|
|
||||||||
Letters to the Editor |
1 Center of Molecular and Structural Biomedicine Institute for Biotechnology and Bioengineering, Universidade do Algarve, Gambelas, Portugal
2 Unit for Pharmacokinetics and Drug Metabolism, Department of Pharmacology, Sahlgrenska Academy at Göteborg University Göteborg, Sweden
3 Institutionen för Biovetenskaper och Näringslära Centrum för Bioteknik Karolinska Institutet Stockholm, Sweden
4 Malaria Research Laboratory Unit of Infectious Diseases Department of Medicine Karolinska University Hospital Karolinska Institute Stockholm, Sweden
5 National Institute of Malariology, Parasitology and Entomology Hanoi, Vietnam
aAddress correspondence to this author at: Malaria Research Unit, Karolinska University Hospital, M9, Plan 2, 17176KS, Stockholm, Sweden. Fax 46 8 51776740; e-mail jose.pedro.gil@ki.se.
| The first 20% of the full text of this article appears below. |
To the Editor:
Vietnam ranks 13th among the 23 countries that must deal with 80% of global deaths from tuberculosis (1). The National Tuberculosis Control Program of Vietnam implemented the WHO DOTS (directly observed therapy, short course) strategy in 1989. The standard treatment regimen for previously untreated patients consists of 2 months of streptomycin, isoniazid (INH), rifampin, and pyrazinamide, followed by 6 months of INH and ethambutol (the 2SHRZ/6HE regimen).
INH, a central component of this chemotherapy, is extensively metabolized by the polymorphic N-acetyltransferase 2 (NAT2) enzyme. N-acetyltransferase 2 (arylamine N-acetyltransferase) (NAT2) gene polymorphisms are associated with individual phenotypes generally classified as INH rapid (homozygous or heterozygous) and slow acetylators. Among the described NAT2 alleles, NAT2*5, *6, *7, 12*, *14, *17, and *19 have been associated with the slow acetylator phenotype, and NAT2*4 and *13 are associated with fast
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |