Drug interactions and the adverse effects that can re-sult are a special concern. Although vitamins are not al-ways thought of as being drugs, these nutrients can in-teract with drugs and result in a variety of effects. Vitamin–drug interactions can produce either a de-crease or an increase in the effectiveness of the drug; conversely, the intake of drugs can affect the disposi-tion of vitamins in the body. Many drugs, such as some laxatives and cholestyramine, can produce vitamin mal-absorption or fecal nutritional loss, resulting in drug-in-duced nutrient depletion and hypovitaminosis. Both fat-soluble and water-soluble vitamins can be affected by drug intake.
Vitamin A absorption from the small intestine requires dietary fat and pancreatic lipase to break down retinyl esters and bile salts to promote the uptake of retinol and carotene. Drugs, such as mineral oil, neomycin and cholestyramine, that can modify lipid absorption from the gastrointestinal tract can impair vitamin A absorp-tion. The use of oral contraceptives can significantly in-crease plasma vitamin A levels.
Since alcohol dehydrogenase is required for the con-version of retinol to retinal, excessive and prolonged ethanol ingestion can impair the physiological function of vitamin A. The decreased conversion of retinol to retinal results from competitive use of the enzyme by ethanol. Night blindness may result, since the visual cy-cle is a retinol-dependent physiological process.
Laxatives and agents that bind bile salts inhibit the gas-trointestinal absorption of vitamin D. The glucocorti-coids in high dosages may interfere with the hepatic me-tabolism of vitamin D. Prolonged administration of hepatic microsomal enzyme inducers, such as pheno-barbital, phenytoin, primidone and glutethimide, can lead to an accelerated degradation of vitamin D3 to form inactive metabolites. The synthesis of vitamin D3 can be impaired by physical and chemical barriers to ul-traviolet light (e.g., sunscreens).
The most common group of drugs that produce vitamin K deficiency are the coumarin anticoagulants. The hy-poprothrombinemic effects of dicumarol can be over-come by administration of vitamin K.
Oral contraceptives decrease the plasma levels of ascor-bic acid. Aspirin also decreases tissue levels of vitamin C. The renal excretion of acidic and basic drugs may be altered when they are coadministered with large doses of vitamin C.
Many drugs interact with folate to affect its absorption, antagonize its biochemical activity, or increase its loss from the body. These drugs include ethanol, phenytoin, and oral contraceptives. Salicylates can compete with folic acid for plasma protein binding. Methotrexate, a cytotoxic agent, is a folate antagonist that inhibits the biosynthesis of this coenzyme.
Many drug classes have been shown either to act as vi-tamin B6 antagonists or to increase vitamin B6 turnover. Alcohol decreases the production of pyridoxal phos-phate, the coenzyme formed from vitamin B6. Hydrazines, such as isoniazid, act as coenzyme inhibitors. Cycloserine, an antitubercular drug, and penicillamine, a chelating agent, inactivate the coenzyme. Steroid hormones, such as those in oral contraceptive preparations, compete with the coenzyme. Pyridoxine can decrease the efficacy of lev-odopa, an antiparkinsonian drug, by stimulating the de-carboxylation of dopa to dopamine in peripheral tissues. Phenobarbital and phenytoin serum levels may be de-creased following pyridoxine supplementation.
Four groups of drugs have been shown to affect the absorption of vitamin B12. These include the oral hypo-glycemic biguanides, colchicine, ethanol, and aminosali-cylic acid.
Drug-induced niacin deficiency has resulted from the use of isonicotinic acid hydrazide, which interferes with the conversion of niacin from tryptophan. Admin-istration of ethanol or the antimetabolites 6-mercaptop-urine and 5-fluorouracil also may lead to niacin defi-ciency. The uricosuric effects of sulfinpyrazone and probenecid may be inhibited by nicotinic acid.
Drugs that increase intestinal motility or induce di-arrhea may decrease riboflavin absorption. Hyperthy-roidism and the administration of thyroxine also reduce riboflavin absorption.
Alcoholics may have both decreased intake and de-creased absorption of thiamine. Liver disease can pre-vent the formation of the active coenzyme.
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