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Co-Amilozide Tablets 5/50mg Bp

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SUMMARY OF PRODUCT CHARACTERISTICS

1    NAME OF THE MEDICINAL PRODUCT

Co-Amilozide Tablets BP 5/50mg

2    QUALITATIVE AND QUANTITATIVE COMPOSITION

Each tablet contains Amiloride Hydrochloride equivalent to 5mg anhydrous amiloride hydrochloride and 50mg Hydrochlorothiazide.

3    PHARMACEUTICAL FORM

Yellow uncoated tablets.

Yellow, circular, biconvex uncoated tablets impressed “C” and the identifying letters “AZ” on either side of a central division line o one face.

4    CLINICAL PARTICULARS

4.1    Therapeutic indications

Potassium-conserving diuretic and antihypertensive.

Co-amilozide is intended for the treatment of patients in whom potassium depletion might be anticipated or suspected. The presence of amiloride hydrochloride minimises the likelihood of potassium loss during vigorous diuresis for long term maintenance therapy. The combination is therefore indicated especially in conditions where potassium balance is particularly important.

1) For the treatment of patients with hypertension, congestive heart failure, or hepatic cirrhosis with ascites and oedema. In hypertension, co-amilozide may be used alone or in combination with other antihypertensive agents.

4.2 Posology and method of administration

Hypertension: Usually half a tablet once daily. If necessary, the daily dosage may be increased to one tablet which may be given as a single or divided dose. Congestive heart failure: Initially half a tablet daily which may be subsequently adjusted if necessary to a maximum of 2 tablets daily. Optimum dosage is determined by the diuretic response and the plasma potassium level. Once diuresis is achieved, reduction in dosage may be attempted for maintenance therapy which may be on an intermittent basis.

Hepatic cirrhosis with ascites: Initiate therapy with a low dose. A single dose of one tablet daily may be increased gradually, if necessary, to achieve an effective diuresis, up to a maximum of 2 tablets daily. Maintenance doses may be lower than those required to initiate diuresis; reduction in the daily dosage should therefore be attempted when the patients weight is stabilised. A gradual weight reduction is especially desirable in cirrhotic patients to reduce the likelihood of untoward reactions associated with diuretic therapy.

Elderly: Dosage in the elderly should be carefully adjusted according to renal function, blood electrolytes and diuretic response. The elderly are more likely to experience hyperkalaemia since renal reserve may be reduced.

Children: Not recommended for use in children under 18 years as safety and efficacy have not been established.

Method of Administration For oral administration.

4.3 Contraindications

Known hypersensitivity to amiloride hydrochloride, hydrochlorothiazide or other sulphonamide derived drugs. Hyperkalaemia (plasma potassium above 5.5mmol/l; other potassium-conserving agents, potassium supplements or potassium-rich food (except in severe and/or refractory cases of hypokalaemia under careful monitoring; anuria; acute renal failure, severe progressive renal disease; severe hepatic failure, precoma associated with hepatic cirrhosis; Addison's disease; hypercalcaemia; diabetic neuropathy; patients with blood urea over 10mmol/l, serum creatinine over 130mmol/l, or with diabetes mellitus require careful monitoring of serum electrolytes and blood urea levels. In renal impairment, use of a potassium-conserving agent may result in rapid development of hyperkalaemia.

Co-amilozide is not recommended for children under 18 years old.

4.4 Special warnings and precautions for use

Renal function should be monitored in cases of impaired renal function as the use of Co-amilozide may results in the rapid development of hyperkalaemia. Thiazide diuretics become ineffective when creatinine levels fall below 30ml/minute.

Electrolyte imbalance and blood urea increases: Hyponatraemia and hypochloraemia may occur when amiloride hydrochloride is used in conjunction with other diuretics. Reversible increases in blood urea levels have been reported accompanying vigorous diuresis, especially when diuretics were used in seriously ill patients, such as those with hepatic cirrhosis with ascites and metabolic alkalosis, or those with resistant oedema. Hyponatraemia may lead to grand mal seizures. Careful monitoring of serum electrolytes and blood urea levels should therefore be carried out when amiloride is given with oral diuretics to such patients. Reports suggest that patients with pre-existing severe liver disease treated with diuretics including amiloride hydrochloride, may experience hepatic encephalopathy, manifested by tremors, confusion and coma, and increased jaundice.

Thiazides may decrease serum PBI levels without signs of thyroid disturbance, calcium excretion is also decreased. Pathological changes in the parathyroid glands accompanied by hypercalcaemia and hypophosphataemia have been seen in a few patients receiving prolonged thiazide therapy. Therapy should be discontinued before carrying out tests for parathyroid function. Hyperuricaemia may occur, or gout may be precipitated, in certain patients receiving thiazides. Increases in cholesterol and triglyceride levels may be associated with thiazide diuretic therapy.

Thiazides may impair glucose tolerance. Diabetes mellitus may be precipitated or aggravated. Dosage adjustment of antidiabetic agents, including insulin, may be required. To minimise the risk of hyperkalaemia in diabetic or suspected diabetic patients, the status of renal function should be determined before initiating therapy with co-amilozide. Therapy should be discontinued at least three days before a glucose tolerance test. Potassium-conserving therapy should be initiated only with caution in severely ill patients in whom metabolic or respiratory acidosis may occur (cardiopulmonary disease, inadequately controlled diabetes). Shifts in acid-base balance of extracellular/intracellular potassium, and the development of acidosis may be associated with rapid increases in plasma potassium.

The possibility that thiazides may activate or exacerbate systemic lupus erythematosus has been reported.

4.5 Interaction with other medicinal products and other forms of interaction

Co-amilozide should not be used concomitantly with spironolactone or triamterene. Hydrochlorothiazide potentiates the actions of other antihypertensive drugs; therefore the dosage of these agents, especially the adrenergic blockers, may need to be reduced when this product is added to the regimen.

Lithium should not generally be given with diuretics because they reduce its renal clearance and add a high risk of lithium toxicity.

Thiazide-containing drugs may increase the responsiveness to tubocurarine. The antihypertensive effect of thiazides may be enhanced in the postsympathectomy patient.

Hydrochlorothiazide may decrease arterial responsiveness to pressor amines such as noradrenaline (norepinephrine), but not enough to preclude their therapeutic usefulness.

Orthostatic hypotension may occur, and may be potentiated by alcohol, barbiturates and narcotics.

Diuretic therapy should be discontinued for 2-3 days before initiation of therapy with an ACE inhibitor to reduce the likelihood of first dose hypotension. If concomitant use is indicated because of demonstrated hypokalaemia, they should be used with caution and with frequent monitoring of serum electrolytes.

Corticosteroids or ACTH may intensify any thiazide-induced electrolyte depletion, particularly hypokalaemia.

NSAIDs may attenuate the diuretic, natriuretic and antihypertensive effects of diuretics.

Co-amilozide can act synergistically with chlorpropamide to increase the risk of hyponatraemia.

4.6. Pregnancy and Lactation

Pregnancy:

The routine use of diuretics in otherwise healthy pregnant women with or without mild oedema is not indicated, because they may be associated with hypovolaemia, increased blood viscosity and decreased placental perfusion. Diuretics do not prevent the development of toxaemia of pregnancy and there is no satisfactory evidence that they are useful for its treatment.

There is limited experience with hydrochlorothiazide during pregnancy, especially during the first trimester. Animal studies are insufficient. Hydrochlorothiazide crosses the placenta. Based on the pharmacological mechanism of action of hydrochlorothiazide its use during the second and third trimester may compromise foeto-placental perfusion and may cause foetal and neonatal effects like icterus, disturbance of electrolyte balance and thrombocytopenia. Hydrochlorothiazide should not be used for gestational oedema, gestational hypertension or preeclampsia due to the risk of decreased plasma volume and placental hypoperfusion, without a beneficial effect on the course of the disease. Hydrochlorothiazide should not be used for essential hypertension in pregnant women except in rare situations where no other treatment could be used.

Lactation:

Hydrochlorothiazide is excreted in human milk in small amounts. Thiazides in high doses causing intense diuresis can inhibit the milk production. The use of co-amilozide during breast feeding is not recommended. If co-amilozide is used during breast feeding, doses should be kept as low as possible.

4.7 Effects on ability to drive and use machines

None known

4.8 Undesirable effects

Although the likelihood of electrolyte imbalance is reduced with co-amilozide, careful check should be kept for such signs of fluid and electrolyte imbalance as hyponatraemia, hypochloraemic alkalosis, hypokalaemia and hypomagnesaemia. It is particularly important to make serum and electrolyte determinations when the patient is vomiting excessively or receiving parenteral fluids. Warning signs or symptoms of fluid or electrolyte imbalance include dryness of mouth, weakness, lethargy, drowsiness, restlessness, seizures, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia and gastrointestinal disturbances such as nausea and vomiting. Hyperkalaemia has been observed in patients receiving amiloride hydrochloride, either alone or in combination with other diuretics, particularly in the aged or in hospital patients with hepatic cirrhosis or congestive heart failure with renal involvement, who were seriously ill, or were undergoing vigorous diuretic therapy. Such patients should be carefully observed for clinical, laboratory and ECG evidence of hyperkalaemia (not always associated with an abnormal ECG). Should hyperkalaemia develop, discontinue treatment immediately and, if necessary, take active measures to reduce the plasma potassium to normal.

Neither potassium supplements nor a potassium rich diet should be used with co-amilozide except under careful monitoring in severe and/or refractory cases of hypokalaemia. Some deaths have bee reported in this group of patients.

Apart from hyperkalaemia, minor side effects are relatively common, significant side effects are infrequent. Reported side effects are generally associated with diuresis, thiazide therapy, or with the underlying disease. No increase in the risk of adverse reactions has been seen over those of the individual components.

General: anaphylactic reaction, back pain, chest pain, fatigue, fever, headache, malaise, neck/shoulder ache, pain in extremities, syncope, weakness. Cardiovascular: angina pectoris, arrhythmias, digitalis toxicity, orthostatic hypotension, necrotising angiitis (vasculitis, cutaneous vasculitis), palpitation and tachycardia.

Digestive: abdominal fullness, abdominal pain, abnormal liver function, activation of probable pre-existing peptic ulcer, anorexia, appetite changes, constipation, cramping, diarrhoea, dyspepsia, flatulence, gastric irritation, GI bleeding, hiccups, jaundice (intrahepatic cholestatic jaundice), nausea, pancreatitis, thirst and vomiting.

Haematological: agranulocytosis, aplastic anaemia, haemolitic anaemia, leucopenia, neutropenia, purpura and thrombocytopenia.

Integumentary: alopecia, diaphoresis, dry mouth, flushing, photosensitivity, puritis, rash, sialadenitis and urticaria.

Metabolic: dehydration, electrolyte imbalance, elevated potassium levels, glycosuria, gout, hyperglycaemia, hyperuricaemia and hyponatraemia. Musculoskeletal: joint pain, leg ache and muscle cramps.

Nervous: dizziness, encephalopathy, paraesthesia, stupor, tremors, vertigo. Psychiatric: decreased libido, depression, insomnia, mental confusion, nervousness, restlessness, sleepiness and somnolence.

Respiratory: cough, dyspnoea and respiratory distress, including pneumonitis, pulmonary oedema.

Special senses: bad taste, increased intra-ocular pressure, nasal congestion, tinnitus, visual disturbance and xanthopsia.

Urogenital: bladder spasm, dysuria, impotence, incontinence, interstitial nephritis, nocturia, polyuria, renal dysfunction including renal failure and urinary frequency.

4.9 Overdose

No specific data is available for the combination; no specific antidote is available and it is not known whether the drug is dialysable.

The most likely signs and symptoms are dehydration and electrolyte imbalance of amiloride overdosage.

Electrolyte depletion (hypokalaemia, hypochloraemia, hyponatraemia) and dehydration are the most common signs and symptoms of hydrochlorothiazide overdosage.

Treatment should be symptomatic and supportive. If hyperkalaemia occurs, active measures should be taken to reduce plasma potassium levels. Therapy should be discontinued and the patient closely observed. Emesis should be induced or gastric lavage performed.

If digitalis has been administered, hypokalaemia may accentuate cardiac arrhythmias.

5    PHARMACOLOGICAL PROPERTIES

5.1    Pharmacodynamic properties

Amiloride hydrochloride is a weak diuretic with potassium-sparing properties. Hydrochlorothiazide is a thiazide diuretic.

Amiloride hydrochloride appears to act mainly on the distal renal tubules. It increases the excretion of sodium and reduces the excretion of potassium.

Thiazides reduce the absorption of electrolytes from the renal tubules, thereby increasing the excretion of sodium and chloride ions, and consequently of water. The excretion of other electrolytes notably potassium and magnesium, is also increased. The excretion of calcium is reduced. Thiazides also reduce carbonic-anhydrase activity so bicarbonate excretion is increased, but this effect is generally small compared with the effect on chloride and does not appreciably alter the pH of urine; they also reduce the glomerular filtration rate. Thiazides also have a hypotensive effect probably partly due to a reduction in peripheral resistance and enhance the effects of other antihypertensive agents. Paradoxically, they have and antidiuretic effect in patients with diabetes insipidus.

5.2 Pharmacokinetic properties

Amiloride is incompletely absorbed from the GI tract; bioavailability of about 50% is reported and is reduced by food. Peak serum concentrations are achieved about 3-4 hours after administration by mouth. It is excreted unchanged in the urine. Amiloride has been estimated to have a serum half-life of 6-9 hours.

Hydrochlorothiazide is fairly rapidly absorbed from the GI tract, and is reported to have a bioavailability of about 65-70%. It has been estimated to have a plasma half-life of about 3-4 hours with a subsequent longer terminal phase; its biological half-life is up to about 15 hours. It is excreted unchanged in the urine. Hydrochlorothiazide crosses the placenta barrier and is excreted in breast milk.

5.3 Preclinical safety data

Not applicable

6.1    List of excipients

The tablets also contain:

Dispersed quinoline yellow lake (E104)

Lactose

Magnesium stearate Maize starch

Microcrystalline cellulose (102) (E460)

6.2    Incompatibilities

None known

6.3    Shelf life

Shelf-life

Two years from the date of manufacture.

Shelf-life after dilution/reconstitution Not applicable.

Shelf-life after first opening Not applicable.

6.4    Special precautions    for storage

Store below 25°C in    a dry place.

Protect from light.

6.5    Nature and contents of container

The product containers are rigid injection moulded polypropylene or injection blow-moulded polyethylene containers with polyfoam wad or polyethylene ullage filler and snap-on polyethylene lids; in case any supply difficulties should arise the alternative is amber glass containers with screw caps and polyfoam wad or cotton wool.

The product may also be supplied in blister packs and cartons:

a)    Carton: White backed folding box board.

b)    Blister pack: (i) 250pm white rigid PVC. (ii) Surface printed 20pm hard temper aluminium foil with 5-7gm2 PVC and PVdC compatible heat seal lacquer on the reverse side.

Pack sizes: 28s, 30s, 56s, 60s, 84s, 90s, 100s, 112s, 120s, 168s, 180s

Product may also be supplied in bulk packs, for reassembly purposes only, in polybags contained in tins, skillets or polybuckets filled with suitable cushioning material. Bulk packs are included for temporary storage of the

finished product before final packaging into the proposed marketing containers.

Maximum size of bulk packs: 25,000.

6.6 Special precautions for disposal

Not applicable

7    MARKETING AUTHORISATION HOLDER

Actavis UK Limited (Trading style: Actavis)

Whiddon Valley Barnstaple North Devon EX32 8NS

8    MARKETING AUTHORISATION NUMBER

PL 0142/0231

9    DATE OF FIRST AUTHORISATION/RENEWAL OF THE AUTHORISATION

17/11/1988 /    14/02/2005

10 DATE OF REVISION OF THE TEXT

21/11/2013