Inherited differences in response to anti-infective drugs were observed several decades ago. Indeed, it is in the field of anti-infective therapy that the importance of polymorphisms in drug disposition was first encountered: the N-acetyltransferase 2 (NAT2) acetylation polymorphism discovered during isoniazid treatment of TB patients (5) was one of the first examples of a pharmacogenetic defect influencing drug biotransformation in human populations. A number of antibiotics and chemotherapeutic agents are substrates of polymorphic phases I and II metabolic pathways and transport genes (Table 2). However, there are currently limited data on the clinical relevance of such genetic variations. In the following, we discuss the current pharmacogenetic knowledge relevant to the treatment of four major diseases and infectious syndromes: HIV, TB, malaria, and sepsis.
What therapy for maximal efficacy What therapy for minimal toxicity No allergic reaction
Figure 1 Genetic markers in the treatment of infection. Genetic determinants of susceptibility define who should be treated, and pharmacogenetic markers help in the choice of therapy.
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