It is not recommended to take concomitantly with sleeping pills, sedatives and preparations containing alcohol.
Increases the concentration in the blood of benzyl-penicillin and tetracyclines. Improves absorption in the intestines of iron preparations (converts trivalent iron into bivalent); can increase the excretion of iron with simultaneous use with deferoxamine.Increases the risk of developing crystalluria in the treatment of salicylates and sulfonamides short-acting, slows the excretion of acids by the kidneys, increases the excretion of drugs that have an alkaline reaction (including alkaloids), reduces the concentration of oral contraceptives in the blood. Increases the total clearance of ethanol. With simultaneous use reduces the chronotropic effect of isoprenaline. Reduces the therapeutic effect of antipsychotic drugs (neuroleptics) - derivatives of phenothiazine, tubular reabsorption of amphetamine and tricyclic antidepressants. Reduces the effectiveness of uricosuric medicines.
Can both increase and decrease the effect of anticoagulant drugs. Paracetamol (or its metabolites) interacts with enzymes involved in vitamin K-dependent synthesis of coagulation factor. Interactions between paracetamol and warfarin or coumarin derivatives may lead to an increase in the international normalized ratio (INR) and an increased risk of bleeding. Patients taking oral anticoagulants should not take long paracetamol without medical supervision.
Ethanol enhances the sedative effect of chlorphenamine. Antidepressants, anti-Parkinsonian and phenothiazine antipsychotic drugs increase the risk of side effects (urinary retention, dryness of the oral mucosa, constipation). Glucocorticosteroids increase the risk of developing glaucoma.
Inductors of microsomal oxidation in the liver (phenytoin, ethanol, barbiturates, rifampicin, phenylbutazone, tricyclic antidepressants) increase the production of hydroxylated active metabolites of paracetamol, which makes it possible to develop severe hepatotoxic reactions even with a slight overdose. Inhibitors of microsomal oxidation (incl. cimetidine) reduce the risk of hepatotoxic effects of paracetamol.
Diflunisal increases the plasma concentration of paracetamol by 50%, increases the hepatotoxicity. Ethanol reduces the concentration of ascorbic acid in the body, and also promotes the development of acute pancreatitis. The use of barbiturates reduces the effectiveness of paracetamol, increases the excretion of ascorbic acid in the urine. Strengthens the effect of hypnotic drugs.
With simultaneous application with chloramphenicol, it is possible to increase the period of its half-elimination from the blood plasma and increase the toxic effect.
Drugs that lead to a delay in emptying the stomach, for example propantheline, can lead to a slow absorption of paracetamol and, thus, delay the onset of its action.
Drugs that lead to accelerated emptying of the stomach, for example metoclopramide, can lead to a faster absorption of paracetamol and, thus, accelerate the onset of its action.
Tropisetron and granisetron antagonists, 5-hydroxytryptamine type 3 can completely inhibit the analgesic effect of paracetamol through pharmacodynamic interaction.
Paracetamol should not be taken together with zidovudine without the recommendation of a doctor because of the increasing tendency to decrease the number of white blood cells (neutropenia).
Continuous combination therapy with more than one analgesic should be avoided; because of the possible summation of side effects.