Irland - Englisch - HPRA (Health Products Regulatory Authority)

sp veterinaria, s.a. - enrofloxacin - oral solution - 100 milligram(s)/millilitre - enrofloxacin - chickens, turkeys - antibacterial

Irland - Englisch - HPRA (Health Products Regulatory Authority)

sp veterinaria, s.a. - enrofloxacin - oral solution - 100 mg/ml - enrofloxacin - fowl - chicken, fowl - turkey - antibacterial

Belgien - Englisch - AFMPS (Agence Fédérale des Médicaments et des Produits de Santé)

kela laboratoria sa-nv - enrofloxacin 100 mg/ml - solution for use in drinking water - 100 mg/ml - enrofloxacin 100 mg/ml - enrofloxacin - poultry

Vereinigte Staaten - Englisch - NLM (National Library of Medicine)

organon llc - alendronate sodium (unii: 2uy4m2u3ra) (alendronic acid - unii:x1j18r4w8p), cholecalciferol (unii: 1c6v77qf41) (cholecalciferol - unii:1c6v77qf41) - fosamax® plus d is indicated for the treatment of osteoporosis in postmenopausal women. in postmenopausal women, fosamax plus d increases bone mass and reduces the incidence of fractures, including those of the hip and spine (vertebral compression fractures). [see clinical studies (14.1).] fosamax plus d is indicated for treatment to increase bone mass in men with osteoporosis [see clinical studies (14.2)]. fosamax plus d alone should not be used to treat vitamin d deficiency. the optimal duration of use has not been determined. the safety and effectiveness of fosamax plus d for the treatment of osteoporosis are based on clinical data of four 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. fosamax plus d 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 (2.3), warnings and precautions (5.1)] - hypocalcemia [see warnings and precautions (5.2)] - hypersensitivity to any component of this product. hypersensitivity reactions including urticaria and angioedema have been reported [see adverse reactions (6.2)]. risk summary available data on the use of fosamax plus vitamin d use in pregnant women are insufficient to inform a drug-associated risk of adverse maternal or fetal outcomes. discontinue fosamax plus d when pregnancy is recognized. alendronate sodium in animal reproduction studies, daily oral administration of alendronate to rats from before mating through the end of gestation or lactation showed decreased postimplantation survival and decreased pup body weight gain starting at doses equivalent to less than half of the highest recommended 40 mg clinical daily dose (based on body surface area, mg/m2 ). oral administration of alendronate to rats during organogenesis resulted in reduced fetal ossification starting at doses 3 times the 40 mg clinical daily dose. no similar fetal effects were observed in pregnant rabbits dosed orally during organogenesis at doses equivalent to approximately 10 times the 40 mg clinical daily dose. delayed or failed delivery of offspring, protracted parturition, and late pregnancy maternal and fetal deaths due to maternal hypocalcemia occurred in rats at oral doses as low as one tenth the 40 mg clinical daily dose (see data). 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 the risk has not been studied. cholecalciferol no data are available for cholecalciferol (vitamin d3 ) in animals. however, administration of high doses of vitamin d2 to pregnant rabbits resulted in abortions and an increased incidence of fetal aortic stenosis. administration of high doses of vitamin d2 to pregnant rats resulted in neonatal death, decreased fetal weight, and impaired osteogenesis of long bones postnatally. (see data.) 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 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 alendronate sodium reproduction studies in rats dosed orally from before mating to the end of gestation or lactation showed decreased postimplantation survival starting at 2 mg/kg/day and decreased body weight gain starting at 1 mg/kg/day, doses equivalent to less than half the 40 mg clinical daily dose based on body surface area, mg/m2 . incidence of incomplete fetal ossification in vertebral, skull, and sternebral bones were increased in rats dosed orally during organogenesis starting at 10 mg/kg/day (approximately 3 times the 40 mg clinical daily dose). no similar fetal effects were observed in pregnant rabbits dosed orally during organogenesis at up to 35 mg/kg/day (equivalent to approximately 10 times the 40 mg clinical daily dose). both total and ionized calcium decreased in pregnant rats dosed orally with 15 mg/kg/day alendronate (approximately 4 times the 40 mg clinical daily dose) resulting in delays and failures of delivery. protracted parturition due to maternal hypocalcemia was observed when rats were treated from before mating through gestation starting at 0.5 mg/kg/day (approximately one tenth the 40 mg clinical daily dose). maternotoxicity (late pregnancy deaths) also occurred in female rats treated orally with 15 mg/kg/day (approximately 4 times the 40 mg clinical daily dose) for varying gestational time periods. these maternal deaths were lessened but not eliminated by cessation of treatment. calcium supplementation in the drinking water or by subcutaneous minipump to rats dosed orally with 15 mg/kg/day alendronate could not ameliorate the hypocalcemia or prevent the dystocia-related maternal and neonatal deaths. however, intravenous calcium supplementation prevented maternal, but not neonatal deaths. administration of high doses (greater than or equal to 10,000 international units/every other day during pregnancy) of ergocalciferol (vitamin d2 ) to pregnant rabbits resulted in abortions and an increased incidence of fetal aortic stenosis. administration of vitamin d2 (40,000 international units/day) to pregnant rats from gestation day 10 to 21 (organogenesis) resulted in neonatal death, decreased fetal weight, and impaired osteogenesis of long bones postnatally. risk summary cholecalciferol and some of its active metabolites pass into breast milk. it is not known whether alendronate is present in human breast milk, affects human milk production, or has effects on the breastfed infant. the developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for fosamax plus d and any potential adverse effects on the breastfed child from fosamax plus d or from the underlying maternal condition. fosamax plus d is not indicated for use in pediatric patients. the safety and efficacy of alendronate were examined in a randomized, double-blind, placebo-controlled two-year study of 139 pediatric patients, aged 4-18 years, with severe osteogenesis imperfecta (oi). one-hundred-and-nine patients were randomized to 5 mg alendronate daily (weight less than 40 kg) or 10 mg alendronate daily (weight greater than or equal to 40 kg) and 30 patients to placebo. the mean baseline lumbar spine bmd z-score of the patients was -4.5. the mean change in lumbar spine bmd z-score from baseline to month 24 was 1.3 in the alendronate-treated patients and 0.1 in the placebo-treated patients. treatment with alendronate did not reduce the risk of fracture. sixteen percent of the alendronate patients who sustained a radiologically-confirmed fracture by month 12 of the study had delayed fracture healing (callus remodeling) or fracture non-union when assessed radiographically at month 24 compared with 9% of the placebo-treated patients. in alendronate-treated patients, bone histomorphometry data obtained at month 24 demonstrated decreased bone turnover and delayed mineralization time; however, there were no mineralization defects. there were no statistically significant differences between the alendronate and placebo groups in reduction of bone pain. the oral bioavailability of alendronate in children was similar to that observed in adults. of the patients receiving fosamax in the fracture intervention trial (fit), 71% (n=2302) were greater than or equal to 65 years of age and 17% (n=550) were greater than or equal to 75 years of age. of the patients receiving fosamax in the united states and multinational osteoporosis treatment studies in women, and osteoporosis studies in men [see clinical studies (14.1, 14.2)] , 45% and 54%, respectively, were 65 years of age or over. no overall differences in efficacy or safety were observed between these patients and younger patients, but greater sensitivity of some older individuals cannot be ruled out. dietary requirements of vitamin d3 are increased in the elderly. fosamax plus d is not recommended for patients with creatinine clearance less than 35 ml/min. no dosage adjustment is necessary in patients with creatinine clearance values between 35-60 ml/min [see clinical pharmacology (12.3)] . alendronate sodium as there is evidence that alendronate is not metabolized or excreted in the bile, no studies were conducted in patients with hepatic impairment. no dosage adjustment is necessary [see clinical pharmacology (12.3)] . cholecalciferol vitamin d3 may not be adequately absorbed in patients who have malabsorption due to inadequate bile production.

Vereinigte Staaten - Englisch - NLM (National Library of Medicine)

organon llc - alendronate sodium (unii: 2uy4m2u3ra) (alendronic acid - unii:x1j18r4w8p) - fosamax® is indicated for the treatment of osteoporosis in postmenopausal women. in postmenopausal women, fosamax increases bone mass and reduces the incidence of fractures, including those of the hip and spine (vertebral compression fractures). [see clinical studies (14.1).] fosamax is indicated for the prevention of postmenopausal osteoporosis [see clinical studies (14.2)]. fosamax is indicated for treatment to increase bone mass in men with osteoporosis [see clinical studies (14.3)] . fosamax is indicated for the treatment of glucocorticoid-induced osteoporosis in men and women receiving glucocorticoids in a daily dosage equivalent to 7.5 mg or greater of prednisone and who have low bone mineral density [see clinical studies (14.4)]. fosamax is indicated for the treatment of paget's disease of bone in men and women. treatment is indicated in patients with paget's disease of bone who have alkaline phosphatase at least two times the upper limit of normal, or those who are symptomatic, or those at risk for future complications from their disease. [see clinical studies (14.5).] the optimal duration of use has not been determined. the safety and effectiveness of fosamax for the treatment of osteoporosis are based on clinical data of four 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. fosamax 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 (2.6); warnings and precautions (5.1)] - do not administer fosamax oral solution to patients at increased risk of aspiration. - hypocalcemia [see warnings and precautions (5.2)] - hypersensitivity to any component of this product. hypersensitivity reactions including urticaria and angioedema have been reported [see adverse reactions (6.2)] . risk summary available data on the use of fosamax in pregnant women are insufficient to inform a drug-associated risk of adverse maternal or fetal outcomes. discontinue fosamax when pregnancy is recognized. in animal reproduction studies, daily oral administration of alendronate to rats from before mating through the end of gestation or lactation showed decreased postimplantation survival and decreased pup body weight gain starting at doses equivalent to less than half of the highest recommended 40 mg clinical daily dose (based on body surface area, mg/m2 ). oral administration of alendronate to rats during organogenesis resulted in reduced fetal ossification starting at doses 3 times the 40 mg clinical daily dose. no similar fetal effects were observed in pregnant rabbits dosed orally during organogenesis at doses equivalent to approximately 10 times the 40 mg clinical daily dose. delayed or failed delivery of offspring, protracted parturition, and late pregnancy maternal and fetal deaths due to maternal hypocalcemia occurred in rats at oral doses as low as one tenth the 40 mg clinical daily dose (see data). 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 the risk has not been studied. 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 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 reproduction studies in rats dosed orally from before mating to the end of gestation or lactation showed decreased postimplantation survival starting at 2 mg/kg/day and decreased body weight gain starting at 1 mg/kg/day, doses equivalent to less than half the 40 mg clinical daily dose based on body surface area, mg/m2 . incidence of incomplete fetal ossification in vertebral, skull, and sternebral bones were increased in rats dosed orally during organogenesis starting at 10 mg/kg/day (approximately 3 times the 40 mg clinical daily dose). no similar fetal effects were observed in pregnant rabbits dosed orally during organogenesis at up to 35 mg/kg/day (equivalent to approximately 10 times the 40 mg clinical daily dose). both total and ionized calcium decreased in pregnant rats dosed orally with 15 mg/kg/day alendronate (approximately 4 times the 40 mg clinical daily dose) resulting in delays and failures of delivery. protracted parturition due to maternal hypocalcemia was observed when rats were treated from before mating through gestation starting at 0.5 mg/kg/day (approximately one tenth the 40 mg clinical daily dose). maternotoxicity (late pregnancy deaths) also occurred in female rats treated orally with 15 mg/kg/day (approximately 4 times the 40 mg clinical daily dose) for varying gestational time periods. these maternal deaths were lessened but not eliminated by cessation of treatment. calcium supplementation in the drinking water or by subcutaneous minipump to rats dosed orally with 15 mg/kg/day alendronate could not ameliorate the hypocalcemia or prevent the dystocia-related maternal and neonatal deaths. however, intravenous calcium supplementation prevented maternal, but not neonatal deaths. risk summary it is not known whether alendronate is present in human breast milk, affects human milk production, or has effects on the breastfed infant. the developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for fosamax and any potential adverse effects on the breastfed child from fosamax or from the underlying maternal condition. fosamax is not indicated for use in pediatric patients. the safety and efficacy of fosamax were examined in a randomized, double-blind, placebo-controlled two-year study of 139 pediatric patients, aged 4-18 years, with severe osteogenesis imperfecta (oi). one-hundred-and-nine patients were randomized to 5 mg fosamax daily (weight less than 40 kg) or 10 mg fosamax daily (weight greater than or equal to 40 kg) and 30 patients to placebo. the mean baseline lumbar spine bmd z-score of the patients was -4.5. the mean change in lumbar spine bmd z-score from baseline to month 24 was 1.3 in the fosamax-treated patients and 0.1 in the placebo-treated patients. treatment with fosamax did not reduce the risk of fracture. sixteen percent of the fosamax patients who sustained a radiologically-confirmed fracture by month 12 of the study had delayed fracture healing (callus remodeling) or fracture non-union when assessed radiographically at month 24 compared with 9% of the placebo-treated patients. in fosamax-treated patients, bone histomorphometry data obtained at month 24 demonstrated decreased bone turnover and delayed mineralization time; however, there were no mineralization defects. there were no statistically significant differences between the fosamax and placebo groups in reduction of bone pain. the oral bioavailability in children was similar to that observed in adults. the overall safety profile of fosamax in osteogenesis imperfecta patients treated for up to 24 months was generally similar to that of adults with osteoporosis treated with fosamax. however, there was an increased occurrence of vomiting in osteogenesis imperfecta patients treated with fosamax compared to placebo. during the 24-month treatment period, vomiting was observed in 32 of 109 (29.4%) patients treated with fosamax and 3 of 30 (10%) patients treated with placebo. in a pharmacokinetic study, 6 of 24 pediatric osteogenesis imperfecta patients who received a single oral dose of fosamax 35 or 70 mg developed fever, flu-like symptoms, and/or mild lymphocytopenia within 24 to 48 hours after administration. these events, lasting no more than 2 to 3 days and responding to acetaminophen, are consistent with an acute-phase response that has been reported in patients receiving bisphosphonates, including fosamax. [see adverse reactions (6.2).] of the patients receiving fosamax in the fracture intervention trial (fit), 71% (n=2302) were greater than or equal to 65 years of age and 17% (n=550) were greater than or equal to 75 years of age. of the patients receiving fosamax in the united states and multinational osteoporosis treatment studies in women, osteoporosis studies in men, glucocorticoid-induced osteoporosis studies, and paget's disease studies [see clinical studies (14.1), (14.3), (14.4), (14.5)], 45%, 54%, 37%, and 70%, respectively, were 65 years of age or over. no overall differences in efficacy or safety were observed between these patients and younger patients, but greater sensitivity of some older individuals cannot be ruled out. fosamax is not recommended for patients with creatinine clearance less than 35 ml/min. no dosage adjustment is necessary in patients with creatinine clearance values between 35-60 ml/min [see clinical pharmacology (12.3)] . as there is evidence that alendronate is not metabolized or excreted in the bile, no studies were conducted in patients with hepatic impairment. no dosage adjustment is necessary [see clinical pharmacology (12.3)] .

Vereinigte Staaten - Englisch - NLM (National Library of Medicine)

merck sharp & dohme corp. - alendronate sodium (unii: 2uy4m2u3ra) (alendronic acid - unii:x1j18r4w8p) - alendronic acid 70 mg - fosamax® is indicated for the treatment of osteoporosis in postmenopausal women. in postmenopausal women, fosamax increases bone mass and reduces the incidence of fractures, including those of the hip and spine (vertebral compression fractures). [see clinical studies (14.1).] fosamax is indicated for the prevention of postmenopausal osteoporosis [see clinical studies (14.2)]. fosamax is indicated for treatment to increase bone mass in men with osteoporosis [see clinical studies (14.3)] . fosamax is indicated for the treatment of glucocorticoid-induced osteoporosis in men and women receiving glucocorticoids in a daily dosage equivalent to 7.5 mg or greater of prednisone and who have low bone mineral density [see clinical studies (14.4)]. fosamax is indicated for the treatment of paget's disease of bone in men and women. treatment is indicated in patients with paget's disease of bone who have alkaline phosphatase at least two times the upper limit of normal, or those who are symptomatic, or those at risk for f

Vereinigte Staaten - Englisch - NLM (National Library of Medicine)

merck sharp & dohme corp. - alendronate sodium (unii: 2uy4m2u3ra) (alendronic acid - unii:x1j18r4w8p), cholecalciferol (unii: 1c6v77qf41) (cholecalciferol - unii:1c6v77qf41) - alendronic acid 70 mg - fosamax® plus d is indicated for the treatment of osteoporosis in postmenopausal women. in postmenopausal women, fosamax plus d increases bone mass and reduces the incidence of fractures, including those of the hip and spine (vertebral compression fractures). [see clinical studies (14.1).] fosamax plus d is indicated for treatment to increase bone mass in men with osteoporosis [see clinical studies (14.2)]. fosamax plus d alone should not be used to treat vitamin d deficiency. the optimal duration of use has not been determined. the safety and effectiveness of fosamax plus d for the treatment of osteoporosis are based on clinical data of four 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. fosamax plus d is contraindicated in

Vereinigte Staaten - Englisch - NLM (National Library of Medicine)

physicians total care, inc. - alendronate sodium (unii: 2uy4m2u3ra) (alendronic acid - unii:x1j18r4w8p), cholecalciferol (unii: 1c6v77qf41) (cholecalciferol - unii:1c6v77qf41) - alendronic acid 70 mg - fosamax® plus d is indicated for: for the treatment of osteoporosis, fosamax plus d increases bone mass and reduces the incidence of fractures, including those of the hip and spine (vertebral compression fractures). fosamax plus d alone should not be used to treat vitamin d deficiency. the safety and effectiveness of fosamax plus d for the treatment of osteoporosis are based on clinical data of four years duration. the optimal duration of use has not been determined. all patients on bisphosphonate therapy should have the need for continued therapy re-evaluated on a periodic basis. - 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 (2.3), warnings and precautions (5.1)] - hypocalcemia [see warnings and precautions (5.2)] - hypersensitivity to any component of this product. hypersensitivity reactions including urticaria and angioedema have

Vereinigte Staaten - Englisch - NLM (National Library of Medicine)

physicians total care, inc. - alendronate sodium (unii: 2uy4m2u3ra) (alendronic acid - unii:x1j18r4w8p) - alendronate sodium 5 mg - fosamax is indicated for: - treatment and prevention of osteoporosis in postmenopausal women for the treatment of osteoporosis, fosamax increases bone mass and reduces the incidence of fractures, including those of the hip and spine (vertebral compression fractures). osteoporosis may be confirmed by the finding of low bone mass (for example, at least 2 standard deviations below the premenopausal mean) or by the presence or history of osteoporotic fracture. (see clinical pharmacology, pharmacodynamics.) for the prevention of osteoporosis, fosamax may be considered in postmenopausal women who are at risk of developing osteoporosis and for whom the desired clinical outcome is to maintain bone mass and to reduce the risk of future fracture. bone loss is particularly rapid in postmenopausal women younger than age 60. risk factors often associated with the development of postmenopausal osteoporosis include early menopause; moderately low bone mass (for example, at least 1 standard deviatio

Australien - Englisch - Department of Health (Therapeutic Goods Administration)

organon pharma pty ltd - alendronate sodium, quantity: 91.37 mg (equivalent: alendronic acid, qty 70 mg); colecalciferol, quantity: 0.1387 mg - tablet, uncoated - excipient ingredients: magnesium stearate; colloidal anhydrous silica; microcrystalline cellulose; lactose; croscarmellose sodium; purified water; gelatin; aluminium starch octenylsuccinate; aluminium sodium silicate; sucrose; medium chain triglycerides - the treatment of osteoporosis in select patients where vitamin d supplementation is recommended.