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P-glycoprotein (Pgp) is a member of the ATP-binding cassette super family of membrane transport proteins, responsible for the efşux of many drugs. It represents a major component of the blood-brain barrier. possessing the potential for important drug interactions to occur by a new mechanism, namely, inhibition of Pgp. A drug to be safely used therapeutically can be reversed by another drug causing P-glycoprotein inhibition, resulting in serious toxic reactions and abuse potential. A 68-year-old male suffering from atrial fibrillation and depression syndrome. The patient has also been treated for atrial fibrillation, and mixed depressive-anxiety disorders. His medications were bupropion hydrochloride (150mg/day), citalopram (10 mg/day), quetiapine (50 mg/day), sulpiride (100 mg/day), sodyum valproate (1000mg/day), lorazepam (3 mg/day), aspirin (100mg/day) and ramipril (2.5mg/day). Under the policlinic control, he recovered from both illnesses with his medication. However, 90 days ago, the patient took in dabigatran 110 mg/day for prevention of secondary to atrial fibrillation. Then, he came to the emergency department with mixed depressive-anxiety disorders. Many other drugs are known to be the substrate of Pgp in vitro, including dabigatran It is necessary to check whether the patients are being treated with drugs such as Pgp modulators before starting dabigatran treatment, to avoid interactions. The activity of the efşux transporter Pgp affects the pharmacokinetic parameters of many drugs and contributes to numerous pharmacokinetic drug-drug interactions. . The role of Pgp for the bioavailability of newer antidepressants and for their interactions with coadministered drugs has not been elucidated thoroughly. For paroxetine, venlafaxine and şuoxetine, the available data indicate that they might be Pgp substrates; whereas for citalopram, the data are conşicting. . very few is known about potential inhibitory characteristics of newer antidepressants on Pgp. Thus far, only şuoxetine has been tested in this regard. In line with the absence of Pgp-substrate characteristics and in agreement with our results, no evidence for a potent interaction was found. So far, there are no studies that systematically examined possible interactions with the newer antidepressants in relevance of Pgp. Antidepressant drugs and their metabolites are substrates of Pgp, and brain concentrations of these drugs are dependent on the activity of this protein. This effect was attributed to the ability of Pgp to act as a pump, which transports the drug from the brain back into circulation at the brain blood barrier. Coadministration of antidepressant drugs and dabigatran may play an important role in drug effectiveness, because it may decrease brain concentrations of antidepressant drugs.