Avoid combination of the drug with barbiturates, anticonvulsants, phenytoin, carbamazepine, rifampicin, zidovudine and other inducers of microsomal liver enzymes.
Paracetamol: reduces the effectiveness of uricosuric medicines. The concomitant use of paracetamol in high doses increases the effect of anticoagulant drugs (a decrease in the synthesis of procoagulant factors in the liver).
Inductors of microsomal oxidation in the liver (phenytoin, barbiturates, rifampicin, phenylbutazone, tricyclic antidepressants), ethanol and hepatotoxic drugs increase the production of hydroxylated active metabolites, which makes it possible to develop severe intoxication even with a slight overdose.
Long-term use of barbiturates reduces the effectiveness of paracetamol.
Ethanol promotes the development of acute pancreatitis.
Prolonged sharing of paracetamol and other non-steroidal anti-inflammatory drugs increases the risk of developing "analgesic" nephropathy and renal papillary necrosis, the onset of the terminal stage of renal failure.
Diflunisal increases the plasma concentration of paracetamol by 50% - the risk of developing hepatotoxicity.
Myelotoxic drugs increase the manifestation, hematotoxicity of the drug.
Diphenhydramine: potentiates the effects of alcohol and drugs;oppressioncentral nervous system. Monoamine oxidase inhibitors increase anticholinergic activity of diphenhydramine.
Ascorbic acid: increases the concentration in the blood of benzylpenicillin and tetracyclines; in a dose of 1 g / day increases the bioavailability of ethinyl estradiol (including that of oral contraceptives).
Reduces the effectiveness of heparin and indirect anticoagulants.
Improves absorption in the intestines of iron preparations (converts trivalent iron into bivalent); can increase the excretion of iron with simultaneous use with deferoxamine.
Acetylsalicylic acid, oral contraceptives, fresh juices and alkaline drink reduce absorption and absorption.
With simultaneous use with acetylsalicylic acid, urinary excretion of ascorbic acid increases and the excretion of acetylsalicylic acid decreases. Acetylsalicylic acid reduces absorption of ascorbic acid by about 30%. Increases the risk of developing crystalluria in the treatment of salicylates and sulfonamides short-acting, slows the excretion of kidney acids, increases the excretion of drugs that have an alkaline reaction (including alkaloids), reduces the concentration of oral contraceptives in the blood.
With simultaneous use reduces the chronotropic effect of isoprenaline. Barbiturates and primidon increase the excretion of ascorbic acid in the urine.
Calcium gluconate: while concomitant use with quinidine may slow intraventricular conduction and increase the toxicity of quinidine.
Forms insoluble complexes with antibiotics of the tetracycline series (reduces the antibacterial effect).
Slows the absorption of tetracyclines, digoxin, oral iron preparations (the interval between their methods should be at least 2 hours).
When combined with thiazide diuretics can increase hypercalcemia, reduce the effect of calcitonin in hypercalcemia.
Reduces the bioavailability of phenytoin.
Pharmaceutically incompatible with carbonates, salicylates, sulfates (forms insoluble or hardly soluble calcium salts).
Reduces the effect of blockers of slow calcium channels.
Rutozide: The pharmacological effect is enhanced by ascorbic acid.