Alcohol and medications

DR MAXWELL ADEYEMI

ALCOHOL consumption is at a phenomenal level across the globe and an increased number of people continue to indulge in alcohol use, especially during festive seasons. Despite this high prevalence, few physicians discuss alcohol use with their patients. In addition, most patients do not consider alcohol a drug capable of interacting with medications.

Several studies have indicated the benefits of moderate alcohol consumption in various disease states. However, the media often discuss these study results without mentioning relevant details about the type of alcoholic beverage used or the patient population involved. They also do not review possible interactions of alcohol with other diseases or medications.

Patients misinterpret such information to rationalise their alcohol use without consulting their physicians. Alcohol has been reported as a risk factor for adverse drug-related hospital admissions.

In light of the prevalence of alcohol consumption, it is essential that doctors and pharmacists enlighten their patients about drug-alcohol interactions. Community pharmacists are at the front line to assist patients in understanding their medications and possible drug interactions.

It is important that community doctors and pharmacists understand various drug-alcohol interactions and explain their clinical significance to patients.

To understand how alcohol can interact with certain medications, it is important to briefly identify the pharmacokinetic and pharmacodynamic interactions involved with alcohol consumption. When alcohol is consumed, about ten per cent undergoes first-pass metabolism in the stomach, intestines and liver.

One of the major enzymes involved in alcohol metabolism is alcohol dehydrogenase, which converts alcohol to acetaldehyde, a toxic compound that is subsequently metabolised by aldehyde dehydrogenase to acetate.

Following first-pass metabolism, alcohol is distributed into various body tissues and exerts its effects. Alcohol is transported back to the liver for metabolism and elimination. In addition to further metabolism in the liver, alcohol is also metabolised by other enzymes such as CYP450 enzymes.

Alcohol is a substrate of these enzymes and, depending on the frequency of alcohol intake, it can also be either an inducer or inhibitor of the enzymes. Chronic, heavy alcohol consumption induces enzyme activities while short-term heavy consumption inhibits its activity by competing with other substrates.

Alcohol intake can alter the pharmacokinetics of medications, including their absorption and metabolism. Conversely, alcohol pharmacokinetics can also be altered by medications. Examples of pharmacodynamic interactions involving alcohol and medications are an increased risk of adverse drug events or an increased susceptibility to the medications’ effects.

Antibiotics

Concomitant use of antibiotics and alcohol can cause or exacerbate adverse effects. Certain reactions have been reported in patients who consume alcoholic preparations while being treated with certain antibiotics.

Isoniazid is metabolised more quickly in chronic heavy alcohol users, which can lead to decreased drug effectiveness and increased risk of isoniazid-associated hepatotoxicity.

Therefore, patients should always be cautioned to avoid alcohol consumption during, and for several days after, antibiotic regimens known to interact with alcohol.

Antihypertensives: Alcohol consumption interacts with some medications taken for hypertension and angina such as nitrates, hydralazine and nitroglycerin. Concomitant use of alcohol with these medications may lead to enhanced orthostatic hypotension, putting patients at risk for injury or falls.

Chronic alcohol use can lead to increased metabolism and decreased effectiveness of the beta-adrenergic blocking agent propranolol, and consumption of verapamil and alcohol has been shown to delay elimination of alcohol, which may lead to prolonged intoxication.

Additionally, there is a positive association between alcohol consumption and blood pressure, and alcohol intake may aggravate hypertension or heart failure. Patients with cardiovascular conditions should consult their healthcare providers regarding alcohol use and potential drug interactions.

Antidiabetics: The use of alcohol in patients with diabetes presents several health issues. Alcohol suppresses gluconeogenesis, the production of glucose from non-glucose sources, which may increase risk for hypoglycemia in diabetic patients. The risk is further increased if the patient uses insulin or oral hypoglycemics.

In addition, heavy alcohol use by diabetics may increase risk for diabetic complications including diabetic neuropathy and retinopathy. For patients on sulfonylureas, such as diamicron, there could be an increased risk of hypoglycemia, especially with the longer-acting first generation sulfonylureas (tolbutamide and chlorpropamide). Diabetic patients on metformin are at an increased risk for lactic acidosis if they consume alcohol heavily.

Anticoagulants [blood thinners]: Alcohol interacts with warfarin, and the consequences of this interaction can lead to significant patient harm. Depending on the frequency of alcohol consumption, alcohol can lead to an increase or decrease in the anticoagulant effect of warfarin. When alcohol is chronically consumed by patients, there is increased metabolism of warfarin, decreasing the drug’s effect and increasing the risk of clot formation.

On the other hand, acute alcohol ingestion appears to decrease warfarin’s metabolism, which can greatly increase the risk for a haemorrhage.

Nonsteroidal Anti-inflammatory Drugs (NSAIDs) and Aspirin: Both NSAIDs and high-dose aspirin are associated with an increased risk of intestinal bleeding, there is a threefold to fivefold increase in the risk of developing a major bleed or an ulcer when NSAIDs are used. Alcohol consumption can irritate the intestinal mucosa and increase gastric acid secretions, which may lead to gastritis. Concomitant use of NSAIDs or aspirin and alcohol can further increase risk of a major intestinal bleed.

Acetaminophen: Marketed as Panadol, Paracetamol [etc], this drug is one of the most frequently used analgesics in the world. In addition to its availability as an over-the-counter product, acetaminophen is also found in combination with many narcotic medications and is among the most commonly prescribed analgesics. In acute overdoses, acetaminophen is associated with liver toxicity.

Acetaminophen is metabolised primarily through the same enzyme involved in alcohol metabolism. When acetaminophen is metabolised, a hepatotoxic metabolite is formed. The body quickly deactivates this metabolite through its stores of glutathione. In an acute overdose where 8 g or more of acetaminophen are consumed, the stores of glutathione are exhausted, and the metabolite accumulation leads to fulminant liver failure.

The possible interaction of alcohol with acetaminophen use depends on the manner in which alcohol is consumed. In chronic alcohol users, the activity of the enzyme that metabolises it is induced, leading to increased toxic metabolite production. In addition, the decreased levels of glutathione in alcoholics further increase risk for liver failure.

Patients who drink more than three alcoholic drinks per day should consult their physician prior to any over-the-counter pain reliever use. So, patients should always be warned about the increased risk of liver injury when acetaminophen-containing products are taken with alcohol.

Analgesics (narcotic)

Opioid medications such as methadone, pethidine, morphine and codeine derivatives are well known for central nervous system effects, including sedation and respiratory depression. Alcohol generally increases the risk of adverse effects of opiates and central nervous system depression.

Contact Dr Maxwell on 631807 or 7575411