Candesartan Cilexetil

Candesartan Cilexetil is used for: Hypertension, Congestive heart failure

Oral Hypertension Adult: Initially, 8 mg once daily, increased if necessary up to 32 mg once daily, doses to be increased at intervals of 4 weeks. Maintenance: 8 mg once daily. Max: 32 mg/day as single or in 2 divided doses. Hypertension with intravascular volume depletion Adult: Initially 4 mg once daily, increased if necessary up to 32 mg daily, doses to be increased at intervals of 4 weeks; usual dose 8 mg once daily Heart failure with impaired left ventricular systolic function when ACE inhibitors are not tolerated | Heart failure with impaired left ventricular systolic function in conjunction with an ACE inhibitor Adult: Initially 4 mg once daily, increased at intervals of at least 2 weeks to ‘target’ dose of 32 mg once daily or to maximum tolerated dose; maximum 32 mg per day

Oral Hypertension Child: 1 to <6 yr Initially, 200 mcg/kg/day. May increase according to response to 50-400 mcg/kg/day. Child: 6 to < 17 years <50 kg: 4-8 mg/day, adjusted according to response to 2-16 mg/day; >50 kg: 8-16 mg/day, adjusted according to response to 4-32 mg/day. All doses may be given as single or in 2 divided doses.

Renal Impairment No dose adjustment necessary for patients with mild renal impairment Initiate thearpy at lower dose if moderate renal impairment

May be taken with or without food.

Hypersensitivity. Pregnancy (2nd and 3rd trimester) and lactation.

Discontinue as soon as pregnancy detected; during the second and third trimesters of pregnancy, drugs that act directly on the renin-angiotensin have been associated with fetal injury that includes hypotension, neonatal skull hypoplasia, anuria, reversible or irreversible renal failure, and death Volume or sodium depletion, preexisting renal insufficiency; aortic or mitral valve stenosis, hypertrophic obstructive cardiomyopathy, renal artery stenosis, primary hyperaldosteronism. Patients with a history of angioedema, urticaria. Hypotension may occur during major surgery and anaesthesia due to suppression of the renin-angiotensin system. Monitor renal function and potassium levels

Pregnancy Therapy can cause fetal harm when administered to a pregnant woman; use of drugs that act on renin-angiotensin system during second and third trimesters of pregnancy reduces fetal renal function and increases fetal and neonatal morbidity and death Most epidemiologic studies examining fetal abnormalities after exposure to antihypertensive use in first trimester have not distinguished drugs affecting the renin-angiotensin system from other antihypertensive agents; when pregnancy is detected, discontinue drug as soon as possible Disease-associated maternal/embryo/fetal risk Hypertension in pregnancy increases maternal risk for pre-eclampsia, gestational diabetes, premature delivery, and delivery complications (e.g., need for cesarean section, and post-partum hemorrhage) Hypertension increases fetal risk for intrauterine growth restriction and intrauterine death; pregnant women with hypertension should be carefully monitored and managed accordingly Pregnant women with chronic heart failure are at increased risk for preterm birth; stroke volume and heart rate increase during pregnancy, increasing cardiac output, especially during the first trimester Heart failure may worsen with pregnancy and may lead to maternal death; closely monitor pregnant patients for destabilization of their heart failure Oligohydramnios in pregnant women who use drugs affecting the renin-angiotensin system in the second and third trimesters of pregnancy can result in the following: reduced fetal renal function leading to anuria and renal failure fetal lung hypoplasia, skeletal deformations, including skull hypoplasia, hypotension and death In the unusual case that there is no appropriate alternative to therapy with drugs affecting renin-angiotensin system for a particular patient, apprise the mother of the potential risk to fetus Perform serial ultrasound examinations to assess intra-amniotic environment; fetal testing may be appropriate, based on the week of pregnancy; patients and physicians should be aware, however, that oligohydramnios may not appear until after the fetus has sustained irreversible injury; if oligohydramnios is observed, consider alternative drug treatment Closely observe infants with histories of in utero exposure to drug for hypotension, oliguria, hyperkalemia or other symptoms of renal impairment; in neonates with a history of in utero exposure, if oliguria or hypotension occurs, support blood pressure and renal perfusion; exchange transfusions or dialysis may be required as a means of reversing hypotension and replacing renal function Lactation Not known whether drug is excreted in human milk, but shown to be present in rat milk; because of potential for serious adverse reactions in breastfed infants, advise a nursing woman that breastfeeding is not recommended during therapy

Lithium: Increases in serum lithium concentrations and toxicity. NSAIDS use may lead to increased risk of renal impairment and loss of antihypertensive effect. Dual inhibition of the renin-angiotensin system: Increased risk of renal impairment, hypotension, and hyperkalemia. May increase serum lithium concentration. K-sparing diuretics, K supplements or salt substitutes containing K may increase risk of hyperkalaemia. Potentially Fatal: Coadministration w/ aliskiren in diabetic patients may increase risk of renal impairment, hypotension and hyperkalemia. Contraindicated (2) aliskiren sparsentan Serious (13) benazepril captopril enalapril fosinopril lisinopril lithium lofexidine moexipril perindopril potassium phosphates, IV quinapril ramipril trandolapril

Side effects of Candesartan Cilexetil : Frequency Not Defined Peripheral edema Dizziness Hypertriglyceridemia Hyperuricemia Fatigue Abdominal pain Diarrhea Nausea Arthralgia Back pain Chest pain Angina Tachycardia MI Palpitation Albuminuria Bronchitis Coughing Pharyngitis Dyspepsia Gastroenteritis Rhinitis URI Rash Angioedema

Candesartan inhibits the binding of angiotensin II to AT1 receptors in many tissues (e.g. vascular smooth muscles, adrenal gland) which leads to vasoconstriction blockade and aldosterone release.