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Valianz HCT

Valianz HCT Drug Interactions

valsartan + hydrochlorothiazide

Manufacturer:

Lloyd

Distributor:

InnoGen Pharmaceuticals
Full Prescribing Info
Drug Interactions
Valsartan-hydrochlorothiazide: The following drug interactions may occur due to both components (valsartan and/or hydrochlorothiazides): Lithium: Reversible increase in serum lithium concentrations and toxicity have been reported during concomitant administration of lithium with ACE inhibitors, angiotensin II receptor antagonists or thiazides. Since renal clearance of lithium is reduced by thiazides, the risk of lithium toxicity may presumably be increased further with Valsartan + Hydrochlorothiazide. Therefore, careful monitoring of serum lithium concentrations is recommended during concomitant use.
Valsartan: The following potential drug interaction may occur due to the valsartan component: Dual blockade of the Renin-Angiotensin-System (RAS) with ARB's, ACEI's, or aliskiren: The concomitant use of ARBs, including valsartan, with other agents acting on the RAS is associated with an increased incidence of hypotension, hyperkalemia, and changes in renal function compared to monotherapy. It is recommended to monitor blood pressure, renal function and electrolytes in patients on valsartan + hydrochlorothiazide and other agents that affect the RAS.
The concomitant use of ARBS - including valsartan - or of ACEIs with aliskiren, should be avoided in patients with severe renal impairment (GFR< 30 mL/min).
The concomitant use of ARBS - including valsartan - or of ACEIs with aliskiren is contraindicated in patients with Type 2 diabetes.
Potassium: Concomitant use with potassium supplements, potassium-sparing diuretics, salt substitutes containing potassium, or other drugs that may alter potassium levels (heparin, etc.) should be used with caution and with frequent monitoring of potassium.
Non-Steroidal Anti-Inflammatory Agents (NSAIDs) including Selective Cyclooxygenase-2 Inhibitors (COX-2 Inhibitors): When angiotensin II antagonists are administered simultaneously with NSAIDs, attenuation of the antihypertensive effect may occur.
Furthermore, in patients who are elderly, volume-depleted (including those on diuretic therapy), or have compromised renal function, concomitant use of angiotensin II antagonists and NSAIDs may lead to an increased risk of worsening of renal function. Therefore, monitoring of renal function is recommended when initiating or modifying the treatment in patients on valsartan who are taking NSAIDs concomitantly.
Hydrochlorothiazide: The following potential drug interactions may occur due to the thiazide component: Lithium: Reversible increases in serum lithium concentrations and toxicity have been reported during concurrent use of ACE inhibitors and thiazides. There is no experience with concomitant use of valsartan and lithium. Therefore, monitoring of serum lithium concentrations is recommended during concurrent use.
Other anti-hypertensive drugs: The thiazides potentiate the antihypertensive action of other antihypertensive drugs (e.g guanethidine, methyldopa, beta-blockers, vasodilators, calcium channel blockers, ACE inhibitors, Angiotensin Receptor Blockers (ARBs) and Direct Renin Inhibitors (DRIs).
Skeletal muscle relaxants: Thiazides, including hydrochlorothiazide, potentiate the action of skeletal muscle relaxants such as curare derivatives.
Medicinal products affecting serum potassium levels: The hypokalemic effect of diuretics may be increased by concomitant administration of kaliuretic diuretics, corticosteroids, ACTH.
Antidiabetic agents: Thiazides may alter glucose tolerance. It may be necessary to adjust the dosage of insulin and oral antidiabetic agents.
Digitalis glycosides: Thiazide-induced hypokalemia or hypomagnesemia may occur as unwanted effects, favoring the onset of digitalis-induced cardiac arrythmias.
NSAIDs and Cox-2 selective inhibitors: Concomitant administration of NSAIDs (e.g salicylic acid derivative, indomethacin) may weaken the diuretic and antihypertensive activity of the thiazide component. Concurrent hypovolemia may include acute renal failure.
Allopurinol: Co-administration of thiazide diuretics (including hydrochlorothiazide) may increase the incidence of hypersensitivity reactions to allopurinol.
Amantadine: Co-administration of thiazide diuretics (including hydrochlorothiazide) may increase the risk of adverse effects caused by amantadine.
Antineoplastic agents (e.g cyclophosphamide, methotrexate): Concomitant use of thiazide diuretics may reduce renal excretion of cytotoxic agents and enhance their myelosuppressive effects.
Anticholinergic agents: The bioavailability of thiazide-type diuretics may be increased by anticholinergic (e.g atropine, biperiden), apparently due to a decrease in gastrointestinal motility and the stomach emptying rate. Conversely prokinetic drugs such as cisapride may decrease the bioavailability of thiazide-type diuretics.
Ion exchange resin: Absorption thiazide diuretics, including hydrochlorothiazide, is decreased by cholestyramine or colestipol. However, staggering the dosage of hydrochlorothiazide and resin such that hydrochlorothiazide is administered at least 4 h before or 4 - 6 h after the administration of resins would potentially minimize the interaction.
Vitamin D: Administration of thiazide diuretics, including hydrochlorothiazide, with vitamin D or with calcium salts may potentiate the rise in serum calcium.
Ciclosporin: Concomitant treatment with ciclosporin may increase the risk of hyperuricemia and gout-type complications.
Calcium salts: Concomitant use of thiazide type diuretics may lead to hypercalcemia by increasing tubular calcium reabsoprtion.
Diazoxide: Thiazide diuretics may enhance the hyperglycemic effect of diazoxide.
Methyldopa: There have been reports in the literature of hemolytic anemia occurring with concomitant us of hydrochlorothiazide band methyldopa.
Alcohol, barbiturates or narcotics: Concomitant administration of thiazide diuretics with alcohol, barbiturates, or narcotics may potentiate orthostatic hypotension.
Pressor amines: Hydrochlorothiazide may reduce the response to pressor amines such as noradrenaline. The clinical significance of this effect is uncertain and not sufficient to preclude their use.
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