BOOTS PARACETAMOL AND CODEINE EXTRA

Adults Two capsules to be taken up to four times a day, doses being repeated not more than every four hours, up to a maximum of eight capsules in 24 hours. Children aged 16 to 18 years One or two capsules every 6 hours when necessary up to a maximum of eight capsules in 24 hours.

The minimum dosing interval is 6 hours. Children aged 12 to 15 years One capsule every 6 hours when necessary up to a maximum of 4 capsules in 24 hours. The minimum dosing interval is 6 hours. 4). Elderly In the elderly, the rate and extent of paracetamol absorption is normal, but plasma half-life is longer, and paracetamol clearance is lower than in young adults.

Elderly patients, especially those who are frail or immobile, may require a reduced dose or frequency of dosing.

Renal impairment:

Patients who have been diagnosed with kidney impairment must seek medical advice before taking this medication. It is recommended, when giving paracetamol to patients with renal failure, to reduce the dose and to increase the minimum interval between each administration to at least 6 hours.

4).

Hepatic impairment:

Patients who have been diagnosed with hepatic impairment or Gilbert’s Syndrome must seek medical advice before taking this medication. 4). 9) Method of administration For oral administration only. 9). Minimum dosing interval: 4 hours for adults and 6 hours for children aged 12 to 18 years.

Treatment goals and discontinuation Before initiating treatment with Boots Paracetamol and Codeine Extra Capsules, treatment duration and treatment goals, should be agreed together with the patient, in accordance with pain management guidelines.

Duration of treatment Do not take for more than 3 days continuously without medical review. The duration of treatment should be as short as possible, and if no effective pain relief is achieved the patients/carers should be advised to seek the views of a healthcare professional.

Adverse events from historical clinical trial data are both infrequent and from small patient exposure. Accordingly, events reported from extensive post-marketing experience at therapeutic/labelled dose and considered attributable are tabulated below by system.

The following convention has been utilized for the classification of undesirable effects: very common (≥1/10), common (≥1/100, <1/10), uncommon (≥1/1,000, <1/100), rare (≥1/10,000, 363 <1/1000), very rare (<1/10,000), not known (cannot be estimated from the available data).

Paracetamol:

System Organ Class Undesirable effect Frequency Blood and lymphatic Thrombocytopenia Agranulocytosis Not known Anaphylaxis Not knownImmune system disorder Allergies (not including angioedema) Rare Respiratory, thoracic and mediastinal disorders Bronchospasm* Not known Hepatobiliary disorders Hepatic dysfunction Not known Cutaneous hypersensitivity reactions including skin rashes, pruritus, sweating, purpura, urticaria and angioedema Very rareSkin and subcutaneous tissue disorders Very rare cases of serious skin reactions have been reported.

Stevens Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), drug induced dermatitis, acute generalised exanthematous pustulosis (AGEP) Very rare Renal and urinary disorders Sterile pyuria (cloudy urine) Very rare Metabolism and nutrition disorders High anion gap metabolic acidosis** Not known * There have been cases of bronchospasm with paracetamol, but these are more likely in asthmatics sensitive to aspirin or other NSAIDs.

4). Pyroglutamic acidosis may occur as a consequence of low glutathione levels in these patients. Caffeine System Organ Class Undesirable effect Frequency Central nervous system Nervousness Dizziness Not known When the recommended paracetamol-caffeine-codeine dosing regimen is combined with dietary caffeine intake, the resulting higher dose of caffeine may increase the potential for caffeine-related adverse effects such as insomnia, restlessness, anxiety, irritability, headaches, gastrointestinal disturbances and palpitations.

Care is advised in the administration of paracetamol to patients with renal or hepatic impairment. The hazards of overdose are greater in those with non-cirrhotic alcoholic liver disease. g. chronic alcoholism) who were treated with paracetamol at therapeutic dose for a prolonged period or a combination of paracetamol and flucloxacillin.

If HAGMA due to pyroglutamic acidosis is suspected, prompt discontinuation of paracetamol and close monitoring is recommended. The measurement of urinary 5-oxoproline may be useful to identify pyroglutamic acidosis as the underlying cause of HAGMA in patients with multiple risk factors.

Glutathione deficiency can also increase the risk of hepatotoxicity with paracetamol use, even at therapeutic doses. 9). Hepatotoxicity at therapeutic dose Cases of paracetamol induced hepatotoxicity, including fatal cases, have been reported in patients taking paracetamol at doses within the therapeutic range.

These cases were reported in patients with one or more risk factors for hepatotoxicity including low body weight (adults <50 kg), renal and hepatic impairment, chronic alcoholism, concomitant intake of hepatotoxic drugs and in acute and chronic malnutrition (low reserves of hepatic glutathione).

Paracetamol should be administered with caution to patients with these risk factors. 9). Dosage adjustment of paracetamol should be considered where there are risk factors for glutathione deficiency or hepatotoxicity and for those of low weight (for adults weighing less than 50kg).

Care should be observed in administering the product to any patient, whose condition may be exacerbated by opioids, including the elderly, who may be sensitive to their central and gastro-intestinal effects, those on concurrent CNS depressant drugs, those with prostatic hypertrophy, hypothyroidism and those with inflammatory or obstructive bowel disorders, Addison's disease or myasthenia gravis.

Hypersensitivity to paracetamol, caffeine, codeine, opioid analgesics or any of the ingredients. Severe liver disease. 4). 6). In patients with respiratory depression, chronic constipation or raised intracranial pressure. In patients for whom it is known they are CYP2D6 ultra-rapid metabolisers.