Dihydropyrimidine Dehydrogenase Testing prior to Treatment with 5-Fluorouracil, Capecitabine, and Tegafur: A Consensus Paper.
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Wörmann Bernhard, Bokemeyer Carsten, Burmeister Thomas, Köhne Claus-Henning, Schwab Matthias, Arnold Dirk, Blohmer Jens-Uwe, Borner Markus, Brucker Sara, Cascorbi Ingolf, Decker Thomas, de Wit Maike, Dietz Andreas, Einsele Hermann, Eisterer Wolfgang, Folprecht Gunnar, Hilbe Wolfgang, Hoffmann Jürgen, Knauf Wolfgang, Kunzmann Volker, Largiadèr Carlo R, Lorenzen Sylvie, Lüftner Diana, Moehler Markus, Nöthen Markus M, Pox Christian, Reinacher-Schick Anke, Scharl Anton, Schlegelberger Brigitte, Seufferlein Thomas, Sinn Marianne, Stroth Matthias, Tamm Ingo, Trümper Lorenz, Wilhelm Martin, Wöll Ewald, Hofheinz Ralf-Dieter
Аннотация
SUMMARY: Among other risk factors associated with increased toxicity, a genetic deficiency in dihydropyrimidine dehydrogenase (DPD), an enzyme responsible for the metabolism of FU, is well known. This is due to variants in the DPD gene (DPYD). Up to 9% of European patients carry a DPD gene variant that decreases enzyme activity, and DPD is completely lacking in approximately 0.5% of patients. Here we describe the clinical and genetic background and summarize recommendations for the genetic testing and tailoring of treatment with 5-FU derivatives. The statement was developed as a consensus statement organized by the German Society for Hematology and Medical Oncology in cooperation with 13 medical associations from Austria, Germany, and Switzerland. Key Messages: (i) Patients should be tested for the 4 most common genetic DPYD variants before treatment with drugs containing FU. (ii) Testing forms the basis for a differentiated, risk-adapted algorithm with recommendations for treatment with FU-containing drugs. (iii) Testing may optionally be supplemented by therapeutic drug monitoring.