Particular drugs can affect the nutritional state, changing the results of biochemical tests or even leading on occasions to clinical undernutrition, overnutrition, or malnutrition.
Appetite may be decreased by anorectic drugs, bulking agents, dexamphetamine, metformin, cardiac glycosides, glucagon, morphine, phenylbutazone, indometacin, cyclophosphamide, fluorouracil, methylphenidate, salbutamol, levodopa, etc, and by drugs that alter taste (griseofulvin, penicillamine, and lincomycin).
Appetite may be increased by sulphonylureas, oral contraceptives, cyproheptadine, chlorpromazine, androgens, anabolic steroids, corticosteroids, insulin, lithium, amitriptyline, pizotifen, clomipramine, benzodiazepines, and metoclopramide.
Malabsorption for more than one nutrient may be induced by neomycin, kanamycin, paromomycin, colchicine, phenindione, chlortetracycline, cholestyramine, colestipol, cyclophosphamide, indometacin, liquid paraffin (fat soluble vitamins), methotrextate, and methyldopa.
Energy metabolism may be stimulated by caffeine, smoking, and some sympathomimetic drugs.
Carbohydrates—Increased blood glucose concentrations may be produced by corticosteroids, thiazide diuretics, diazoxide, oral contraceptives, and phenytoin. Hypoglycaemia may be produced by propranolol and by alcohol (as well as by sulphonylureas, metformin and insulin).
Lipids—Plasma total cholesterol may be raised by thiazides (for example, chlorthalidone, hydrochlorothiazide), by phenobarbital, chlorpromazine, some oral contraceptives, and large intakes of boiled coffee. As well as specific cholesterol lowering drugs, aspirin, colchicine, prazosin, clonidine, neomycin, phenformin, and sulphinpyrazone may lower total cholesterol.
Plasma high density lipoprotein cholesterol may be raised by phenytoin, ethanol, cimetidine, valproate, carbamazine, terbutaline, and prazosin. It may be lowered by danazol, propranolol, and oxprenolol.
Plasma triglycerides may be raised by propranolol, ethanol, and (oestrogenic) oral contraceptives. They may be lowered by norethisterone.
Protein—Nitrogen balance may be made negative by corticosteroids, vaccines, and tetracyclines. It may be made positive by insulin or anabolic steroids. Plasma amino acids may be increased by tranylcypromine and lowered by oral contraceptives. Plasma phenylalanine may be raised by trimethoprim and methotrexate.
Thiamin absorption can be reduced by ethanol.
Riboflavin status may be lowered by oral contraceptives and by chlorpromazine.
Niacin may be antagonised by isoniazid.
Vitamin B-6 may be antagonised by isoniazid, hydralazine, cycloserine, penicillamine, oral contraceptives, oestrogens, hydrocortisone, imipramine, levodopa, piperazine, and pyrazinamide.
Folate may be antagonised by ethanol, phenytoin, oral contraceptives (uncommonly), cycloserine, triamterine, and cholestyramine. In addition several drugs owe their antibacterial action to antagonism of folate metabolism—more in microbial than mammalian cells—pyrimethamine, trimethoprin, and pentamidine. Methotrexate is a potent folate antagonist which has more effect on rapidly dividing cells—for example, cancer cells.
Vitamin B-12 absorption may be impaired by slow K, cimetidine, ranitidine, metformin, colchicine, trifluroperazine, and by high doses of vitamin C, cholestyramine, and methotrexate. Prolonged nitrous oxide anaesthesia oxidizes vitamin B-12 in vivo. Smoking and oral contraceptives reduce the plasma concentration.
Vitamin C—Plasma concentrations are lowered by oral contraceptives, smoking, aspirin, and tetracycline. Ascorbate excretion is increased by corticosteroids, phenylbutazone and sulfinpyrazone.
Vitamin A plasma concentration is increased by oral contraceptives. Absorption may be reduced by liquid paraffin and cholestyramine.
Vitamin D status is lowered by anticonvulsants—for example, phenytoin, phenobarbitone, and when these are taken in high dose for long periods rickets can occur.
Vitamin E is antagonised by iron in premature newborns. Fish oils (refined) increase requirements.
Vitamin K—Coumarin drugs—for example warfarin—are antimetabolites. Purgatives and intestinal antibiotics, such as neomycin, tetracyclines, and sulphonamides, may remove the contribution from colonic bacteria. Salicylates and cholestyramine may reduce absorption, and some cephalosporin antibiotics antagonise the vitamin K-epoxide cycle.
Potassium—Drugs are important causes of potassium depletion: purgatives and laxatives increase faecal loss; thiazide diuretics and frusemide and ethacrynic acid increase renal loss.
Other drugs that may increase urinary potassium are penicillin, glucocorticoids, liquorice, outdated tetracycline, gentamicin, and alcohol. Insulin can lower serum potassium. Drugs that raise serum potassium include ACE inhibitors, spironolactone, succinylcholine, triamterene, and potassium compounds.
Calcium—Absorption may be increased by aluminium hydroxide or by cholestyramine and decreased by phosphates and corticosteroids. Thiazide diuretics decrease urinary calcium excretion. Gentamicin, dactinomycin, frusemide, and ethacrynic acid increase it.
Iron—Gastrointestinal bleeding from aspirin and NSAIDS depletes the body’s iron. Allopurinol, fructose, and ascorbic acid increase absorption. Antacids, phosphates, and tetracycline decrease it. Oral contraceptives tend to increase serum iron.
Iodine—Sulphonylureas, phenylbutazone, amiodorone, and lithium can cause goitre; they interfere with iodine uptake in the gland. Serum protein bound iodine is increased by oral contraceptives, x-ray contrast media, and potassium iodide, and decreased by phenytoin.
Phosphate absorption is decreased by aluminium or calcium compounds.
Zinc depletion from increased urinary excretion may be produced by thiazide diuretics and frusemide, by cisplatin, penicillamine, and alcohol.
Magnesium depletion from increased urinary loss may be produced by thiazides and frusemide, cisplatin, alcohol, aminoglycosides, amphotericin, ciclosporin, and gentamicin.
Source – ABC OF NUTRITION, Stewart Truswell, BMJ Publishing Group, 2003
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