One of the factors that can alter the response to drugs is the concurrent administration of other drugs. There are several mechanisms by which drugs may interact, but most can be categorized as pharmacokinetic (absorption, distribution, metabolism, excretion), pharmacodynamic (additive, synergistic, or antagonistic effects), or combined interactions. The general principles of pharmacokinetics are discussed in Chapters 3 and 4; the general principles of pharmacodynamics in Chapter 2.
Botanical medications ("herbals") may interact with each other or with conventional drugs. Unfortunately, botanicals are much less well studied than other drugs, so information about their interactions is scanty. Pharmacodynamic interactions are described in Chapter 64. Pharmacokinetic interactions that have been documented (eg, St. John's wort) are listed in Table 66–1.
Table 66–1 Important Drug Interactions. |Favorite Table|Download (.pdf)
Table 66–1 Important Drug Interactions.
|Drug or Drug Group||Properties Promoting Drug Interaction||Clinically Documented Interactions|
|Alcohol||Chronic alcoholism results in enzyme induction. Acute alcoholic intoxication tends to inhibit drug metabolism (whether person is alcoholic or not). Severe alcohol-induced hepatic dysfunction may inhibit ability to metabolize drugs. Disulfiram-like reaction in the presence of certain drugs. Additive central nervous system depression with other central nervous system depressants.|
Acetaminophen: [NE] Increased formation of hepatotoxic acetaminophen metabolites (in chronic alcoholics).
Acitretin: [P] Increased conversion of acitretin to etretinate (teratogenic).
Anticoagulants, oral: [NE] Increased hypoprothrombinemic effect with acute alcohol intoxication.
Central nervous system depressants: [HP] Additive or synergistic central nervous system depression.
Insulin: [NE] Acute alcohol intake may increase hypoglycemic effect of insulin (especially in fasting patients).
Drugs that may produce a disulfiram-like reaction:
Cephalosporins: [NP] Disulfiram-like reactions are noted with cefamandole, cefoperazone, cefotetan, and moxalactam.
Chloral hydrate: [NP] Mechanism not established.
Disulfiram: [HP] Inhibited aldehyde dehydrogenase.
Metronidazole: [NP] Mechanism not established.
Sulfonylureas: [NE] Chlorpropamide is most likely to produce a disulfiram-like reaction; acute alcohol intake may increase hypoglycemic effect (especially in fasting patients).
|Allopurinol||Inhibits hepatic drug-metabolizing enzymes. Febuxostat (another drug used in gout) will also inhibit the metabolism of azathioprine and mercaptopurine.|
Anticoagulants, oral: [NP] Increased hypoprothrombinemic effect.
Azathioprine: [P] Decreased azathioprinedetoxification resulting in increased azathioprine toxicity.
Mercaptopurine: [P] Decreased mercaptopurine metabolism resulting in increased mercaptopurine toxicity.
|Antacids||Antacids may adsorb drugs in gastrointestinal tract, thus reducing absorption. Antacids tend to speed gastric emptying, thus delivering drugs to absorbing sites in the intestine more quickly. Some antacids (eg, magnesium hydroxide with aluminum hydroxide) alkalinize the urine somewhat, thus altering excretion of drugs sensitive to urinary pH.|
Atazanavir: [NP] Decreased absorption of atazanavir (requires acid for absorption).
Digoxin: [NP] Decreased gastrointestinal absorption of digoxin.
Indinavir: [NP] Decreased absorption of indinavir (requires acid for absorption).
Iron: [P] Decreased gastrointestinal absorption of iron with calcium-containing antacids.
Itraconazole: [P] Reduced gastrointestinal absorption of itraconazole due to increased pH (itraconazole requires acid for dissolution).
Ketoconazole: [P] Reduced gastrointestinal absorption of ketoconazole due to increased pH (ketoconazole requires acid for dissolution).
Quinolones: [HP] Decreased ...
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