevant doses, can produce adverse effects on male reproductive tissues. the impact of these findings on male fertility is not clear [see nonclinical toxicology (13.1)]. safety and effectiveness 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) ]. of the 911 patients treated with diclofenac sodium topical solution 1.5% 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 topical solution 1.5% 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 topical solution 1.5% for this elderly population. diclofenac sodium (dye kloe' fen ak soe' dee um) topical solution, usp 2% read the medication guide that comes with diclofenac sodium topical solution first. be sure that you read, understand and follow these instructions for use before you use diclofenac sodium topical solution for the first time. important: for use on the skin only (topical). do not get diclofenac sodium topical solution in your eyes, nose or mouth. before you use diclofenac sodium topical solution: diclofenac sodium topical solution comes in a pump bottle from your healthcare provider. if you are using a diclofenac sodium topical solution pump bottle follow the steps below: before you use diclofenac sodium topical solution pump bottle for the first time, you will need to prime the pump. to prime the pump, remove the cap (see figure a ) and fully press the top of the pump all the way down 4 times while holding the bottle in an upright position (see figure b ). dispense this portion of the medicine into a tissue or paper towel and throw it away in a trash can. the pump is now ready to use. you should not need to prime the pump again. steps for using diclofenac sodium topical solution pump bottle: step 1: wash your hands with soap and water before applying diclofenac sodium topical solution. step 2: remove the bottle cap and press the pump head down firmly and fully to dispense diclofenac sodium topical solution into the palm of your hand. release the pump head and then press the pump head down firmly and fully a second time. when you use your diclofenac sodium topical solution pump bottle, you can hold the bottle at an angle. put 2 pumps of diclofenac sodium topical solution on your hand (see figure c ).   step 3: apply diclofenac sodium topical solution evenly around the front, back, and sides of your knee. diclofenac sodium topical solution should be applied without massaging the knee (see figures d and e ).   step 4: repeat steps 2 and 3 for your other knee if your healthcare provider has prescribed diclofenac sodium topical solution for both knees. step 5: wash your hands with soap and water right away after applying diclofenac sodium topical solution. step 6: replace the cap on the bottle and store in an upright position. after you use diclofenac sodium topical solution: do not: how should i store diclofenac sodium topical solution? keep diclofenac sodium topical solution and all medicines out of the reach of children. this instructions for use has been approved by the u.s. food and drug administration. distributed by: aurobindo pharma usa, inc. 279 princeton-hightstown road east windsor, nj 08520 issued: november 2022 relabeled by: preferred pharmaceuticals inc.

Hoa Kỳ - Tiếng Anh - NLM (National Library of Medicine)

physicians total care, inc. - progesterone (unii: 4g7ds2q64y) (progesterone - unii:4g7ds2q64y) - progesterone 100 mg - prometrium capsules are indicated for use in the prevention of endometrial hyperplasia in nonhysterectomized postmenopausal women who are receiving conjugated estrogens tablets. they are also indicated for use in secondary amenorrhea. prometrium capsules should not be used in women with any of the following conditions: - prometrium capsules should not be used in patients with known hypersensitivity to its ingredients. prometrium capsules contain peanut oil and should never be used by patients allergic to peanuts. - undiagnosed abnormal genital bleeding. - known, suspected, or history of cancer of the breast. - active deep vein thrombosis, pulmonary embolism or history of these conditions. - active or recent (e.g., within the past year) arterial thromboembolic disease (e.g., stroke, myocardial infarction). - liver dysfunction or disease. - known or suspected pregnancy. there is no indication for prometrium capsules in pregnancy. there appears to be little or no increased risk of birth defects in chi

Hoa Kỳ - Tiếng Anh - NLM (National Library of Medicine)

horizon therapeutics usa, inc. - diclofenac sodium (unii: qtg126297q) (diclofenac - unii:144o8ql0l1) - diclofenac sodium 20 mg in 1 g - pennsaid is indicated for the treatment of the pain of osteoarthritis of the knee(s). pennsaid 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 pennsaid, 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 pennsaid use between about 20 and 30 weeks of gestation, and avoid pennsaid use at about 30 weeks of ge

Hoa Kỳ - Tiếng Anh - NLM (National Library of Medicine)

taro pharmaceuticals u.s.a., inc. - diclofenac sodium (unii: qtg126297q) (diclofenac - unii:144o8ql0l1) - diclofenac sodium topical solution is indicated for the treatment of the pain of osteoarthritis of the knee(s). 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 topical solution use between about 20 and

Hoa Kỳ - Tiếng Anh - NLM (National Library of Medicine)

lupin pharmaceuticals, inc. - diclofenac sodium (unii: qtg126297q) (diclofenac - unii:144o8ql0l1) - diclofenac sodium topical solution is indicated for the treatment of the pain of osteoarthritis of the knee(s). diclofenac sodium topical solution 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 topical solution, 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 topical solution use between about 20 and 30 weeks of gestation, and avoid diclofenac sodium topical solution 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 topical solution, 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 malformations were observed in mice, rats, or rabbits given diclofenac 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 162 mg diclofenac sodium via diclofenac sodium topical solution, 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 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 the fetal ductus arteriosus: avoid use of nsaids in women at about 30 weeks gestation and later in pregnancy, because nsaids, including diclofenac sodium topical solution, 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 topical solution treatment extends beyond 48 hours, consider monitoring with ultrasound for oligohydramnios. if oligohydramnios occurs, discontinue diclofenac sodium topical solution and follow up according to clinical practice (see data) . labor or delivery: there are no studies on the effects of diclofenac sodium topical solution during labor or delivery. in animal studies, nsaids, including diclofenac 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: reproductive and developmental studies in animals demonstrated that diclofenac sodium administration during organogenesis did not produce malformations 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 topical solution, 162 mg diclofenac sodium/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 a study in which pregnant rats were orally administered 2 or 4 mg/kg diclofenac (0.12 and 0.24 times the mrhd, respectively, based on bsa comparison) from gestation day 15 through lactation day 21, significant maternal toxicity (peritonitis, mortality) was noted. these maternally toxic doses were associated with dystocia, prolonged gestation, reduced fetal weights and growth, and reduced fetal survival. diclofenac has been shown to cross the placental barrier in mice and rats. in published studies, diclofenac administration to pregnant rats prolonged gestation and produced liver toxicity and neuronal loss in offspring (1 mg/kg, ip; 0.06 times the mrhd based on bsa comparison), impaired nephrogenesis in the kidney (3.6 mg/kg, ip; 0.2 times the mrhd based on bsa comparison), and caused adverse effects on the developing testes (6.1 mg/kg, oral; 0.4 times the mrhd based on bsa comparison). 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 diclofenac sodium topical solution and any potential adverse effects on the breastfed infant from the diclofenac sodium topical solution 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 topical solution, 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 diclofenac sodium topical solution, in women who have difficulties conceiving or who are undergoing investigation of infertility. males: published studies in adult male rodents report that diclofenac, at clinically relevant doses, can produce adverse effects on male reproductive tissues. the impact of these findings on male fertility is not clear [see nonclinical toxicology (13.1) ]. safety and effectiveness 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)]. of the 911 patients treated with diclofenac sodium topical solution 1.5% 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 topical solution 1.5% 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 topical solution 1.5% for this elderly population.

Hoa Kỳ - Tiếng Anh - NLM (National Library of Medicine)

preferred pharmaceuticals, inc. - diclofenac sodium (unii: qtg126297q) (diclofenac - unii:144o8ql0l1) - diclofenac sodium topical solution is indicated for the treatment of the pain of osteoarthritis of the knee(s). diclofenac sodium topical solution is contraindicated in the following patients: risk summary use of nsaids, including diclofenac sodium topical solution, 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 topical solution use between about 20 and 30 weeks of gestation, and avoid diclofenac sodium topical solution 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 topical solution, 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 i

Hoa Kỳ - Tiếng Anh - NLM (National Library of Medicine)

lupin pharmaceuticals, inc. - diclofenac sodium (unii: qtg126297q) (diclofenac - unii:144o8ql0l1) - diclofenac sodium topical solution is indicated for the treatment of the pain of osteoarthritis of the knee(s). diclofenac sodium topical solution 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 topical solution, 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 topical solution use between about 20 and 30 weeks of gestation, and avoid diclofenac sodium topical solution 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 topical solution, 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 malformations were observed in mice, rats, or rabbits given diclofenac 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 162 mg diclofenac sodium via diclofenac sodium topical solution, 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 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 the fetal ductus arteriosus: avoid use of nsaids in women at about 30 weeks gestation and later in pregnancy, because nsaids, including diclofenac sodium topical solution, 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 topical solution treatment extends beyond 48 hours, consider monitoring with ultrasound for oligohydramnios. if oligohydramnios occurs, discontinue diclofenac sodium topical solution and follow up according to clinical practice (see data) . labor or delivery: there are no studies on the effects of diclofenac sodium topical solution during labor or delivery. in animal studies, nsaids, including diclofenac 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: reproductive and developmental studies in animals demonstrated that diclofenac sodium administration during organogenesis did not produce malformations 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 topical solution, 162 mg diclofenac sodium/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 a study in which pregnant rats were orally administered 2 or 4 mg/kg diclofenac (0.12 and 0.24 times the mrhd, respectively, based on bsa comparison) from gestation day 15 through lactation day 21, significant maternal toxicity (peritonitis, mortality) was noted. these maternally toxic doses were associated with dystocia, prolonged gestation, reduced fetal weights and growth, and reduced fetal survival. diclofenac has been shown to cross the placental barrier in mice and rats. in published studies, diclofenac administration to pregnant rats prolonged gestation and produced liver toxicity and neuronal loss in offspring (1 mg/kg, ip; 0.06 times the mrhd based on bsa comparison), impaired nephrogenesis in the kidney (3.6 mg/kg, ip; 0.2 times the mrhd based on bsa comparison), and caused adverse effects on the developing testes (6.1 mg/kg, oral; 0.4 times the mrhd based on bsa comparison). 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 diclofenac sodium topical solution and any potential adverse effects on the breastfed infant from the diclofenac sodium topical solution 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 topical solution, 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 diclofenac sodium topical solution, in women who have difficulties conceiving or who are undergoing investigation of infertility. males: published studies in adult male rodents report that diclofenac, at clinically relevant doses, can produce adverse effects on male reproductive tissues. the impact of these findings on male fertility is not clear [see nonclinical toxicology (13.1) ]. safety and effectiveness 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)]. of the 911 patients treated with diclofenac sodium topical solution, 1.5% 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 topical solution, 1.5% 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 topical solution, 1.5% for this elderly population.

Hoa Kỳ - Tiếng Anh - NLM (National Library of Medicine)

physicians total care, inc. - albuterol sulfate (unii: 021sef3731) (albuterol - unii:qf8svz843e) - albuterol sulfate 108 ug - ventolin hfa is indicated for the treatment or prevention of bronchospasm in patients 4 years of age and older with reversible obstructive airway disease. ventolin hfa is indicated for the prevention of exercise-induced bronchospasm in patients 4 years of age and older. ventolin hfa is contraindicated in patients with a history of hypersensitivity to albuterol or any other components of ventolin hfa. rare cases of hypersensitivity reactions, including urticaria, angioedema, and rash have been reported after the use of albuterol sulfate. teratogenic effects: pregnancy category c. there are no adequate and well-controlled studies of ventolin hfa or albuterol sulfate in pregnant women. during worldwide marketing experience, various congenital anomalies, including cleft palate and limb defects, have been reported in the offspring of patients being treated with albuterol. some of the mothers were taking multiple medications during their pregnancies. no consistent pattern of defects can be discerned, and a relatio