Egyesült Államok - angol - NLM (National Library of Medicine)

glenmark pharmaceuticals inc., usa - pimecrolimus (unii: 7kyv510875) (pimecrolimus - unii:7kyv510875) - pimecrolimus cream, 1% is contraindicated in individuals with a history of hypersensitivity to pimecrolimus or any of the components of the cream. pregnancy category c there are no adequate and well-controlled studies with pimecrolimus cream, 1% in pregnant women. therefore, pimecrolimus cream, 1% should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. in dermal embryofetal developmental studies, no maternal or fetal toxicity was observed up to the highest practicable doses tested, 10 mg/kg/day (1% pimecrolimus cream) in rats (0.14x mrhd based on body surface area) and 10 mg/kg/day (1% pimecrolimus cream) in rabbits (0.65x mrhd based on auc comparisons). the 1% pimecrolimus cream was administered topically for 6 hours/day during the period of organogenesis in rats and rabbits (gestational days 6 to 21 in rats and gestational days 6 to 20 in rabbits). a second dermal embryofetal development study was conducted in rats using pimecrolimus cream applied dermally to pregnant rats (1 g cream/kg body weight of 0.2%, 0.6% and 1% pimecrolimus cream) from gestation day 6 to 17 at doses of 2, 6, and 10 mg/kg/day with daily exposure of approximately 22 hours. no maternal, reproductive, or embryo-fetal toxicity attributable to pimecrolimus was noted at 10 mg/kg/day (0.66x mrhd based on auc comparisons), the highest dose evaluated in this study. no teratogenicity was noted in this study at any dose. a combined oral fertility and embryofetal developmental study was conducted in rats and an oral embryofetal developmental study was conducted in rabbits. pimecrolimus was administered during the period of organogenesis (2 weeks prior to mating until gestational day 16 in rats, gestational days 6 to 18 in rabbits) up to dose levels of 45 mg/kg/day in rats and 20 mg/kg/day in rabbits. in the absence of maternal toxicity, indicators of embryofetal toxicity (post-implantation loss and reduction in litter size) were noted at 45 mg/kg/day (38x mrhd based on auc comparisons) in the oral fertility and embryofetal developmental study conducted in rats. no malformations in the fetuses were noted at 45 mg/kg/day (38x mrhd based on auc comparisons) in this study. no maternal toxicity, embryotoxicity or teratogenicity were noted in the oral rabbit embryofetal developmental toxicity study at 20 mg/kg/day (3.9x mrhd based on auc comparisons), which was the highest dose tested in this study. a second oral embryofetal development study was conducted in rats. pimecrolimus was administered during the period of organogenesis (gestational days 6 to 17) at doses of 2, 10 and 45 mg/kg/day. maternal toxicity, embryolethality and fetotoxicity were noted at 45 mg/kg/day (271x mrhd based on auc comparisons). a slight increase in skeletal variations that were indicative of delayed skeletal ossification was also noted at this dose. no maternal toxicity, embryolethality or fetotoxicity were noted at 10 mg/kg/day (16x mrhd based on auc comparisons). no teratogenicity was noted in this study at any dose. a second oral embryofetal development study was conducted in rabbits. pimecrolimus was administered during the period of organogenesis (gestational days 7 to 20) at doses of 2, 6 and 20 mg/kg/day. maternal toxicity, embryotoxicity and fetotoxicity were noted at 20 mg/kg/day (12x mrhd based on auc comparisons). a slight increase in skeletal variations that were indicative of delayed skeletal ossification was also noted at this dose. no maternal toxicity, embryotoxicity or fetotoxicity were noted at 6 mg/kg/day (5x mrhd based on auc comparisons). no teratogenicity was noted in this study at any dose. an oral peri- and post-natal developmental study was conducted in rats. pimecrolimus was administered from gestational day 6 through lactational day 21 up to a dose level of 40 mg/kg/day. only 2 of 22 females delivered live pups at the highest dose of 40 mg/kg/day. postnatal survival, development of the f1 generation, their subsequent maturation and fertility were not affected at 10 mg/kg/day (12x mrhd based on auc comparisons), the highest dose evaluated in this study. pimecrolimus was transferred across the placenta in oral rat and rabbit embryofetal developmental studies. it is not known whether this drug is excreted in human milk. because of the potential for serious adverse reactions in nursing infants from pimecrolimus, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother. pimecrolimus cream, 1% is not indicated for use in children less than 2 years of age. the long-term safety and effects of pimecrolimus cream, 1% on the developing immune system are unknown three phase 3 pediatric trials were conducted involving 1,114 subjects 2 to 17 years of age. two trials were 6-week randomized vehicle-controlled trials with a 20-week open-label phase and one was a vehicle-controlled (up to 1 year) safety trial with the option for sequential topical corticosteroid use. of these subjects 542 (49%) were 2 to 6 years of age. in the short-term trials, 11% of pimecrolimus cream, 1% subjects did not complete these trials and 1.5% of pimecrolimus cream, 1%, subjects discontinued due to adverse events. in the one-year trial, 32% of pimecrolimus cream, 1%, subjects did not complete this trial and 3% of pimecrolimus cream, 1%, subjects discontinued due to adverse events. most discontinuations were due to unsatisfactory therapeutic effect. the most common local adverse event in the short-term trials of pimecrolimus cream, 1% in pediatric subjects ages 2 to 17 was application site burning (10% vs. 13% vehicle); the incidence in the long-term trial was 9% pimecrolimus cream, 1% vs. 7% vehicle [see adverse reactions (6.1)]. adverse events that were more frequent (>5%) in subjects treated with pimecrolimus cream, 1% compared to vehicle were headache (14% vs. 9%) in the short-term trial. nasopharyngitis (26% vs. 21%), influenza (13% vs. 4%), pharyngitis (8% vs. 3%), viral infection (7% vs. 1%), pyrexia (13% vs. 5%), cough (16% vs. 11%), and headache (25% vs. 16%) were increased over vehicle in the 1-year safety trial [see adverse reactions (6.1)]. in 843 subjects ages 2 to 17 years treated with pimecrolimus cream, 1%9 (0.8%) developed eczema herpeticum (5 on pimecrolimus cream alone and 4 on pimecrolimus cream, 1% used in sequence with corticosteroids). in 211 subjects on vehicle alone, there were no cases of eczema herpeticum. the majority of adverse events were mild to moderate in severity. two phase 3 trials were conducted involving 436 infants age 3 months to 23 months. one 6-week randomized vehicle-controlled trial with a 20-week open-label phase and one safety trial, up to one year, were conducted. in the 6-week trial, 11% of pimecrolimus cream, 1% and 48% of vehicle subjects did not complete this trial; no subject in either group discontinued due to adverse events. infants on pimecrolimus cream, 1% had an increased incidence of some adverse events compared to vehicle. in the 6-week vehicle-controlled trial these adverse events included pyrexia (32% vs. 13% vehicle), uri (24% vs. 14%), nasopharyngitis (15% vs. 8%), gastroenteritis (7% vs. 3%), otitis media (4% vs. 0%), and diarrhea (8% vs. 0%). in the open-label phase of the trial, for infants who switched to pimecrolimus cream, 1% from vehicle, the incidence of the above-cited adverse events approached or equaled the incidence of those subjects who remained on pimecrolimus cream, 1%. in the 6 month safety data, 16% of pimecrolimus cream, 1% and 35% of vehicle subjects discontinued early and 1.5% of pimecrolimus cream, 1% and 0% of vehicle subjects discontinued due to adverse events. infants on pimecrolimus cream, 1% had a greater incidence of some adverse events as compared to vehicle. these included pyrexia (30% vs. 20%), uri (21% vs. 17%), cough (15% vs. 9%), hypersensitivity (8% vs. 2%), teething (27% vs. 22%), vomiting (9% vs. 4%), rhinitis (13% vs. 9%), viral rash (4% vs. 0%), rhinorrhea (4% vs. 0%), and wheezing (4% vs. 0%). the systemic exposure to pimecrolimus from pimecrolimus cream, 1% was investigated in 28 pediatric subjects with atopic dermatitis (20% to 80% bsa involvement) between the ages of 8 months to 14 yrs. following twice daily application for three weeks, blood concentrations of pimecrolimus were <2 ng/ml with 60% (96/161) of the blood samples having blood concentration below the limit of quantification (0.5 ng/ml). however, more children (23 children out of the total 28 children investigated) had at least one detectable blood level as compared to the adults (12 adults out of the total 52 adults investigated) over a 3-week treatment period. due to the erratic nature of the blood levels observed, no correlation could be made between amount of cream, degree of bsa involvement, and blood concentrations. in general, the blood concentrations measured in adult atopic dermatitis subjects were comparable to those seen in the pediatric population. in a second group of 30 pediatric subjects aged 3 to 23 months with 10% to 92% bsa involvement, following twice daily application for three weeks, blood concentrations of pimecrolimus were <2.6 ng/ml with 65% (75/116) of the blood samples having blood concentration below 0.5ng/ml, and 27% (31/116) below the limit of quantification (0.1 ng/ml) for these trials. overall, a higher proportion of detectable blood levels was seen in the pediatric subject population as compared to adult population. this increase in the absolute number of positive blood levels may be due to the larger surface area to body mass ratio seen in these younger subjects. in addition, a higher incidence of upper respiratory symptoms/infections was also seen relative to the older age group in the pk trials. at this time, a causal relationship between these findings and pimecrolimus cream, 1% use cannot be ruled out. nine (9) subjects ≥65 years old received pimecrolimus cream, 1% in phase 3 trials. clinical trials of pimecrolimus cream, 1% did not include sufficient numbers of subjects aged 65 and over to assess efficacy and safety.

Egyesült Államok - angol - NLM (National Library of Medicine)

glenmark pharmaceuticals inc., usa - rufinamide (unii: wfw942pr79) (rufinamide - unii:wfw942pr79) - rufinamide tablets are indicated for adjunctive treatment of seizures associated with lennox-gastaut syndrome in pediatric patients 1 year of age and older and in adults. rufinamide is contraindicated in patients with familial short qt syndrome [see warnings and precautions (5.3) ]. pregnancy exposure registry there is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to aeds, such as rufinamide, during pregnancy. encourage women who are taking rufinamide during pregnancy to enroll in the north american antiepileptic drug (naaed) pregnancy registry by calling 1-888-233-2334 or visiting http://www.aedpregnancyregistry.org. risk summary there are no adequate data on the developmental risks associated with use of rufinamide in pregnant women. in animal reproduction studies, oral administration of rufinamide resulted in developmental toxicity in pregnant rats and rabbits at clinically relevant doses [see data] . 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. the background risk of major birth defects and miscarriage for the indicated population is unknown. data animal data oral administration of rufinamide (0, 20, 100, or 300 mg/kg/day) to pregnant rats throughout organogenesis resulted in decreased fetal weight and increased incidence of fetal skeletal abnormalities at 100 and 300 mg/kg/day, which were associated with maternal toxicity. the maternal plasma exposure (auc) at the no- adverse effect dose (20 mg/kg/day) for developmental toxicity was less than that in humans at the maximum recommended human dose (mrhd) of 3200 mg/day. oral administration of rufinamide (0, 30, 200, or 1000 mg/kg/day) to pregnant rabbits throughout organogenesis resulted in embryofetal death, decreased fetal body weight, and increased incidence of fetal visceral and skeletal abnormalities at doses of 200 and 1000 mg/kg/day. the high dose (1000 mg/kg/day) was associated with abortion. plasma exposure (auc) at the no-adverse effect dose (30 mg/kg/day) was less than that in humans at the mrhd. when rufinamide was orally administered (0, 5, 30, or 150 mg/kg/day) to pregnant rats throughout pregnancy and lactation, decreased offspring growth and survival were observed at all doses tested. a no-effect dose for adverse effects on pre- and postnatal development was not established. at the lowest dose tested (5 mg/kg/day), plasma exposure (auc) was less than that in humans at the mrhd. risk summary there are no data on the presence of rufinamide in human milk, the effects on the breastfed infant, or the effects of the drug on milk production. the developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for rufinamide and any potential adverse effects on the breastfed infant from rufinamide or from the underlying maternal condition. contraception use of rufinamide may reduce the effectiveness of hormonal contraceptives containing ethinyl estradiol or norethindrone. advise women of reproductive potential taking rufinamide who are using a contraceptive containing ethinyl estradiol and norethindrone to use an additional non-hormonal form of contraception [see drug interactions (7.3) and clinical pharmacology (12.3)] . infertility the effect of rufinamide on fertility in humans has not been established. oral administration of rufinamide (20, 60, 200, and 600 mg/kg/day) to male and female rats prior to mating, during mating, and during early gestation (females only) resulted in the impairment of fertility at all dose levels tested. the no-effect dose was not established. the plasma exposure level at 20 mg/kg was approximately 0.2 times the human plasma auc at the mrhd [see nonclinical toxicology ( error! hyperlink reference not valid. )]. safety and effectiveness have been established in pediatric patients 1 to 17 years of age. the effectiveness of rufinamide in pediatric patients 4 years of age and older was based upon an adequate and well-controlled trial of rufinamide that included both adults and pediatric patients, 4 years of age and older, with lennox gastaut syndrome. the effectiveness in patients 1 to less than 4 years was based upon a bridging pharmacokinetic and safety study [see dosage and administration (2.1), adverse reactions ( error! hyperlink reference not valid. ), and clinical studies ( error! hyperlink reference not valid. ) ]. the pharmacokinetics of rufinamide in the pediatric patients, ages 1 to less than 4 years of age is similar to children older than 4 years of age and adults [see clinical pharmacology (12.3)] . safety and effectiveness in pediatric patients below the age of 1 year has not been established. oral administration of rufinamide (0, 15, 50, or 150 mg/kg) to young rats for 10 weeks starting on postnatal day 7 resulted in decreased brain weights at the mid and high doses and neurobehavioral impairment (learning and memory deficit, altered startle response, decreased locomotor activity) and decreased growth (decreased body weight) at the highest dose tested. the no-effect dose for adverse effects on postnatal development in rats (15 mg/kg) was associated with a plasma exposure (auc) lower than that in humans at the maximum recommended human dose (mrhd) of 3200 mg/day. clinical studies of rufinamide did not include sufficient numbers of subjects aged 65 and over to determine whether they respond differently from younger subjects. in general, dose selection for an elderly patient should be cautious, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy. pharmacokinetics of rufinamide in the elderly are similar to that in the young subjects [see clinical pharmacology (12.3) ]. rufinamide pharmacokinetics in patients with severe renal impairment (creatinine clearance < 30 ml/min) was similar to that of healthy subjects. dose adjustment in patients undergoing dialysis should be considered [see clinical pharmacology (12.3) ]. use of rufinamide in patients with severe hepatic impairment (child-pugh score 10 to 15) is not recommended. caution should be exercised in treating patients with mild (child-pugh score 5 to 6) to moderate (child-pugh score 7 to 9) hepatic impairment.

Egyesült Államok - angol - NLM (National Library of Medicine)

glenmark pharmaceuticals inc., usa - esomeprazole magnesium (unii: r6dxu4way9) (esomeprazole - unii:n3pa6559ft) - adults 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. pediatric patients 12 years to 17 years of age 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 delayed-release capsules are indicated for the maintenance of healing of ee in adults. controlled studies do not extend beyond 6 months. adults 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. pediatric patients 12 years to 17 years of age esomeprazole magnes

Egyesült Államok - angol - NLM (National Library of Medicine)

glenmark pharmaceuticals inc. usa - lacosamide (unii: 563ks2pqy5) (lacosamide - unii:563ks2pqy5) - lacosamide tablets are indicated for the treatment of partial-onset seizures in patients 4 years of age and older. additional pediatric use information is approved for ucb, inc.’s vimpat® (lacosamide) tablets. however, due to ucb, inc.’s marketing exclusivity rights, this drug product is not labeled with that information. none. pregnancy exposure registry there is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to antiepileptic drugs (aeds), such as lacosamide, during pregnancy. encourage women who are taking lacosamide during pregnancy to enroll in the north american antiepileptic drug (naaed) pregnancy registry by calling 1-888-233-2334 or visiting http://www.aedpregnancyregistry.org/. risk summary available data from the north american antiepileptic drug (naaed) pregnancy registry, a prospective cohort study, case reports, and a case series with lacosamide use in pregnant women are insufficient to identify a drug associated risk of major birth defects, miscarriage or other

Egyesült Államok - angol - NLM (National Library of Medicine)

glenmark pharmaceuticals inc., usa - sodium phenylbutyrate (unii: nt6k61736t) (phenylbutyric acid - unii:7wy7ybi87e) - sodium phenylbutyrate tablets are indicated as adjunctive therapy in the chronic management of patients with urea cycle disorders involving deficiencies of carbamylphosphate synthetase (cps), ornithine transcarbamylase (otc), or argininosuccinic acid synthetase (as). it is indicated in all patients with neonatal-onset deficiency (complete enzymatic deficiency, presenting within the first 28 days of life). it is also indicated in patients with late-onset disease (partial enzymatic deficiency, presenting after the first month of life) who have a history of hyperammonemic encephalopathy. it is important that the diagnosis be made early and treatment initiated immediately to improve survival. any episode of acute hyperammonemia should be treated as a life-threatening emergency. sodium phenylbutyrate tablets must be combined with dietary protein restriction and, in some cases, essential amino acid supplementation (see nutritional supplementation subsection of the dosage and administration section). previously, neonatal-onset disease was almost universally fatal within the first year of life, even when treated with peritoneal dialysis and essential amino acids or their nitrogen-free analogs. however, with hemodialysis, use of alternative waste nitrogen excretion pathways (sodium phenylbutyrate, sodium benzoate, and sodium phenylacetate), dietary protein restriction, and, in some cases, essential amino acid supplementation, the survival rate in newborns diagnosed after birth but within the first month of life is almost 80%. most deaths have occurred during an episode of acute hyperammonemic encephalopathy. patients with neonatal-onset disease have a high incidence of mental retardation. those who had iq tests administered had an incidence of mental retardation as follows: ornithine transcarbamylase deficiency, 100% (14/14 patients tested); argininosuccinic acid synthetase deficiency, 88% (15/17 patients tested); and carbamylphosphate synthetase deficiency, 57% (4/7 patients tested). retardation was severe in the majority of the retarded patients. in patients diagnosed during gestation and treated prior to any episode of hyperammonemic encephalopathy, survival is 100%, but even in these patients, most subsequently demonstrate cognitive impairment or other neurologic deficits. in late-onset deficiency patients, including females heterozygous for ornithine transcarbamylase deficiency, who recover from hyperammonemic encephalopathy and are then treated chronically with sodium phenylbutyrate and dietary protein restriction, the survival rate is 98%. the two deaths in this group of patients occurred during episodes of hyperammonemic encephalopathy. however, compliance with the therapeutic regimen has not been adequately documented to allow evaluation of the potential for sodium phenylbutyrate tablets and dietary protein restriction to prevent mental deterioration and recurrence of hyperammonemic encephalopathy if carefully adhered to. the majority of these patients tested (30/46 or 65%) have iq’s in the average to low average/borderline mentally retarded range. reversal of preexisting neurologic impairment is not likely to occur with treatment and neurologic deterioration may continue in some patients. even on therapy, acute hyperammonemic encephalopathy recurred in the majority of patients for whom the drug is indicated. sodium phenylbutyrate tablets may be required lifelong unless orthotopic liver transplantation is elected. (see clinical pharmacology, pharmacodynamics subsection for the biochemical effects of sodium phenylbutyrate tablets). sodium phenylbutyrate tablets should not be used to manage acute hyperammonemia, which is a medical emergency.

Egyesült Államok - angol - NLM (National Library of Medicine)

glenmark pharmaceuticals inc., usa - bumetanide (unii: 0y2s3xuq5h) (bumetanide - unii:0y2s3xuq5h) - bumetanide injection is indicated for the treatment of edema associated with congestive heart failure, hepatic and renal disease, including the nephrotic syndrome. almost equal diuretic response occurs after oral and parenteral administration of bumetanide. therefore, if impaired gastrointestinal absorption is suspected or oral administration is not practical, bumetanide should be given by the intramuscular or intravenous route. successful treatment with bumetanide following instances  of allergic reactions  to  furosemide  suggests a lack of cross-sensitivity. bumetanide is contraindicated in anuria. although bumetanide can be used to induce diuresis in renal insufficiency, any marked increase in blood urea nitrogen or creatinine, or the development of oliguria during therapy of patients with progressive renal disease, is an indication for discontinuation of treatment with bumetanide. bumetanide is also contraindicated in patients in hepatic coma or in states of severe electrolyte depletion until the conditi

Egyesült Államok - angol - NLM (National Library of Medicine)

glenmark pharmaceuticals inc., usa - teriflunomide (unii: 1c058ikg3b) (teriflunomide - unii:1c058ikg3b) - teriflunomide tablets are indicated for the treatment of relapsing forms of multiple sclerosis (ms), to include clinically isolated syndrome, relapsing-remitting disease, and active secondary progressive disease, in adults. teriflunomide tablets are contraindicated in/with: risk summary teriflunomide is contraindicated for use in pregnant women and females of reproductive potential not using effective contraception because of the potential for fetal harm based on animal data [see contraindications (4) and warnings and precautions (5.2)]. in animal reproduction studies in rat and rabbit, oral administration of teriflunomide during organogenesis caused teratogenicity and embryolethality at plasma exposures (auc) lower than that at the maximum recommended human dose (mrhd) of 14 mg/day [see data] . available human data from pregnancy registries, clinical trials, pharmacovigilance cases, and published literature are too limited to draw any conclusions, but they do not clearly indicate increased birth defects or m

Egyesült Államok - angol - NLM (National Library of Medicine)

glenmark pharmaceuticals inc., usa - omeprazole (unii: kg60484qx9) (omeprazole - unii:kg60484qx9) - omeprazole 10 mg - omeprazole delayed-release capsules are indicated for short-term treatment of active duodenal ulcer in adults. most patients heal within four weeks. some patients may require an additional four weeks of therapy. eradication of h. pylori has been shown to reduce the risk of duodenal ulcer recurrence. triple therapy omeprazole delayed-release capsules in combination with clarithromycin and amoxicillin, is indicated for treatment of patients with h. pylori infection and duodenal ulcer disease (active or up to 1-year history) to eradicate h. pylori in adults. dual therapy omeprazole delayed-release capsules in combination with clarithromycin are indicated for treatment of patients with h. pylori infection and duodenal ulcer disease to eradicate h. pylori in adults. among patients who fail therapy, omeprazole delayed-release capsules with clarithromycin is more likely to be associated with the development of clarithromycin resistance as compared with triple therapy. in patients who fail therapy, susceptibilit

Egyesült Államok - angol - NLM (National Library of Medicine)

glenmark pharmaceuticals inc., usa - topiramate (unii: 0h73wjj391) (topiramate - unii:0h73wjj391) - topiramate 25 mg - topiramate tablets are indicated as initial monotherapy for the treatment of partial-onset or primary generalized tonic‑clonic seizures in patients 2 years of age and older. topiramate tablets are indicated as adjunctive therapy for the treatment of partial-onset seizures, primary generalized tonic-clonic seizures, and seizures associated with lennox-gastaut syndrome in patients 2 years of age and older. topiramate tablets are indicated for the preventive treatment of migraine in patients 12 years of age and older. none. pregnancy exposure registry there is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to topiramate during pregnancy. patients should be encouraged to enroll in the north american antiepileptic drug (naaed) pregnancy registry if they become pregnant. this registry is collecting information about the safety of antiepileptic drugs during pregnancy. to enroll, patients can call the toll-free number 1-888-233-2334. information about the north american drug pregnancy

Egyesült Államok - angol - NLM (National Library of Medicine)

glenmark generics inc. usa - sulfamethoxazole (unii: je42381tnv) (sulfamethoxazole - unii:je42381tnv), trimethoprim (unii: an164j8y0x) (trimethoprim - unii:an164j8y0x) - sulfamethoxazole 400 mg - to reduce the development of drug-resistant bacteria and maintain the effectiveness of sulfamethoxazole and trimethoprim tablets usp and other antibacterial drugs, sulfamethoxazole and trimethoprim tablets usp 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 empiric selection of therapy. urinary tract infections: for the treatment of urinary tract infections due to susceptible strains of the following organisms: escherichia coli , klebsiella species, enterobacter species, morganella morganii , proteus mirabilis and proteus vulgaris . it is recommended that initial episodes of uncomplicated urinary tract infections be treated with a single effective antibacterial agent rather than the combination. acute ot