Enhanced Antithrombotic Effect of Warfarin
Enhanced Antithrombotic Effect of Warfarin
A 58-year-old Caucasian man was receiving long-term anticoagulation with warfarin for the prevention of ischemic stroke; his international normalized ratio (INR) had been stable. His INR increased when he began consistent, low-dose beer consumption for its perceived cardiovascular protection. After he stopped drinking the alcohol, his anticoagulation control improved and returned to previous levels. Information on the effects of alcohol, particularly beer, is limited in nonalcoholic patients who receive warfarin therapy. This case reveals a potential for low-dose beer consumption to elevate INR. We propose that the increased antithrombotic effect of warfarin involved protein-binding interactions and decreased warfarin metabolism through the cytochrome P450 (CYP) enzyme system. Concurrent administration of aspirin and other drugs that are metabolized through or are inhibitors of the CYP system may have enhanced the interaction that occurred in this patient. Caution should be used whenever warfarin and alcohol in any amount are taken together, especially in patients receiving many drugs, and close monitoring of the INR is warranted.
Anticoagulation with warfarin is often challenging because of the various confounding factors that can influence its antithrombotic effect, which is measured with the international normalized ratio (INR). These confounders include genetic, medical, and dietary factors. The influence of alcohol -- a dietary factoranticoagulation in nonalcoholic patients was studied in three trials evaluating the short-term effect of 10-20 oz of wine (28.2-56.4 g of alcohol). Each trial showed that wine consumption had no effect on anticoagulation control. Data about the effect of other forms of alcohol on anticoagulation control in non-alcoholic patients without liver disease are lacking. Also limited is information on the effect of a consistent, low intake of alcohol, which may be used to prevent cardiovascular events in patients with medically complex conditions who are taking many drugs.
An inverse relationship between low-to-moderate alcohol consumption and the risk of cardiovascular disease and mortality has been suggested. The connection is stronger with low-to-moderate wine consumption, which has a relative risk (RR) of 0.68 (95% confidence interval [CI] 0.59-0.77) for vascular disease, than with beer intake (RR 0.78, 95% CI 0.70-0.86). With regard to beer consumption, one to seven drinks/week (where one drink equals one bottle of beer or 11.6 g of alcohol) is associated with an RR of 0.78 (95% CI 0.67-0.91) for death from coronary heart disease (CHD) and an RR of 0.90 (95% CI 0.83-0.97) for death from all causes. Although men with CHD usually have been excluded from these types of studies or grouped in study populations without preexisting disease, a distinction between who benefits and who does not is often lacking. In fact, one evaluation of alcohol consumption in men with CHD revealed no significant benefit or harm with regular, light drinking (1-14 drinks/wk). Regardless of the findings, reports in the media often do not portray the specific details and may lead to patients starting low-dose alcohol regimens on their own because of the perceived benefits.
One risk of alcohol intake is the potential for interactions with concurrent drugs. Information is available on alcohol-drug interactions in people who drink large amounts for long periods; however, evidence of the effect of short-term and low-to-moderate drinking on various drugs is limited. Alcohol can interact with drugs through various mechanisms, including alteration of hepatic metabolism and interference with plasma protein binding. Data on how the other constituents of alcoholic beverages may influence the effects of drugs are lacking.
A patient was receiving long-term warfarin therapy; his INRwas stable. After he started consuming low doses of alcohol (6 oz of beer, 5.3 g of alcohol) every other day for its cardiovascular benefits, his INRincreased.
A 58-year-old Caucasian man was receiving long-term anticoagulation with warfarin for the prevention of ischemic stroke; his international normalized ratio (INR) had been stable. His INR increased when he began consistent, low-dose beer consumption for its perceived cardiovascular protection. After he stopped drinking the alcohol, his anticoagulation control improved and returned to previous levels. Information on the effects of alcohol, particularly beer, is limited in nonalcoholic patients who receive warfarin therapy. This case reveals a potential for low-dose beer consumption to elevate INR. We propose that the increased antithrombotic effect of warfarin involved protein-binding interactions and decreased warfarin metabolism through the cytochrome P450 (CYP) enzyme system. Concurrent administration of aspirin and other drugs that are metabolized through or are inhibitors of the CYP system may have enhanced the interaction that occurred in this patient. Caution should be used whenever warfarin and alcohol in any amount are taken together, especially in patients receiving many drugs, and close monitoring of the INR is warranted.
Anticoagulation with warfarin is often challenging because of the various confounding factors that can influence its antithrombotic effect, which is measured with the international normalized ratio (INR). These confounders include genetic, medical, and dietary factors. The influence of alcohol -- a dietary factoranticoagulation in nonalcoholic patients was studied in three trials evaluating the short-term effect of 10-20 oz of wine (28.2-56.4 g of alcohol). Each trial showed that wine consumption had no effect on anticoagulation control. Data about the effect of other forms of alcohol on anticoagulation control in non-alcoholic patients without liver disease are lacking. Also limited is information on the effect of a consistent, low intake of alcohol, which may be used to prevent cardiovascular events in patients with medically complex conditions who are taking many drugs.
An inverse relationship between low-to-moderate alcohol consumption and the risk of cardiovascular disease and mortality has been suggested. The connection is stronger with low-to-moderate wine consumption, which has a relative risk (RR) of 0.68 (95% confidence interval [CI] 0.59-0.77) for vascular disease, than with beer intake (RR 0.78, 95% CI 0.70-0.86). With regard to beer consumption, one to seven drinks/week (where one drink equals one bottle of beer or 11.6 g of alcohol) is associated with an RR of 0.78 (95% CI 0.67-0.91) for death from coronary heart disease (CHD) and an RR of 0.90 (95% CI 0.83-0.97) for death from all causes. Although men with CHD usually have been excluded from these types of studies or grouped in study populations without preexisting disease, a distinction between who benefits and who does not is often lacking. In fact, one evaluation of alcohol consumption in men with CHD revealed no significant benefit or harm with regular, light drinking (1-14 drinks/wk). Regardless of the findings, reports in the media often do not portray the specific details and may lead to patients starting low-dose alcohol regimens on their own because of the perceived benefits.
One risk of alcohol intake is the potential for interactions with concurrent drugs. Information is available on alcohol-drug interactions in people who drink large amounts for long periods; however, evidence of the effect of short-term and low-to-moderate drinking on various drugs is limited. Alcohol can interact with drugs through various mechanisms, including alteration of hepatic metabolism and interference with plasma protein binding. Data on how the other constituents of alcoholic beverages may influence the effects of drugs are lacking.
A patient was receiving long-term warfarin therapy; his INRwas stable. After he started consuming low doses of alcohol (6 oz of beer, 5.3 g of alcohol) every other day for its cardiovascular benefits, his INRincreased.
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