title: [Caffeine and antiepileptic drugs: experimental and clinical data].
abstract: BACKGROUND
  Caffeine, a methylxanthine derivative, is contained in coffee or tea, chocolate as well as in some beverages. In addition, it may be added to some analgesics. At high doses, similarly to other methylxanthine derivatives (theophylline, pentoxifylline) caffeine induces seizure activity in rodents.
  
  
  OBJECTIVE
  If caffeine intake from coffee drinking resulting in pharmacologically active plasma caffeine concentrations--can lead to diverse interactions with other medications.
  
  
  RESULTS
  Since 90s of the XX century, there are experimental data available pointing to the caffeine-induced impairment of the protective activity of a number of antiepileptic drugs in basic models of epilepsy in rodents. Acute caffeine, in doses far below its convulsive potential (almost 10-20 fold lower than the ED50 of the methylxanthine of 2.03 mmol/kg for the induction of seizures), produced a significant reduction in the anticonvulsant effects of carbamazepine, phenobarbital, phenytoin, and valproate against maximal electroshock-induced seizures in mice. This interaction was pharmacodynamic in nature since caffeine did not affect the plasma concentrations of these anti-epileptics. Interestingly, there was no tolerance to this hazardous effect of caffeine since its administration at the same dosages (0.12-0.24 mmollkg) also resulted in the impairment of the protection provided by antiepileptic drugs, this effect being even more pronounced in the case of phenobarbital and carbamazepine. In case of newer antiepileptics, both acute and chronic caffeine decreased the protective potential of gabapentin and topiramate but not that of lamotrigine and tiagabine.
  
  
  CONCLUSIONS
  The existing clinical data confirm the experimental results in that caffeine intake in epileptic patients results in increased seizure frequency. It may be concluded that epileptic patients should limit their daily intake of caffeine.
authors.affiliation: Katedra i Zakład Patofizjologii, Akademia Medyczna im. F. Skubiszewskiego, Lublin.
authors.forename: Katarzyna
authors.initials: K
authors.lastname: Jankiewicz
authors.forename: Magdalena
authors.initials: M
authors.lastname: Chrościńska-Krawczyk
authors.forename: Barbara
authors.initials: B
authors.lastname: Błaszczyk
authors.forename: Stanisław J
authors.initials: SJ
authors.lastname: Czuczwar
mesh_terms: D000818:Animals; D000927:Anticonvulsants / Q000494:pharmacology*; D002110:Caffeine / Q000494:pharmacology*; D002220:Carbamazepine / Q000037:antagonists & inhibitors; D004305:Dose-Response Relationship, Drug; D004347:Drug Interactions; D004597:Electroshock; D006801:Humans; D000077213:Lamotrigine; D051379:Mice; D009557:Nipecotic Acids / Q000494:pharmacology; D010634:Phenobarbital / Q000037:antagonists & inhibitors; D010672:Phenytoin / Q000037:antagonists & inhibitors; D012640:Seizures / Q000139:chemically induced*; D000078308:Tiagabine; D014227:Triazines / Q000494:pharmacology; D014635:Valproic Acid / Q000037:antagonists & inhibitors
chemical_list: D000927:Anticonvulsants; D009557:Nipecotic Acids; D014227:Triazines; D002220:Carbamazepine; D002110:Caffeine; D014635:Valproic Acid; D010672:Phenytoin; D000077213:Lamotrigine; D010634:Phenobarbital; D000078308:Tiagabine