Valsartan 80 mg and hydrochlorothiazide 12.5 mg tab
Valsartan 160 mg and hydrochlorothiazide 12.5 mg tab
Valsartan 160 mg and hydrochlorothiazide 25 mg tab
Valsartan 320 mg and hydrochlorothiazide 12.5 mg tab
Valsartan 320 mg and hydrochlorothiazide 25 mg tab
As initial therapy: 160 mg/12.5 mg once daily; titrate as needed according to response after 1-2 weeks of therapy. As add-on or replacement therapy in patients with inadequately controlled blood pressure on either valsartan or hydrochlorothiazide monotherapy: Valsartan 80-320 mg and hydrochlorothiazide 12.5-25 mg once daily; titrate as needed according to response after 3-4 weeks of therapy. Max: Valsartan 320 mg and hydrochlorothiazide 25 mg daily.
Severe (GFR <30 mL/min): Contraindicated.
Mild to moderate: Max: Valsartan 80 mg; no adjustment is required on hydrochlorothiazide. Severe: Contraindicated.
Hypersensitivity to sulfonamide-derived drugs. Refractory hypokalaemia, hyponatraemia, hypercalcemia, symptomatic hyperuricaemia, anuria, and biliary obstructive disorders. Severe renal (GFR <30 mL/min) and hepatic impairment. Pregnancy. Concomitant use with aliskiren-containing products in patients with diabetes mellitus or renal impairment (GFR <60 mL/min).
Patient with heart failure, history of MI, unstented unilateral/bilateral renal artery stenosis, aortic or mitral stenosis, pre-diabetes or diabetes mellitus, history of gout or familial predisposition to gout, history of angioedema, Na or volume depletion; moderate or high cholesterol level, parathyroid disease (prolonged use). Patient undergoing surgery. Mild to moderate renal and hepatic impairment (without cholestasis). Lactation.
Significant: Fluid or electrolyte imbalance (e.g. hypokalaemia, hyponatraemia, hypochloraemic alkalosis, hypomagnesaemia, hypercalcaemia), symptomatic hypotension (particularly in salt- or volume-depleted patients), increased risk of non-melanoma skin cancer (basal cell carcinoma and squamous cell carcinoma), exacerbation or activation of SLE, impaired glucose tolerance, increased cholesterol, triglycerides and uric acid; photosensitivity, choroidal effusion with visual field defect, acute transient myopia, acute angle-closure glaucoma, renal function deterioration and/or increases in serum creatinine (particularly in patients with low renal blood flow). Rarely, angioedema of the face, lips, tongue, pharynx, larynx, or glottis. Blood and lymphatic system disorders: Neutropenia. Ear and labyrinth disorders: Tinnitus. Eye disorders: Blurred vision. Gastrointestinal disorders: Abdominal pain, diarrhoea. General disorders and administration site conditions: Fatigue. Investigations: Increased bilirubin, urea or liver enzymes. Musculoskeletal and connective tissue disorders: Muscle spasm, rhabdomyolysis, arthralgia, myalgia. Nervous system disorders: Dizziness, headache, paraesthesia. Respiratory, thoracic and mediastinal disorders: Nasopharyngitis, cough, non-cardiogenic pulmonary oedema. Skin and subcutaneous tissue disorders: Bullous dermatitis, alopecia. Vascular disorders: Syncope, vasculitis.
Avoid prolonged exposure to sunlight and UV rays, wear sunscreen or protective clothing when going outdoors.
Monitor blood pressure, heart rate; serum electrolytes (e.g. K, Mg, Na) and renal function periodically. Observe for signs of fluid or electrolyte imbalance.
Symptoms: Nausea, somnolence, hypovolaemia, electrolyte disturbances, dehydration, hypotension, tachycardia, bradycardia, depressed level of consciousness, circulatory collapse and/or shock. Management: Supportive and symptomatic treatment. May induce vomiting if ingestion is recent. In case of hypotension, place the patient in a supine position with salt and volume supplementation. Hydrochlorothiazide may be removed by haemodialysis.
May decrease the excretion of lithium, increasing the risk of lithium toxicity. May increase the therapeutic effects of other antihypertensive agents. Concomitant use with NSAIDs diminish the therapeutic effect and may cause a significant decrease in renal function.
Valsartan: Enhanced hyperkalaemic effect with K-sparing diuretics (e.g. spironolactone, triamterene, amiloride), K supplements, K-containing salt substitutes and other drugs that may increase K levels (e.g. heparin).
Hydrochlorothiazide: May diminish the therapeutic effect of antidiabetic agents. Increased risk of hyponatraemia with antidepressants (e.g SSRIs), antiepileptics (e.g. carbamazepine, oxcarbazepine) and antipsychotics. Increases the risk of digitalis toxicity. May increase the incidence of hypersensitivity reactions to allopurinol. May reduce the renal excretion and potentiate the myelosuppressive effects of cytotoxic agents (e.g. cyclophosphamide, methotrexate). Increased serum concentration with anticholinergic agents (e.g. atropine, biperiden). May reduce or delay absorption with colestyramine and colestipol. Administration with vitamin D may potentiate the rise in serum Ca. May decrease the excretion of Ca salts and if continued, it can result in hypercalcaemia and metabolic alkalosis. May enhance the hyperglycaemic effect of diazoxide. Concomitant administration with barbiturates and opioids may potentiate orthostatic hypotension. May reduce the response to pressor amines (e.g. norepinephrine). Enhanced hypokalaemic effect with kaliuretic diuretics, corticosteroids, corticotropin, amphotericin B, and carbenoxolone. May increase risk of torsades de pointes with certain antiarrhythmics, certain antipsychotics and other drugs known to induce torsades de pointes. May increase the risk of adverse effects of amantadine. Potentially Fatal:
Valsartan: Increased risk of hypotension, hyperkalaemia, and changes in renal function with aliskiren in patients with diabetes mellitus or renal impairment (GFR <60 mL/min).
Alcohol may potentiate the hypotensive effect of hydrochlorothiazide.
May lead to a false-negative aldosterone/renin ratio (ARR). May interfere with parathyroid function tests and may decrease serum iodine (protein-bound) without signs of thyroid disturbance.
Description: Valsartan is an angiotensin II receptor antagonist producing its blood pressure lowering effects by selectively blocking the binding of angiotensin II to AT1 receptors, thereby antagonising angiotensin I-induced vasoconstriction, aldosterone release, catecholamine release, arginine vasopressin release, water intake, and hypertrophic responses.
Hydrochlorothiazide inhibits the reabsorption of Na in the distal renal tubules causing an increase in the excretion of Na and water along with K and hydrogen ions. Onset: Valsartan: Approx 2 hours.
Hydrochlorothiazide: Diuresis: Approx 2 hours. Duration: Valsartan: 24 hours.
Hydrochlorothiazide: 6-12 hours. Pharmacokinetics: Absorption: Valsartan: Rapidly absorbed from the gastrointestinal tract. Bioavailability: 25%. Time to peak plasma concentration: 2-4 hours.
Hydrochlorothiazide: Rapidly and well-absorbed from the gastrointestinal tract. Bioavailability: Approx 65-75%. Time to peak plasma concentration: Approx 1-5 hours. Distribution: Valsartan: Volume of distribution: 17 L. Plasma protein binding: 95%, mainly to albumin.
Hydrochlorothiazide: Crosses the placenta and enters breast milk. Volume of distribution: 3.6-7.8 L/kg. Plasma protein binding: Approx 40-68%. Metabolism: Valsartan: Metabolised to inactive metabolite, valeryl 4-hydroxy valsartan.
Hydrochlorothiazide: Not metabolised. Excretion: Valsartan: Mainly via faeces (83%) and urine (approx 13%) as unchanged drug. Elimination half-life: Approx 6 hours.
Hydrochlorothiazide: Mainly via urine (≥61% as unchanged drug). Elimination half-life: Approx 6-15 hours.
Store below 30°C. Protect from light and moisture.