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IntroductionUntil recently, erythromycin and the newer macrolide antibiotics have been used extensively in the treatment of infectious processes in patients receiving anticoagulant therapy. Furthermore, macrolides have been part of the recommendations for endocarditis prophylaxis in those patients who were unable to take penicillins [1, 2]. However, it is well known that macrolides inhibit cytochrome P450, which appears to be the most common metabolic enzyme in human liver tissue. It is involved in the metabolism of many drugs, including oral anticoagulants. Several reports have confirmed that macrolides can potentiate the effect of oral anticoagulants [3, 4]. We report a new case in whom erythromycin potentiated acenocoumarol anticoagulant treatment.A 68-year-old man was treated with acenocoumarol for 14 years because he was a heart double-valve prosthesis carrier. Anticoagulation control presented no major problem under acenocoumarol, 3 mg/day, as his international normalized ratio (INR) stayed in the range 3–4.5. He started oral erythromycin ethylsuccinate 1.5 g/day for an upper respiratory tract infection. A week later, in a routine control, his INR was found to be 15. There was no macroscopic bleeding. No other drugs were being administered at that time. Results of a blood cell count, platelet count, and liver function tests were
Acta Haematologica – Karger
Published: Oct 1, 1999
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