Spojené státy - angličtina - NLM (National Library of Medicine)

bryant ranch prepack - olmesartan medoxomil (unii: 6m97xtv3hd) (olmesartan - unii:8w1iqp3u10) - olmesartan medoxomil tablets are indicated for the treatment of hypertension in adults and children six years of age and older, 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. there are no controlled trials demonstrating risk reduction with olmesartan medoxomil. 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. it may be used alone or in combination with other antihypertensive agents. do not co-administer aliskiren with olmesartan medoxomil in patients with diabetes [see drug interactions (7.3)]. risk summary olmesartan medoxomil 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. 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. in animal reproduction studies, olmesartan medoxomil treatment during organogenesis resulted in increased embryofetal toxicity in rats at doses lower than maternally toxic doses. when pregnancy is detected, discontinue olmesartan medoxomil as soon as possible. consider alternative antihypertensive therapy during pregnancy. 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. clinical considerations disease-associated maternal and/or embryo/fetal risk 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. fetal/neonatal adverse reactions oligohydramnios in pregnant women who use drugs affecting the renin-angiotensin system in the second and third trimesters of pregnancy can result in the following: reduced fetal renal function leading to anuria and renal failure, fetal lung hypoplasia, skeletal deformations, including skull hypoplasia, hypotension and death. in patients taking olmesartan medoxomil tablets during pregnancy, perform serial ultrasound examinations to assess the intra-amniotic environment. fetal testing may be appropriate, based on the week of gestation. 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 olmesartan medoxomil for hypotension, oliguria, and hyperkalemia. in neonates with a history of in utero exposure to olmesartan medoximil, if oliguria or hypotension occurs, utilize measures to maintain adequate blood pressure and renal perfusion. exchange transfusions or dialysis may be required as a means of reversing hypotension and supporting renal function. data animal data no teratogenic effects were observed when olmesartan medoxomil was administered to pregnant rats at oral doses up to 1000 mg/kg/day (240 times the maximum recommended human dose (mrhd) on a mg/m 2 basis) or pregnant rabbits at oral doses up to 1 mg/kg/day (half the mrhd on a mg/m 2 basis; higher doses could not be evaluated for effects on fetal development as they were lethal to the does). in rats, significant decreases in pup birth weight and weight gain were observed at doses ≥1.6 mg/kg/day, and delays in developmental milestones (delayed separation of ear auricula, eruption of lower incisors, appearance of abdominal hair, descent of testes, and separation of eyelids) and dose-dependent increases in the incidence of dilation of the renal pelvis were observed at doses ≥ 8 mg/kg/day. the no observed effect dose for developmental toxicity in rats is 0.3 mg/kg/day, about one-tenth the mrhd of 40 mg/day. risk summary there is no information regarding the presence of olmesartan in human milk, the effects on the breastfed infant, or the effects on milk production. olmesartan is secreted at low concentration in the milk of lactating rats (see data) . because of the potential for adverse effects on the nursing infant, a decision should be made whether to discontinue nursing or discontinue the drug, taking into account the importance of the drug to the mother. data presence of olmesartan in milk was observed after a single oral administration of 5 mg/kg [ 14 c] olmesartan medoxomil to lactating rats. the antihypertensive effects of olmesartan medoxomil were evaluated in one randomized, double-blind clinical study in pediatric patients 1 to 16 years of age [see clinical studies (14.2)] . the pharmacokinetics of olmesartan medoxomil were evaluated in pediatric patients 1 to 16 years of age [see clinical pharmacology (12.3)] . olmesartan medoxomil was generally well tolerated in pediatric patients, and the adverse experience profile was similar to that described for adults. olmesartan medoxomil has not been shown to be effective for hypertension in children <6 years of age. use of olmesartan medoxomil in children <1 year of age is not recommended [see warnings and precautions (5.2)]. the renin-angiotensin-aldosterone system (raas) plays a critical role in kidney development. raas blockade has been shown to lead to abnormal kidney development in very young mice. administering drugs that act directly on the renin-angiotensin aldosterone system (raas) can alter normal renal development. of the total number of hypertensive patients receiving olmesartan medoxomil in clinical studies, more than 20% were 65 years of age and over, while more than 5% were 75 years of age and older. no overall differences in effectiveness or safety were observed between elderly 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 [see clinical pharmacology (12.3)] . increases in auc 0-∞ and c max were observed in patients with moderate hepatic impairment compared to those in matched controls, with an increase in auc of about 60%. no initial dosage adjustment is recommended for patients with moderate to marked hepatic dysfunction [see clinical pharmacology (12.3)] . patients with renal insufficiency have elevated serum concentrations of olmesartan compared to subjects with normal renal function. after repeated dosing, the auc was approximately tripled in patients with severe renal impairment (creatinine clearance <20 ml/min). no initial dosage adjustment is recommended for patients with moderate to marked renal impairment (creatinine clearance <40 ml/min) [see dosage and administration (2.1), warnings and precautions (5.4) and clinical pharmacology (12.3)] . the antihypertensive effect of olmesartan medoxomil was smaller in black patients (usually a low-renin population), as has been seen with ace inhibitors, beta-blockers and other angiotensin receptor blockers.

Spojené státy - angličtina - NLM (National Library of Medicine)

bionpharma inc. - enalapril maleate (unii: 9o25354epj) (enalaprilat anhydrous - unii:q508q118jm) - enalapril maleate oral solution is indicated for the treatment of symptomatic heart failure, usually in combination with diuretics and digitalis. in these patients, enalapril maleate oral solution increases survival and decreases the frequency of hospitalization. in clinically stable asymptomatic patients with left ventricular dysfunction (ejection fraction ≤35 percent), enalapril maleate oral solution decreases the rate of development of overt heart failure and decreases the incidence of hospitalization for heart failure. enalapril is contraindicated in patients with: - a history of angioedema or hypersensitivity related to previous treatment with an angiotensin converting enzyme (ace) inhibitor. [see warnings and precautions ( 5.2)] - hereditary or idiopathic angioedema. [see warnings and precautions ( 5.2)] do not co-administer aliskiren with enalapril in patients with diabetes [see drug interactions ( 7.2)] . enalapril is contraindicated in combination with a neprilysin inhibitor (e.g., sacubitril). do not administer enalapril within 36 hours of switching to or from sacubitril/valsartan, a neprilysin inhibitor [see warnings and precautions ( 5.2)] . risk summary enalapril 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. 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. when pregnancy is detected, discontinue enalapril as soon as possible. the estimated background risk of major birth defects and miscarriage for the indicated population(s) are unknown. in the general u.s. population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2 to 4% and 15 to 20%, respectively. clinical considerations adverse reactions in the fetus or in neonates with a history of in utero exposure to enalapril maleate. use of drugs that act on the renin-angiotensin system during the second and third trimesters of pregnancy can result in the following: reduced fetal renal function leading to anuria and renal failure, oligohydramnios, 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. perform serial ultrasound examinations to assess the intra-amniotic environment. fetal testing may be appropriate, based on the week of pregnancy. patients and physicians should be aware, however, that oligohydraminos may not appear until after the fetus has sustained irreversible injury. closely observe infants with histories of in utero exposure to enalapril for hypotension, oliguria, and hyperkalemia. if oliguria or hypotension occurs in neonates with a history of in utero exposure to enalapril, support blood pressure and renal perfusion. exchange transfusions or dialysis may be required as a means of reversing hypotension and substituting for disordered renal function. risk summary enalapril and enalaprilat have been detected in human breast milk. because of the potential for severe adverse reactions in the breastfed infant, including hypotension, hyperkalemia, and renal impairment, advise women not to breastfeed during treatment with enalapril. neonates with a history of in utero exposure to enalapril maleate if oliguria or hypotension occurs, direct attention toward support of 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. enalapril, which crosses the placenta, has been removed from neonatal circulation by peritoneal dialysis with some clinical benefit, and theoretically may be removed by exchange transfusion, although there is no experience with the latter procedure. pediatric patients with heart failure or asymptomatic left ventricular dysfunction  safety and effectiveness of enalapril have not been established in pediatric patients with heart failure or asymptomatic left ventricular dysfunction. this drug is known to be substantially excreted by the kidney, and the risk of adverse 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. ace inhibitors, including enalapril, as monotherapy have an effect on blood pressure that is less in black patients than in non-blacks. use a lower initial dose of enalapril in patients undergoing hemodialysis and in patients whose egfr is ≤ 30 ml/min [see clinical pharmacology ( 12.3)] .

Spojené státy - angličtina - NLM (National Library of Medicine)

bryant ranch prepack - lisinopril (unii: e7199s1ywr) (lisinopril anhydrous - unii:7q3p4bs2fd) - lisinopril tablets are indicated for the treatment of hypertension in adult patients and pediatric patients 6 years of age and older to lower blood pressure. lowering blood pressure lowers the risk of fatal and non-fatal 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. 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 1 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. lisinopril tablets may be administered alone or with other antihypertensive agents [see clinical studies ( 14.1 )] . lisinopril tablets are indicated to reduce signs and symptoms of systolic heart failure [see clinical studies ( 14.2 )] . lisinopril tablets are indicated for the reduction of mortality in treatment of hemodynamically stable patients within 24 hours of acute myocardial infarction. patients should receive, as appropriate, the standard recommended treatments such as thrombolytics, aspirin and beta-blockers [see clinical studies ( 14.3 )] . lisinopril tablets are contraindicated in combination with a neprilysin inhibitor (e.g., sacubitril). do not administer lisinopril tablets within 36 hours of switching to or from sacubitril/valsartan, a neprilysin inhibitor [see warnings and precautions (5.2)]. lisinopril tablets are contraindicated in patients with: - a history of angioedema or hypersensitivity related to previous treatment with an angiotensin converting enzyme inhibitor - hereditary or idiopathic angioedema do not co-administer aliskiren with lisinopril tablets in patients with diabetes [see drug interactions ( 7.4 )]. risk summary lisinopril 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. 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. when pregnancy is detected, discontinue lisinopril as soon as possible. the estimated background risk of major birth defects and miscarriage for the indicated population(s) are unknown. in the general u.s. population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively. clinical considerations disease-associated maternal and/or embryo/fetal risk 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. fetal/neonatal adverse reactions oligohydramnios in pregnant women who use drugs affecting the renin-angiotensin system in the second and third trimesters of pregnancy can result in the following: reduced fetal renal function leading to anuria and renal failure, fetal lung hypoplasia and 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. perform serial ultrasound examinations to assess the intra-amniotic environment. fetal testing may be appropriate, based on the week of pregnancy. 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 lisinopril for hypotension, oliguria, and hyperkalemia. if oliguria or hypotension occur in neonates with a history of in utero exposure to lisinopril, support blood pressure and renal perfusion. exchange transfusions or dialysis may be required as a means of reversing hypotension and substituting for disordered renal function.  risk summary no data are available regarding the presence of lisinopril in human milk or the effects of lisinopril on the breast fed infant or on milk production. lisinopril is present in rat milk. because of the potential for severe adverse reactions in the breastfed infant, advise women not to breastfeed during treatment with lisinopril. antihypertensive effects and safety of lisinopril have been established in pediatric patients aged 6 to 16 years [see dosage and administration ( 2.1 ) and clinical studies ( 14.1 )] . no relevant differences between the adverse reaction profile for pediatric patients and adult patients were identified. safety and effectiveness of lisinopril have not been established in pediatric patients under the age of 6 or in pediatric patients with glomerular filtration rate < 30 ml/min/1.73 m2 [see dosage and administration ( 2.1 ), clinical pharmacology ( 12.3 ), and clinical studies ( 14.1 )] . neonates with a history of in utero exposure to lisinopril if oliguria or hypotension occurs, direct attention toward support of 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. no dosage adjustment with lisinopril is necessary in elderly patients. in a clinical study of lisinopril in patients with myocardial infarctions (gissi-3 trial) 4,413 (47%) were 65 and over, while 1,656 (18%) were 75 and over. in this study, 4.8 % of patients aged 75 years and older discontinued lisinopril treatment because of renal dysfunction vs. 1.3% of patients younger than 75 years. no other differences in safety or effectiveness were observed between elderly and younger patients, but greater sensitivity of some older individuals cannot be ruled out. ace inhibitors, including lisinopril, have an effect on blood pressure that is less in black patients than in non blacks. dose adjustment of lisinopril is required in patients undergoing hemodialysis or whose creatinine clearance is ≤ 30 ml/min. no dose adjustment of lisinopril is required in patients with creatinine clearance >30 ml/min [see dosage and administration ( 2.4 ) and clinical pharmacology ( 12.3 )] .

Spojené státy - angličtina - NLM (National Library of Medicine)

bryant ranch prepack - lisinopril (unii: e7199s1ywr) (lisinopril anhydrous - unii:7q3p4bs2fd) - lisinopril tablets are indicated for the treatment of hypertension in adult patients and pediatric patients 6 years of age and older to lower blood pressure. lowering blood pressure lowers the risk of fatal and non-fatal 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. 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 1 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. lisinopril tablets may be administered alone or with other antihypertensive agents [see clinical studies ( 14.1 )] . lisinopril tablets are indicated to reduce signs and symptoms of systolic heart failure [see clinical studies ( 14.2 )] . lisinopril tablets are indicated for the reduction of mortality in treatment of hemodynamically stable patients within 24 hours of acute myocardial infarction. patients should receive, as appropriate, the standard recommended treatments such as thrombolytics, aspirin and beta-blockers [see clinical studies ( 14.3 )] . lisinopril tablets are contraindicated in combination with a neprilysin inhibitor (e.g., sacubitril). do not administer lisinopril tablets within 36 hours of switching to or from sacubitril/valsartan, a neprilysin inhibitor [see warnings and precautions (5.2)]. lisinopril tablets are contraindicated in patients with: - a history of angioedema or hypersensitivity related to previous treatment with an angiotensin converting enzyme inhibitor - hereditary or idiopathic angioedema do not co-administer aliskiren with lisinopril tablets in patients with diabetes [see drug interactions ( 7.4 )]. risk summary lisinopril 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. 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. when pregnancy is detected, discontinue lisinopril as soon as possible. the estimated background risk of major birth defects and miscarriage for the indicated population(s) are unknown. in the general u.s. population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively. clinical considerations disease-associated maternal and/or embryo/fetal risk 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. fetal/neonatal adverse reactions oligohydramnios in pregnant women who use drugs affecting the renin-angiotensin system in the second and third trimesters of pregnancy can result in the following: reduced fetal renal function leading to anuria and renal failure, fetal lung hypoplasia and 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. perform serial ultrasound examinations to assess the intra-amniotic environment. fetal testing may be appropriate, based on the week of pregnancy. 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 lisinopril for hypotension, oliguria, and hyperkalemia. if oliguria or hypotension occur in neonates with a history of in utero exposure to lisinopril, support blood pressure and renal perfusion. exchange transfusions or dialysis may be required as a means of reversing hypotension and substituting for disordered renal function.  risk summary no data are available regarding the presence of lisinopril in human milk or the effects of lisinopril on the breast fed infant or on milk production. lisinopril is present in rat milk. because of the potential for severe adverse reactions in the breastfed infant, advise women not to breastfeed during treatment with lisinopril. antihypertensive effects and safety of lisinopril have been established in pediatric patients aged 6 to 16 years [see dosage and administration ( 2.1 ) and clinical studies ( 14.1 )] . no relevant differences between the adverse reaction profile for pediatric patients and adult patients were identified. safety and effectiveness of lisinopril have not been established in pediatric patients under the age of 6 or in pediatric patients with glomerular filtration rate < 30 ml/min/1.73 m2 [see dosage and administration ( 2.1 ), clinical pharmacology ( 12.3 ), and clinical studies ( 14.1 )] . neonates with a history of in utero exposure to lisinopril if oliguria or hypotension occurs, direct attention toward support of 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. no dosage adjustment with lisinopril is necessary in elderly patients. in a clinical study of lisinopril in patients with myocardial infarctions (gissi-3 trial) 4,413 (47%) were 65 and over, while 1,656 (18%) were 75 and over. in this study, 4.8 % of patients aged 75 years and older discontinued lisinopril treatment because of renal dysfunction vs. 1.3% of patients younger than 75 years. no other differences in safety or effectiveness were observed between elderly and younger patients, but greater sensitivity of some older individuals cannot be ruled out. ace inhibitors, including lisinopril, have an effect on blood pressure that is less in black patients than in non blacks. dose adjustment of lisinopril is required in patients undergoing hemodialysis or whose creatinine clearance is ≤ 30 ml/min. no dose adjustment of lisinopril is required in patients with creatinine clearance >30 ml/min [see dosage and administration ( 2.4 ) and clinical pharmacology ( 12.3 )] .

Spojené státy - angličtina - NLM (National Library of Medicine)

remedyrepack inc. - losartan potassium (unii: 3st302b24a) (losartan - unii:jms50mpo89) - losartan potassium tablets are indicated for the treatment of hypertension in adults and pediatric patients 6 years of age and older, to lower blood pressure. lowering blood pressure lowers the risk of fatal and nonfatal cardiovascular (cv) events, primarily strokes and myocardial infarction. these benefits have been seen in controlled trials of antihypertensive drugs from a wide variety of pharmacologic classes including losartan. 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 1 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. losartan potassium tablets may be administered with other antihypertensive agents.  losartan potassium tablets are indicated to reduce the risk of stroke in patients with hypertension and left ventricular hypertrophy, but there is evidence that this benefit does not apply to black patients [see use in specific populations (8.6) and clinical pharmacology (12.3)]. losartan potassium tablets are indicated for the treatment of diabetic nephropathy with an elevated serum creatinine and proteinuria (urinary albumin to creatinine ratio ≥300 mg/g) in patients with type 2 diabetes and a history of hypertension. in this population, losartan potassium tablet reduces the rate of progression of nephropathy as measured by the occurrence of doubling of serum creatinine or end stage renal disease (need for dialysis or renal transplantation) [see clinical studies (14.3)]. losartan potassium tablets are contraindicated: •in patients who are hypersensitive to any component of this product. •for coadministration with aliskiren in patients with diabetes. risk summary losartan potassium 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. 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. when pregnancy is detected, discontinue losartan potassium tablets as soon as possible (see clinical considerations). 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. clinical considerations disease-associated maternal and/or embryo/fetal risk hypertension in pregnancy increases the maternal risk for pre-eclampsia, gestational diabetes, premature delivery, and delivery complications (e.g., need for cesarean section, 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. fetal/neonatal adverse reactions oligohydramnios in pregnant women who use drugs affecting the renin-angiotensin system in the second and third trimesters of pregnancy can result in the following: 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 reninangiotensin system for a particular patient, apprise the mother of the potential risk to the fetus. in patients taking losartan potassium 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 losartan potassium tablets, unless it is 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 neonates with histories of in utero exposure to losartan potassium tablets for hypotension, oliguria, and hyperkalemia. in neonates with a history of in utero exposure to losartan potassium tablets, 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 replacing renal function. data animal data losartan potassium was administered orally to rats during the period of late gestation through lactation (gestation day 15 through lactation day 20) at doses of 10, 25, and 100 mg/kg/day. losartan potassium has been shown to produce adverse effects in rat fetuses and neonates, including decreased body weight, delayed physical and behavioral development, mortality and renal toxicity. with the exception of neonatal weight gain (which was affected at doses as low as 10 mg/kg/day), doses associated with these effects exceeded 25 mg/kg/day (approximately three times the maximum recommended human dose of 100 mg on a mg/m 2 basis). these findings are attributed to drug exposure in late gestation and during lactation. significant levels of losartan and its active metabolite were shown to be present in rat fetal plasma during late gestation and in rat milk. risk summary  it is not known whether losartan is excreted in human milk, but significant levels of losartan and its active metabolite were shown to be present in rat milk. because of the potential for adverse effects on the nursing infant, a decision should be made whether to discontinue nursing or discontinue the drug, taking into account the importance of the drug to the mother. antihypertensive effects of losartan potassium tablets have been established in hypertensive pediatric patients aged 6 to 16 years. safety and effectiveness have not been established in pediatric patients under the age of 6 or in pediatric patients with glomerular filtration rate <30 ml/min/1.73 m 2 [see dosage and administration (2.1), clinical pharmacology (12.3), and clinical studies (14.1)] . of the total number of patients receiving losartan potassium tablets in controlled clinical studies for hypertension, 391 patients (19%) were 65 years and over, while 37 patients (2%) were 75 years and over. in a controlled clinical study for renal protection in type 2 diabetic patients with proteinuria, 248 patients (33%) were 65 years and over. in a controlled clinical study for the reduction in the combined risk of cardiovascular death, stroke and myocardial infarction in hypertensive patients with left ventricular hypertrophy, 2857 patients (62%) were 65 years and over, while 808 patients (18%) were 75 years and over. no overall differences in effectiveness or safety were observed between these patients and younger patients, but greater sensitivity of some older individuals cannot be ruled out. in the life study, black patients with hypertension and left ventricular hypertrophy treated with atenolol were at lower risk of experiencing the primary composite endpoint compared with black patients treated with losartan potassium tablets (both cotreated with hydrochlorothiazide in the majority of patients). the primary endpoint was the first occurrence of stroke, myocardial infarction or cardiovascular death, analyzed using an intention-to-treat (itt) approach. in the subgroup of black patients (n=533, 6% of the life study patients), there were 29 primary endpoints among 263 patients on atenolol (11%, 26 per 1000 patient-years) and 46 primary endpoints among 270 patients (17%, 42 per 1000 patient-years) on losartan potassium tablets. this finding could not be explained on the basis of differences in the populations other than race or on any imbalances between treatment groups. in addition, blood pressure reductions in both treatment groups were consistent between black and non-black patients. given the difficulty in interpreting subset differences in large trials, it cannot be known whether the observed difference is the result of chance. however, the life study provides no evidence that the benefits of losartan potassium tablets on reducing the risk of cardiovascular events in hypertensive patients with left ventricular hypertrophy apply to black patients [see clinical studies (14.2)] . patients with renal insufficiency have elevated plasma concentrations of losartan and its active metabolite compared to subjects with normal renal function. no dose adjustment is necessary in patients with renal impairment unless a patient with renal impairment is also volume depleted [see dosage and administration (2.3), warnings and precautions (5.3) and clinical pharmacology (12.3)] . the recommended starting dose of losartan potassium tablet is 25 mg in patients with mild-to-moderate hepatic impairment. following oral administration in patients with mild-to-moderate hepatic impairment, plasma concentrations of losartan and its active metabolite were, respectively, 5 times and 1.7 times those seen in healthy volunteers. losartan potassium tablets have not been studied in patients with severe hepatic impairment [see dosage and administration (2.4) and clinical pharmacology (12.3)] .

Spojené státy - angličtina - NLM (National Library of Medicine)

bryant ranch prepack - benazepril hydrochloride (unii: n1sn99t69t) (benazeprilat - unii:jrm708l703) - benazepril hydrochloride 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 mm hg 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. it may be used alone or in combination with thiazide diuretics. benazepril hydrochloride tablets are contraindicated in patients: benazepril hydrochloride tablets are contraindicated in combination with a neprilysin inhibitor (e.g., sacubitril). do not administer benazepril hydrochloride tablets within 36 hours of switching to or from sacubitril/valsartan, a neprilysin inhibitor [see warnings and precautions (5.2)]. do not coadminister aliskiren with angiotensin receptor blockers, ace inhibitors; including benazepril hydrochloride tablets in patients with diabetes [see drug interactions (7.4)] . risk summary benazepril hydrochloride 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. 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. when pregnancy is detected, discontinue benazepril hydrochloride as soon as possible. the estimated background risk 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 general u.s. population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2-4% and 15-20%, respectively. clinical considerations disease-associated maternal and/or embryo/fetal risk 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. fetal/neonatal adverse reactions oligohydramnios in pregnant women who use drugs affecting the renin-angiotensin system in the second and third trimesters of pregnancy can result in the following: reduced fetal renal function leading to anuria and renal failure, fetal lung hypoplasia and 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. perform serial ultrasound examinations to assess the intra-amniotic environment. fetal testing may be appropriate, based on the week of pregnancy. 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 benazepril hydrochloride for hypotension, oliguria, and hyperkalemia. if oliguria or hypotension occur in neonates with a history of in utero exposure to benazepril hydrochloride, support blood pressure and renal perfusion. exchange transfusions or dialysis may be required as a means of reversing hypotension and substituting for disordered renal function. minimal amounts of unchanged benazepril and of benazeprilat are excreted into the breast milk of lactating women treated with benazepril. a newborn child ingesting entirely breast milk would receive less than 0.1% of the mg/kg maternal dose of benazepril and benazeprilat. the antihypertensive effects of benazepril hydrochloride have been evaluated in a double-blind study in pediatric patients 7 to 16 years of age [see clinical pharmacology (12.3)]. the pharmacokinetics of benazepril hydrochloride have been evaluated in pediatric patients 6 to 16 years of age [see clinical pharmacology (12.3)]. infants below the age of 1 year should not be given benazepril hydrochloride because of the risk of effects on kidney development. safety and effectiveness of benazepril hydrochloride have not been established in pediatric patients less than 6 years of age or in children with glomerular filtration rate < 30 ml/min/1.73m² [see dosage and administration (2.1) and clinical pharmacology 12.3)]. of the total number of patients who received benazepril in u.s. clinical studies of benazepril hydrochloride, 18% were 65 or older while 2% were 75 or older. no overall differences in effectiveness or safety were observed between these patients and younger patients, and other reported clinical experience has not identified differences in responses between the elderly and younger patients, but greater sensitivity of some older individuals cannot be ruled out. benazepril and benazeprilat are substantially excreted by the kidney. 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)] . ace inhibitors, including benazepril hydrochloride, as monotherapy, have an effect on blood pressure that is less in black patients than in non-blacks. dose adjustment of benazepril hydrochloride is required in patients undergoing hemodialysis or whose creatinine clearance is ≤ 30 ml/min. no dose adjustment of benazepril hydrochloride is required in patients with creatinine clearance > 30 ml/min [see dosage and administration (2.2) and clinical pharmacology (12.3)] .

Spojené státy - angličtina - NLM (National Library of Medicine)

remedyrepack inc. - benazepril hydrochloride (unii: n1sn99t69t) (benazeprilat - unii:jrm708l703) - benazepril hcl 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 mm hg 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. it may be used alone or in combination with thiazide diuretics. benazepril hcl tablets are contraindicated in patients: - who are hypersensitive to benazepril or to any other ace inhibitor - with a history of angioedema with or without previous ace inhibitor treatment benazepril hcl is contraindicated in combination with a neprilysin inhibitor (e.g., sacubitril). do not administer benazepril hcl within 36 hours of switching to or from sacubitril/valsartan, a neprilysin inhibitor [see warnings and precautions (5.2)]. do not co-administer aliskiren with angiotensin receptor blockers, ace inhibitors; including benazepril hcl tablets in patients with diabetes [see drug interactions (7.4)]. risk summary benazepril hcl 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. 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. when pregnancy is detected, discontinue benazepril hcl as soon as possible. the estimated background risk 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 general u.s. population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively. clinical considerations disease-associated maternal and/or embryo/fetal risk 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. fetal/neonatal adverse reactions oligohydramnios in pregnant women who use drugs affecting the renin-angiotensin system in the second and third trimesters of pregnancy can result in the following: reduced fetal renal function leading to anuria and renal failure, fetal lung hypoplasia and 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. perform serial ultrasound examinations to assess the intra-amniotic environment. fetal testing may be appropriate, based on the week of pregnancy. 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 benazepril hcl for hypotension, oliguria, and hyperkalemia. if oliguria or hypotension occur in neonates with a history of in utero exposure to benazepril hcl, support blood pressure and renal perfusion. exchange transfusions or dialysis may be required as a means of reversing hypotension and substituting for disordered renal function . minimal amounts of unchanged benazepril and of benazeprilat are excreted into the breast milk of lactating women treated with benazepril. a newborn child ingesting entirely breast milk would receive less than 0.1% of the mg/kg maternal dose of benazepril and benazeprilat. the antihypertensive effects of benazepril hcl have been evaluated in a double-blind study in pediatric patients 7 to 16 years of age [see clinical pharmacology (12.3)]. the pharmacokinetics of benazepril hcl have been evaluated in pediatric patients 6 to 16 years of age [see clinical pharmacology (12.3)]. infants below the age of 1 year should not be given benazepril hcl because of the risk of effects on kidney development. safety and effectiveness of benazepril hcl have not been established in pediatric patients less than 6 years of age or in children with glomerular filtration rate < 30 ml/min/1.73 m² [see  dosage and administration (2.1) and clinical pharmacology (12.3)]. of the total number of patients who received benazepril in u.s. clinical studies of benazepril hcl, 18% were 65 or older while 2% were 75 or older. no overall differences in effectiveness or safety were observed between these patients and younger patients, and other reported clinical experience has not identified differences in responses between the elderly and younger patients, but greater sensitivity of some older individuals cannot be ruled out. benazepril and benazeprilat are substantially excreted by the kidney. 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)] . ace inhibitors, including benazepril hcl, as monotherapy, have an effect on blood pressure that is less in black patients than in non-blacks.  dose adjustment of benazepril hcl is required in patients undergoing hemodialysis or whose creatinine clearance is ≤ 30 ml/min. no dose adjustment of benazepril hcl is required in patients with creatinine clearance > 30 ml/min [see  dosage and administration (2.2) and clinical pharmacology (12.3)].

Spojené státy - angličtina - NLM (National Library of Medicine)

amneal pharmaceuticals of new york llc - benazepril hydrochloride (unii: n1sn99t69t) (benazeprilat - unii:jrm708l703) - benazepril hydrochloride 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 mm hg 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. it may be used alone or in combination with thiazide diuretics. benazepril hydrochloride tablets are contraindicated in patients: - who are hypersensitive to benazepril or to any other ace inhibitor - with a history of angioedema with or without previous ace inhibitor treatment benazepril hydrochloride is contraindicated in combination with a neprilysin inhibitor (e.g., sacubitril). do not administer benazepril hydrochloride within 36 hours of switching to or from sacubitril/valsartan, a neprilysin inhibitor [see warnings and precautions (5.2)]. do not co-administer aliskiren with angiotensin receptor blockers, ace inhibitors; including benazepril hydrochloride tablets in patients with diabetes [see drug interactions (7.4)]. risk summary benazepril hydrochloride 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. 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. when pregnancy is detected, discontinue benazepril hydrochloride as soon as possible. the estimated background risk 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 general u.s. population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively. clinical considerations disease-associated maternal and/or embryo/fetal risk 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. fetal/neonatal adverse reactions oligohydramnios in pregnant women who use drugs affecting the renin-angiotensin system in the second and third trimesters of pregnancy can result in the following: reduced fetal renal function leading to anuria and renal failure, fetal lung hypoplasia and 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. perform serial ultrasound examinations to assess the intra-amniotic environment. fetal testing may be appropriate, based on the week of pregnancy. 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 benazepril hydrochloride for hypotension, oliguria, and hyperkalemia. if oliguria or hypotension occur in neonates with a history of in utero exposure to benazepril hydrochloride, support blood pressure and renal perfusion. exchange transfusions or dialysis may be required as a means of reversing hypotension and substituting for disordered renal function. minimal amounts of unchanged benazepril and of benazeprilat are excreted into the breast milk of lactating women treated with benazepril. a newborn child ingesting entirely breast milk would receive less than 0.1% of the mg/kg maternal dose of benazepril and benazeprilat. the antihypertensive effects of benazepril hydrochloride have been evaluated in a double-blind study in pediatric patients 7 to 16 years of age [see clinical pharmacology (12.3)]. the pharmacokinetics of benazepril hydrochloride have been evaluated in pediatric patients 6 to 16 years of age [see clinical pharmacology (12.3)]. infants below the age of 1 year should not be given benazepril hydrochloride because of the risk of effects on kidney development. safety and effectiveness of benazepril hydrochloride have not been established in pediatric patients less than 6 years of age or in children with glomerular filtration rate < 30 ml/min/1.73 m² [see dosage and administration (2.1)  and clinical pharmacology (12.3)]. of the total number of patients who received benazepril in u.s. clinical studies of benazepril hydrochloride, 18% were 65 or older while 2% were 75 or older. no overall differences in effectiveness or safety were observed between these patients and younger patients, and other reported clinical experience has not identified differences in responses between the elderly and younger patients, but greater sensitivity of some older individuals cannot be ruled out. benazepril and benazeprilat are substantially excreted by the kidney. 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)] . ace inhibitors, including benazepril hydrochloride, as monotherapy, have an effect on blood pressure that is less in black patients than in non-blacks. dose adjustment of benazepril hydrochloride is required in patients undergoing hemodialysis or whose creatinine clearance is ≤ 30 ml/min. no dose adjustment of benazepril hydrochloride is required in patients with creatinine clearance > 30 ml/min [see dosage and administration (2.2)  and clinical pharmacology (12.3)].

Spojené státy - angličtina - NLM (National Library of Medicine)

remedyrepack inc. - telmisartan (unii: u5syw473rq) (telmisartan - unii:u5syw473rq) - 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)]. risk summary telmisartan 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 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. clinical considerations disease-associated maternal and/or embryo/fetal risk 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. fetal/neonatal adverse reactions 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 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, unless it is 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)] . data animal data 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/m 2 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/m 2 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/m 2 basis, the maximum recommended human dose of telmisartan (80 mg/day). risk summary 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. data 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)]. neonates with a history of in utero exposure to telmisartan 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 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 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)] .

Spojené státy - angličtina - NLM (National Library of Medicine)

northwind pharmaceuticals, llc - benazepril hydrochloride (unii: n1sn99t69t) (benazeprilat - unii:jrm708l703) - benazepril hydrochloride 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 mm hg 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. it may be used alone or in combination with thiazide diuretics. benazepril hydrochloride tablets are contraindicated in patients: - who are hypersensitive to benazepril or to any other ace inhibitor - with a history of angioedema with or without previous ace inhibitor treatment benazepril hydrochloride is contraindicated in combination with a neprilysin inhibitor (e.g., sacubitril). do not administer benazepril hydrochloride within 36 hours of switching to or from sacubitril/valsartan, a neprilysin inhibitor [see warnings and precautions (5.2)]. do not co-administer aliskiren with angiotensin receptor blockers, ace inhibitors; including benazepril hydrochloride tablets in patients with diabetes [see drug interactions (7.4)]. risk summary benazepril hydrochloride 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. 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. when pregnancy is detected, discontinue benazepril hydrochloride as soon as possible. the estimated background risk 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 general u.s. population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively. clinical considerations disease-associated maternal and/or embryo/fetal risk 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. fetal/neonatal adverse reactions oligohydramnios in pregnant women who use drugs affecting the renin-angiotensin system in the second and third trimesters of pregnancy can result in the following: reduced fetal renal function leading to anuria and renal failure, fetal lung hypoplasia and 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. perform serial ultrasound examinations to assess the intra-amniotic environment. fetal testing may be appropriate, based on the week of pregnancy. 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 benazepril hydrochloride for hypotension, oliguria, and hyperkalemia. if oliguria or hypotension occur in neonates with a history of in utero exposure to benazepril hydrochloride, support blood pressure and renal perfusion. exchange transfusions or dialysis may be required as a means of reversing hypotension and substituting for disordered renal function . minimal amounts of unchanged benazepril and of benazeprilat are excreted into the breast milk of lactating women treated with benazepril. a newborn child ingesting entirely breast milk would receive less than 0.1% of the mg/kg maternal dose of benazepril and benazeprilat. the antihypertensive effects of benazepril hydrochloride have been evaluated in a double-blind study in pediatric patients 7 to 16 years of age [see clinical pharmacology (12.3)]. the pharmacokinetics of benazepril hydrochloride have been evaluated in pediatric patients 6 to 16 years of age [see clinical pharmacology (12.3)]. infants below the age of 1 year should not be given benazepril hydrochloride because of the risk of effects on kidney development. safety and effectiveness of benazepril hydrochloride have not been established in pediatric patients less than 6 years of age or in children with glomerular filtration rate < 30 ml/min/1.73 m² [see dosage and administration (2.1)  and  clinical pharmacology (12.3)]. of the total number of patients who received benazepril in u.s. clinical studies of benazepril hydrochloride, 18% were 65 or older while 2% were 75 or older. no overall differences in effectiveness or safety were observed between these patients and younger patients, and other reported clinical experience has not identified differences in responses between the elderly and younger patients, but greater sensitivity of some older individuals cannot be ruled out. benazepril and benazeprilat are substantially excreted by the kidney. 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)] . ace inhibitors, including benazepril hydrochloride, as monotherapy, have an effect on blood pressure that is less in black patients than in non-blacks. dose adjustment of benazepril hydrochloride is required in patients undergoing hemodialysis or whose creatinine clearance is ≤ 30 ml/min. no dose adjustment of benazepril hydrochloride is required in patients with creatinine clearance > 30 ml/min [see dosage and administration (2.2)  and  clinical pharmacology (12.3)].