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Avoiding alcohol-related prescribing problems

Continuing his series on prescribing problems Professor Hugh McGavock discusses two issues associated with alcohol use and misuse

Continuing his series on prescribing problems Professor Hugh McGavock discusses two issues associated with alcohol use and misuse

Alcohol, the liver and prescribing

Previous generations, when offering a drink, often asked ‘what's your poison?'. They were much more scientific than they knew, for alcohol is a potent hepatocellular poison and, even in moderate amounts, temporarily disrupts liver function.

The majority of Western populations drink alcohol – some occasionally, some regularly and moderately, and some excessively.

That truism is important for the prescriber, because alcohol has paradoxical effects on P450 liver enzymes, which metabolise other drugs. These effects depend on the individual's drinking habits.

Occasional drinking

This inhibits members of the P450 enzyme group, reducing the metabolism of many drugs and leading to an increase in their plasma concentration. The BNF (appendix 1) has two columns citing drugs whose plasma concentration and therapeutic effects are enhanced by the concurrent occasional use of alcohol1.

Chronic heavy drinking

In contrast, alcohol misuse induces these same enzymes, increasing drug metabolism and leading to a reduced plasma drug concentration – and, therefore, therapeutic failure. The BNF does not describe this reverse effect of alcohol in chronic drinkers and alcoholics. In this situation, there is a high risk of therapeutic failure in patients taking the following:

• warfarin

• tolbutamide

• doxycycline

• antidepressants

• antipsychotics

• benzodiazepines

• paracetamol.

In particular, beware paracetamol overdose in chronic drinkers. Because of enzyme induction, their livers produce more of the toxic paracetamol metabolite N-acetyl-p-benzoquinone imine (NAPBQI), which is the common cause of death in paracetamol poisoning. Therefore, alcoholics and heavy drinkers should be warned to avoid paracetamol.

Alcohol itself is metabolised stepwise by two enzymes, alcohol dehydrogenase and aldehyde dehydrogenase, and to a lesser extent by a P450 enzyme. Unfortunately, the availability of these enzymes for alcohol is limited, and the metabolic capacity is saturated after only a few drinks.

The remaining alcohol is slowly metabolised over the next 12 hours or more.

Antabuse-like reactions

Most prescribers know the alcohol aversion drug disulfiram (Antabuse) causes a progressive series of very unpleasant symptoms, depending on the dose of alcohol consumed. These include vomiting, flushing, headache, palpitations and – if the alcohol intake is large – hypotension and collapse (see the contraindications to disulfiram prescribing in the BNF, chapter 4.10).

But many prescribers are unaware that a number of commonly prescribed drugs may cause a similar reaction. These are:

• cephalosporins

• metronidazole

• sulfonamides

• isoniazid

• griseofulvin

• sulphonylureas

• nitrofurantoin

• nitrates.

Most of these are not mentioned in the BNF and only some patients will experience such an effect. As with disulfiram, the severity of the reaction between these drugs and alcohol is proportional to the dose of alcohol and, at worst, convulsions and death may result.

Hugh McGavock is visiting professor of prescribing science at the University of Ulster and course organiser of GP continuing clinical education at the Northern Ireland Medical and Dental Training Agency

This is an extract from Pitfalls in Prescribing and How to Avoid Them. Pulse readers can buy the book at the specially discounted price of £15.00 plus P&P (usual price £18.99 plus P&P). To claim the discount, please visit Radcliffe Publishing's website at and enter the discount code PPLSE9 at the checkout. Alternatively, please order via 01235 528820 quoting the same code. Offer ends 28 August 2009.


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