Slow-K^® Tablets 600mg

Potassium chloride 600mg PhEur

Excipients: also includes sucrose.

For a full list of excipients see 6.1.

Pale orange, round, biconvex, sugar-coated modified release tablets.

The correction and/or prevention of hypokalaemia in those patients who cannot tolerate and/or refuse to take liquid or effervescent potassium chloride, or when there is a problem of compliance with these preparations.

Slow-K is taken orally. It is important that the tablets should be swallowed whole, with fluid, during meals, whilst the patient is sitting upright.

Adults:

The dosage of Slow-K should be adapted to the cause, degree and duration of potassium depletion. 2 to 3 tablets daily are usually an adequate supplement. In states of severe potassium deficiency, a higher dose of 9 to 12 tablets daily may be needed.

If the dosage exceeds 16mmol K⁺ (2 tablets) it should be taken in divided doses. Where intermittent diuretic therapy is being used, it is advisable to give Slow-K on intervening days between administration of the diuretic. The response to treatment should preferably be monitored by repeat determination of plasma potassium and Slow-K continued until the hypokalaemia has been corrected.

Children: Not recommended.

Elderly: No special dosage regime is usually necessary, but concurrent renal insufficiency should be taken into account (See Section 4.4 “Special warnings and precautions”).

Hypersensitivity to potassium administration, eg hyperkalaemic periodic paralysis, congenital paramyotonia, or hypersensitivity to any of the excipients. Marked renal failure (even when not yet associated with manifest hyperkalaemia), untreated Addison's Disease, hyporeninaemic hypoaldosteronism, acute dehydration, hyperkalaemia and conditions involving extensive cell destruction (eg severe burns).

All solid forms of potassium medication are contra-indicated in the presence of obstructions in the digestive tract (eg resulting from compression of the oesophagus due to dilation of the left atrium or from stenosis of the gut).

In cases of metabolic acidosis, the hypokalaemia should be treated not with potassium chloride but with an alkaline potassium salt (eg potassium bicarbonate).

Concomitant treatment with potassium sparing diuretics (eg triamterene and amiloride) and aldosterone antagonists (eg spironolactone and eplerenone (see also section 4.5 Interactions with other medicaments and other forms of interaction).

If a patient under treatment with Slow-K develops severe vomiting, severe abdominal pains or flatulence, or gastro-intestinal haemorrhage, the preparation should be withdrawn at once, because in the presence of an obstruction it could conceivably give rise to ulceration or perforation (see also section 4.8 Undesirable effects).

Oral potassium preparations should be prescribed with particular caution in patients with a history of peptic ulcer.

Caution should be exercised when prescribing solid oral potassium preparations, particularly in high dosage, in patients concurrently receiving anticholinergics, because of their potential to slow gastro-intestinal motility (see also section 4.5 Interactions with other medicaments and other forms of interaction).

Patients with ostomies may have altered intestinal transit times and are better treated with other forms of potassium salts.

In patients suffering from impaired renal function, special care should be exercised when prescribing potassium salts owing to the risk of their producing hyperkalaemia. Monitoring of the serum electrolytes is particularly necessary in patients with diseases of the heart or kidneys.

In some patients, diuretic-induced magnesium deficiency will prevent restoration of intracellular deficits of potassium, so that hypomagnesaemia should be corrected at the same time as hypokalaemia.

Patients with rare hereditary problems of fructose intolerance, glucose-galactose malabsorption or sucrase-isomaltase insufficiency should not take this medicine.

Drugs which interfere with potassium excretion may promote hyperkalaemia when given together with Slow-K.

Combined treatment with the following increase the risk of hyperkalaemia: ACE inhibitors, angiotensin-II-receptor antagonists, ciclosporin, NSAIDs, β-blockers, heparin, digoxin, potassium sparing diuretics (see Section 4.3 Contra-indications).

Pregnancy

For Slow-K no clinical data on exposed pregnancies are available.

There is no indication in animal studies of direct or indirect harmful effects with respect to pregnancy, embryonal/fetal development, parturition or postnatal development (see also section 5.3 Preclinical safety data).

As a general rule, no drugs should be taken during the first 3 months of pregnancy, and the benefits and risks of taking drugs should be carefully considered throughout the whole of pregnancy, solid forms of oral potassium preparations should be given to pregnant women only if clearly needed.

Lactation

The excretion of potassium in milk has not been studied in animals or human.

The normal K⁺ content of human milk is about 13mmol/litre. Since oral potassium becomes part of the body's potassium pool, provided this is not excessive, Slow-K can be expected to have little or no effect on the potassium level in human milk.

Slow-K should only be given during breast-feeding when the expected benefit to the mother outweighs the potential risk to the baby.

None known.

Side effects are rare with Slow-K, as any excess potassium is rapidly excreted in the urine.

Gastrointestinal tract: Rare: oral potassium preparations may provoke gastro-intestinal disturbances (nausea, vomiting, abdominal pains, diarrhoea) necessitating either a reduction in dosage or withdrawal of medication (see Section 4.4 “Special warnings and precautions for use”). Isolated cases: obstruction, bleeding and ulceration, with or without perforation of the upper or lower GIT, have been reported, usually associated with other factors known to predispose a patient to these effects (eg delayed GIT transit time, obstruction of GIT).

Skin: Rare: Pruritus and/or skin rash, urticaria.

Electrolytes: Hyperkalaemia may develop in patients having difficulty with either renal potassium excretion or potassium metabolism.

Signs and symptoms: Mainly cardiovascular (hypotension, shock, ventricular arrhythmias, bundle-branch block, ventricular fibrillation leading possibly to cardiac arrest) and neuromuscular (paraesthesiae, convulsions, areflexia, flaccid paralysis of striated muscle leading possibly to respiratory paralysis). Beside elevation of serum potassium concentration, typical ECG changes are also encountered (increasing amplitude and peaking of T waves, disappearance of P wave, widening of QRS complex and S-T segment depression).

Treatment: Gastric lavage, administration of cation exchange agents, infusion of glucose and insulin, forced diuresis and possibly peritoneal dialysis or haemodialysis.

Pharmacotherapeutic group: Potassium supplement

ATC code: A12 BA01

The potassium chloride in Slow-K is finely distributed in a neutral wax base, from which it is gradually released over a period of 3 to 6 hours during its passage through the digestive tract. This special form of potassium substitution therapy is designed to avoid high localised concentrations of potassium chloride which might irritate or damage the mucosa. The potassium chloride in Slow-K is completely absorbed in the intestinal tract.

The potassium chloride in Slow-K has been shown to be completely absorbed; occasionally patients may notice “ghost” tablet cores in the faeces, these do not contain any potassium.

Following a single dose of Slow-K, potassium chloride is released over a period of approximately 4 hours. Renal excretion of potassium chloride following ingestion of Slow-K occurs 30 to 60 minutes later than when the same dose is given in the form of a solution. In the presence of a normal potassium balance, 90% of the potassium supplied by Slow-K is excreted renally within 8 hours, and more than 98% by 24 hours.

The acute and repeated-dose oral toxicity of potassium chloride (KCl) in animals is low. Gastrointestinal irritant effects have been observed in rhesus monkeys at high oral dosages of Slow-K. Some positive results in in-vitro genotoxicity assays were attributed to very high concentrations of KCl. Carcinogenicity studies in rats administered KCl in-feed were negative. Limited information from developmental studies in rodents indicates there is no ill effect on offspring. There is no evidence from animal experiments that KCl exerts any teratogenic effects or reproductive toxicity which would be relevant to man.

Cetostearyl alcohol

Gelatin

Magnesium stearate

Acacia

Titanium dioxide (E171)

Talc

Sucrose

Red iron oxide (E172)

Yellow iron oxide (E172)

Carnauba wax

None known.

5 years.

Do not store above 30°C. Keep the container tightly closed.

Polypropylene Securitainer with polyethylene cap containing 100 tablets.

None.

Alliance Pharmaceuticals Ltd

Avonbridge House

Bath Road

Chippenham

Wiltshire

SN15 2BB

PL16853/0014

25 June 1998

16 March 2012