Interactions between food and drugs may inadvertently reduce or increase the drug effect. The majority of clinically relevant food-drug interactions are caused by food-induced changes in the bioavailability of the drug. Since the bioavailability and clinical effect of most drugs are correlated, the bioavailability is an important pharmacokinetic effect parameter. However, in order to evaluate the clinical relevance of a food-drug interaction, the impact of food intake on the clinical effect of the drug has to be quantified as well. As a result of quality review in healthcare systems, healthcare providers are increasingly required to develop methods for identifying and preventing adverse food-drug interactions. In this review of original literature, we have tried to provide both pharmacokinetic and clinical effect parameters of clinically relevant food-drug interactions. The most important interactions are those associated with a high risk of treatment failure arising from a significantly reduced bioavailability in the fed state. Such interactions are frequently caused by chelation with components in food (as occurs with alendronic acid, clodronic acid, didanosine, etidronic acid, penicillamine and tetracycline) or dairy products (ciprofloxacin and norfloxacin), or by other direct interactions between the drug and certain food components (avitriptan, indinavir, itraconazole solution, levodopa, melphalan, mercaptopurine and perindopril). In addition, the physiological response to food intake, in particular gastric acid secretion, may reduce the bioavailability of certain drugs (ampicillin, azithromycin capsules, didanosine, erythromycin stearate or enteric coated, and isoniazid). For other drugs, concomitant food intake may result in an increase in drug bioavailability either because of a food-induced increase in drug solubility (albendazole, atovaquone, griseofulvin, isotretinoin, lovastatin, mefloquine, saquinavir and tacrolimus) or because of the secretion of gastric acid (itraconazole capsules) or bile (griseofulvin and halofantrine) in response to food intake. For most drugs, such an increase results in a desired increase in drug effect, but in others it may result in serious toxicity (halofantrine).

Food-Drug Interactions

The quantitative aspects of the disposition in man of 12 antituberculosis drugs [isoniazid, rifampicin, (rifampin), ethambutol, para-aminosalicylic acid, pyrazinamide, streptomycin, kanamycin, ethionamide, cycloserine, capreomycin, viomycin and thiacetazone] are reviewed. Isoniazid appears to be the only agent for which plasma concentrations and clearance are related to hereditary differences in acetylator status and for which there is an appreciable ‘first-pass’ effect. Recent data cast doubt on the suggestion that isoniazid may be more hepatotoxic for rapid as opposed to slow acetylators. Continuous administration of rifampicin leads to induction of enzymes in the liver with a concomitant decrease in maximum plasma concentrations, the time required to achieve this level, elimination half-life, and area under the plasma concentration-time curve (AUC). Coadministration of para-aminosalicylic acid leads to increases in the serum concentrations and elimination half-life of isoniazid.

Clinical Pharmacokinetics of the Antituberculosis Drugs

https://www.fip.org/files/fip/BPS/BCS/Monographs/Isoniazid.pdf

Biowaiver monographs for immediate release solid oral dosage forms: Isoniazid

nationColorado Health Sciences Center, usa; Infectious Diseases Pharmacokinetics Laboratory, National Jewish Medical and Research Center, Denver, Colorado, usa; Clinical Investigational Unit, Ottawa General Hospital, Ottawa, Ontario, canada.

Therapeutic implications of drug interactions in the treatment of human immunodeficiency virus-related tuberculosis.

Pharmacological and clinical aspects of antiepileptic drug use in the elderly

Pharmacokinetic interactions of oral timolol maleate 10 mg, with food (3566 kJ), single oral doses of prazosin 1 mg and dihydralazine 25 mg, and with a 1 week pretreatment with phenobarbitone 100 mg daily were examined in a randomized crossover study in 12 healthy volunteers. After fasting, the peak level (Cmax = 29.1 +/- 3.2 ng/ml; mean +/- SEM) was reached at 1.3 +/- 0.1 h (Tmax). The total area under the serum concentration-time curve (AUC0-infinity) was 154.4 +/- 33.8 ng x h/ml, total clearance (Cltot) 751.5 +/- 90.6 ml/min, renal clearance (Clren) 97.2 +/- 10.1 ml/min, elimination half-life (t1/2) 2.9 +/- 0.3 h and 24-h recovery in urine (X0u-24) 11.1 +/- 1.4% of the dose. Food and prazosin did not significantly affect the fate of timolol maleate. Dihydralazine enhanced Cmax (38.2 +/- 4.6 ng/ml) only when compared to phenobarbitone treatment, and did not affect any other parameters. Phenobarbitone pretreatment somewhat lowered Cmax (25.5 +/- 3.9 ng/ml), AUC0-infinity (117.5 +/- 22.1; p less than 0.05 vs food) and X0u-24 (8.7 +/- 1.2%), evidently by increasing Cltot (957.5 +/- 116.9 ml/min; p less than 0.05 vs food), but it did not affect Clren. It is concluded that the pharmacokinetics of timolol maleate can be altered to a limited extent in opposite directions by dihydralazine and phenobarbitone.

Pharmacokinetic interactions of timolol with vasodilating drugs, food and phenobarbitone in healthy human volunteers

Influence of various diets on the bioavailability of isoniazid

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Pharmacokinetic interactions of timolol with vasodilating drugs, food and phenobarbitone in healthy human volunteers

Influence of various diets on the bioavailability of isoniazid