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Active ingredient and strength
Indapamide hemihydrate 2.5mg
Excipients: Sodium lauryl sulphate, lactose, microcrystalline cellulose, magnesium stearate, hypromellose, titanium dioxide, polyethylene glycol, carmine BPC Aluminium lake, sunset yellow aluminium lake, indigo carmine aluminium lake.

Therapeutic properties
Essential hypertension

Mechanism of Action
Indapamide is an indoline antihypertensive/diuretic. Chemically indapamide has a sulphonamide group in common with other diuretics but also has an indoline moiety. The N-N bond has similarities to hydralazine that is a direct vasodilator. It does not have a thiazide ring.

In clinical trials daily doses of indapamide between 0.5 mg and 5.0 mg produce dose-related antihypertensive effects. Generally, doses of 2.5 mg and 5.0 mg are indistinguishable but are distinguishable from placebo and doses of 0.5 mg and 1.0 mg.

The effect of indapamide at doses of 2.5 mg daily are approximately equal to those obtained with conventional doses of other anti-hypertensive/diuretics.

The antihypertensive action appears to predominantly involve extra-renal mechanisms including normalisation of vascular hyperreactivity to vasopressor amines and a reduction in peripheral resistance. There is little cardiac: inotropic, chronotropic, output or rhythm effect. Indapamide does not provoke glucose intolerance and has no adverse effect upon triglycerides, LDL-cholesterol, or LDL/HDL cholesterol ratio.

Indapamide is rapidly and completely absorbed from the gastrointestinal tract after oral administration, estimates of the degree of absorption ranging from 80-93%. Peak plasma concentrations are achieved at approximately 3.5 hours. It is preferentially and reversibly taken up by the erythrocytes in blood, the whole blood/ plasma ratio being approximately 6:1 at peak concentration decreasing to 3.5:1 after eight hours.

Within the red cell, indapamide is almost completely bound to carbonic anhydrase, however, the activity of the enzyme is not inhibited by this binding. Red cell binding has been shown in-vitro to be substantially decreased by chlorthalidone and acetazolamide. These latter two agents have greater affinity for the binding site than indapamide. Within plasma indapamide is approximately 76-79% bound to human plasma proteins, however, the specific proteins involved have not been identified.

Volume of distribution for indapamide is large, having been estimated as 25-27 I from blood concentrations and 110 I from plasma concentrations. The major route of elimination in man is the urine where up to 60-70% of a dose is excreted within 48 hours. Between 5- 7% is excreted unchanged, the rest being metabolised. Up to 19 metabolites have been identified although the majority are minor.

Hydroxylation of the indoline ring gives rise to the major metabolite. It is thought to be active, however, this remains to be confirmed. 18% of the metabolites in urine appear as conjugates, 14% as conjugates with glucuronic acid and 4% as conjugates with sulphate.

The renal clearance of unchanged indapamide is low, being estimated at 0.3 l/h while systemic clearance is approximately 1.2 1/h. This reflects the importance of hepatic clearance. Approximately 16-23% of a dose is eliminated in the faeces. The plasma elimination half-life has been estimated to be between 14-18 hours.

The bioavailability of indapamide is not significantly altered by administration with food or magnesium hydroxide or aluminium hydroxide. Renal failure, however, increases plasma concentrations by about 20%. Little is known about the effect of age or impaired hepatic function.

Hypersensitivity to indapamide or other sulphonamide-derived agents. Severe renal or hepatic impairment. Pregnancy and breast feeding. Recent cerebrovascular accident.

Adverse Effects
Most adverse effects have been mild and transient. Serum potassium may fall although it usually remains within the normal range. The fall may be sufficient, however, to cause hypokalaemia in some patients, Serum urate levels may rise slightly but gout has rarely been reported. Asthenia, headache, gastrointestinal disturbances and rash have also been reported.

Thiazide and related diuretics may decrease urinary calcium excretion and cause a slight and transitory rise in plasma calcium, however hypercalcaemia from this cause is extremely rare. Frank hypercalcaemia if it arises may be due to previously unrecognised hyperparathyroidism. Treatment with indapamide should be withdrawn before the investigation of parathyroid function. An increase in blood glucose may occur during treatment, however, indapamide does not appear to adversely affect glucose tolerance or alter glucose metabolism, even in diabetic hypertensive patients.

Warnings and Precautions
Hypokalaemia and other fluid and electrolyte imbalances: Periodic determinations of serum electrolytes should be performed at appropriate intervals. In addition, patients should be observed for clinical signs of fluid or electrolyte imbalance, such as hyponatraemia, hypochloraemic alkalosis, or hypokalaemia. Warning signs include dry mouth, thirst, weakness, fatigue, lethargy, drowsiness, restlessness, muscle pains or cramps, hypotension, oliguria, tachycardia and gastrointestinal disturbance. Electrolyte determinations are particularly important in patients who are vomiting excessively or receiving parenteral fluids, in patients subject to electrolyte imbalance (including those with heart failure, kidney disease and cirrhosis), and in patients on a salt restricted diet.

The risk of hypokalaemia secondary to diuresis and natriuresis is increased when larger doses are used, when the diuresis is brisk, when severe cirrhosis is present and during concomitant use of corticosteroids or ACTH. Interference with adequate oral intake of electrolytes will also contribute to hypokalaemia. Hypokalaemia can sensitise or exaggerate the response of the heart to the toxic effects of digitalis, such as increased ventricular irritability.

Dilutional hyponatraemia may occur in oedematous patients; the appropriate treatment is restriction of water rather than administration of salt, except in rare instances when the hyponatraemia is life threatening. However, in actual salt depletion, appropriate replacement is the treatment of choice.

Any chloride deficit that may occur during treatment is generally mild and usually does not require specific treatment except in extraordinary circumstances as in liver or renal disease.

Hyperuricaemia and Gout: Serum concentrations of uric acid increased by an average of 1.0mg/100mL in patients treated with indapamide, and frank gout may be precipitated in certain patients receiving indapamide. Serumconcentrations of uric acid should, therefore, be monitored periodically during treatment.

Renal Impairment: Indapamide, like the thiazides, should be used with caution in patients with severe renal disease, as reduced plasma volume may exacerbate or precipitate azotaemia. If progressive renal impairment is observed in a patient receiving indapamide, withholding or discontinuing diuretic therapy should be considered. Renal function tests should be performed periodically during treatment with indapamide.

Impaired Hepatic Function: Indapamide, like the thiazides, should be used with caution in patients with impaired hepatic function or progressive liver disease, since minor alterations of fluid and electrolyte balance may precipitate hepatic coma.

Calcium Excretion: Calcium excretion is decreased by diuretics pharmacologically related to indapamide. In long-term studies of hypertensive patients, however, serum concentrations of calcium increased only slightly with indapamide.

Prolonged treatment with medicines pharmacologically related to indapamide may in rare instances be associated with hypercalcaemia and hypophosphataemia secondary to physiologic changes in the parathyroid gland, however, the common complications of hyperparathyroidism, such as renal lithiasis, bone resorption and peptic ulcer, have not been seen.

Treatment should be discontinued before tests for parathyroid function are performed. Like the thiazides, indapamide may decrease serum PBI levels without signs of thyroid disturbance.

Interaction with Systemic Lupus Erythematosus: Thiazides have exacerbated or activated systemic lupus erythematosus and this possibility should be considered with indapamide as well.

Indapamide is a drug substance that may induce a positive reaction during antidoping control tests. Athletes may need to be cautious about taking Napamide.

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