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MANAGEMENT OF CHRONIC PROBLEMS INTERACTIONS BETWEEN ALCOHOL AND DRUGS A. Leary,* T. MacDonald† SUMMARY concerned. Alcohol may alter the effects of the drug; drug In western society alcohol consumption is common as is may change the effects of alcohol; or both may occur. the use of therapeutic drugs. It is not surprising therefore The interaction between alcohol and drug may be that concomitant use of these should occur frequently. The pharmacokinetic, with altered absorption, metabolism or consequences of this combination vary with the dose of elimination of the drug, alcohol or both.2 Alcohol may drug, the amount of alcohol taken, the mode of affect drug pharmacokinetics by altering gastric emptying administration and the pharmacological effects of the drug or liver metabolism. Drugs may affect alcohol kinetics by concerned. Interactions may be pharmacokinetic or altering gastric emptying or inhibiting gastric alcohol pharmacodynamic, and while coincidental use of alcohol dehydrogenase (ADH).3 This may lead to altered tissue may affect the metabolism or action of a drug, a drug may concentrations of one or both agents, with resultant toxicity. equally affect the metabolism or action of alcohol. Alcohol- The results of concomitant use may also be principally drug interactions may differ with acute and chronic alcohol pharmacodynamic, with combined alcohol and drug effects ingestion, particularly where toxicity is due to a metabolite occurring at the receptor level without important changes rather than the parent drug. There is both inter- and intra- in plasma concentration of either. Some interactions have individual variation in the response to concomitant drug both kinetic and dynamic components and, where this is and alcohol use. Interactions are also age-dependent and so, the final combined result may be difficult to predict. become more frequent in the elderly, a group who are Alcohol-drug interactions differ not only with amount often using several drugs simultaneously. This article aims of alcohol taken but also with pattern of alcohol intake. to give an overview of the principles behind alcohol-drug When intake is acute, there is usually inhibition of the interactions, and to discuss in more detail some of those enzymes of drug metabolism. Alternatively, chronic alcohol most commonly seen in clinical practice. abuse may lead to enzyme induction, increasing drug metabolism. The clinical results may then vary depending GENERAL PRINCIPLES on whether toxicity is due to the parent drug or one of its Alcohol consumption is widespread in many countries metabolites. The main problem in clinical practice is the where it is taken for its pleasant taste and mood-altering unpredictability of the effect of alcohol on drug metabolism, effects. Unfortunately abuse of alcohol is also common, particularly given the variable nature of alcohol ingestion making it the foremost drug of abuse worldwide. Alcohol- by most patients. In addition, patients with heavy alcohol related problems are a frequent reason for consulting the use often have unreliable drug compliance. doctor, and are a contributory factor in 20-40% of hospital The elderly take more drugs than the young, have more admissions.1 Alcohol-associated medical disorders are coincidental pathology to their main illness, and also show common in the elderly. In addition, alcoholics are often age-related changes in pharmacokinetics and undiagnosed before admission to hospital. Indeed, unless pharmacodynamics. They are thus at greater risk of alcohol- the diagnosis is clear on admission, or unless acute alcohol drug interactions. Community surveys of the elderly have withdrawal supervenes during the hospital stay, the diagnosis shown that between 25% and 38% of those who responded of alcoholism is frequently missed. used alcohol together with at least one drug with the known An interaction between pharmacologically-active potential to produce adverse effects in combination.4 The compounds can be described as a combined action resulting elderly often have impaired homeostatic responses, and may from their concomitant use that deviates from the expected have reduced renal and hepatic function. They frequently additive effect of the compounds. The result may be have increased end-organ sensitivity to drugs and alcohol; potentiation or antagonism of one or both.2 Many people this is particularly true of the central nervous system and take prescription drugs; therefore interactions between combined use of CNS depressants and alcohol may be alcohol and drugs occur commonly, and are seen frequently dangerous.5 The elderly are at increased risk of hypotension in clinical practice (Table 1). The consequences of when nitrates are taken in conjunction with alcohol, and at accompanying alcohol and drug use vary with the dose of increased risk of over-anticoagulation from simultaneous drug and amount of alcohol taken, with the mode of use of warfarin and alcohol.5 The effects on memory of administration of the drug, and with the effects of the drug alcohol use add further to the problems of compliance with therapy often seen in this patient group. *Clinical Lecturer and Honorary Specialist Registrar, Department of Clinical Pharmacology and Therapeutics, CLINICAL PHARMACOLOGY OF ALCOHOL Ninewells Hospital and Medical School, Alcohol is rapidly absorbed from the gastrointestinal tract. Dundee DD1 9SY The small intestine is the main site of absorption, although †Professor of Clinical Pharmacology and there is also some absorption from the gastric mucosa. There Pharmacoepidemiology, Medicines Monitoring Unit, is considerable inter- and intra-individual variability in University of Dundee absorption, particularly if there is concomitant ingestion of food.6 Higher concentrations of alcohol irritate the gastric Proc R Coll Physicians Edinb 1999; 29:137-143 137 MANAGEMENT OF CHRONIC PROBLEMS TABLE 1 Drugs that commonly interact with alcohol. Type of agent Examples Consequences of interaction with alcohol CNS depressants benzodiazepines, sedation, psychomotor impairment tricyclic antidepressants, with concomitant use sedative antihistamines Agents provoking tolbutamide, metronidazole, ‘antabuse’ reaction; worse in heavier drinkers disulfiram-like reactions sulfonamides, some cephalosporins Analgesics paracetamol increased hepatotoxity in heavy drinkers (may occur at therapeutic doses) Vasodilators methyldopa, nitrates, hydralazine hypotension, unexpected collapse Antidiabetic agents long-acting oral hypoglycaemics hypoglycaemia due to impairment of liver gluconeogenesis by alcohol Coumarin anticoagulants warfarin hepatic enzyme induction interferes with anticoagulant control NSAIDs aspirin, others synergistic effect on gastric mucosa with increased risk of bleeding Anticonvulsants phenytoin, (others) enzyme induction with chronic alcohol excess may affect metabolism H2 blockers cimetidine, ranitidine inhibit gastric ADH, increasing blood alcohol (at low doses of alcohol only) mucosa causing pyloric spasm and, consequently, slow down of alcohol, the barrier to systemic toxicity provided by FPM absorption of alcohol and drugs. can be overcome, and FPM falls to 10% or lower.11,13,14 Alcohol (ethanol) is a small molecule that is both water Whilst the majority of FPM occurs in the hepatocytes, a and lipid-soluble and, once absorbed, easily permeates all small proportion occurs at the level of the gastric mucosa. organs, affecting their function. Initially alcohol is Cytoplasmic ADH in the hepatocytes and gastric mucosal distributed throughout the body water. The apparent cells oxidise ethanol to acetaldehyde with the loss of H+ volume of distribution is reduced with age because of which reduces NAD to NADH. When alcohol is used to decreased total body water. Once absorbed there is excess, large amounts of reducing equivalents accumulate redistribution into the cellular compartment; inebriation leading to a variety of metabolic derangements including and, subsequently, sedation occur when blood alcohol hyperlactic-acidaemia and hyperuricaemia. Gastric ADH concentrations (BACs) are already falling. In inebriating levels are lower in women than in men, lower in Orientals doses (BAC > 0.5 mg/ml of blood), ethanol disorganises than in Caucasians, and lower in alcoholics than in non- the lipid bilayers of neural cell membranes, interfering with alcoholics.1,15 This may partly explain the higher BACs synaptic function and impairing neurotransmitter release.2 achieved for the same dose in alcoholics compared to non- There is inhibition of cell membrane ATPase, impaired alcoholics. The ADH activity of the stomach is 100 times function of cholinergic muscarinic receptors, and a less than that of the liver, and so the relatively small reduction in cytoplasmic calcium concentrations in certain contribution of gastric ADH to the metabolism of alcohol regions of the brain. The sedative and anxiolytic effects of suggests other causes for these differences.3 Acetaldehyde alcohol, as well as the motor incoordination seen with higher is further converted to acetic acid by aldehyde doses, are mediated via gamma-aminobutyric acid (GABA) dehydrogenase (AIDH). The rate of elimination of alcohol type-A receptor activation.7,8 Blockade of the GABA varies between individuals from 70-150 mg/kg/hr and is receptor by partial inverse agonists significantly attenuates independent of dose. There is little intra-subject variability. the intoxicating effects of ethanol.9 Genetic animal models The microsomal ethanol oxidizing system (MEOS)
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