США - англійська - NLM (National Library of Medicine)

greenstone llc - risedronate sodium hemi-pentahydrate (unii: hu2yaq274o) (risedronic acid - unii:km2z91756z), risedronate sodium monohydrate (unii: f67l43ut5c) (risedronic acid - unii:km2z91756z) - risedronate sodium anhydrous 30.1 mg - risedronate sodium delayed-release is indicated for the treatment of osteoporosis in postmenopausal women. in postmenopausal women, risedronate sodium has been shown to reduce the incidence of vertebral fractures and a composite endpoint of nonvertebral osteoporosis-related fractures [see clinical studies (14.1) ].  the optimal duration of use has not been determined. the safety and effectiveness of risedronate sodium delayed-release for the treatment of osteoporosis are based on clinical data of one year duration. all patients on bisphosphonate therapy should have the need for continued therapy re-evaluated on a periodic basis. patients at low-risk for fracture should be considered for drug discontinuation after 3 to 5 years of use. patients who discontinue therapy should have their risk for fracture re-evaluated periodically. risedronate sodium delayed-release is contraindicated in patients with the following conditions: - abnormalities of the esophagus which delay esophageal emptying such as stricture or achalasia [see warnings and precautions (5.2) ] - inability to stand or sit upright for at least 30 minutes [see dosage and administration (2) , warnings and precautions (5.2) ] - hypocalcemia [see  warnings and precautions (5.3) ] - known hypersensitivity to any component of this product. angioedema, generalized rash, bullous skin reactions, stevens-johnson syndrome and toxic epidermal necrolysis have been reported [see  adverse reactions (6.2) ] risk summary available data on use of risedronate sodium delayed-release in pregnant women are insufficient to inform drug-associated risk of adverse maternal or fetal outcomes. discontinue risedronate sodium delayed-release when pregnancy is recognized. in animal reproduction studies, daily oral administration of risedronate to pregnant rats during organogenesis decreased neonatal survival and body weight at doses approximately 5 and 26 times, respectively, the highest recommended human daily dose of 30 mg (based on body surface area, mg/m2 ), the dose indicated for treatment of paget’s disease. a low incidence of cleft palate was observed in fetuses of dams treated at doses approximately equal to the 30 mg human daily dose. delayed skeletal ossification was observed in fetuses of dams treated at approximately 2.5 to 5 times the 30 mg human daily dose. periparturient mortality due to maternal hypocalcemia occurred in dams and neonates upon daily oral administration of risedronate to pregnant rats during mating and/or gestation starting at doses equivalent to the 30 mg daily human dose. bisphosphonates are incorporated into the bone matrix, from which they are gradually released over a period of weeks to years. the amount of bisphosphonate incorporated into adult bone available for release into the systemic circulation is directly related to the dose and duration of bisphosphonate use. consequently, based on mechanism of action of bisphosphonates, there is a potential risk of fetal harm, predominantly skeletal, if a woman becomes pregnant after completing a course of bisphosphonate therapy. the impact of variables such as time between cessation of bisphosphonate therapy to conception, the particular bisphosphonate used, and the route of administration (intravenous versus oral) on this risk has not been studied. the estimated background risk of major birth defects and miscarriage for the indicated populations is unknown. all pregnancies have a background risk of birth defects, loss, or other adverse outcomes. in the u.s. general population, the estimated background risks of major birth defects and miscarriage in clinically recognized pregnancies is 2-4% and 15-20%, respectively. data animal d ata in animal studies, pregnant rats received risedronate sodium during organogenesis at doses 1 to 26 times the human paget’s disease dose of 30 mg/day (based on body surface area, mg/m2 ). survival of neonates was decreased in rats treated during gestation with oral doses approximately 5 times the human dose and body weight was decreased in neonates from dams treated with approximately 26 times the human dose. a low incidence of cleft palate was observed in fetuses from female rats treated with oral doses approximately equal to the human dose. the number of fetuses exhibiting incomplete ossification of sternebrae or skull of dams treated with approximately 2.5 times the human dose was significantly increased compared to controls. both incomplete ossification and unossified sternebrae were increased in fetuses of dams treated with oral doses approximately 5 times the human dose. no significant ossification effects were seen in fetuses of rabbits treated with oral doses approximately 7 times the human dose (the highest dose tested). however, 1 of 14 litters were aborted and 1 of 14 litters were delivered prematurely. periparturient mortality due to maternal hypocalcemia occurred in dams and neonates when pregnant rats were treated daily during mating and/or gestation with oral doses equivalent to the human dose or higher. risk summary there are no data to assess the presence of risedronate in human milk, the effects on the breastfed infant, or the effects on milk production. a small degree of lacteal transfer occurred in nursing rats. the concentration of the drug in animal milk does not necessarily predict the concentration of drug in human milk. however, when a drug is present in animal milk, it is likely that the drug will be present in human milk. the developmental and health benefits of breast-feeding should be considered along with the mother’s clinical need for risedronate sodium delayed-release and any potential adverse effects on the breast-fed child from risedronate sodium delayed-release or from the underlying maternal condition. data animal data risedronate was detected in neonates of lactating rats given a single oral dose of risedronate at 24-hours post-dosing, indicating a small degree of lacteal transfer. infertility there are no data available in humans. female and male fertility may be impaired based on animal studies demonstrating adverse effects of risedronate sodium delayed-release on fertility parameters [see nonclinical toxicology (13.1) ] . risedronate sodium delayed-release is not indicated for use in pediatric patients. the safety and effectiveness of risedronate sodium immediate-release was assessed in a one-year, randomized, double-blind, placebo-controlled study of 143 pediatric patients (94 received risedronate) with osteogenesis imperfecta (oi). the enrolled population was predominantly patients with mild oi (85% type-i), aged 4 to less than 16 years, 50% male and 82% caucasian, with a mean lumbar spine bmd z-score of -2.08 (2.08 standard deviations below the mean for age-matched controls). patients received either a 2.5 mg (less than or equal to 30 kg body weight) or 5 mg (greater than 30 kg body weight) daily oral dose. after one year, an increase in lumbar spine bmd in the risedronate sodium immediate-release group compared to the placebo group was observed. however, treatment with risedronate sodium immediate-release did not result in a reduction in the risk of fracture in pediatric patients with oi. in risedronate sodium immediate-release treated subjects, no mineralization defects were noted in paired bone biopsy specimens obtained at baseline and month 12. the overall safety profile of risedronate in oi patients treated for up to 12 months was generally similar to that of adults with osteoporosis. however, there was an increased incidence of vomiting compared to placebo. in this study, vomiting was observed in 15% of children treated with risedronate sodium immediate-release and 6% of patients treated with placebo. other adverse reactions reported in greater than or equal to 10% of patients treated with risedronate sodium immediate-release and with a higher frequency than placebo were: pain in the extremity (21% with risedronate sodium immediate-release versus 16% with placebo), headache (20% versus 8%), back pain (17% versus 10%), pain (15% versus 10%), upper abdominal pain (11% versus 8%), and bone pain (10% versus 4%). of the patients receiving risedronate sodium delayed-release in postmenopausal osteoporosis studies, 59% were 65 and over, while 13% were 75 and over. no overall differences in safety or effectiveness were observed between these patients and younger patients, 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. risedronate sodium delayed-release is not recommended for use in patients with severe renal impairment (creatinine clearance less than 30 ml/min) because of lack of clinical experience. no dosage adjustment is necessary in patients with a creatinine clearance greater than or equal to 30 ml/min. no studies have been performed to assess risedronate sodium’s safety or efficacy in patients with hepatic impairment. risedronate is not metabolized in human liver preparations. dosage adjustment is unlikely to be needed in patients with hepatic impairment.

США - англійська - NLM (National Library of Medicine)

greenstone llc - sirolimus (unii: w36zg6ft64) (sirolimus - unii:w36zg6ft64) - sirolimus is indicated for the prophylaxis of organ rejection in patients aged 13 years or older receiving renal transplants. in patients at low- to moderate-immunologic risk, it is recommended that sirolimus be used initially in a regimen with cyclosporine and corticosteroids; cyclosporine should be withdrawn 2 to 4 months after transplantation [see dosage and administration (2.2) ]. in patients at high-immunologic risk (defined as black recipients and/or repeat renal transplant recipients who lost a previous allograft for immunologic reason and/or patients with high panel-reactive antibodies [pra; peak pra level >80%]), it is recommended that sirolimus be used in combination with cyclosporine and corticosteroids for the first year following transplantation [see dosage and administration (2.3) , clinical studies (14.3) ]. cyclosporine withdrawal has not been studied in patients with banff grade 3 acute rejection or vascular rejection prior to cyclosporine withdrawal, those who are dialysis-dependent, those

Філіппіни - англійська - FDA (Food And Drug Administration)

greenstone pharma'l h.k. inc - methyl salicylate , menthol , eucalyptus oil - liniment oil - 27 mg/ 25 mg/ 6 mg per 100 ml

Філіппіни - англійська - FDA (Food And Drug Administration)

greenstone pharma'l h.k., inc - methyl salicylate , menthol , camphor - ointment - 80mcg/75mcg/26mcg per gram ointment

США - англійська - 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

США - англійська - NLM (National Library of Medicine)

greenstone llc - triazolam (unii: 1hm943223r) (triazolam - unii:1hm943223r) - triazolam 0.125 mg - triazolam is indicated for the short-term treatment of insomnia (generally 7 to 10 days) in adults. triazolam is contraindicated in: pregnancy exposure registry there is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to psychiatric medications, including triazolam, during pregnancy. healthcare providers are encouraged to register patients by calling the national pregnancy registry for psychiatric medications at 1-866-961-2388 or visiting online at https://womensmentalhealth.org/pregnancyregistry/. risk summary neonates born to mothers using benzodiazepines late in pregnancy have been reported to experience symptoms of sedation and/or neonatal withdrawal [see warnings and precautions (5.10) and clinical considerations] . available data from published observational studies of pregnant women exposed to benzodiazepines do not report a clear association with benzodiazepines and major birth defects (see data ). the background risk of major birth defects and miscarriage for the indic

США - англійська - NLM (National Library of Medicine)

greenstone llc - piroxicam (unii: 13t4o6vmam) (piroxicam - unii:13t4o6vmam) - piroxicam 10 mg - piroxicam is indicated: piroxicam is contraindicated in the following patients: risk summary use of nsaids, including piroxicam, 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 piroxicam use between about 20 and 30 weeks of gestation, and avoid piroxicam use at about 30 weeks of gestation and later in pregnancy (see error! hyperlink reference not valid. , error! hyperlink reference not valid. ) . premature closure of fetal ductus arteriosus use of nsaids, including piroxicam, 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 in rats and rabbits, there was no evidence of teratogenicity at exposures up to 5 and 10 times the maximum recommended human dose (mrhd), respectively. in rat studies with piroxicam, fetotoxicity (postimplantation loss) was observed at exposures 2 times the mrhd, and delayed parturition and an increased incidence of stillbirth were noted at doses equivalent to the mrhd of piroxicam. 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 piroxicam, 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 piroxicam, can cause premature closure of the fetal ductus arteriosus (see error! hyperlink reference not valid. ) . 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 piroxicam treatment extends beyond 48 hours, consider monitoring with ultrasound for oligohydramnios. if oligohydramnios occurs, discontinue piroxicam and follow up according to clinical practice (see error! hyperlink reference not valid. ) . labor or delivery there are no studies on the effects of piroxicam during labor or delivery. in animal studies, nsaids, including piroxicam 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 pregnant rats administered piroxicam at 2, 5, or 10 mg/kg/day during the period of organogenesis (gestation days 6 to 15) demonstrated increased post-implantation losses with 5 and 10 mg/kg/day of piroxicam (equivalent to 2 and 5 times the mrhd, of 20 mg respectively, based on a mg/m2 body surface area [bsa]). there were no drug-related developmental abnormalities noted in offspring. gastrointestinal tract toxicity was increased in pregnant rats in the last trimester of pregnancy compared to non-pregnant rats or rats in earlier trimesters of pregnancy. pregnant rabbits administered piroxicam at 2, 5, or 10 mg/kg/day during the period of organogenesis (gestation days 7 to 18) demonstrated no drug-related developmental abnormalities in offspring (up to 10 times the mrhd based on a mg/m2 bsa). in a pre- and post-natal development study in which pregnant rats were administered piroxicam at 2, 5, or 10 mg/kg/day on gestation day 15 through delivery and weaning of offspring, reduced weight gain and death were observed in dams at 10 mg/kg/day (5 times the mrhd based on a mg/m2 bsa) starting on gestation day 20. treated dams revealed peritonitis, adhesions, gastric bleeding, hemorrhagic enteritis and dead fetuses in utero. parturition was delayed and there was an increased incidence of stillbirth in all piroxicam-treated groups (at doses equivalent to the mrhd). postnatal development could not be reliably assessed due to the absence of maternal care secondary to severe maternal toxicity. risk summary limited data from 2 published reports that included a total of 6 breastfeeding women and 2 infants showed piroxicam is excreted in human milk at approximately 1% to 3% of the maternal concentration. no accumulation of piroxicam occurred in milk relative to that in maternal plasma during treatment. the developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for piroxicam and any potential adverse effects on the breastfed infant from the piroxicam or from the underlying maternal condition. infertility females based on the mechanism of action, the use of prostaglandin-mediated nsaids, including piroxicam, 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 piroxicam, in women who have difficulties conceiving or who are undergoing investigation of infertility. piroxicam has not been investigated in pediatric patients. the safety and effectiveness of piroxicam 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)] .

США - англійська - NLM (National Library of Medicine)

greenstone llc - risedronate sodium hemi-pentahydrate (unii: hu2yaq274o) (risedronic acid - unii:km2z91756z), risedronate sodium monohydrate (unii: f67l43ut5c) (risedronic acid - unii:km2z91756z) - risedronate sodium is indicated for the treatment and prevention of osteoporosis in postmenopausal women. in postmenopausal women with osteoporosis, risedronate sodium reduces the incidence of vertebral fractures and a composite endpoint of nonvertebral osteoporosis-related fractures [see clinical studies ( 14.1 , 14.2 ) ]. risedronate sodium is indicated for treatment to increase bone mass in men with osteoporosis. risedronate sodium is indicated for the treatment and prevention of glucocorticoid-induced osteoporosis in men and women who are either initiating or continuing systemic glucocorticoid treatment (daily dosage of greater than or equal to 7.5 mg of prednisone or equivalent) for chronic diseases. patients treated with glucocorticoids should receive adequate amounts of calcium and vitamin d. risedronate sodium is indicated for treatment of paget’s disease of bone in men and women. the optimal duration of use has not been determined. the safety and effectiveness of risedronate sodium for the treatment of osteoporosis are based on clinical data of three years duration. all patients on bisphosphonate therapy should have the need for continued therapy re-evaluated on a periodic basis. patients at low-risk for fracture should be considered for drug discontinuation after 3 to 5 years of use. patients who discontinue therapy should have their risk for fracture re-evaluated periodically. risedronate sodium is contraindicated in patients with the following conditions: - abnormalities of the esophagus which delay esophageal emptying such as stricture or achalasia [see warnings and precautions ( 5.1 ) ] - inability to stand or sit upright for at least 30 minutes [see dosage and administration ( 2 ), warnings and precautions ( 5.1 ) ] - hypocalcemia [see warnings and precautions ( 5.2 ) ] - known hypersensitivity to risedronate sodium or any of its excipients. angioedema, generalized rash, bullous skin reactions, stevens-johnson syndrome and toxic epidermal necrolysis have been reported [see adverse reactions ( 6.2 ) ] risk summary available data on the use of risedronate sodium in pregnant women are insufficient to inform a drug-associated risk of adverse maternal or fetal outcomes. discontinue risedronate sodium when pregnancy is recognized. in animal reproduction studies, daily oral administration of risedronate to pregnant rats during organogenesis decreased neonatal survival and body weight at doses approximately 5 and 26 times, respectively, the highest recommended human daily dose of 30 mg (based on body surface area, mg/m2 ). a low incidence of cleft palate was observed in fetuses of dams treated at doses approximately equal to the 30 mg human daily dose. delayed skeletal ossification was observed in fetuses of dams treated at approximately 2.5 to 5 times the 30 mg human daily dose. periparturient mortality due to maternal hypocalcemia occurred in dams and neonates upon daily oral administration of risedronate to pregnant rats during mating and/or gestation starting at doses equivalent to the 30 mg daily human dose. bisphosphonates are incorporated into the bone matrix, from which they are gradually released over a period of years. the amount of bisphosphonate incorporated into adult bone and available for release into the systemic circulation is directly related to the dose and duration of bisphosphonate use. consequently, based on the mechanism of action of bisphosphonates, there is a potential risk of fetal harm, predominantly skeletal, if a woman becomes pregnant after completing a course of bisphosphonate therapy. the impact of variables such as time between cessation of bisphosphonate therapy to conception, the particular bisphosphonate used, and the route of administration (intravenous versus oral) on this risk has not been studied. the estimated background risk of major birth defects and miscarriage for the indicated populations is unknown. all pregnancies have a background risk of birth defects, loss, or other adverse outcomes. in the u.s. general population, the estimated background risks of major birth defects and miscarriage in clinically recognized pregnancies is 2-4% and 15-20%, respectively. data animal data in animal studies, pregnant rats received risedronate sodium during organogenesis at doses equivalent to 1 to 26 times the 30 mg human daily dose (based on body surface area, mg/m2 ). survival of neonates was decreased in dams treated during gestation with oral doses approximately 5 times the human dose, and body weight was decreased in neonates of dams treated with approximately 26 times the human dose. a low incidence of cleft palate was observed in fetuses of dams treated with oral doses approximately equal to the human dose. the number of fetuses exhibiting incomplete ossification of sternebrae or skull of dams treated with approximately 2.5 times the human dose was significantly increased compared to controls. both incomplete ossification and unossified sternebrae were increased in fetuses of dams treated with oral doses approximately 5 times the human dose. no significant ossification effects were seen in fetuses of rabbits treated with oral doses approximately 7 times the human dose (the highest dose tested). however, 1 of 14 litters were aborted and 1 of 14 litters were delivered prematurely. periparturient mortality due to maternal hypocalcemia occurred in dams and neonates when pregnant rats were treated daily during mating and/or gestation with oral doses equivalent to the human dose or higher. risk summary there are no data on the presence of risedronate in human milk, the effects on the breastfed infant, or the effects on milk production. a small degree of lacteal transfer occurred in nursing rats. the concentration of the drug in animal milk does not necessarily predict the concentration of drug in human milk. however, when a drug is present in animal milk, it is likely that the drug will be present in human milk. the developmental and health benefits of breast-feeding should be considered along with the mother’s clinical need for risedronate sodium and any potential adverse effects on the breast-fed child from risedronate sodium or from the underlying maternal condition. data animal data risedronate was detected in neonates of lactating rats given a single oral dose of risedronate at 24-hours post-dosing, indicating a small degree of lacteal transfer. risedronate sodium is not indicated for use in pediatric patients. the safety and effectiveness of risedronate was assessed in a one-year, randomized, double-blind, placebo-controlled study of 143 pediatric patients (94 received risedronate) with osteogenesis imperfecta (oi). the enrolled population was predominantly patients with mild osteogenesis imperfecta (85% type-i), aged 4 to less than 16 years, 50% male and 82% caucasian, with a mean lumbar spine bmd z-score of -2.08 (2.08 standard deviations below the mean for age-matched controls). patients received either a 2.5 mg (less than or equal to 30 kg body weight) or 5 mg (greater than 30 kg body weight) daily oral dose. after one year, an increase in lumbar spine bmd in the risedronate group compared to the placebo group was observed. however, treatment with risedronate did not result in a reduction in the risk of fracture in pediatric patients with osteogenesis imperfecta. in risedronate sodium-treated subjects, no mineralization defects were noted in paired bone biopsy specimens obtained at baseline and month 12. the overall safety profile of risedronate in oi patients treated for up to 12 months was generally similar to that of adults with osteoporosis. however, there was an increased incidence of vomiting compared to placebo. in this study, vomiting was observed in 15% of children treated with risedronate and 6% of patients treated with placebo. other adverse events reported in greater than or equal to 10% of patients treated with risedronate and with a higher frequency than placebo were: pain in the extremity (21% with risedronate versus 16% with placebo), headache (20% versus 8%), back pain (17% versus 10%), pain (15% versus 10%), upper abdominal pain (11% versus 8%), and bone pain (10% versus 4%). of the patients receiving risedronate sodium in postmenopausal osteoporosis studies [see clinical studies ( 14 ) ], 47% were between 65 and 75 years of age, and 17% were over 75. the corresponding proportions were 26% and 11% in glucocorticoid-induced osteoporosis trials, and 40% and 26% in paget’s disease trials. no overall differences in efficacy between geriatric and younger patients were observed in these studies. in the male osteoporosis trial, 28% of patients receiving risedronate sodium were between 65 and 75 years of age and 9% were over 75. the lumbar spine bmd response for risedronate sodium compared to placebo was 5.6% for subjects less than 65 years and 2.9% for subjects greater than or equal to 65 years. no overall differences in safety between geriatric and younger patients were observed in the risedronate sodium trials, but greater sensitivity of some older individuals cannot be ruled out. risedronate sodium is not recommended for use in patients with severe renal impairment (creatinine clearance less than 30 ml/min) because of lack of clinical experience. no dosage adjustment is necessary in patients with a creatinine clearance greater than or equal to 30 ml/min. no studies have been performed to assess risedronate’s safety or efficacy in patients with hepatic impairment. risedronate is not metabolized in human liver preparations. dosage adjustment is unlikely to be needed in patients with hepatic impairment.

США - англійська - NLM (National Library of Medicine)

greenstone llc - sildenafil citrate (unii: bw9b0ze037) (sildenafil - unii:3m7ob98y7h) - sildenafil is indicated for the treatment of pulmonary arterial hypertension (who group i) in adults to improve exercise ability and delay clinical worsening. the delay in clinical worsening was demonstrated when sildenafil was added to background epoprostenol therapy [see clinical studies (14)] . studies establishing effectiveness were short-term (12 to 16 weeks), and included predominately patients with new york heart association (nyha) functional class ii–iii symptoms and idiopathic etiology (71%) or associated with connective tissue disease (ctd) (25%). limitation of use: adding sildenafil to bosentan therapy does not result in any beneficial effect on exercise capacity [see clinical studies (14)] . sildenafil is contraindicated in patients with: - concomitant use of organic nitrates in any form, either regularly or intermittently, because of the greater risk of hypotension [see warnings and precautions (5.2)] . - concomitant use of riociguat, a guanylate cyclase stimulator. pde-5 inhibitors, including s

США - англійська - NLM (National Library of Medicine)

pd-rx pharmaceuticals, inc. - sertraline hydrochloride (unii: uti8907y6x) (sertraline - unii:quc7nx6wmb) - sertraline 50 mg - sertraline hydrochloride is indicated for the treatment of the following [see clinical studies (14)] : - major depressive disorder (mdd) - obsessive-compulsive disorder (ocd) - panic disorder (pd) - posttraumatic stress disorder (ptsd) - social anxiety disorder (sad) - premenstrual dysphoric disorder (pmdd) sertraline hydrochloride is contraindicated in patients: - taking, or within 14 days of stopping, maois, (including the maois linezolid and intravenous methylene blue) because of an increased risk of serotonin syndrome [see warnings and precautions (5.2), drug interactions (7.1)] . - taking pimozide [see drug interactions (7.1)] . - with known hypersensitivity to sertraline (e.g., anaphylaxis, angioedema) [see adverse reactions (6.1, 6.2)]. in addition to the contraindications for all sertraline hydrochloride formulations listed above, sertraline hydrochloride oral solution is contraindicated in patients: - taking disulfiram. sertraline hydrochloride oral solution contains alcohol, and concomi