Source:http://www4.wiwiss.fu-berlin.de/dailymed/resource/drugs/3901
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| dailymed-drugs:3901 | rdf:type | http://www4.wiwiss.fu-berli... | lld:dailymed |
| dailymed-drugs:3901 | rdf:type | dailymed-instance:drugs | lld:dailymed |
| dailymed-drugs:3901 | rdfs:label | Benazepril Hydrochloride and Hydrochlorothiazide (Tablet, Film Coated) | lld:dailymed |
| dailymed-drugs:3901 | dailymed-instance:dosage | Benazepril is an effective treatment of hypertension in once-daily doses of 10 to 80 mg, while hydrochlorothiazide is effective in doses of 12.5 to 50 mg per day. In clinical trials of benazepril/hydrochlorothiazide combination therapy using benazepril doses of 5 to 20 mg and hydrochlorothiazide doses of 6.25 to 25 mg, the antihypertensive effects increased with increasing dose of either component. The side effects of benazepril are generally rare and apparently independent of dose; those of hydrochlorothiazide are a mixture of dose-dependent phenomena (primarily hypokalemia) and dose-independent phenomena (e.g., pancreatitis), the former much more common than the latter. Therapy with any combination of benazepril and hydrochlorothiazide will be associated with both sets of dose-independent side effects, but regimens in which benazepril is combined with low doses of hydrochlorothiazide produce minimal effects on serum potassium. In clinical trials of benazepril hydrochloride and hydrochlorothiazide tablets, the average change in serum potassium was near zero in subjects who received 5/6.25 mg or 20/12.5 mg, but the average subject who received 10/12.5 mg or 20/25 mg experienced a mild reduction in serum potassium, similar to that experienced by the average subject receiving the same dose of hydrochlorothiazide monotherapy. To minimize dose-independent side effects, it is usually appropriate to begin combination therapy only after a patient has failed to achieve the desired effect with monotherapy.<br/>Dose Titration Guided by Clinical Effect: A patient whose blood pressure is not adequately controlled with benazepril monotherapy may be switched to benazepril hydrochloride and hydrochlorothiazide tablets 10/12.5 or benazepril hydrochloride and hydrochlorothiazide tablets 20/12.5. Further increases of either or both components could depend on clinical response. The hydrochlorothiazide dose should generally not be increased until 2 to 3 weeks have elapsed. Patients whose blood pressures are adequately controlled with 25 mg of daily hydrochlorothiazide, but who experience significant potassium loss with this regimen, may achieve similar blood-pressure control without electrolyte disturbance if they are switched to benazepril hydrochloride and hydrochlorothiazidetablets 5/6.25.<br/>Replacement Therapy: The combination may be substituted for the titrated individual components.<br/>Use in Renal Impairment: Regimens of therapy with benazepril hydrochloride and hydrochlorothiazide tablets need not take account of renal function as long as the patient's creatinine clearance is>30 mL/min/1.73m(serum creatinine roughly���3 mg/dL or 265��mol/L). In patients with more severe renal impairment, loop diuretics are preferred to thiazides, so benazepril hydrochloride and hydrochlorothiazide tablets are not recommended . | lld:dailymed |
| dailymed-drugs:3901 | dailymed-instance:descripti... | Benazepril hydrochloride is a white to off-white crystalline powder, soluble (>100 mg/mL) in water, in ethanol, and in methanol. Benazepril hydrochloride's chemical name is 3-[[1-(ethoxycarbonyl)-3-phenyl-(1S)-propyl]amino]-2,3,4,5-tetrahydro-2-oxo-1H-1-(3S)-benzazepine-1-acetic acid monohydrochloride; its structural formula is: Its molecular formula is CHNO���HCl, and its molecular weight is 460.96. Benazeprilat, the active metabolite of benazepril, is a nonsulfhydryl angiotensin-converting enzyme inhibitor. Benazepril is converted to benazeprilat by hepatic cleavage of the ester group. Hydrochlorothiazide USP is a white, or practically white, practically odorless, crystalline powder. It is slightly soluble in water; freely soluble in sodium hydroxide solution, in n-butylamine, and in dimethylformamide; sparingly soluble in methanol; and insoluble in ether, in chloroform, and in dilute mineral acids. Hydrochlorothiazide's chemical name is 6-chloro-3,4-dihydro-2H-1,2,4-benzothiadiazine-7-sulfonamide 1,1-dioxide; its structural formula is: Its molecular formula is CHClNOS, and its molecular weight is 297.73. Hydrochlorothiazide is a thiazide diuretic. Benazepril hydrochloride and hydrochlorothiazide tablets are a combination of benazepril hydrochloride and hydrochlorothiazide USP. The tablets are formulated for oral administration with a combination of 5, 10, or 20 mg of benazepril hydrochloride and 6.25, 12.5, or 25 mg of hydrochlorothiazide USP. The inactive ingredients are: anhydrous lactose, black iron oxide, colloidal silicon dioxide, crospovidone, hypromellose, polydextrose, polyethylene glycol, pregelatinized starch, stearic acid, talc, titanium dioxide, triacetin and yellow iron oxide. | lld:dailymed |
| dailymed-drugs:3901 | dailymed-instance:clinicalP... | Mechanism of Action: Benazepril and benazeprilat inhibit angiotensin-converting enzyme (ACE) in human subjects and in animals. ACE is a peptidyl dipeptidase that catalyzes the conversion of angiotensin I to the vasoconstrictor substance, angiotensin II. Angiotensin II also stimulates aldosterone secretion by the adrenal cortex. Inhibition of ACE results in decreased plasma angiotensin II, which leads to decreased vasopressor activity and to decreased aldosterone secretion. The latter decrease may result in a small increase of serum potassium. Hypertensive patients treated with benazepril alone for up to 52 weeks had elevations of serum potassium of up to 0.2 mEq/L. Similar patients treated with benazepril and hydrochlorothiazide for up to 24 weeks had no consistent changes in their serum potassium . Removal of angiotensin II negative feedback on renin secretion leads to increased plasma renin activity. In animal studies, benazepril had no inhibitory effect on the vasopressor response to angiotensin II and did not interfere with the hemodynamic effects of the autonomic neurotransmitters acetylcholine, epinephrine, and norepinephrine. ACE is identical to kininase, an enzyme that degrades bradykinin. Whether increased levels of bradykinin, a potent vasodepressor peptide, play a role in the therapeutic effects of benazepril hydrochloride and hydrochlorothiazide remains to be elucidated. While the mechanism through which benazepril lowers blood pressure is believed to be primarily suppression of the renin-angiotensin-aldosterone system, benazepril has an antihypertensive effect even in patients with low-renin hypertension. Hydrochlorothiazide is a thiazide diuretic. Thiazides affect the renal tubular mechanisms of electrolyte reabsorption, directly increasing excretion of sodium and chloride in approximately equivalent amounts. Indirectly, the diuretic action of hydrochlorothiazide reduces plasma volume, with consequent increases in plasma renin activity, increases in aldosterone secretion, increases in urinary potassium loss, and decreases in serum potassium. The renin-aldosterone link is mediated by angiotensin, so coadministration of an ACE inhibitor tends to reverse the potassium loss associated with these diuretics. The mechanism of the antihypertensive effect of thiazides is unknown.<br/>Pharmacokinetics and Metabolism: Following oral administration of benazepril hydrochloride and hydrochlorothiazide, peak plasma concentrations of benazepril are reached within 0.5 to 1 hours. As determined by urinary recovery, the extent of absorption is at least 37%. The absorption of hydrochlorothiazide is somewhat slower (1 to 2.5 hours) and somewhat more complete (50% to 80%). In fasting subjects, the rate and extent of absorption of benazepril and hydrochlorothiazide from benazepril hydrochloride and hydrochlorothiazide tablets are not different, respectively, from the rate and extent of absorption of benazepril and hydrochlorothiazide from immediate-release monotherapy formulations. The absorption of benazepril from benazepril hydrochloride tablets is not influenced by the presence of food in the gastrointestinal tract, but possible effects of food upon absorption of either component from benazepril hydrochloride and hydrochlorothiazide tablets have not been studied. The reported studies of food effects on hydrochlorothiazide absorption have been inconclusive. The absorption of hydrochlorothiazide is increased by agents that reduce gastrointestinal motility, but it is reported to be reduced by 50% in patients with congestive heart failure. Cleavage of the ester group (primarily in the liver) converts benazepril to its active metabolite, benazeprilat. Peak plasma concentrations of benazeprilat are reached 1 to 2 hours after drug intake in the fasting state and 2 to 4 hours after drug intake in the nonfasting state. The serum protein binding of benazepril is about 96.7% and that of benazeprilat about 95.3%, as measured by equilibrium dialysis; on the basis of in vitro studies, the degree of protein binding should be unaffected by age, hepatic dysfunction, or���over the concentration range of 0.24 to 23.6��mol/L���concentration. Hydrochlorothiazide is not metabolized. Its apparent volume of distribution is 3.6 to 7.8 L/kg, and its measured plasma protein binding is 67.9%. The drug also accumulates in red blood cells, so that whole blood levels are 1.6 to 1.8 times those measured in plasma. In studies of rats givenC-benazepril, benazepril and its metabolites crossed the blood-brain barrier only to an extremely low extent. Multiple doses of benazepril did not result in accumulation in any tissue except the lung, where, as with other ACE inhibitors in similar studies, there was a slight increase in concentration due to slow elimination in that organ. Some placental passage occurred when benazepril was administered to pregnant rats. In humans, hydrochlorothiazide crosses the placenta freely, and levels in umbilical-cord blood are similar to those in the maternal circulation. Benazepril is almost completely metabolized to benazeprilat, which has much greater ACE inhibitory activity than benazepril, and to the glucuronide conjugates of benazepril and benazeprilat. Only trace amounts of an administered dose of benazepril can be recovered unchanged in the urine; about 20% of the dose is excreted as benazeprilat, 4% as benazepril glucuronide, and 8% as benazeprilat glucuronide. In patients with hepatic dysfunction due to cirrhosis, levels of benazeprilat are essentially unaltered. Similarly, the pharmacokinetics of benazepril and benazeprilat do not appear to be influenced by age. The kinetics of benazepril are dose-proportional within the dosage range of 5 to 20 mg. Small deviations from dose proportionality were observed when the broader range of 2 to 80 mg was studied, possibly due to the saturable binding of the compound to ACE. The effective half-life of accumulation of benazeprilat following multiple dosing of benazepril hydrochloride is 10 to 11 hours. Thus, steady-state concentrations of benazeprilat should be reached after 2 or 3 doses of benazepril hydrochloride given once daily. During chronic administration (28 days) of once-daily doses of benazepril between 5 mg and 20 mg, the kinetics did not change, and there was no significant accumulation. Accumulation ratios based on AUC and urinary recovery of benazeprilat were 1.19 and 1.27, respectively. When dialysis was started 2 hours after ingestion of 10 mg of benazepril, approximately 6% of benazeprilat was removed in 4 hours of dialysis. The parent compound, benazepril, was not detected in the dialysate. Benazepril and benazeprilat are cleared predominantly by renal excretion in healthy subjects with normal renal function. Nonrenal (i.e., biliary) excretion accounts for approximately 11% to 12% of benazeprilat excretion in healthy subjects. In patients with renal failure, biliary clearance may compensate to an extent for deficient renal clearance. The disposition of benazepril and benazeprilat in patients with mild-to-moderate renal insufficiency (creatinine clearance>30 mL/min) is similar to that in patients with normal renal function. In patients with creatinine clearance���30 mL/min, peak benazeprilat levels and the initial (alpha phase) half-life increase, and time to steady state may be delayed . Thiazide diuretics are eliminated by the kidney, with a terminal half-life of 5 to 15 hours. In a study of patients with impaired renal function (mean creatinine clearance of 19 mL/min), the half-life of hydrochlorothiazide elimination was lengthened to 21 hours.<br/>Pharmacodynamics: Single and multiple doses of 10 mg or more of benazepril cause inhibition of plasma ACE activity by at least 80% to 90% for at least 24 hours after dosing. For up to 4 hours after a 10 mg dose, pressor responses to exogenous angiotensin I were inhibited by 60% to 90%. Administration of benazepril to patients with mild-to-moderate hypertension results in a reduction of both supine and standing blood pressure to about the same extent, with no compensatory tachycardia. Symptomatic postural hypotension is infrequent, although it can occur in patients who are salt and/or volume depleted . In single-dose studies, benazepril lowered blood pressure within 1 hour, with peak reductions achieved 2 to 4 hours after dosing. The antihypertensive effect of a single dose persisted for 24 hours. In multiple-dose studies, once-daily doses of 20 to 80 mg decreased seated pressure (systolic/diastolic) 24 hours after dosing by about 6 to 12/4 to 7 mmHg. The reductions at trough are about 50% of those seen at peak. Four dose-response studies of benazepril monotherapy using once-daily dosing were conducted in 470 mild-to-moderate hypertensive patients not using diuretics. The minimal effective once-daily dose of benazepril was 10 mg; further falls in blood pressure, especially at morning trough, were seen with higher doses in the studied dosing range (10 to 80 mg). In studies comparing the same daily dose of benazepril given as a single morning dose or as a twice-daily dose, blood pressure reductions at the time of morning trough blood levels were greater with the divided regimen. During chronic therapy with benazepril, the maximum reduction in blood pressure with any given dose is generally achieved after 1 to 2 weeks. The antihypertensive effects of benazepril have continued during therapy for at least 2 years. Abrupt withdrawal of benazepril has not been associated with a rapid increase in blood pressure. In patients with mild-to-moderate hypertension, total daily doses of benazepril hydrochloride 20 to 40 mg were similar in effectiveness to total daily doses of captopril 50 to 100 mg, hydrochlorothiazide 25 to 50 mg, nifedipine SR 40 to 80 mg, and propranolol 80 to 160 mg. The antihypertensive effects of benazepril were not appreciably different in patients receiving high- or low-sodium diets. In hemodynamic studies in dogs, blood pressure reduction was accompanied by a reduction in peripheral arterial resistance, with an increase in cardiac output and renal blood flow and little or no change in heart rate. In normal human volunteers, single doses of benazepril caused an increase in renal blood flow but had no effect on glomerular filtration rate. In clinical trials of benazepril/hydrochlorothiazide using benazepril doses of 5 to 20 mg and hydrochlorothiazide doses of 6.25 to 25 mg, the antihypertensive effects were sustained for at least 24 hours, and they increased with increasing dose of either component. Although benazepril monotherapy is somewhat less effective in blacks than in nonblacks, the efficacy of combination therapy appears to be independent of race. By blocking the renin-angiotensin-aldosterone axis, administration of benazepril tends to reduce the potassium loss associated with the diuretic. In clinical trials of benazepril hydrochloride and hydrochlorothiazide, the average change in serum potassium was near zero in subjects who received 5/6.25 mg or 20/12.5 mg, but the average subject who received 10/12.5 mg or 20/25 mg experienced a mild reduction in serum potassium, similar to that experienced by the average subject receiving the same dose of hydrochlorothiazide monotherapy. | lld:dailymed |
| dailymed-drugs:3901 | dailymed-instance:activeIng... | dailymed-ingredient:Benazep... | lld:dailymed |
| dailymed-drugs:3901 | dailymed-instance:contraind... | Benazepril hydrochloride and hydrochlorothiazide tablets are contraindicated in patients who are anuric. Benazepril hydrochloride and hydrochlorothiazide is also contraindicated in patients who are hypersensitive to benazepril, to any other ACE inhibitor, to hydrochlorothiazide, or to other sulfonamide-derived drugs. Hypersensitivity reactions are more likely to occur in patients with a history of allergy or bronchial asthma. | lld:dailymed |
| dailymed-drugs:3901 | dailymed-instance:supply | Benazepril Hydrochloride and Hydrochlorothiazide Tablets are available containing benazepril 5 mg and hydrochlorothiazide 6.25 mg, benazepril 10 mg and hydrochlorothiazide 12.5 mg, benazepril 20 mg and hydrochlorothiazide 12.5 mg or benazepril 20 mg and hydrochlorothiazide 25 mg. The 5 mg/6.25 mg tablets are beige film-coated, oval, biconvex, beveled edge, scored tablets debossed with M 725 on one side of the tablet and scored on the other side. They are available as follows: NDC 0378-4725-01bottles of 100 tablets NDC 0378-4725-05bottles of 500 tablets The 10 mg/12.5 mg tablets are beige film-coated, round, biconvex, beveled edge, scored tablets debossed with M above the score and 735 below the score on one side of the tablet and blank on the other side. They are available as follows: NDC 0378-4735-01bottles of 100 tablets NDC 0378-4735-05bottles of 500 tablets The 20 mg/12.5 mg tablets are beige film-coated, capsule-shaped, biconvex, beveled edge, scored tablets debossed with M to the left of the score and 745 to the right of the score on one side of the tablet and blank on the other side. They are available as follows: NDC 0378-4745-01bottles of 100 tablets NDC 0378-4745-05bottles of 500 tablets The 20 mg/25 mg tablets are beige film-coated, oval, biconvex, beveled edge, scored tablets debossed with M to the left of the score and 775 to the right of the score on one side of the tablet and blank on the other side. They are available as follows: NDC 0378-4775-01bottles of 100 tablets NDC 0378-4775-05bottles of 500 tablets Store at 20��to 25��C (68��to 77��F). [See USP for Controlled Room Temperature.] PROTECT FROM MOISTURE AND LIGHT. Dispense in a tight, light-resistant container as defined in the USP using a child-resistant closure. | lld:dailymed |
| dailymed-drugs:3901 | dailymed-instance:boxedWarn... | USE IN PREGNANCY: When used in pregnancy during the second and third trimesters, ACE inhibitors can cause injury and even death to the developing fetus. When pregnancy is detected, benazepril hydrochloride and hydrochlorothiazide should be discontinued as soon as possible. See WARNINGS: Fetal/Neonatal Morbidity and Mortality. | lld:dailymed |
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| dailymed-drugs:3901 | dailymed-instance:overdosag... | No specific information is available on the treatment of overdosage with benazepril hydrochloride and hydrochlorothiazide; treatment should be symptomatic and supportive. Therapy with benazepril hydrochloride and hydrochlorothiazide should be discontinued, and the patient should be observed. Dehydration, electrolyte imbalance, and hypotension should be treated by established procedures. Single oral doses of 1 g/kg of benazepril caused reduced activity in mice, and doses of 3 g/kg were associated with significant lethality. Reduction of activity in rats was not seen until they had received doses of 5 g/kg, and doses of 6 g/kg were not lethal. In single-dose studies of hydrochlorothiazide, most rats survived doses up to 2.75 g/kg. Data from human overdoses of benazepril are scanty, but the most common manifestation of human benazepril overdosage is likely to be hypotension. In human hydrochlorothiazide overdose, the most common signs and symptoms observed have been those of dehydration and electrolyte depletion (hypokalemia, hypochloremia, hyponatremia). If digitalis has also been administered, hypokalemia may accentuate cardiac arrhythmias. Laboratory determinations of serum levels of benazepril and its metabolites are not widely available, and such determinations have, in any event, no established role in the management of benazepril overdose. No data are available to suggest physiological maneuvers (e.g., maneuvers to change the pH of the urine) that might accelerate elimination of benazepril and its metabolites. Benazeprilat is only slightly dialyzable, but dialysis might be considered in overdosed patients with severely impaired renal function . Angiotensin II could presumably serve as a specific antagonist-antidote in the setting of benazepril overdose, but angiotensin II is essentially unavailable outside of scattered research facilities. Because the hypotensive effect of benazepril is achieved through vasodilation and effective hypovolemia, it is reasonable to treat benazepril overdose by infusion of normal saline solution. | lld:dailymed |
| dailymed-drugs:3901 | dailymed-instance:genericMe... | Benazepril Hydrochloride and Hydrochlorothiazide | lld:dailymed |
| dailymed-drugs:3901 | dailymed-instance:fullName | Benazepril Hydrochloride and Hydrochlorothiazide (Tablet, Film Coated) | lld:dailymed |
| dailymed-drugs:3901 | dailymed-instance:adverseRe... | Benazepril hydrochloride and hydrochlorothiazide has been evaluated for safety in over 2500 patients with hypertension; over 500 of these patients were treated for at least 6 months, and over 200 were treated for more than 1 year. The reported side effects were generally mild and transient, and there was no relationship between side effects and age, sex, race, or duration of therapy. Discontinuation of therapy due to side effects was required in approximately 7% of U.S. patients treated with benazepril hydrochloride and hydrochlorothiazide and in 4% of patients treated with placebo. The most common reasons for discontinuation of therapy with benazepril hydrochloride and hydrochlorothiazide in U.S. studies were cough , "dizziness" (1%), headache (0.6%), and fatigue (0.6%). The side effects considered possibly or probably related to study drug that occurred in U.S. placebo-controlled trials in more than 1% of patients treated with benazepril hydrochloride and hydrochlorothiazide are shown in the table below. Other side effects considered possibly or probably related to study drug that occurred in U.S. placebo-controlled trials in 0.3% to 1% of patients treated with benazepril hydrochloride and hydrochlorothiazide were the following: Angioedema: Edema of the lips or face without other manifestations of angioedema (0.3%). See WARNINGS: Angioedema. Cardiovascular: Hypotension (seen in 0.6% of patients), postural hypotension (0.3%), palpitations, and flushing. Gastrointestinal: Vomiting, diarrhea, dyspepsia, anorexia, and constipation. Neurologic and Psychiatric: Insomnia, nervousness, paresthesia, libido decrease, dry mouth, taste perversion, and tinnitus. Dermatologic: Rash and sweating. Other: Gout, urinary frequency, arthralgia, myalgia, asthenia, and pain (including chest pain and abdominal pain). Other adverse experiences reported in 0.3% or more of benazepril hydrochloride and hydrochlorothiazide patients in U.S. controlled clinical trials, and rarer events seen in postmarketing experience, were the following; asterisked entries occurred in more than 1% of patients (in some, a causal relationship to benazepril hydrochloride and hydrochlorothiazide is uncertain): Angioedema: Edema of the lips or face without other manifestations of angioedema. See WARNINGS: Angioedema. Cardiovascular: Syncope, peripheral vascular disorder, and tachycardia. Body as a Whole: Infection, back pain*, flu syndrome*, fever, chills, and neck pain. Dermatologic: Photosensitivity and pruritus. Gastrointestinal: Gastroenteritis, flatulence, and tooth disorder. Neurologic and Psychiatric: Hypesthesia, abnormal vision, abnormal dreams, and retinal disorder. Respiratory: Upper respiratory infection*, epistaxis, bronchitis, rhinitis*, sinusitis*, and voice alteration. Other: Conjunctivitis, arthritis, urinary tract infection, alopecia, and urinary frequency*.<br/>Fetal/Neonatal Morbidity and Mortality: See WARNINGS: Fetal/Neonatal Morbidity and Mortality. Monotherapy with benazepril has been evaluated for safety in over 6000 patients. In clinical trials, the observed adverse reactions to benazepril were similar to those seen in trials of benazepril hydrochloride and hydrochlorothiazide. In postmarketing experience with benazepril, there have been rare reports of Stevens-Johnson syndrome, pancreatitis, hemolytic anemia, pemphigus, and thrombocytopenia. Another potentially important adverse experience, eosinophilic pneumonitis, has been attributed to other ACE inhibitors. Hydrochlorothiazide has been extensively prescribed for many years, but there has not been enough systematic collection of data to support an estimate of the frequency of the observed adverse reactions. Within organ-system groups, the reported reactions are listed here in decreasing order of severity, without regard to frequency. Cardiovascular: Orthostatic hypotension (may be potentiated by alcohol, barbiturates, or narcotics). Digestive: Pancreatitis, jaundice (intrahepatic cholestatic) , sialadenitis, vomiting, diarrhea, cramping, nausea, gastric irritation, constipation, and anorexia. Neurologic: Vertigo, lightheadedness, transient blurred vision, headache, paresthesia, xanthopsia, weakness, and restlessness. Musculoskeletal: Muscle spasm. Hematologic: Aplastic anemia, agranulocytosis, leukopenia, and thrombocytopenia. Metabolic: Hyperglycemia, glycosuria, and hyperuricemia. Hypersensitivity: Necrotizing angiitis, Stevens-Johnson syndrome, respiratory distress (including pneumonitis and pulmonary edema), purpura, urticaria, rash, and photosensitivity.<br/>Clinical Laboratory Test Findings: Serum Electrolytes: See PRECAUTIONS. Creatinine: Minor reversible increases in serum creatinine were observed in patients with essential hypertension treated with benazepril hydrochloride and hydrochlorothiazide. Such increases occurred most frequently in patients with renal artery stenosis . PBI and Tests of Parathyroid Function: See PRECAUTIONS. Other (Causal Relationships Unknown): Other clinically important changes in standard laboratory tests were rarely associated with benazepril hydrochloride and hydrochlorothiazide administration. Elevations in blood urea nitrogen, uric acid, glucose, SGOT, and SGPT have been reported. In the somewhat larger patient population exposed to benazepril monotherapy in U.S. trials, the same abnormalities were reported, together with scattered accounts of hyponatremia, melena, electrocardiographicchanges, leukopenia, eosinophilia, and proteinuria. | lld:dailymed |
| dailymed-drugs:3901 | dailymed-instance:indicatio... | Benazepril hydrochloride and hydrochlorothiazide tablets are indicated for the treatment of hypertension. This fixed combination drug is not indicated for the initial therapy of hypertension . In using benazepril hydrochloride and hydrochlorothiazide, consideration should be given to the fact that another angiotensin-converting enzyme inhibitor, captopril, has caused agranulocytosis, particularly in patients with renal impairment or collagen-vascular disease. Available data are insufficient to show that benazepril does not have a similar risk . Black patients receiving ACE inhibitors have been reported to have a higher incidence of angioedema compared to nonblacks. | lld:dailymed |
| dailymed-drugs:3901 | dailymed-instance:represent... | http://www4.wiwiss.fu-berli... | lld:dailymed |
| dailymed-drugs:3901 | dailymed-instance:routeOfAd... | http://www4.wiwiss.fu-berli... | lld:dailymed |
| dailymed-drugs:3901 | dailymed-instance:name | Benazepril Hydrochloride and Hydrochlorothiazide | lld:dailymed |
| http://www4.wiwiss.fu-berli... | dailymed-instance:producesD... | dailymed-drugs:3901 | lld:dailymed |