Соединенные Штаты - английский - NLM (National Library of Medicine)

preferred pharmaceuticals inc. - alendronate sodium (unii: 2uy4m2u3ra) (alendronic acid - unii:x1j18r4w8p) - alendronate sodium tablets, usp are indicated for the treatment of osteoporosis in postmenopausal women. in postmenopausal women, alendronate sodium tablets, usp increases bone mass and reduces the incidence of fractures, including those of the hip and spine (vertebral compression fractures). [see clinical studies (14.1).] alendronate sodium tablets, usp are indicated for the prevention of postmenopausal osteoporosis [see clinical studies (14.2)]. alendronate sodium tablets, usp are indicated for treatment to increase bone mass in men with osteoporosis [see clinical studies (14.3)]. alendronate sodium tablets, usp are 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)]. alendronate sodium tablets, usp are 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 alendronate sodium 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. alendronate sodium tablets are contraindicated in patients with the following conditions: risk summary available data on the use of alendronate sodium in pregnant women are insufficient to inform a drug-associated risk of adverse maternal or fetal outcomes. discontinue alendronate sodium 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 the 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 alendronate sodium and any potential adverse effects on the breastfed child from alendronate sodium or from the underlying maternal condition. alendronate sodium is not indicated for use in pediatric patients. the safety and efficacy of alendronate sodium 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 sodium daily (weight less than 40 kg) or 10 mg alendronate sodium 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 sodium-treated patients and 0.1 in the placebo-treated patients. treatment with alendronate sodium did not reduce the risk of fracture. sixteen percent of the alendronate sodium 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 sodium-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 sodium 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 alendronate sodium in osteogenesis imperfecta patients treated for up to 24 months was generally similar to that of adults with osteoporosis treated with alendronate sodium. however, there was an increased occurrence of vomiting in osteogenesis imperfecta patients treated with alendronate sodium compared to placebo. during the 24-month treatment period, vomiting was observed in 32 of 109 (29.4%) patients treated with alendronate sodium 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 alendronate sodium 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 alendronate sodium. [see adverse reactions (6.2).] of the patients receiving alendronate sodium 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 alendronate sodium 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. alendronate sodium 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)] .

Соединенные Штаты - английский - NLM (National Library of Medicine)

nucare pharmaceuticals,inc. - alendronate sodium (unii: 2uy4m2u3ra) (alendronic acid - unii:x1j18r4w8p) - alendronate sodium tablets are indicated for the treatment of osteoporosis in postmenopausal women. in postmenopausal women, alendronate sodium tablets increase bone mass and reduce the incidence of fractures, including those of the hip and spine (vertebral compression fractures). [see clinical studies (14.1).] alendronate sodium tablets are indicated for the prevention of postmenopausal osteoporosis [see clinical studies (14.2)] . alendronate sodium tablets are indicated for treatment to increase bone mass in men with osteoporosis [see clinical studies (14.3)] . alendronate sodium tablets are 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)] . al

Соединенные Штаты - английский - NLM (National Library of Medicine)

twi pharmaceuticals, inc. - testosterone (unii: 3xmk78s47o) (testosterone - unii:3xmk78s47o) - warning: secondary exposure to testosterone see full prescribing information for complete boxed warning. - virilization has been reported in children who were secondarily exposed to testosterone gel (5.2, 6.2). - children should avoid contact with unwashed or unclothed application sites in men using testosterone gel (2.2, 5.2). - healthcare providers should advise patients to strictly adhere to recommended instructions for use (2.2, 5.2, 17). - testosterone gel 1.62% is contraindicated in men with carcinoma of the breast or known or suspected carcinoma of the prostate [see warnings and precautions (5.1) and adverse reactions (6.1)]. - testosterone gel 1.62% is contraindicated in women who are pregnant. testosterone gel 1.62% can cause virilization of the female fetus when administered to a pregnant woman. pregnant women need to be aware of the potential for transfer of testosterone from men treated with testosterone gel 1.62%. if a pregnant woman is exposed to testosterone gel 1.62%, she should be apprised of the potential hazard to the fetus [see warnings and precautions (5.2) and use in specific populations (8.1)] . risk summary testosterone gel 1.62% is contraindicated in pregnant women. testosterone is teratogenic and may cause fetal harm when administered to a pregnant woman based on data from animal studies and its mechanism of action [see contraindications (4) and clinical pharmacology (12.1)] . exposure of a female fetus to androgens may result in varying degrees of virilization. in animal developmental studies, exposure to testosterone in utero resulted in hormonal and behavioral changes in offspring and structural impairments of reproductive tissues in female and male offspring. these studies did not meet current standards for nonclinical development toxicity studies. data animal data in developmental studies conducted in rats, rabbits, pigs, sheep and rhesus monkeys, pregnant animals received intramuscular injection of testosterone during the period of organogenesis. testosterone treatment at doses that were comparable to those used for testosterone replacement therapy resulted in structural impairments in both female and male offspring. structural impairments observed in females included increased ano-genital distance, phallus development, empty scrotum, no external vagina, intrauterine growth retardation, reduced ovarian reserve, and increased ovarian follicular recruitment. structural impairments seen in male offspring included increased testicular weight, larger seminal tubular lumen diameter, and higher frequency of occluded tubule lumen. increased pituitary weight was seen in both sexes. testosterone exposure in utero also resulted in hormonal and behavioral changes in offspring. hypertension was observed in pregnant female rats and their offspring exposed to doses approximately twice those used for testosterone replacement therapy. risk summary androgel 1.62% is not indicated for use in women. infertility testis disorder, testicular atrophy, and oligospermia have been identified during use of androgel 1.62% [see adverse reactions (6.1, 6.2)] . during treatment with large doses of exogenous androgens, including androgel 1.62%, spermatogenesis may be suppressed through feedback inhibition of the hypothalamic-pituitary-testicular axis [see warnings and precautions (5.8)] . reduced fertility is observed in some men taking testosterone replacement therapy. testicular atrophy, subfertility, and infertility have also been reported in men who abuse anabolic androgenic steroids [see drug abuse and dependence (9.2)] . with either type of use, the impact on fertility may be irreversible. the safety and effectiveness of testosterone gel 1.62% in pediatric patients less than 18 years old has not been established. improper use may result in acceleration of bone age and premature closure of epiphyses. there have not been sufficient numbers of geriatric patients involved in controlled clinical studies utilizing testosterone gel 1.62% to determine whether efficacy in those over 65 years of age differs from younger subjects. of the 234 patients enrolled in the clinical trial utilizing testosterone gel 1.62%, 21 were over 65 years of age. additionally, there is insufficient long-term safety data in geriatric patients to assess the potentially increased risks of cardiovascular disease and prostate cancer. geriatric patients treated with androgens may also be at risk for worsening of signs and symptoms of bph. no studies were conducted involving patients with renal impairment. no studies were conducted in patients with hepatic impairment. testosterone gel 1.62% contains testosterone, a schedule iii controlled substance in the controlled substances act. drug abuse is intentional non-therapeutic use of a drug, even once, for its rewarding psychological and physiological effects. abuse and misuse of testosterone are seen in male and female adults and adolescents. testosterone, often in combination with other anabolic androgenic steroids (aas), and not obtained by prescription through a pharmacy, may be abused by athletes and bodybuilders. there have been reports of misuse by men taking higher doses of legally obtained testosterone than prescribed and continuing testosterone despite adverse events or against medical advice. serious adverse reactions have been reported in individuals who abuse anabolic androgenic steroids and include cardiac arrest, myocardial infarction, hypertrophic cardiomyopathy, congestive heart failure, cerebrovascular accident, hepatotoxicity, and serious psychiatric manifestations, including major depression, mania, paranoia, psychosis, delusions, hallucinations, hostility and aggression. the following adverse reactions have also been reported in men: transient ischemic attacks, convulsions, hypomania, irritability, dyslipidemias, testicular atrophy, subfertility, and infertility. the following additional adverse reactions have been reported in women: hirsutism, virilization, deepening of voice, clitoral enlargement, breast atrophy, male-pattern baldness, and menstrual irregularities. the following adverse reactions have been reported in male and female adolescents: premature closure of bony epiphyses with termination of growth, and precocious puberty. because these reactions are reported voluntarily from a population of uncertain size and may include abuse of other agents, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure. continued abuse of testosterone and other anabolic steroids, leading to addiction is characterized by the following behaviors: - taking greater dosages than prescribed - continued drug use despite medical and social problems due to drug use - spending significant time to obtain the drug when supplies of the drug are interrupted - giving a higher priority to drug use than other obligations - having difficulty in discontinuing the drug despite desires and attempts to do so - experiencing withdrawal symptoms upon abrupt discontinuation of use physical dependence is characterized by withdrawal symptoms after abrupt drug discontinuation or a significant dose reduction of a drug. individuals taking supratherapeutic doses of testosterone may experience withdrawal symptoms lasting for weeks or months which include depressed mood, major depression, fatigue, craving, restlessness, irritability, anorexia, insomnia, decreased libido and hypogonadotropic hypogonadism. drug dependence in individuals using approved doses of testosterone for approved indications has not been documented. instruction for use testosterone (tes-tos-ter-one) gel ciii 1.62% for topical use read this instructions for use for testosterone gel 1.62% before you start using it and each time you get a refill. there may be new information. this leaflet does not take the place of talking to your healthcare provider about your medical condition or treatment. applying testosterone gel 1.62%: - testosterone gel 1.62% comes in a pump. - before applying testosterone gel 1.62% make sure that your shoulders and upper arms are clean, dry, and that there is no broken skin. - testosterone gel 1.62% is to be applied to the area of your shoulders and upper arms that will be covered by a short sleeve t-shirt (see figure a). do not apply testosterone gel 1.62% to any other parts of your body such as your stomach area (abdomen), penis, scrotum, chest, armpits (axillae), or knees. (figure a) if you are using testosterone gel 1.62% pump: - before using a new bottle of testosterone gel 1.62 % for the first time, you will need to remove the cap and then prime the pump. to prime the testosterone gel 1.62% pump, slowly push the pump all the way down 3 times, over the sink drain. do not use any testosterone gel 1.62% that came out while priming. wash it down the sink to avoid accidental exposure to others. your testosterone gel 1.62% pump is now ready to use. - remove the cap from the pump. then, put the spout opening at the top of the pump where the medicine comes out over the palm of your hand and slowly push the pump all the way down. apply testosterone gel 1.62% to the application site. you may also apply testosterone gel 1.62% directly to the application site. your healthcare provider will tell you the number of times to press the pump for each dose. - wash your hands with soap and water right away. find your dose as prescribed by your healthcare provider how should i store testosterone gel 1.62%? - store testosterone gel 1.62% at room temperature between 59ºf to 86ºf (15ºc to 30ºc). - when it is time to throw away the pump, safely throw away used testosterone gel 1.62% in household trash. be careful to prevent accidental exposure of children or pets. - keep testosterone gel 1.62% away from fire. keep testosterone gel 1.62% and all medicines out of the reach of children. this instructions for use has been approved by the u.s. food and drug administration manufactured for: twi pharmaceuticals usa, inc. paramus, nj 07652 manufactured by: twi pharmaceuticals, inc. taoyuan city, 32063, taiwan revised: 07/22

Соединенные Штаты - английский - NLM (National Library of Medicine)

marlex pharmaceuticals inc - alendronate sodium (unii: 2uy4m2u3ra) (alendronic acid - unii:x1j18r4w8p) - alendronate sodium tablets are indicated for the treatment of osteoporosis in postmenopausal women. in postmenopausal women, alendronate sodium tablets increase bone mass and reduce the incidence of fractures, including those of the hip and spine (vertebral compression fractures). [see clinical studies ( 14.1 ).] alendronate sodium tablets are indicated for the prevention of postmenopausal osteoporosis [see clinical studies ( 14.2 )] . alendronate sodium tablets are indicated for treatment to increase bone mass in men with osteoporosis [ see clinical studies ( 14.3 )] . alendronate sodium tablets are 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 )] . alendronate sodium tablets are 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

Соединенные Штаты - английский - NLM (National Library of Medicine)

pd-rx pharmaceuticals, inc. - citalopram hydrobromide (unii: i1e9d14f36) (citalopram - unii:0dhu5b8d6v) - citalopram tablets are indicated for the treatment of major depressive disorder (mdd) in adults [see clinical studies ( 14)] . citalopram tablets are contraindicated in patients: • taking, or within 14 days of stopping, maois (including maois such as linezolid or intravenous methylene blue) because of an increased risk of serotonin syndrome [see warnings and precautions ( 5.3), drug interactions ( 7)] . • taking pimozide because of risk of qt prolongation [see drug interactions ( 7)] . • with known hypersensitivity to citalopram or any of the inactive ingredients in citalopram tablets. reactions have included angioedema and anaphylaxis [see adverse reactions ( 6.2)] . pregnancy exposure registry there is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to antidepressants during pregnancy. healthcare providers are encouraged to register patients by calling the national pregnancy registry for antidepressants at 1-844-405-6185 or visiting online at https://womensmentalhealth.org/research/pregnancyregistry/antidepressants . risk summary based on data from published observational studies, exposure to ssris, particularly in the month before delivery, has been associated with a less than 2-fold increase in the risk of postpartum hemorrhage [see warnings and precautions ( 5.4) and clinical considerations] . available data from published epidemiologic studies and postmarketing reports with citalopram use in pregnancy have not established an increased risk of major birth defects or miscarriage. published studies demonstrated that citalopram levels in both cord blood and amniotic fluid are similar to those observed in maternal serum. there are risks of persistent pulmonary hypertension of the newborn (pphn) (see data) and/or poor neonatal adaptation with exposure to selective serotonin reuptake inhibitors (ssris), including citalopram, during pregnancy . there also are risks associated with untreated depression in pregnancy (see clinical considerations) . in animal reproduction studies, citalopram caused adverse embryo/fetal effects at doses that caused maternal toxicity (see data) . the estimated background risk of major birth defects and miscarriage for the indicated population is unknown. all pregnancies have a background risk of birth defect, loss, or other adverse outcomes. in the u.s. general population, the estimated background risk of major birth defects and miscarriage in the clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively. clinical considerations disease-associated maternal and/or embryo/fetal risk women who discontinue antidepressants during pregnancy are more likely to experience a relapse of major depression than women who continue antidepressants. this finding is from a prospective longitudinal study of 201 pregnant women with a history of major depressive disorder who were euthymic and taking antidepressants at the beginning of pregnancy. consider the risk of untreated depression when discontinuing or changing treatment with antidepressant medication during pregnancy and postpartum. maternal adverse reactions use of citalopram tablet in the month before delivery may be associated with an increased risk of postpartum hemorrhage [see warnings and precautions ( 5.4)] . fetal/neonatal adverse reactions neonates exposed to citalopram and other ssris late in third trimester have developed complications requiring prolonged hospitalization, respiratory support, and tube feeding. such complications can arise immediately upon delivery. reported clinical findings have included respiratory distress, cyanosis, apnea, seizures, temperature instability, feeding difficulty, vomiting, hypoglycemia, hypotonia, hypertonia, hyperreflexia, tremor, jitteriness, irritability, and constant crying. these findings are consistent with either a direct toxic effect of ssris or possibly, a drug discontinuation syndrome. it should be noted that, in some cases, the clinical picture is consistent with serotonin syndrome [see warnings and precautions ( 5.3)] . data human data exposure during late pregnancy to ssris may have an increased risk for persistent pulmonary hypertension of the newborn (pphn). pphn occurs in 1- 2 per 1,000 live births in the general population and is associated with substantial neonatal morbidity and mortality. animal data citalopram was administered orally to pregnant rats during the period of organogenesis at doses of 32, 56, and 112 mg/kg/day, which are approximately 8, 14, and 27 times the maximum recommended human dose (mrhd) of 40 mg, based on mg/m 2 body surface area. citalopram caused maternal toxicity of cns clinical signs and decreased weight gain at 112 mg/kg/day, which is 27 times the mrhd. at this maternally toxic dose, citalopram decreased embryo/fetal growth and survival and increased fetal abnormalities (including cardiovascular and skeletal defects). the no observed adverse effect level (noael) for maternal and embryofetal toxicity is 56 mg/kg/day, which is approximately 14 times the mrhd. citalopram was administered orally to pregnant rabbits during the period of organogenesis at doses up to 16 mg/kg/day, which is approximately 8 times the mrhd of 40 mg, based on mg/m 2 body surface area. no maternal or embryofetal toxicity was observed. the noael for maternal and embryofetal toxicity is 16 mg/kg/day, which is approximately 8 times the mrhd. citalopram was administered orally to pregnant rats during late gestation and lactation periods at doses of 4.8, 12.8, and 32 mg/kg/day, which are approximately 1, 3, and 8 times the mrhd of 40 mg, based on mg/m 2 body surface area. citalopram increased offspring mortality during the first 4 days of birth and decreased offspring growth at 32 mg/kg/day, which is approximately 8 times the mrhd. the noael for developmental toxicity is 12.8 mg/kg/day, which is approximately 3 times the mrhd. in a separate study, similar effects on offspring mortality and growth were seen when dams were treated throughout gestation and early lactation at doses ≥ 24 mg/kg/day, which is approximately 6 times the mrhd. a noael was not determined in that study. risk summary data from the published literature report the presence of citalopram in human milk at relative infant doses ranging between 0.7 to 9.4% of the maternal weight-adjusted dosage and a milk/plasma ratio ranging between 0.78 to 4.3. there are reports of breastfed infants exposed to citalopram experiencing irritability, restlessness, excessive somnolence, decreased feeding, and weight loss (see clinical considerations). there is no information about effects of citalopram on milk production. the developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for citalopram and any potential adverse effects on the breastfed child from citalopram or from the underlying maternal condition. clinical considerations monitor breastfeeding infants for adverse reactions, such as irritability, restlessness, excessive somnolence, decreased feeding, and weight loss. the safety and effectiveness of citalopram have not been established in pediatric patients. two placebo-controlled trials in 407 pediatric patients with mdd have been conducted with citalopram, and the data were not sufficient to support use in pediatric patients. antidepressants increase the risk of suicidal thoughts and behaviors in pediatric patients [see boxed warning, warnings  and precautions ( 5.1)] . decreased appetite and weight loss have been observed in association with the use of ssris in pediatric patients. of 4,422 patients in clinical studies of citalopram, 1,357 were 60 and over, 1,034 were 65 and over, and 457 were 75 and over. in two pharmacokinetic studies, citalopram auc was increased by 23% and 30%, respectively, in subjects ≥ 60 years of age as compared to younger subjects, and its half-life was increased by 30% and 50%, respectively [see clinical pharmacology ( 12.3)] . therefore, the maximum recommended dosage in patients 60 years of age and older is lower than younger patients [see dosage and administration ( 2.3), warnings and precautions ( 5.2)] . ssris, including citalopram, have been associated with cases of clinically significant hyponatremia in elderly patients, who may be at greater risk for this adverse reaction [see warnings and precautions ( 5.9)] . increased citalopram exposure occurs in patients with hepatic impairment. the maximum recommended dosage of citalopram is lower in patients with hepatic impairment [see dosage and administration ( 2.3), clinical pharmacology ( 12.3)]. citalopram (citalopram hbr) is not a controlled substance. animal studies suggest that the abuse liability of citalopram is low. citalopram has not been systematically studied in humans for its potential for abuse, tolerance, or physical dependence. the premarketing clinical experience with citalopram did not reveal any drug-seeking behavior. however, these observations were not systematic and it is not possible to predict, on the basis of this limited experience, the extent to which a cns-active drug will be misused, diverted, and/or abused once marketed. consequently, health care providers should carefully evaluate citalopram patients for history of drug abuse and follow such patients closely, observing them for signs of misuse or abuse (e.g., development of tolerance, incrementations of dose, drug-seeking behavior).

Соединенные Штаты - английский - NLM (National Library of Medicine)

nucare pharmaceuticals,inc. - ketoconazole (unii: r9400w927i) (ketoconazole - unii:r9400w927i) - ketoconazole tablets are not indicated for treatment of onychomycosis, cutaneous dermatophyte infections, or candida infections. ketoconazole tablets should be used only when other effective antifungal therapy is not available or tolerated and the potential benefits are considered to outweigh the potential risks. ketoconazole tablets are indicated for the treatment of the following systemic fungal infections in patients who have failed or who are intolerant to other therapies: blastomycosis, coccidioidomycosis, histoplasmosis, chromomycosis, and paracoccidioidomycosis. ketoconazole tablets should not be used for fungal meningitis because it penetrates poorly into the cerebrospinal fluid. drug interactions coadministration of a number of cyp3a4 substrates such as dofetilide, quinidine cisapride and pimozide is contraindicated with ketoconazole tablets. coadministration with ketoconazole can cause elevated plasma concentrations of these drugs and may increase or prolong both therapeutic and adverse effects to s

Соединенные Штаты - английский - NLM (National Library of Medicine)

preferred pharmaceuticals, inc. - lithium carbonate (unii: 2bmd2gna4v) (lithium cation - unii:8h8z5uer66) - lithium is a mood-stabilizing agent indicated as monotherapy for the treatment of bipolar i disorder: lithium is contraindicated in patients with known hypersensitivity to any inactive ingredient in the lithium carbonate tablet or capsule or lithium citrate products [see adverse reactions (6)]. risk summary: lithium may cause harm when administered to a pregnant woman. early voluntary reports to international birth registries suggested an increase in cardiovascular malformations, especially for ebstein’s anomaly, with first trimester use of lithium. subsequent case-control and cohort studies indicate that the increased risk for cardiac malformations is likely to be small; however, the data are insufficient to establish a drug-associated risk. there are concerns for maternal and/or neonatal lithium toxicity during late pregnancy and the postpartum period [see clinical considerations]. published animal developmental and toxicity studies in mice and rats report an increased incidence of fetal mortality, dec

Соединенные Штаты - английский - NLM (National Library of Medicine)

eton pharmaceuticals, inc. - hydrocortisone (unii: wi4x0x7bpj) (hydrocortisone - unii:wi4x0x7bpj) - alkindi sprinkle is indicated as replacement therapy in pediatric patients with adrenocortical insufficiency. alkindi sprinkle is contraindicated in patients with hypersensitivity to hydrocortisone or to any of the ingredients in alkindi sprinkle. anaphylactic reactions have occurred in patients receiving corticosteroids [see adverse reactions (6.2)] . risk summary untreated adrenocortical insufficiency in pregnancy can result in a high rate of complications, including maternal mortality. the use of physiologic doses of hydrocortisone is not expected to cause major birth defects, miscarriage and adverse maternal and fetal outcomes. available data from observational studies with hydrocortisone use in pregnancy have not identified a clear drug-associated risk of major birth defects, miscarriage or adverse maternal or fetal outcomes (see data ). the estimated background risk of major birth defects and miscarriage for the indicated population is unknown. in the u.s. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2–4% and 15–20%, respectively. data human data available data from observational studies with hydrocortisone use in pregnant women have not identified a clear drug-associated risk of major birth defects, miscarriage or adverse maternal or fetal outcomes. evidence from published epidemiologic studies suggest that there may be a small increased risk of cleft lip with or without cleft palate associated with first trimester systemic corticosteroid use in pregnant patients. however, the data are limited and report inconsistent findings, and studies have important methodological limitations, including non-randomized design, retrospective data collection, lack of dose-response data and the inability to control for confounders, such as underlying maternal disease and use of concomitant medications. in addition, unlike other corticosteroids, hydrocortisone is enzymatically deactivated by the placenta and therefore, limits fetal exposure. animal data corticosteroids have been shown to be teratogenic in many species when given in doses equivalent to the human dose. animal studies in which corticosteroids have been given to pregnant mice, rats and rabbits without adrenocortical insufficiency have yielded an increased incidence of cleft palate in the offspring. risk summary cortisol is present in human milk. the use of hydrocortisone at a physiologic dose for adrenocortical insufficiency is not expected to adversely affect the breastfed infant or milk production. there are no data on the presence of hydrocortisone in breast milk, the effect on the breastfed infant or on milk production. the developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for alkindi sprinkle and any potential adverse effects on the breastfed infant from alkindi sprinkle or from the underlying maternal condition. the safety and effectiveness of alkindi sprinkle have been established in pediatric patients for replacement therapy of adrenocortical insufficiency and the information on this use is discussed throughout the labeling. use of alkindi sprinkle in pediatric patients is supported by use in pediatric patients for adrenocortical insufficiency with another hydrocortisone product, along with supportive pharmacokinetic and safety data in 24 pediatric patients with adrenocortical insufficiency. no new adverse reactions were identified [see adverse reactions (6) and clinical pharmacology (12.3)] . alkindi sprinkle are oral granules contained within capsules that must be opened and not swallowed whole to administer the granules. additionally, alkindi sprinkle granules should not be administered via nasogastric or gastric tubes as they may cause tube blockage [see dosage and administration (2.2)] . instructions for use alkindi® sprinkle(ælˈkɪndi spr-en-kle) (hydrocortisone) oral granules read this instructions for use before you start using alkindi sprinkle, and each time you get a refill. there may be new information. this information does not take the place of talking to your healthcare provider about your child's medical condition or treatment. important information you need to know before giving alkindi sprinkle - alkindi sprinkle comes in a capsule that must be opened before use. - do not let your child swallow the capsule. small children may choke. - do not let your child chew or crush the granules in the capsule. - do not let the capsules get wet as this may make some of the granules stick to the capsule. - your healthcare provider will decide the right dose of alkindi sprinkle for your child. follow your healthcare provider's instructions for the dose of alkindi sprinkle to give your child. - ask your healthcare provider or pharmacist if you are not sure how to prepare or give the prescribed dose of alkindi sprinkle to your child. - call your healthcare provider if granules come back up into your child's mouth (regurgitation) or your child has vomiting after swallowing alkindi sprinkle. your child may not have received the full dose of alkindi sprinkle and another dose of alkindi sprinkle may be needed. - your child may sometimes pass the alkindi sprinkle granules in their stools (bowel movement). it does not mean that alkindi sprinkle is not working. do not give your child another dose of alkindi sprinkle. supplies needed to give alkindi sprinkle: - alkindi sprinkle capsule(s) for prescribed dose - 1 spoon - soft food such as yogurt or pureed fruit or sip of fluids such as water, milk, breastmilk or formula preparing and giving alkindi sprinkle: step 1: check the expiration date on the alkindi sprinkle bottle. do not use alkindi sprinkle after the expiration date on the bottle has passed. step 2: remove the prescribed dose of alkindi sprinkle capsules from the bottle. step 6: giving alkindi sprinkle alkindi sprinkle can be given (a) with food onto a spoon, (b) without food onto a spoon, or (c) directly into the child's mouth. do not add the granules to a fluid before giving alkindi sprinkle because it can result in less than the full dose given and it may leave a bitter taste in the mouth. (c) directly onto the child's tongue. pour all granules that make up the prescribed dose directly onto the child's tongue. tap the capsule to make sure all granules are removed. the alkindi sprinkle granules should be given and swallowed within 5 minutes to avoid a bitter taste. step 7: give fluids after giving alkindi sprinkle, give a sip of fluids such as water, milk, breastmilk or formula right away to make sure all granules are swallowed. throwing away (disposal of) alkindi sprinkle: ask your pharmacist how to throw away medicines you no longer use. how should i store alkindi sprinkle? - store alkindi sprinkle at room temperature between 68°f to 77°f (20°c to 25°c). - store in the original bottle to protect from light. - after the bottle has been opened, use the alkindi sprinkle capsules within 60 days. keep alkindi sprinkle and all medicines out of the reach of children. alkindi sprinkle is manufactured for eton pharmaceuticals, inc. by glatt pharmaceutical services gmbh & co. kg werner-glatt-strasse 1, binzen, baden-wuerttemberg, 79589, germany alkindi® is a registered trademark of diurnal limited. alkindi is covered by the following us patents: 9,649,280; 9,675,559; 9,717,740; and other patents in other countries internationally. for more information, go to www.alkindisprinkle.com or call 1-833-343-2500. this instructions for use has been approved by the u.s. food and drug administration. revised: 12/2022

Соединенные Штаты - английский - NLM (National Library of Medicine)

marlex pharmaceuticals, inc. - alendronate sodium (unii: 2uy4m2u3ra) (alendronic acid - unii:x1j18r4w8p) - alendronate sodium tablets are indicated for the treatment of osteoporosis in postmenopausal women. in postmenopausal women, alendronate sodium tablets increase bone mass and reduce the incidence of fractures, including those of the hip and spine (vertebral compression fractures). [ see clinical studies (14.1).] alendronate sodium tablets are indicated for the prevention of postmenopausal osteoporosis [ see clinical studies (14.2)]. alendronate sodium tablets are indicated for treatment to increase bone mass in men with osteoporosis [see clinical studies ( 14.3)]. alendronate sodium tablets are 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)]. alendronate sodium tablets are indicated for the treatment of paget’s disease of bone in men and women. treatment is indicated in patients with paget's disease of bon

Соединенные Штаты - английский - NLM (National Library of Medicine)

exelan pharmaceuticals inc. - alendronate sodium (unii: 2uy4m2u3ra) (alendronic acid - unii:x1j18r4w8p) - alendronate sodium tablets, usp are indicated for the treatment of osteoporosis in postmenopausal women. in postmenopausal women, alendronate sodium tablets, usp increases bone mass and reduces the incidence of fractures, including those of the hip and spine (vertebral compression fractures). [see clinical studies (14.1).] alendronate sodium tablets, usp are indicated for the prevention of postmenopausal osteoporosis [see clinical studies (14.2)]. alendronate sodium tablets, usp are indicated for treatment to increase bone mass in men with osteoporosis [see clinical studies (14.3)]. alendronate sodium tablets, usp are 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)]. alendronate sodium tablets, usp are indicated for the treatment of paget's disease of bone in men and women. treatment is indicated in patients with page