Drug and alcohol interactions
Drug and alcohol interactions
(Adapted from Drug / Alcohol Interactions – When to be Cautious. Adapted from
O’Hagan J, Robinson R, Whiteside E. Alcohol and Drug Problems: Handbook for
Health Professionals. Wellington: Alcohol Advisory Council, 1993.)
Drug-alcohol interactions are frequently encountered because they are widely used substances.
Ethanol is metabolised in the liver by a variety of enzymes – mainly alcohol and
acetaldehyde dehydrogenses but also by the microsomal enzymes. Chronic
ingestion of alcohol stimulates these enzymes and speeds up the metabolism of
alcohol and other drugs metabolised by the liver. Acute isolated alcohol intoxication
inhibits the enzyme systems and slows down the metabolism and clearance of some
The interactions may be antagonistic, synergistic, potentiating or mutually
neutralising in their effect. Ethanol is basically a central nervous system depressant
and therefore will have an additive effect when given with tranquillisers, sedatives,
sleeping drugs etc., whereas stimulants amphetamine, caffeine, cocaine and possibly
nicotine should have an antagonistic effect when co-administered with alcohol. ASPRIN: NSAIDs
Moderate prolongation of bleeding time and mucosal irritation.
Patients should be warned of the possibility of this interaction especially if they are taking prolonged courses of treatment with non-steroidal anti-inflammatory agents. Gastrointestinal irritation due to these drugs may be worsened by concomitant alcohol intake. When possible, advise no or low alcohol intake.
Acute alcohol intake, even in moderate dosage, potentiates the action of coumarin anticoagulants by competitive inhibition of their hepatic enzyme metabolism. In alcoholics the half-life of warfarin is reduced due to alcohol-induced induction of liver microsomal enzymes.
The most critical factor is that alcohol intake is relatively constant from day to day. For practical purposes it may be desirable to advise patients to avoid alcohol.
Increased metabolism of phenytoin can occur with heavy drinking; this can result in
the drug failing to control epilepsy.
Advise to minimise or avoid alcohol. If choose to continue drinking advise a regular
intake is safer and to avoid binges.
Enhanced sedation, agitation, sleep disturbance. Ability to drive or operate
machinery may be grossly impaired. Patients being treated with tricyclic
antidepressants who take alcohol may show both unusual and unexpected
behavioural disorders. These are usually most noticeable during the first few days of
tricyclic antidepressant therapy.
Original MAOIs may have caused hypertension (due to the tyramine content of some
alcoholic drinks, notably beers and wines) the new MAOIs do not have this effect.
Advise to minimise or avoid alcohol.
Cimetidine and ranitidine but not famotidine inhibit gastric A.D.H. increasing alcohol
absorption, blood levels and clinical effects.
Patients taking H2 blockers should be warned to limit alcohol intake especially when
driving or using machinery etc.
ANTIDIABETIC AGENTS: BIGUANIDES (METFORMIN), INSULIN,
Acute ingestion of alcohol by patients on insulin or an oral hypoglycaemic drug
carries the risk of severe hypoglycaemia due to the hypoglycaemic effects of alcohol.
In patients on metaformin dosage, an increased risk of lactic acidosis must also be
considered. In alcoholics there is induction of hepatic microsomal enzymes and a
reduced half-life of chlorpropamide and tolbutamide.
Alcohol should only be taken moderately; if therapy is accompanied by calorie
restricted diet then alcohol may not be allowed at all.
The hypotensive effect of these drugs may be enhanced due to synergism with the
vasodilator effects of alcohol. Alcohol increases the absorption of propranolol.
Advise to minimise or avoid alcohol. Advise lifestyle interventions for hypertension. If
chooses to continue to drink, try downward titration of antihypertensive dose.
e.g. barbitiruates, non barbiturate sedatives, hypnotics, minor tranquillisers,
benzodiazepines, opioid narcotics.
Alcohol will enhance the CNS depressant effect. Suicide or accidental death are common especially if alcohol is combined with barbiturates, or opioid narcotics.
Recommend avoiding these combinations especially when driving, where there is suicide risk or severe obstructive airways disease.
e.g. butyrophenones (haloperidol), phenothiazines (including depot-injections),
triaxanthenes (thiothixene), atypical antipyschotics: respridone, alanzapine and
The combination is contraindicated in patients who might perform potentially hazardous tasks such as driving.
Taking alcohol, even in small quantities, after the administration of disulfiram (Antabuse) evokes an extremely unpleasant syndrome of systemic reactions. This effect is due to the inhibition of the oxidation of acetaldehyde, the primary metabolite of alcohol causing an increase of acetaldehyde in the blood. Citrated calcium carbimide (Dipsan) has the same action and uses as disulfiram.
Patients should be given a cardiovascular assessment before starting treatment. OTHER DRUGS WHICH PRODUCE DISULFIRAM-LIKE EFFECTS IN THE
PRESENCE OF ALCOHOL
e.g. griseofulvin, metronidazole, sulphonylureas, ornidazole, tinidazole.
Other drugs, whose therapeutic use is quite distinct from the treatment of chronic alcoholism, may produce a disulfiram-like interaction with alcohol. With some, the mechanism involved is thought to be an inhibition of acetaldehyde dehydrogenase.
Patients should be warned against the possibility of interactions with alcohol.
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