Indications for LOTENSIN HCT:
Hypertension (not for initial therapy).
Switching from monotherapy with either component: initially 10/12.5mg once daily; may increase after 2–3 weeks as needed up to max 20/25mg daily. Or, substitute for individually titrated components.
History of ACEI-associated or other angioedema. Anuria. Sulfonamide allergy. Concomitant neprilysin inhibitors (eg, sacubitril); do not administer benazepril/HCT within 36hrs of switching to or from sacubitril/valsartan. Concomitant aliskiren in patients with diabetes.
Fetal toxicity may develop; discontinue if pregnancy is detected. Discontinue if angioedema, laryngeal edema, jaundice or marked elevations of hepatic enzymes develop. Salt/volume depletion; correct prior to initiation. Severe CHF. Renal or hepatic impairment. Dialysis (esp. high-flux membrane). Renal artery stenosis. Monitor WBCs in renal or collagen vascular disease. Surgery. Postsympathectomy. SLE. Diabetes. Gout. Hypercalcemia; avoid. Acute myopia. Secondary angle-closure glaucoma. Monitor BP, electrolytes and renal function periodically. Black patients may have higher rate of angioedema than non-Black patients. Neonates. Pregnancy (Cat.D); avoid. Nursing mothers: not recommended.
ACE inhibitor + diuretic (thiazide).
See Contraindications. Increased risk of angioedema with concomitant mTOR inhibitors (eg, temsirolimus, sirolimus, everolimus) or neprilysin inhibitors. Potassium or potassium-sparing diuretics may cause hyperkalemia. May increase lithium levels. Dual inhibition of the renin-angiotensin system with ARBs, ACEIs, or aliskiren may increase risk of hypotension, hyperkalemia, renal function changes; monitor closely. Avoid concomitant aliskiren in renal impairment (CrCl <60mL/min). May be antagonized by, and renal toxicity potentiated by, NSAIDs, including selective COX-2 inhibitors (monitor renal function periodically in elderly and/or volume depleted). Potentiated by antihypertensives, anticholinergics. Potentiates skeletal muscle relaxants. Antagonizes norepinephrine. Orthostatic hypotension potentiated by alcohol, CNS depressants. Thiazide-induced hypokalemia or hypomagnesemia may predispose patients to digoxin toxicity. Adjust antidiabetic drugs. Renal excretion may be reduced and myelosuppression enhanced with antineoplastic agents. Antagonized by pro-kinetic drugs. Increased risk of hyperuricemia with cyclosporine. Anion exchange resins; administer at least 4hrs before or 4–6hrs after resin administration. Nitritoid reactions with concomitant injectable gold (eg, sodium aurothiomalate); rare. May interfere with parathyroid test.
Dizziness, fatigue, orthostatic hypotension, headache, cough, hypertonia, vertigo, nausea, impotence, somnolence, electrolyte imbalance; rare: hepatic failure.
Renal (primarily), biliary.