미국 - 영어 - NLM (National Library of Medicine)

evofem, inc. - lactic acid, l- (unii: f9s9ffu82n) (lactic acid, l- - unii:f9s9ffu82n), citric acid monohydrate (unii: 2968phw8qp) (anhydrous citric acid - unii:xf417d3psl), potassium bitartrate (unii: npt6p8p3uu) (tartaric acid - unii:w4888i119h) - phexxi is indicated for the prevention of pregnancy in females of reproductive potential for use as an on-demand method of contraception. limitations of use phexxi is not effective for the prevention of pregnancy when administered after intercourse [see dosage and administration (2.1)]. risk summary there is no use for phexxi in pregnancy; therefore, discontinue phexxi during pregnancy. there are no data with the use of phexxi in pregnant women or animals. in the u.s. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2 to 4 percent and 15 to 20 percent, respectively. risk summary there are no data on the presence of lactic acid, citric acid, and potassium bitartrate or their metabolites in human milk, the effects on the breastfed infant, or the effects on milk production. the safety and effectiveness of phexxi have been established in females of reproductive potential. efficacy is expected to be the same for post-menarchal females

몰타 - 영어 - Medicines Authority

beecham group plc 980 great west road, brentford, middlesex, tw8 9gs, united kingdom - lactic acid, salicylic acid - cutaneous solution - lactic acid 15 % (w/w) salicylic acid 16.7 % (w/w) - other dermatological preparations

미국 - 영어 - NLM (National Library of Medicine)

bristol-myers squibb pharma company - warfarin sodium (unii: 6153cwm0cl) (warfarin - unii:5q7zvv76ei) - warfarin sodium 1 mg - coumadin® is indicated for: limitations of use coumadin has no direct effect on an established thrombus, nor does it reverse ischemic tissue damage. once a thrombus has occurred, however, the goals of anticoagulant treatment are to prevent further extension of the formed clot and to prevent secondary thromboembolic complications that may result in serious and possibly fatal sequelae. coumadin is contraindicated in: • pregnancy coumadin is contraindicated in women who are pregnant except in pregnant women with mechanical heart valves, who are at high risk of thromboembolism [see warnings and precautions (5.7) and use in specific populations (8.1)] . coumadin can cause fetal harm when administered to a pregnant woman. coumadin exposure during pregnancy causes a recognized pattern of major congenital malformations (warfarin embryopathy and fetotoxicity), fatal fetal hemorrhage, and an increased risk of spontaneous abortion and fetal mortality. if coumadin is used during pregnancy or if the patient becomes pregn

미국 - 영어 - NLM (National Library of Medicine)

washington homeopathic products - sarcolacticum ac - to relieve the symptoms of muscular weakness. indications: sarcolacticum ac   muscular weakness if symptoms persist/worsen or if pregnant/nursing, stop use and consult your practitioner.

미국 - 영어 - NLM (National Library of Medicine)

washington homeopathic products - lacticum ac - to relieve the symptoms of nausea. indications: lacticum ac   nausea if symptoms persist/worsen or if pregnant/nursing, stop use and consult your practitioner.

미국 - 영어 - NLM (National Library of Medicine)

international laboratories, llc - citalopram hydrobromide (unii: i1e9d14f36) (citalopram - unii:0dhu5b8d6v) - citalopram 40 mg - citalopram tablets usp are indicated for the treatment of depression. the efficacy of citalopram in the treatment of depression was established in 4-6 week, controlled trials of outpatients whose diagnosis corresponded most closely to the dsm-lii and dsm-lli-r category of major depressive disorder (see clinical pharmacology ). a major depressive episode (dsm-lv) implies a prominent and relatively persistent (nearly every day for at least 2 weeks) depressed or dysphoric mood that usually interferes with daily functioning, and includes at least five of the following nine symptoms: depressed mood, loss of interest in usual activities, significant change in weight and/or appetite, insomnia or hypersomnia, psychomotor agitation or retardation, increased fatigue, feelings of guilt or worthlessness, slowed thinking or impaired concentration, a suicide attempt or suicidal ideation. the antidepressant action of citalopram in hospitalized depressed patients has not been adequately studied. the efficacy of citalopram in

미국 - 영어 - NLM (National Library of Medicine)

mylan pharmaceuticals inc. - esomeprazole magnesium (unii: r6dxu4way9) (esomeprazole - unii:n3pa6559ft) - esomeprazole 20 mg - esomeprazole magnesium delayed-release capsules are indicated for the short-term treatment (4 to 8 weeks) in the healing and symptomatic resolution of diagnostically confirmed ee in adults. for those patients who have not healed after 4 to 8 weeks of treatment, an additional 4- to 8-week course of esomeprazole magnesium delayed-release capsules may be considered. esomeprazole magnesium delayed-release capsules are indicated for the short-term treatment (4 to 8 weeks) for the healing of ee in pediatric patients 12 years to 17 years of age. esomeprazole magnesium delayed-release capsules are indicated for the maintenance of healing of ee in adults. controlled studies do not extend beyond 6 months. esomeprazole magnesium delayed-release capsules are indicated for short-term treatment (4 to 8 weeks) of heartburn and other symptoms associated with gerd in adults. esomeprazole magnesium delayed-release capsules are indicated for short-term treatment (4 weeks) of heartburn and other symptoms associated with gerd in pediatric patients 12 years to 17 years of age. esomeprazole magnesium delayed-release capsules are indicated for the reduction in the occurrence of gastric ulcers associated with continuous nsaid therapy in adult patients at risk for developing gastric ulcers. patients are considered to be at risk due to their age (60 years and older) and/or documented history of gastric ulcers. controlled studies do not extend beyond 6 months. eradication of h. pylori has been shown to reduce the risk of duodenal ulcer recurrence. esomeprazole magnesium delayed-release capsules in combination with amoxicillin and clarithromycin are indicated for the treatment of adult patients with h. pylori infection and duodenal ulcer disease (active or history of within the past 5 years) to eradicate h. pylori . in patients who fail therapy, susceptibility testing should be done. if resistance to clarithromycin is demonstrated or susceptibility testing is not possible, alternative antimicrobial therapy should be instituted [see clinical pharmacology (12.4) and the prescribing information for clarithromycin] . esomeprazole magnesium delayed-release capsules are indicated for the long-term treatment of pathological hypersecretory conditions, including zollinger-ellison syndrome, in adults. there are no adequate and well-controlled studies with esomeprazole in pregnant women. esomeprazole is the s-isomer of omeprazole. available epidemiologic data fail to demonstrate an increased risk of major congenital malformations or other adverse pregnancy outcomes with first trimester omeprazole use (see data) . reproduction studies in rats and rabbits resulted in dose-dependent embryo-lethality at omeprazole doses that were approximately 3.4 to 34 times an oral human dose of 40 mg (based on a body surface area for a 60 kg person). teratogenicity was not observed in animal reproduction studies with administration of oral esomeprazole magnesium in rats and rabbits with doses about 68 times and 42 times, respectively, an oral human dose of 40 mg (based on a body surface area basis for a 60 kg person). changes in bone morphology were observed in offspring of rats dosed through most of pregnancy and lactation at doses equal to or greater than approximately 34 times an oral human dose of 40 mg. when maternal administration was confined to gestation only, there were no effects on bone physeal morphology in the offspring at any age (see data) . the estimated background risks of major birth defects and miscarriage for the indicated population are 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. esomeprazole is the s-isomer of omeprazole. four epidemiological studies compared the frequency of congenital abnormalities among infants born to women who used omeprazole during pregnancy with the frequency of abnormalities among infants of women exposed to h2 -receptor antagonists or other controls. a population-based retrospective cohort epidemiological study from the swedish medical birth registry, covering approximately 99% of pregnancies, from 1995 to 1999, reported on 955 infants (824 exposed during the first trimester with 39 of these exposed beyond first trimester, and 131 exposed after the first trimester) whose mothers used omeprazole during pregnancy. the number of infants exposed in utero to omeprazole that had any malformation, low birth weight, low apgar score, or hospitalization was similar to the number observed in this population. the number of infants born with ventricular septal defects and the number of stillborn infants was slightly higher in the omeprazole-exposed infants than the expected number in this population. a population-based retrospective cohort study covering all live births in denmark from 1996 to 2009, reported on 1,800 live births whose mothers used omeprazole during the first trimester of pregnancy and 837,317 live births whose mothers did not use any proton pump inhibitor. the overall rate of birth defects in infants born to mothers with first trimester exposure to omeprazole was 2.9% and 2.6% in infants born to mothers not exposed to any proton pump inhibitor during the first trimester. a retrospective cohort study reported on 689 pregnant women exposed to either h2 -blockers or omeprazole in the first trimester (134 exposed to omeprazole) and 1,572 pregnant women unexposed to either during the first trimester. the overall malformation rate in offspring born to mothers with first trimester exposure to omeprazole, an h2 -blocker, or were unexposed was 3.6%, 5.5%, and 4.1%, respectively. a small prospective observational cohort study followed 113 women exposed to omeprazole during pregnancy (89% with first trimester exposures). the reported rate of major congenital malformations was 4% in the omeprazole group, 2% in controls exposed to non-teratogens, and 2.8% in disease paired controls. rates of spontaneous and elective abortions, preterm deliveries, gestational age at delivery, and mean birth weight were similar among the groups. several studies have reported no apparent adverse short-term effects on the infant when single dose oral or intravenous omeprazole was administered to over 200 pregnant women as premedication for cesarean section under general anesthesia. omeprazole reproductive studies conducted with omeprazole in rats at oral doses up to 138 mg/kg/day (about 34 times an oral human dose of 40 mg on a body surface area basis) and in rabbits at doses up to 69.1 mg/kg/day (about 34 times an oral human dose of 40 mg on a body surface area basis) during organogenesis did not disclose any evidence for a teratogenic potential of omeprazole. in rabbits, omeprazole in a dose range of 6.9 to 69.1 mg/kg/day (about 3.4 to 34 times an oral human dose of 40 mg on a body surface area basis) administered during organogenesis produced dose-related increases in embryo-lethality, fetal resorptions, and pregnancy disruptions. in rats, dose-related embryo/fetal toxicity and postnatal developmental toxicity were observed in offspring resulting from parents treated with omeprazole at 13.8 to 138.0 mg/kg/day (about 3.4 to 34 times an oral human dose of 40 mg on a body surface area basis), administered prior to mating through the lactation period. esomeprazole no effects on embryo-fetal development were observed in reproduction studies with esomeprazole magnesium in rats at oral doses up to 280 mg/kg/day (about 68 times an oral human dose of 40 mg on a body surface area basis) or in rabbits at oral doses up to 86 mg/kg/day (about 41 times an oral human dose of 40 mg on a body surface area basis) administered during organogenesis. a pre- and postnatal developmental toxicity study in rats with additional endpoints to evaluate bone development was performed with esomeprazole magnesium at oral doses of 14 to 280 mg/kg/day (about 3.4 to 68 times an oral human dose of 40 mg on a body surface area basis). neonatal/early postnatal (birth to weaning) survival was decreased at doses equal to or greater than 138 mg/kg/day (about 34 times an oral human dose of 40 mg on a body surface area basis). body weight and body weight gain were reduced and neurobehavioral or general developmental delays in the immediate post-weaning timeframe were evident at doses equal to or greater than 69 mg/kg/day (about 17 times an oral human dose of 40 mg on a body surface area basis). in addition, decreased femur length, width and thickness of cortical bone, decreased thickness of the tibial growth plate and minimal to mild bone marrow hypocellularity were noted at doses equal to or greater than 14 mg/kg/day (about 3.4 times an oral human dose of 40 mg on a body surface area basis). physeal dysplasia in the femur was observed in offspring of rats treated with oral doses of esomeprazole magnesium at doses equal to or greater than 138 mg/kg/day (about 34 times an oral human dose of 40 mg on a body surface area basis). effects on maternal bone were observed in pregnant and lactating rats in a pre- and postnatal toxicity study when esomeprazole magnesium was administered at oral doses of 14 to 280 mg/kg/day (about 3.4 to 68 times an oral human dose of 40 mg on a body surface area basis). when rats were dosed from gestational day 7 through weaning on postnatal day 21, a statistically significant decrease in maternal femur weight of up to 14% (as compared to placebo treatment) was observed at doses equal to or greater than 138 mg/kg/day (about 34 times an oral human dose of 40 mg on a body surface area basis). a pre- and postnatal development study in rats with esomeprazole strontium (using equimolar doses compared to esomeprazole magnesium study) produced similar results in dams and pups as described above. a follow-up developmental toxicity study in rats with further time points to evaluate pup bone development from postnatal day 2 to adulthood was performed with esomeprazole magnesium at oral doses of 280 mg/kg/day (about 68 times an oral human dose of 40 mg on a body surface area basis) where esomeprazole administration was from either gestational day 7 or gestational day 16 until parturition. when maternal administration was confined to gestation only, there were no effects on bone physeal morphology in the offspring at any age. esomeprazole is the s-isomer of omeprazole and limited data suggest that omeprazole may be present in human milk. there are no clinical data on the effects of esomeprazole 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 esomeprazole magnesium delayed-release capsules and any potential adverse effects on the breastfed infant from esomeprazole magnesium delayed-release capsules or from the underlying maternal condition. the safety and effectiveness of esomeprazole magnesium delayed-release capsules have been established in pediatric patients 12 years to 17 years for short-term treatment (4 to 8 weeks) for healing of ee. use of esomeprazole magnesium delayed-release capsules for this indication is supported by evidence from adequate and well-controlled studies in adults with additional safety and pharmacokinetic data in pediatric patients 1 year to 17 years of age. the safety profile in pediatric patients 1 year to 17 years of age was similar to adults [see adverse reactions (6.1), clinical pharmacology (12.3), clinical studies (14.4)] . the safety and effectiveness of esomeprazole magnesium delayed-release capsules have been established in pediatric patients 12 years to 17 years of age for the short-term treatment (4 weeks) of heartburn and other symptoms associated with gerd. use of esomeprazole magnesium delayed-release capsules for this indication is supported by evidence from adequate and well-controlled studies in adults with additional safety and pharmacokinetic data in pediatric patients 1 year to 17 years of age. the safety profile in pediatric patients 1 year to 17 years of age was similar to adults [see adverse reactions (6.1), clinical pharmacology (12.3), clinical studies (14.4)] . the safety and effectiveness of esomeprazole for the risk reduction of nsaid-associated gastric ulcer, h. pylori eradication to reduce the risk of duodenal ulcer recurrence and treatment of pathological hypersecretory conditions have not been established in pediatric patients. in a juvenile rat toxicity study, esomeprazole was administered with both magnesium and strontium salts at oral doses about 34 to 68 times a daily human dose of 40 mg based on body surface area. increases in death were seen at the high dose, and at all doses of esomeprazole, there were decreases in body weight, body weight gain, femur weight and femur length, and decreases in overall growth [see nonclinical toxicology (13.2)] . of the total number of patients who received esomeprazole in clinical trials, 1459 were 65 to 74 years of age and 354 patients were 75 years of age and older. no overall differences in safety and efficacy were observed between the elderly and younger individuals, and other reported clinical experience has not identified differences in responses between elderly and younger patients, but greater sensitivity of some older individuals cannot be ruled out. in patients with severe hepatic impairment (child-pugh class c) exposure to esomeprazole substantially increased compared to healthy subjects. dosage modification of esomeprazole is recommended for patients with severe hepatic impairment for the healing of ee, risk reduction of nsaid-associated gastric ulcer, h. pylori eradication to reduce the risk of duodenal ulcer recurrence, and pathological hypersecretory conditions including zollinger-ellison syndrome [see dosage and administration (2.1), clinical pharmacology (12.3)] . in patients with mild to moderate liver impairment (child-pugh classes a and b), no dosage adjustment is necessary. esomeprazole magnesium delayed-release capsules, usp (es″ oh mep′ ra zole mag nee′ zee um) giving esomeprazole magnesium delayed-release capsules with water through a nasogastric tube (ng tube) esomeprazole magnesium delayed-release capsules: this instructions for use has been approved by the u.s. food and drug administration. the brands listed are trademarks of their respective owners. manufactured for: mylan pharmaceuticals inc. morgantown, wv 26505   u.s.a. manufactured by: mylan laboratories limited hyderabad — 500 096, india revised: 11/2023 75100442 mx:esome:r8m/mx:mg:esome:r5m

미국 - 영어 - NLM (National Library of Medicine)

mylan pharmaceuticals inc. - telmisartan (unii: u5syw473rq) (telmisartan - unii:u5syw473rq) - telmisartan 20 mg - telmisartan tablets are indicated for the treatment of hypertension, to lower blood pressure. lowering blood pressure reduces the risk of fatal and nonfatal cardiovascular events, primarily strokes and myocardial infarctions. these benefits have been seen in controlled trials of antihypertensive drugs from a wide variety of pharmacologic classes including the class to which this drug principally belongs. control of high blood pressure should be part of comprehensive cardiovascular risk management, including, as appropriate, lipid control, diabetes management, antithrombotic therapy, smoking cessation, exercise, and limited sodium intake. many patients will require more than one drug to achieve blood pressure goals. for specific advice on goals and management, see published guidelines, such as those of the national high blood pressure education program’s joint national committee on prevention, detection, evaluation, and treatment of high blood pressure (jnc). numerous antihypertensive drugs, from a variety of pharmacologic classes and with different mechanisms of action, have been shown in randomized controlled trials to reduce cardiovascular morbidity and mortality, and it can be concluded that it is blood pressure reduction, and not some other pharmacologic property of the drugs, that is largely responsible for those benefits. the largest and most consistent cardiovascular outcome benefit has been a reduction in the risk of stroke, but reductions in myocardial infarction and cardiovascular mortality also have been seen regularly. elevated systolic or diastolic pressure causes increased cardiovascular risk, and the absolute risk increase per mmhg is greater at higher blood pressures, so that even modest reductions of severe hypertension can provide substantial benefit. relative risk reduction from blood pressure reduction is similar across populations with varying absolute risk, so the absolute benefit is greater in patients who are at higher risk independent of their hypertension (for example, patients with diabetes or hyperlipidemia), and such patients would be expected to benefit from more aggressive treatment to a lower blood pressure goal. some antihypertensive drugs have smaller blood pressure effects (as monotherapy) in black patients, and many antihypertensive drugs have additional approved indications and effects (e.g., on angina, heart failure, or diabetic kidney disease). these considerations may guide selection of therapy. telmisartan tablets may be used alone or in combination with other antihypertensive agents [see clinical studies (14.1)] . telmisartan tablets are indicated for reduction of the risk of myocardial infarction, stroke, or death from cardiovascular causes in patients 55 years of age or older at high risk of developing major cardiovascular events who are unable to take ace inhibitors. high risk for cardiovascular events can be evidenced by a history of coronary artery disease, peripheral arterial disease, stroke, transient ischemic attack, or high-risk diabetes (insulin-dependent or non-insulin dependent) with evidence of end-organ damage [see clinical studies (14.2)] . telmisartan tablets can be used in addition to other needed treatment (such as antihypertensive, antiplatelet or lipid-lowering therapy) [see clinical studies (14.2)] . studies of telmisartan in this setting do not exclude the possibility that telmisartan may not preserve a meaningful fraction of the effect of the ace inhibitor to which it was compared. consider using the ace inhibitor first, and, if it is stopped for cough only, consider re-trying the ace inhibitor after the cough resolves. use of telmisartan with an ace inhibitor is not recommended [see warnings and precautions (5.6)] . telmisartan tablets are contraindicated in patients with known hypersensitivity (e.g., anaphylaxis or angioedema) to telmisartan or any other component of this product [see adverse reactions (6.2)] . do not co-administer aliskiren with telmisartan tablets in patients with diabetes [see drug interactions (7)] . telmisartan tablets can cause fetal harm when administered to a pregnant woman. use of drugs that act on the renin-angiotensin system during the second and third trimesters of pregnancy reduces fetal renal function and increases fetal and neonatal morbidity and death (see clinical considerations) . most epidemiologic studies examining fetal abnormalities after exposure to antihypertensive use in the first trimester have not distinguished drugs affecting the renin-angiotensin system from other antihypertensive agents. studies in rats and rabbits with telmisartan showed fetotoxicity only at maternally toxic doses (see data) . when pregnancy is detected, discontinue telmisartan tablets as soon as possible. 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 clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively. hypertension in pregnancy increases the maternal risk for pre-eclampsia, gestational diabetes, premature delivery, and delivery complications (e.g., need for cesarean section, and post-partum hemorrhage). hypertension increases the fetal risk for intrauterine growth restriction and intrauterine death. pregnant women with hypertension should be carefully monitored and managed accordingly. use of drugs that act on the ras in the second and third trimesters of pregnancy can result in the following: oligohydramnios, reduced fetal renal function leading to anuria and renal failure, fetal lung hypoplasia, skeletal deformations, including skull hypoplasia, hypotension, and death. in the unusual case that there is no appropriate alternative to therapy with drugs affecting the renin-angiotensin system for a particular patient, apprise the mother of the potential risk to the fetus. in patients taking telmisartan tablets during pregnancy, perform serial ultrasound examinations to assess the intra-amniotic environment. fetal testing may be appropriate, based on the week of gestation. if oligohydramnios is observed, discontinue telmisartan tablets, unless they are considered lifesaving for the mother. patients and physicians should be aware, however, that oligohydramnios may not appear until after the fetus has sustained irreversible injury. closely observe infants with histories of in utero exposure to telmisartan for hypotension, oliguria, and hyperkalemia. if oliguria or hypotension occurs, support blood pressure and renal perfusion. exchange transfusions or dialysis may be required as a means of reversing hypotension and/or substituting for disordered renal function [see use in specific populations (8.4)] . no teratogenic effects were observed when telmisartan was administered to pregnant rats at oral doses of up to 50 mg/kg/day and to pregnant rabbits at oral doses up to 45 mg/kg/day. in rabbits, embryolethality associated with maternal toxicity (reduced body weight gain and food consumption) was observed at 45 mg/kg/day [about 12 times the maximum recommended human dose (mrhd) of 80 mg on a mg/m2 basis]. in rats, maternally toxic (reduction in body weight gain and food consumption) telmisartan doses of 15 mg/kg/day (about 1.9 times the mrhd on a mg/m2 basis), administered during late gestation and lactation, were observed to produce adverse effects in neonates, including reduced viability, low birth weight, delayed maturation, and decreased weight gain. the no-observed-effect doses for developmental toxicity in rats and rabbits, 5 and 15 mg/kg/day, respectively, are about 0.64 and 3.7 times, on a mg/m2 basis, the maximum recommended human dose of telmisartan (80 mg/day). there is no information regarding the presence of telmisartan in human milk, the effects on the breastfed infant, or the effects on milk production. telmisartan is present in the milk of lactating rats (see data) . because of the potential for serious adverse reactions in the breastfed infant including hypotension, hyperkalemia and renal impairment, advise a nursing woman not to breastfeed during treatment with telmisartan tablets. telmisartan was present in the milk of lactating rats at concentrations 1.5 to 2 times those found in plasma from 4 to 8 hours after administration. safety and effectiveness in pediatric patients have not been established [see clinical pharmacology (12.3)] . if oliguria or hypotension occurs, support blood pressure and renal perfusion. exchange transfusions or dialysis may be required as a means of reversing hypotension and/or substituting for disordered renal function. of the total number of patients receiving telmisartan tablets in hypertension clinical studies, 551 (19%) were 65 to 74 years of age and 130 (4%) were 75 years or older. no overall differences in effectiveness and safety were observed in these patients compared to 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. of the total number of patients receiving telmisartan tablets in the cardiovascular risk reduction study (ontarget), the percentage of patients ≥ 65 to < 75 years of age was 42%; 15% of patients were ≥ 75 years old. no overall differences in effectiveness and safety were observed in these patients compared to 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. monitor carefully and uptitrate slowly in patients with biliary obstructive disorders or hepatic insufficiency [see warnings and precautions (5.4)] .

미국 - 영어 - NLM (National Library of Medicine)

merck sharp & dohme llc - ertapenem sodium (unii: 2t90ke67l0) (ertapenem - unii:g32f6eid2h) - ertapenem 1 g - invanz is indicated for the treatment of adult patients and pediatric patients (3 months of age and older) with complicated intra-abdominal infections due to escherichia coli , clostridium clostridioforme , eubacterium lentum , peptostreptococcus species, bacteroides fragilis , bacteroides distasonis , bacteroides ovatus , bacteroides thetaiotaomicron , or bacteroides uniformis . invanz is indicated for the treatment of adult patients and pediatric patients (3 months of age and older) with complicated skin and skin structure infections, including diabetic foot infections without osteomyelitis due to staphylococcus aureus (methicillin susceptible isolates only), streptococcus agalactiae , streptococcus pyogenes , escherichia coli , klebsiella pneumoniae , proteus mirabilis , bacteroides fragilis , peptostreptococcus species, porphyromonas asaccharolytica , or prevotella bivia . invanz has not been studied in diabetic foot infections with concomitant osteomyelitis [see clinical studies (14)]. invanz is indicated for the treatment of adult patients and pediatric patients (3 months of age and older) with community acquired pneumonia due to streptococcus pneumoniae (penicillin susceptible isolates only) including cases with concurrent bacteremia, haemophilus influenzae (beta-lactamase negative isolates only), or moraxella catarrhalis . invanz is indicated for the treatment of adult patients and pediatric patients (3 months of age and older) with complicated urinary tract infections including pyelonephritis due to escherichia coli , including cases with concurrent bacteremia, or klebsiella pneumoniae . invanz is indicated for the treatment of adult patients and pediatric patients (3 months of age and older) with acute pelvic infections including postpartum endomyometritis, septic abortion and post-surgical gynecological infections due to streptococcus agalactiae, escherichia coli , bacteroides fragilis, porphyromonas asaccharolytica, peptostreptococcus species, or prevotella bivia . invanz is indicated in adults for the prevention of surgical site infection following elective colorectal surgery. to reduce the development of drug-resistant bacteria and maintain the effectiveness of invanz and other antibacterial drugs, invanz should be used only to treat or prevent infections that are proven or strongly suspected to be caused by susceptible bacteria. when culture and susceptibility information are available, they should be considered in selecting or modifying antibacterial therapy. in the absence of such data, local epidemiology and susceptibility patterns may contribute to the empiric selection of therapy. - invanz is contraindicated in patients with known hypersensitivity to any component of this product or to other drugs in the same class or in patients who have demonstrated anaphylactic reactions to beta-lactams. - due to the use of lidocaine hcl as a diluent, invanz administered intramuscularly is contraindicated in patients with a known hypersensitivity to local anesthetics of the amide type. risk summary available data from a small number of post-marketing cases with invanz use in pregnancy are insufficient to inform any drug-associated risks for major birth defects, miscarriage, or adverse maternal or fetal outcomes. in animal reproduction studies after intravenous administration of ertapenem during the period of organogenesis, there was no evidence of developmental malformations in rats at systemic exposures (auc) up to approximately 1.2 times the human exposure at the maximum recommended human dose (mrhd) and in mice at doses up to approximately 3 times the mrhd based on body surface area comparison. in pregnant rats administered ertapenem during organogenesis through lactation, fetal toxicity, developmental delays, and impaired reproduction did not occur in first generation offspring at systemic exposures (auc) approximately 1.2 times the human exposure at the mrhd (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 clinically recognized pregnancies is 2 to 4% and 15 to 20%, respectively. data animal data in pregnant rats, intravenous administration of ertapenem dosages of up to 700 mg/kg/day (approximately 1.2 times the mrhd based on auc) during the period of organogenesis (gestation days [gd] 6-20) revealed no maternal or embryofetal effects. pregnant mice intravenously administered ertapenem dosages of up to 700 mg/kg/day (approximately 3 times the mrhd based on body surface area comparison) during the period of organogenesis (gd 6-15) showed slight decreases in average fetal weight and an associated decrease in the average number of ossified sacrocaudal vertebrae. there were no maternal effects at any dosage. in a pre-postnatal study in rats, ertapenem administered to pregnant rats at dosages up to 700 mg/kg/day (approximately 1.2 times the mrhd based on auc) during organogenesis through lactation, (gd 6 until lactation day (ld) 20) did not result in fetal toxicity, developmental delays, or impaired reproduction in first generation offspring, and fetal deaths and malformations were not increased in second generation offspring. risk summary ertapenem is present in human milk (see data) . there are no data on the effects on the breastfed infant or the effects on milk production. the developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for invanz and any potential adverse effects on the breastfed infant from invanz or from the underlying maternal condition. data the concentration of ertapenem in breast milk from 5 lactating women with pelvic infections (5 to 14 days postpartum) measured at random time points daily for 5 consecutive days following the last 1 g dose of intravenous therapy (3 to 10 days of therapy) showed low levels. the concentration of ertapenem in breast milk within 24 hours of the last dose of therapy in all 5 women ranged from (<0.13 (lower limit of quantitation) to 0.38 mcg/ml), although peak concentrations were not assessed. by day 5 after discontinuation of therapy, the level of ertapenem was undetectable in the breast milk of 4 women and below the lower limit of quantitation (<0.13 mcg/ml) in 1 woman. the concentration of ertapenem in transitional milk observed in this study may not reflect the concentration of ertapenem in mature milk. safety and effectiveness of invanz in pediatric patients 3 months to 17 years of age are supported by evidence from adequate and well-controlled trials in adults, pharmacokinetic data in pediatric patients, and additional data from comparator-controlled trials in pediatric patients 3 months to 17 years of age [see indications and usage (1.1), (1.2), (1.3), (1.4) and (1.5) and clinical studies (14.2)] . invanz is not recommended in infants under 3 months of age as no data are available. invanz is not recommended in the treatment of meningitis in the pediatric population due to lack of sufficient csf penetration. of the 1,835 patients in phase 2b/3 trials treated with invanz, approximately 26 percent were 65 and over, while approximately 12 percent were 75 and over. no overall differences in safety or effectiveness were observed between these patients and younger patients. 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. this drug is known to be substantially excreted by the kidney, and the risk of toxic reactions to this drug may be greater in patients with impaired renal function. because elderly patients are more likely to have decreased renal function, care should be taken in dose selection, and it may be useful to monitor renal function [see dosage and administration (2.2)]. dosage adjustment is necessary in patients with creatinine clearance 30 ml/min or less [see dosage and administration (2.4) and clinical pharmacology (12.3)] . the pharmacokinetics of ertapenem in patients with hepatic impairment have not been established. of the total number of patients in clinical trials, 37 patients receiving ertapenem 1 g daily and 36 patients receiving comparator drugs were considered to have child-pugh class a, b, or c liver impairment. the incidence of adverse experiences in patients with hepatic impairment was similar between the ertapenem group and the comparator groups.

미국 - 영어 - NLM (National Library of Medicine)

dr.reddy's laboratories ltd - zoledronic acid (unii: 6xc1pad3kf) (zoledronic acid anhydrous - unii:70hz18ph24) - zoledronic acid anhydrous 5 mg in 100 ml - zoledronic acid injection is indicated for treatment of osteoporosis in postmenopausal women. in postmenopausal women with osteoporosis, diagnosed by bone mineral density (bmd) or prevalent vertebral fracture, zoledronic acid injection reduces the incidence of fractures (hip, vertebral and non-vertebral osteoporosis-related fractures). in patients at high risk of fracture, defined as a recent low-trauma hip fracture, zoledronic acid injection reduces the incidence of new clinical fractures [see clinical studies (14.1)]. zoledronic acid injection is indicated for prevention of osteoporosis in postmenopausal women [see clinical studies (14.2)] . zoledronic acid injection is indicated for treatment to increase bone mass in men with osteoporosis [see clinical studies (14.3)]. zoledronic acid injection is indicated for the treatment and prevention of glucocorticoid-induced osteoporosis in men and women who are either initiating or continuing systemic glucocorticoids in a daily dosage equivalent to 7.5 mg or greater of prednisone and who are expected to remain on glucocorticoids for at least 12 months [see clinical studies (14.4)]. zoledronic acid injection is indicated for treatment of paget's disease of bone in men and women. treatment is indicated in patients with paget’s disease of bone with elevations in serum alkaline phosphatase of two times or higher than the upper limit of the age-specific normal reference range, or those who are symptomatic, or those at risk for complications from their disease [see clinical studies (14.5) ]. the safety and effectiveness of zoledronic acid injection for the treatment of osteoporosis is based on clinical data of three 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. 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. zoledronic acid injection is contraindicated in patients with the following conditions:   - hypocalcemia [see warnings and precautions (5.2) ] - creatinine clearance less than 35 ml/min and in those with evidence of acute renal impairment due to an increased risk of renal failure [see warnings and precautions (5.3) ]. - known hypersensitivity to zoledronic acid or any components of zoledronic acid injection. hypersensitivity reactions including urticaria, angioedema, and anaphylactic reaction/shock have been reported [see adverse reactions (6.2) ] . risk summary available data on the use of zoledronic acid in pregnant women are insufficient to inform a drug-associated risk of adverse maternal or fetal outcomes. discontinue zoledronic acid when pregnancy is recognized. in animal reproduction studies, daily subcutaneous administration of zoledronic acid to pregnant rats during organogenesis resulted in increases in fetal skeletal, visceral, and external malformations, decreases in postimplantation survival, and decreases in viable fetuses and fetal weight starting at doses equivalent to 2 times the recommended human 5 mg intravenous dose (based on auc). subcutaneous administration of zoledronic acid to rabbits during organogenesis did not cause adverse fetal effects at up to 0.4 times the human 5 mg intravenous dose (based on body surface area, mg/m2 ), but resulted in maternal mortality and abortion associated with hypocalcemia starting at doses equivalent to 0.04 times the human 5 mg intravenous dose. subcutaneous dosing of female rats from before mating through gestation and lactation and allowed to deliver caused maternal dystocia and periparturient mortality, increases in stillbirths and neonatal deaths, and reduced pup body weight starting at doses equivalent to 0.1 times the human 5 mg intravenous dose (based on auc). (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 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 to 4% and 15 to 20%, respectively. data animal data in pregnant rats given daily subcutaneous doses of zoledronic acid of 0.1, 0.2, or 0.4 mg/kg during organogenesis, fetal skeletal, visceral, and external malformations, increases in pre-and post-implantation loss, and decreases in viable fetuses and fetal weight were observed at 0.2 and 0.4 mg/kg/day (equivalent to 2 and 4 times the human 5 mg intravenous dose, based on auc). adverse fetal skeletal effects at 0.4 mg/kg/day (4 times the human 5 mg dose) included unossified or incompletely ossified bones, thickened, curved or shortened bones, wavy ribs, and shortened jaw. other adverse fetal effects at this dose included reduced lens, rudimentary cerebellum, reduction or absence of liver lobes, reduction of lung lobes, vessel dilation, cleft palate, and edema. skeletal variations were observed in all groups starting at 0.1 mg/kg/day (1.2 times the human 5 mg dose). signs of maternal toxicity including reduced body weight and food consumption were observed at 0.4 mg/kg/day (4 times the human 5 mg dose). in pregnant rabbits given daily subcutaneous doses of zoledronic acid of 0.01, 0.03, or 0.1 mg/kg during gestation no adverse fetal effects were observed up to 0.1 mg/kg/day (0.4 times the human 5 mg intravenous dose, based on body surface area, mg/m2 ). maternal mortality and abortion were observed in all dose groups (starting at 0.04 times the human 5 mg dose). adverse maternal effects were associated with drug-induced hypocalcemia. in female rats given daily subcutaneous doses of 0.01, 0.03, or 0.1 mg/kg, beginning 15 days before mating and continuing through gestation, parturition and lactation, dystocia and periparturient mortality were observed in pregnant rats allowed to deliver starting at 0.01 mg/kg/day (0.1 times the human 5 mg intravenous dose, based on auc). also, there was an increase in stillbirths and a decrease in neonate survival starting at 0.03 mg/kg/day (0.3 times the human 5 mg dose), while the number of viable newborns and pup body weight on postnatal day 7 were decreased at 0.1 mg/kg/day (equivalent to the human 5 mg dose). maternal and neonatal deaths were considered related to drug-induced periparturient hypocalcemia. risk summary there are no data on the presence of zoledronic acid in human milk, the effects on the breastfed infant, or the effects on milk production. the developmental and health benefits of breast-feeding should be considered along with the mother’s clinical need for zoledronic acid and any potential adverse effects on the breast-fed child from zoledronic acid or from the underlying maternal condition. infertility there are no data available in humans. female fertility may be impaired based on animal studies demonstrating adverse effects of zoledronic acid on fertility parameters [see nonclinical toxicology (13.1)]. zoledronic acid injection is not indicated for use in children.   the safety and effectiveness of zoledronic acid was studied in a one-year active controlled trial of 152 pediatric subjects (74 receiving zoledronic acid). the enrolled population was subjects with severe osteogenesis imperfecta, aged 1 to 17 years, 55% male, 84% caucasian, with a mean lumbar spine bmd of 0.431 gm/cm2 , which is 2.7 standard deviations below the mean for age-matched controls (bmd z-score of -2.7). at one year, increases in bmd were observed in the zoledronic acid treatment group. however, changes in bmd in individual patients with severe osteogenesis imperfecta did not necessarily correlate with the risk for fracture or the incidence or severity of chronic bone pain. the adverse events observed with zoledronic acid use in children did not raise any new safety findings beyond those previously seen in adults treated for paget’s disease of bone and treatment of osteoporosis including osteonecrosis of the jaw (onj) and renal impairment. however, adverse reactions seen more commonly in pediatric patients included pyrexia (61%), arthralgia (26%), hypocalcemia (22%) and headache (22%). these reactions, excluding arthralgia, occurred most frequently within three days after the first infusion and became less common with repeat dosing. no cases of onj or renal impairment were observed in this study. because of long-term retention in bone, zoledronic acid injection should only be used in children if the potential benefit outweighs the potential risk. plasma zoledronic acid concentration data was obtained from 10 patients with severe osteogenesis imperfecta (4 in the age group of 3 to 8 years and 6 in the age group of 9 to 17 years) infused with 0.05 mg/kg dose over 30 minutes. mean cmax and auc(0-last) was 167 ng/ml and 220 ng.h/ml respectively. the plasma concentration time profile of zoledronic acid in pediatric patients represent a multi-exponential decline, as observed in adult cancer patients at an approximately equivalent mg/kg dose. the combined osteoporosis trials included 4863 zoledronic acid injection-treated patients who were at least 65 years of age, while 2101 patients were at least 75 years old. no overall differences in efficacy or safety were observed between patients under 75 years of age with those at least 75 years of age, except that the acute phase reactions occurred less frequently in the older patients. of the patients receiving zoledronic acid injection in the osteoporosis study in men, glucocorticoid-induced osteoporosis, and paget’s disease studies, 83, 116 and 132 patients, respectively were 65 years of age or over, while 68 patients, respectively were at least 75 years of age. however, because decreased renal function occurs more commonly in the elderly, special care should be taken to monitor renal function. zoledronic acid injection is contraindicated in patients with creatinine clearance less than 35 ml/min and in those with evidence of acute renal impairment. there are no safety or efficacy data to support the adjustment of the zoledronic acid injection dose based on baseline renal function. therefore, no dosage adjustment is required in patients with a creatinine clearance of greater than or equal to 35 ml/min [see warnings and precautions (5.3) , clinical pharmacology (12.3) ]. risk of acute renal failure may increase with underlying renal disease and dehydration secondary to fever, sepsis, gastrointestinal losses, diuretic therapy, advanced age, etc. [see adverse reactions (6.2) ]. zoledronic acid injection is not metabolized in the liver. no clinical data are available for use of zoledronic acid injection in patients with hepatic impairment.