Lisinopril + Hydrochlorothiazide

Generic Medicine Info
Indications and Dosage
Mild to moderate hypertension
Adult: As tablets containing lisinopril (mg)/hydrochlorothiazide (mg): 10/12.5, 20/12.5. Usual: 1 tablet once daily, may increase to 2 tablets once daily if needed.
Renal Impairment
≤30Not recommended.
May be taken with or without food.
Hypersensitivity to sulphonamide drugs. Patients with anuria, aortic stenosis or hyperkalaemia. History of angioneurotic oedema related to use of ACE inhibitors. Hereditary or idiopathic angioedema. Lactation.
Special Precautions
Hepatic cirrhosis, severe heart failure, oedema, renal impairment (including haemodialysis patients), unilateral renal artery stenosis, hepatic impairment, diabetes, gout, hyperuricaemia, left ventricular hypertrophy and/or ventricular ectopics (extrasystoles), electrolyte disturbances (e.g. hyperkalaemia), collagen vascular disease, valvular stenosis, renovascular hypertension, hypercholesterolemia. Before, during or immediately after anaesthesia; surgery. Assess renal function before initiation. Patients with hypertension should be stabilised on individual components before starting combination. Therapy should not be started after MI if systolic blood pressure <100 mmHg. Hypotension may occur after initial dose in patients who are hypovolaemic and/or salt depleted (diuretic should be discontinued for 2-3 days and then lisinopril initiated alone). Discontinue before carrying parathyroid function test.
Adverse Reactions
Volume depletion and electrolyte imbalance (eg hyperkalaemia); dry mouth, thirst; lethargy, drowsiness; muscle pain, cramps; hypotension; hypersensitivity reactions eg, rashes, photosensitivity, thrombocytopenia, jaundice, pancreatitis; fatigue; weakness; may precipitate an attack of gout (hyperuricaemia); impotence, hyperglycaemia; anorexia, gastric irritation, nausea, vomiting, constipation, diarrhoea; sialadenitis; dizziness; hypercalcaemia; headache; cough; chest pain; angioneurotic oedema; occasional increase in liver enzymes and serum bilirubin; renal function deterioration; alopecia; oliguria/anuria; urticaria, pruritis; diaphoresis.
Potentially Fatal: Seizures; cholestatic jaundice; neutropenia and agranulocytosis (with or without myeloid hyperplasia); acute renal failure, oliguria; progressive azotemia; haemolytic anaemia; angioedema associated with laryngeal oedema.
Symptoms: hypotension, bradycardia may occur; electrolyte depletion and dehydration from excessive diuresis. Treatment: symptom specific and supportive; induction of emesis and/or gastric lavage, correction of dehydration, electrolyte imbalance and hypotension with IV solution.
Drug Interactions
Antacids may decrease the bioavailability of ACE inhibitors; aprotinin may decrease effects of lisinopril during infusion. Sympathomimetics and indomethacin may decrease antihypertensive effects. Increased risk of hyperkalaemia with eplerenone, potassium sparing diuretics, ciclosporine, trimethoprim, corticosteroids. May increase toxic effects of gold sodium thiomalate. Increased risk of hypoglycaemia with insulin and oral antidiabetics. Increased risk of hypovolaemia (and resulting renal failure) with loop diuretics. Concurrent use with β-blockers may increase hyperglycaemic effects in type 2 DM. NSAIDs may exacerbate renal impairment; narcotics, antipsychotics and alcohol may enhance hypotensive effects. Cholestyramine and colestipol resins may reduce absorption of hydrochlorothiazide; leave 2 hr between doses. Potassium containing salt substitutes may increase risk of hyperkalaemia.
Potentially Fatal: Potentiates bone marrow suppression caused by anticancer drugs eg azathioprine, mercaptopurine; reduces renal clearance and increases toxicity of lithium (monitor lithium levels especially in 1st 4 wk); increased risk of hypokalaemia with corticosteroids, prolongs paralysis caused by tubocurarine; increased risk of nephrotoxicity with ciclosporin, aminoglycosides, salicylates, increased risk of cardiac toxicity in hypokalaemia with cardiac glycosides.
Food Interaction
Hydrochlorothiazide peak serum levels may be decreased if taken with food. Avoid dong quai (if using for hypertension as it exerts estrogenic activity), ephedra, yohimbe, ginseng (may worsen hypertension) and garlic (increased hypertensive effect).
Lab Interference
False-positive urine acetone determination results using Na nitroprusside. Increases serum K and BUN/serum creatinine.
Description: Lisinopril competitively inhibits ACE from converting angiotensin I to angiotensin II resulting in increased plasma renin activity and reduced aldosterone secretion, causing reduced BP and sodium and water retention. Hydrochlorothiazide increases renal excretion of sodium and chloride and reduces cardiac load. The two drugs exert additive effects in hypertension.
Onset: Lisinopril: 1 hr; hydrochlorothiazide: diuresis: approx 2 hr.
Duration: Lisinopril: 24 hr; hydrochlorothiazide: 6-12 hr.
Absorption: Lisinopril: Well absorbed, unaffected by food; peak effect: approx 6 hr. Hydrochlorothiazide: approx 50-80%; peak effect: 4-6 hr.
Distribution: Plasma protein binding: lisinopril: 25%; hydrochlorothiazide: 68%. Distribution of hydrochlorothiazide: 3.6-7.8 L/kg.
Metabolism: Lisinopril: Not significantly metabolised. Hydrochlorothiazide: Not metabolised.
Excretion: Half-life elimination: lisinopril: 11-12 hr; hydrochlorothiazide: 5.6-14.8 hr. Excretion: lisinopril Mainly via urine as unchanged drug (lisinopril and hydrochlorothiazide).
Store below 25°C.
Disclaimer: This information is independently developed by MIMS based on Lisinopril + Hydrochlorothiazide from various references and is provided for your reference only. Therapeutic uses, prescribing information and product availability may vary between countries. Please refer to MIMS Product Monographs for specific and locally approved prescribing information. Although great effort has been made to ensure content accuracy, MIMS shall not be held responsible or liable for any claims or damages arising from the use or misuse of the information contained herein, its contents or omissions, or otherwise. Copyright © 2021 MIMS. All rights reserved. Powered by
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