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Australian Journal of Pharmacy : June 2005
Casebook_LH_June05.qxd 13/05/2005 10:24 AM Page 4 ucation Metoclopramide Metronidazole . Mexilitene Nicorandil . Opiates Oral contraceptives Paracetamol Stimulants, for example, amphetamines, cocaine Tetracyclines, for example, doxycyline Thiamine Tinidazole Tramadol Verapamil Warfarin Zopiclone Zolpidem Metoclopramide increases the rate of absorption of alcohol A disulfiram-like reaction (symptoms of flushing, palpitations, tachycardia, nausea, vomiting) may occur with concomitant use. Reports are inconsistent but caution is advised. Enhanced impairment to drive or operate machinery. Concurrent use of nicorandil may increase the hypotensive effect. NSAIDS and COX-2 Inhibitors May increase bleeding time, plus may increase the risk of gastrointestinal side effects, including ulceration or haemorrhage Increase the risk of CNS depression. Alcohol serum concentrations and CNS effects may be increased. Chronic consumption of alcohol may increase the risk of paracetamol-induced liver damage. Temporary arousal. Chronic alcohol consumption results in faster doxycycline clearance. Acute alcohol consumption may increase tetracycline absorption. Alcohol inhibits absorption of thiamine. 4 2 2 2 2 1 4 2 4 5 2 Concurrent use may result in disulfiram-like effects such as abdominal cramps, vomiting, tachycardia 1 and flushing; it is recommended that alcohol not be used concurrently with tinidazole, or for three days after discontinuing tinidazole therapy. Increased risk of CNS depression. Increased and prolonged CNS effects of alcohol affecting coordination and judgment. The chronic consumption of alcohol in high amounts may increase the clearance of warfarin. However, moderate or small alcohol doses do not alter the anticoagulant effect of warfarin. May increase the CNS depressant effects. May increase the CNS depressant effects. 1 4 5 2 2 Definitions of significance levels [Adapted from (15)]: 1: Potentially severe or life-threatening interaction; occurrence has been suspected, established or probable in well controlled studies. Contraindicated drug combinations may also have this number. 2: Interaction may cause deterioration in a patient’s clinical status; occurrence suspected, established or probable in well controlled studies. 3: Interaction causes minor effects; occurrence suspected, established or probable in well controlled studies. 4: Interaction may cause moderate-to-major effects; data are very limited. 5: Interaction may cause minor-to-major effects; occurrence is unlikely or there is not good evidence of an altered clinical effect. of alcohol use and then interpreting the significance in the person’s total disease state management. The wide range of effects of alcohol may be disguised with other expected adverse effects of medication, for example, postural hypotension. Many alcohol-dependent people require no medication when withdrawing from alcohol. Supportive care including information on the withdrawal syndrome, monitoring, reassurance and a low-stimulus environment are effective in reducing withdrawal severity. If medication is required, a benzodiazepine loading dose technique is usually employed. The patient is given repeated doses of diazepam until symptoms have diminished to an acceptable level.8 prosate, naltrexone or disulfiram but often in conjunction with cognitive therapy.8,12 being trialled. Alcohol and drug interactions Alcohol is a potent central nervous system depressant. The com- Long-term management may require the use of acamMonthly injections of naloxone are also bination of alcohol and other drugs can have potentially unpredictable and dangerous effects. The more drugs taken with alcohol the harder to predict the effects on the user. In addition, the use of drugs with hepatotoxic risk will be increased with the use of alcohol, for example, flucloxacillin, ketoconazole, methotrexate, paracetamol and terbinafine. Patients suffering alcoholism are also likely to be vitamin and mineral deficient. Alcohol and paracetamol Although it is a widely held view that chronic alcohol use amplifies the risk of paracetamol hepatotoxicity (even at therapeutic doses) the bulk of evidence for this association is weak. At the moment, the possibility that repeated therapeutic doses of paracetamol may rarely result in hepatotoxicity in chronic alcohol users cannot be entirely dismissed. However, avoiding paracetamol and substituting a NSAID for pain relief increases the overall risk of gastrointestinal bleeding in heavy drinkers.13 tions of alcohol. Table One summarises some drug interacTHE AUSTRALIAN JOURNAL OF PHARMACY VOL.86 JUNE 2005 473