Benazepril / hydrochlorothiazide Side Effects
Some side effects of benazepril / hydrochlorothiazide may not be reported. Always consult your doctor or healthcare specialist for medical advice. You may also report side effects to the FDA.
For the Consumer
Applies to benazepril / hydrochlorothiazide: oral tablet
Along with its needed effects, benazepril / hydrochlorothiazide may cause some unwanted effects. Although not all of these side effects may occur, if they do occur they may need medical attention.
Check with your doctor immediately if any of the following side effects occur while taking benazepril / hydrochlorothiazide:Less common
- Blurred vision
- decreased urination
- dizziness, faintness, or lightheadedness when getting up suddenly from a lying or sitting position
- dry mouth
- fast, slow, or irregular heartbeat
- muscle cramps or pain
- numbness, tingling, pain, or weakness in the hands or feet
- rapid breathing
- sunken eyes
- unusual tiredness or weakness
- weakness and heaviness of the legs
- wrinkled skin
Some side effects of benazepril / hydrochlorothiazide may occur that usually do not need medical attention. These side effects may go away during treatment as your body adjusts to the medicine. Also, your health care professional may be able to tell you about ways to prevent or reduce some of these side effects. Check with your health care professional if any of the following side effects continue or are bothersome or if you have any questions about them:Less common
- decreased interest in sexual intercourse
- excessive muscle tone
- feeling of constant movement of self or surroundings
- inability to have or keep an erection
- loss in sexual ability, desire, drive, or performance
- muscle stiffness
- muscle tension or tightness
- sensation of spinning
- sleepiness or unusual drowsiness
For Healthcare Professionals
Applies to benazepril / hydrochlorothiazide: oral tablet
Cardiovascular effects include postural hypotension or dizziness in 3% to 6% of patients. Postural hypotension can result in syncope, particularly in elderly patients. Angioneurotic edema is rare, but potentially serious, and may require dose reduction or discontinuation of therapy. Hydrochlorothiazide (HCTZ)-induced hypokalemia can predispose some patients to experience significant cardiac arrhythmias, including ventricular ectopy and complete AV heart block. This is much less likely with the addition of benazepril because ACE inhibitors may decrease serum aldosterone levels.
A 68-year-old man with a history of myocardial infarction (MI) developed dyspnea, chest tightness, a low grade fever, dizziness, sweating, and vomiting associated with cyanosis, a mild leukocytosis, radiographic evidence of pulmonary edema, clinical evidence of hypovolemia, and respiratory acidosis. MI and infection were ruled out; the patient recovered after restoration of his intravascular volume with saline and albumin. The only precipitating factor per history was the ingestion of HCTZ, which the patient had taken without incidence for two years. Rechallenge resulted in recurrent acute pulmonary edema. Other signs of hypersensitivity, such as rash and eosinophilia, were absent.
Patients with intestinal angioedema generally present with abdominal pain (with or without nausea or vomiting) and in some cases there was no prior history of facial angioedema, and C-1 esterase levels were normal. These symptoms resolve after stopping the ACE inhibitor.
Hypersensitivity reactions to angiotensin converting enzyme (ACE) inhibitors may be life threatening. Angioedema of the face, extremities, lips, tongue, glottis and/or pharynx have been reported rarely in patients receiving ACE inhibitors. In addition, intestinal angioedema has been reported in patients treated with ACE inhibitors. It is recommended that any patient with dyspnea, dysphagia, or significant facial angioedema stop therapy immediately and avoid ACE inhibitor therapy in general. Other hypersensitivity reactions associated with benazepril have included dermatitis, rash, flushing and pruritus.
Hypersensitivity (usually nausea, vomiting, diarrhea, and rash) has been reported in less than 1% of patients receiving hydrochlorothiazide. Rare cases of acute pulmonary edema, interstitial cystitis, and interstitial nephritis, and anaphylaxis have also been reported.
Nervous system side effects include headache in 5% to 13%, fatigue in 5%, dizziness in 5%, and somnolence or vertigo in 1% of patients. Rare cases of cerebrovascular insufficiency have been associated with HCTZ-induced intravascular volume depletion.
Respiratory side effects are unusual. An increase in cough or rhinitis occurs in 2% to 3% of patients. There have been approximately 30 case reports of acute noncardiogenic pulmonary edema associated with the use of HCTZ.
A retrospective study has revealed a significantly higher incidence of discontinuation of angiotensin converting enzyme inhibitor therapy due to cough among black patients compared with non-black patients (9.6% vs. 2.4%).
Gastrointestinal side effects are rare. General abdominal pain or diarrhea has been reported in 2% of patients. Rare cases of acute pancreatitis and cholecystitis have been associated with the use of HCTZ.
Thiazide diuretics may increase serum cholesterol and triglycerides, resulting in increased risk of cholesterol gallstone formation. Reports of bowel strictures associated with thiazide ingestion have been reported in the 1960's, although these patients were on a combination HCTZ-potassium product.
Although HCTZ has been used to treat nephrogenic diabetes insipidus, a case report in which the drug was believed to have caused this condition has been reported.
New or worsened renal insufficiency has been reported in 2% of patients on benazepril alone (defined as a 150% increase in baseline serum creatinine). This may be exacerbated by HCTZ-induced intravascular volume depletion. Risk factors include preexisting renal insufficiency, renal artery stenosis, hypovolemia, or sodium depletion. Rare cases of interstitial nephritis have been associated with HCTZ.
A 67-year-old white woman with hypothyroidism, hypercalcemia, depression, and hypertension developed facial erythema, headaches, tremors, confusion, and personality changes associated with a new positive ANA and anti-nRNP, and skin biopsy consistent with lupus erythematosus while taking HCTZ, levothyroxine, and amitriptyline. The eruption resolved upon discontinuation of HCTZ, but she later developed a higher ANA titer associated with symptomatic diffuse interstitial pulmonary infiltrates. She was successfully treated with corticosteroids.
Dermatologic reactions associated with HCTZ include erythema annular centrifugum, acute eczematous dermatitis, morbilliform or leukocytoclastic vasculitis, erythema multiforme (including Stevens-Johnson syndrome), and exfoliative dermatitis (including toxic epidermal necrolysis). In addition, a rare, distinct entity with clinical and laboratory features indistinguishable from those of subacute cutaneous lupus erythematosus has been associated with HCTZ.
The usual metabolic disorder, hypokalemia, associated with the use of HCTZ is much less likely with the addition of benazepril because ACE inhibitors may decrease serum aldosterone levels. By the same token, the mild hyperkalemia, although clinically insignificant, that often accompanies the use of ACE inhibitors, is much less likely due to HCTZ-induced kaliuresis. HCTZ can induce metabolic alkalosis, hyponatremia, hypomagnesemia, hypercalcemia, hyperglycemia, and elevated serum uric acid levels. It may also increase serum cholesterol.
Since HCTZ may increase total serum cholesterol by 11%, LDL lipoprotein cholesterol by 12%, and VLDL lipoprotein cholesterol levels by 50%, and may reduce insulin secretion, it should be used with caution in diabetic patients and in those with hypercholesterolemia.
Hyperuricemia may be an important consideration in patients with a history of gout. Hypophosphatemia and low serum magnesium concentrations may occur, but are usually clinically insignificant except in malnourished patients.
Endocrinologic problems associated with thiazide diuretics include glucose intolerance and a potentially deleterious effect on the lipid profile. This may be important in some patients with or who are at risk for diabetes or coronary artery disease.
A prospective study of 34 patients who received oral thiazide diuretics for 14 years without interruption revealed an increased mean fasting blood glucose level after treatment. Withdrawal of thiazide therapy for seven months in 10 of the patients resulted in mean reductions of 10% in fasting blood glucose and 25% in the 2-hour glucose tolerance test value. A control group was not reported.
Hematologic side effects are rare, and include cases of anemia, immune-complex hemolytic anemia, aplastic anemia, and thrombocytopenia.
In two studies, 1 of 2,014 and 1 of 1,357 patients developed decreased hemoglobin during benazepril therapy. Neither patient required stopping the drug.
There are rare case reports of HCTZ-induced immune hemolytic anemia. The following illustrates a fatal case:
A 53-year-old man with hypertension developed nausea, vomiting, diarrhea, and progressive anorexia and weakness associated with scleral icterus, anemia with spherocytosis, dark red urine with proteinuria, bilirubinemia, and hemoglobinuria, and elevated lactic dehydrogenase levels 18 months after beginning HCTZ and methyldopa. Haptoglobin was less than 50 mg/dl. Direct and indirect Coombs' tests were positive. The patient died suddenly; autopsy revealed no obvious cause of death, left ventricular hypertrophy, and mild coronary atherosclerosis.
General musculoskeletal pains have occasionally been associated with the use of HCTZ.
Ocular side effects have included idiosyncratic reactions to the hydrochlorothiazide component resulting in acute transient myopia and acute angle-closure glaucoma.
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