medigraphic.com
Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán

2008, Número 1

<< Anterior Siguiente >>

Rev Invest Clin 2008; 60 (1)


Polimorfismos en los genes CYP450 y NAT2 y metabolismo de fármacos para el tratamiento antituberculosis estandarizado

Castillejos-López MJ, García-Sancho MC, Quiñones-Falconi F, Pérez-Padilla JR

Idioma: Español
Referencias bibliográficas: 60
Paginas: 47-57
Archivo PDF: 132.82 Kb.


RESUMEN

Se ha descrito un incremento en la frecuencia de fracaso al Tratamiento Acortado Estrictamente Supervisado (TAES) en países con elevadas tasas de resistencia. Este incremento odría ser debido a que las dosis estandarizadas del TAES se traducen en dosis plasmáticas insuficientes. Varios miembros de la superfamilia de enzimas del citocromo P450 (CYP) catalizan la oxidación de fármacos considerándose que las diferencias en los polimorfismos de P450 podrían explicar las variaciones en la velocidad de acetilación y en la disposición a fármacos. Las personas con acetilación lenta de INH tienen un riesgo mayor de toxicidad, ya que el grado de inhibición debida a la INH de distintas isoformas del citocromo P450 (CYP2C19 y CYP3A) es dependiente de la concentración de INH. El efecto inhibitorio de la INH se ha descrito también para CYP12, CYP2C9 y CYP2E1. La INH se metaboliza a través de la enzima N-acetiltransferasa 2 (NAT2). La gran variabilidad intra e interétnica en la velocidad de acetilación se asocia con los polimorfismos de NAT2. Los pacientes con acetilación rápida tienen concentraciones plasmáticas de INH insuficientes que inducen fracaso terapéutico. El estudio de los genotipos de P450 y de NAT2 permitirá predecir una dosis de INH terapéutica e individualizada.


REFERENCIAS (EN ESTE ARTÍCULO)

  1. Global tuberculosis control - surveillance, planning, financing. WHO Report 2007. WHO/HTM/TB/2007.376. Disponible en: http://www.who.int/tb/publications/global_report/2007/en/ index.html

  2. Organización Mundial de la Salud, Control Mundial de la Tuberculosis 2007. Resultados principales. Disponible en: http:// www. who. int/tb/publications global report/2007/ download_centre/en/index.html

  3. World Health Organization. The five elements of DOTS. Disponible en: http://www.who.int/tb/dots/whatisdots/en/ index.html

  4. Secretaría de Salud. Modificación a la Norma Oficial Mexicana NOM-006-SSA2-1993, Para la prevención y control de la tuberculosis en la atención primaria a la salud. Diario Oficial de la Federación, Martes 27 de septiembre de 2005.

  5. World Health Organization, 2006. The Stop TB Strategy. http:/ /www.who.int/tb/publications/2006/stoptb_strategy_sp.pdf).

  6. Pablos-Mendez A, Raviglione MC, Laszlo A, Binkin N, Rieder HL, Bustreo F, et al. Global surveillance for antituberculosisdrug resistance, 1994-1997. World Health Organization-International Union against Tuberculosis and Lung Disease Working Group on Anti-Tuberculosis Drug Resistance Surveillance. N Engl J Med 1998; 338: 1641-9.

  7. Van den Broek J, Borgdorff MW, Pakker NG, Chum HJ, Klokke AH, Senkoro KP, et al. HIV-1 infection as a risk factor for the development of tuberculosis: a case-control study in Tanzania. Int J Epidemiol 1993; 22: 1159-65.

  8. Storla DG, Rahim Z, Islam MA, Plettner S, Begum V, Myrvang B, et al. Drug resistance of Mycobacterium tuberculosis in the Sunamganj District of Bangladesh. Scand J Infect Dis 2007; 39: 142-5.

  9. Chen J, Li NX, Wan KL, Yang GJ, Wang Q. Analysis on risk factors of drug resistance for tuberculosis in Sichuan and Anhui Provinces. Sichuan Da Xue Xue Bao Yi Xue Ban 2007; 38: 135-7.

  10. Cox H, Kebede Y, Allamuratova S, Ismailov G, Davletmuratova Z, Byrnes G, et al. Tuberculosis recurrence and mortality after successful treatment: impact of drug resistance. PLoS Med 2006; 3: e384. Published online 2006 October 3. doi: 10.1371/ journal.pmed.0030384.

  11. Wang GJ, Xu JY, Wang GB, Zhen XA, Gao SY, Du CM. Impact of anti-tuberculosis drug resistance on treatment outcome of pulmonary tuberculosis patients receiving directly observed treatment strategy in Henan Province, China. Zhonghua Jie He He Hu Xi Za Zhi 2006; 29: 527-30.

  12. Davies PD. The role of DOTS in tuberculosis treatment and control. Am J Respir Med 2003; 2: 203-9.

  13. Kimerling ME, Phillips P, Patterson P, Hall M, Robinson CA, Dunlap NE. Low serum antimycobacterial drug levels in non- HIV-infected tuberculosis patients. Chest 1998; 113: 1178-83.

  14. Tappero JW, Bradford WZ, Agerton TB, Hopewell P, Reingold AL, Lockman S, et al. Serum Concentrations of antimycobacterial drugs in patients with pulmonary tuberculosis in Botswana. CID 2005; 41: 461-9.

  15. Yew WW. Clinically significant interactions with drugs used in the treatment of tuberculosis. Drug Saf 2002; 25: 111-33.

  16. Desta Z, Soukhova NV, Flockhart DA. Inhibition of cytochrome P450 (CYP450) isoforms by isoniazid: potent inhibition of CYP2C19 and CYP3A. Antimicrob Agents Chemother 2001; 45: 382-92.

  17. Narita M, Ashkin D, Hollender ES, Pitchenik AE. Paradoxical worsening of tuberculosis following antiretroviral therapy in patients with AIDS. Am J Respir Crit Care Med 1998; 158: 157-61.

  18. McIlleron H, Meintjes G, Burman WJ, Maartens G. Complications of antiretroviral therapy in patients with tuberculosis: drug interactions, toxicity, and immune reconstitution inflammatory syndrome. J Infect Dis 2007; 196(Suppl 1): S63-S75.

  19. Matteelli A, Regazzi M, Villani P, De Iaco G, Cusato M, Carvalho AC, et al. Multiple-dose pharmacokinetics of efavirenz with and without the use of rifampicin in HIV-positive patients. Curr HIV Res 2007; 5: 349-53.

  20. Centers for Disease Control and Prevention (CDC). Acquired rifamycin resistance in persons with advanced HIV disease being treated for active tuberculosis with intermittent rifamycin-based regimens. MMWR Morb Mortal Wkly Rep 2002; 51: 214-15.

  21. Nolan CM, Williams DL, Cave MD, Eisenach KD, el-Hajj H, Hooton TM, et al. Evolution of rifampin resistance in human immunodeficiency virus-associated tuberculosis. Am J Respir Crit Care Med 1995; 152: 1067-71.

  22. Bishai WR, Graham NM, Harrington S, Page C, Moore-Rice K, Hooper N, Chaisson RE. Brief report: rifampin-resistant tuberculosis in a patient receiving rifabutin prophylaxis. N Engl J Med 1996; 334: 1573-76.

  23. Bradford WZ, Martin JN, Reingold AL, Schecter GF, Hopewell PC, Small PM. The changing epidemiology of acquired drugresistant tuberculosis in San Francisco, USA. Lancet 1996; 348: 928-31.

  24. Lutfey M, Della-Latta P, Kapur V, Palumbo LA, Gurner D, Stotzky G, et al. Independent origin of mono-rifampin-resistant Mycobacterium tuberculosis in patients with AIDS. Am J Respir Crit Care Med 1996; 153: 837-40.

  25. Ridzon R, Whitney CG, McKenna MT, Taylor JP, Ashkar SH, Nitta AT, et al. Risk factors for rifampin mono-resistant tuberculosis. Am J Respir Crit Care Med 1998; 157: 1881-4.

  26. Gurumurthy P, Ramachandran G, Hemanth Kumar AK, Rajasekaran S, Padmapriyadarsini C, Swaminathan S, et al. Decreased bioavailability of rifampin and other antituberculosis drugs in patients with advanced human immunodeficiency virus disease. Antimicrob Agents Chemother 2004; 48: 4473-5.

  27. Barry M, Gibbons S, Back D, Mulcahy F. Protease inhibitors in patients with HIV disease. Clinically important pharmacokinetic considerations. Clin Pharmacokinet 1997; 32: 194-209.

  28. Kirschner D. Dynamics of co-infection with M. Tuberculosis and HIV-1. Theor Popul Biol 1999; 55: 94-109.

  29. Alavez-Ramírez J, Castellanos JR, Esteva L, Flores JA, Fuentes- Allen JL, García-Ramos G, Gómez G, López-Estrada J. Withinhost population dynamics of antibiotic-resistant M. tuberculosis. Math Med Biol 2007; 24: 35-56.

  30. Nebert DW, Adesnik M, Coon MJ, Estabrook RW, Gonzalez FJ, Guengerich FP, et al. The P450 gene superfamily: recommended nomenclature. DNA 1987; 6: 1-11.

  31. Miranda GE, Ostrosky P. Bases científicas de las respuestas idiosincráticas en la terapéutica. El papel del gen CYP2D6. Acta Médica Grupo Ángeles 2004; 2: 59-63.

  32. Soya SS, Padmaja N, Adithan C. Genetic polymorphisms of CYP2E1 and GSTP1 in a South Indian population-comparison with North Indians, Caucasians and Chinese. Asian Pac J Cancer Prev 2005; 6: 315-19.

  33. Garcia-Martin E, Martinez C, Ladero JM, Agundez JA. Interethnic and intraethnic variability of CYP2C8 and CYP2C9 polymorphisms in healthy individuals. Mol Diagn Ther 2006; 10: 29-40.

  34. Dorne JL. Impact of inter-individual differences in drug metabolism and pharmacokinetics on safety evaluation. Fundam Clin Pharmacol 2004; 18: 609-20.

  35. Schwarz UI. Clinical relevance of genetic polymorphisms in the human CYP2C9 gene. Eur J Clin Invest 2003; 33(Suppl 2): 23-30.

  36. Bertz RJ, Granneman GR. Use in vitro and in vivo data to estimate the likelihood of metabolic pharmacokinetic interactions. Clinical Pharmacokinet 1997; 32: 210-58.

  37. Goldstein JA. Clinical relevance of genetic polymorphisms in the human CYP2C subfamily. Br J Clin Pharmacol 2001; 52: 349-55.

  38. Llerena A, Dorado P, O’Kirwan F, Jepson R, Linicio J, Wong ML. Lower frequency of CYP2C9*2 in Mexican-Americans compared to Spaniards. Pharmacogenomics J 2004; 4: 403-6.

  39. Thier R, Bruning T, Roos PH, Rihs HP, Golka K, Ko Y, Bolt HM. Markers of genetic susceptibility in human environmental hygiene and toxicology: the role of selected CYP, NAT and GST genes. Int J Hyg Environ Health 2003; 206: 149-71.

  40. Rossini A, Lima SS, Raposo DC, Faria M, Albano RM, Pinto LF. CYP2A6 and CYP2E1 polymorphisms in a Brazilian population living in Rio de Janeiro. Braz J Med Biol Res 2006; 39: 195-201.

  41. Huang YS, Chern HD, Su WJ, Wu JC, Chang SC, Chiang CH, et al. Cytochrome P450 2E1 genotype and the susceptibility to antituberculosis drug-induced hepatitis. Hepatology 2003; 37: 924-30.

  42. Vuilleumier N, Rossier MF, Chiappe A, Degoumois F, Dayer P, Mermillod B, et al. CYP2E1 genotype and isoniazid-induced hepatotoxicity in patients treated for latent tuberculosis. Eur J Clin Pharmacol 2006; 62: 423-29.

  43. Madan A, Graham RA, Carroll KM, Mudra DR, Burton LA, Krueger LA, et al. Effects of prototypical microsomal enzyme inducers on cytochrome P450 expression in cultured human hepatocytes. Drug Metab Dispos 2003; 31: 421-31.

  44. Hesse LM, Sakai Y, Vishnuvardhan D, Li AP, von Moltke LL, Greenblatt DJ. Effect of bupropion on CYP2B6 and CYP3A4 catalytic activity, immunoreactive protein and mRNA levels in primary human hepatocytes: comparison with rifampicin. J Pharm Pharmacol 2003; 55: 1229-39.

  45. Rae JM, Johnson MD, Lippman ME, Flockhart DA. Rifampin is a selective, pleiotropic inducer of drug metabolism genes in human hepatocytes: studies with cDNA and oligonucleotide expression arrays. J Pharmacol Exp Ther 2001; 299: 849-57.

  46. Reinach B, de Sousa G, Dostert P, Ings R, Gugenheim J, Rahmani R. Comparative effects of rifabutin and rifampicin on cytochromes P450 and UDP-glucuronosyl-transferases expression in fresh and cryopreserved human hepatocytes. Chem Biol Interact 1999; 121: 37-48.

  47. Gerbal-Chaloin S, Pascussi JM, Pichard-Garcia L, Daujat M, Waechter F, Fabre JM, et al. Induction of CYP2C genes in human hepatocytes in primary culture. Drug Metab Dispos 2001; 29: 242-51.

  48. Chen B, Li JH, Xu YM, Wang J, Cao XM. The influence of NAT2 genotypes on the plasma concentration of isoniazid and acetylisoniazid in Chinese pulmonary tuberculosis patients. Clin Chim Acta 2006; 365: 104-8.

  49. Xie HG, Xu ZH, Ou-Yang DS, Shu Y, Yang DL, Wang JS, et al. Meta-analysis of phenotype and genotype of NAT2 deficiency in Chinese populations. Pharmacogenetics 1997; 7: 503-14.

  50. Straka RJ, Burkhardt RT, Lang NP, Vang T, Hadsall KZ, Tsai MY. Verified predominance of slow acetylator phenotype Nacetyltransferase 2 (NAT2) in a Hmong population residing in Minnesota. Biopharm Drug Dispos 2006; 27: 299-304.

  51. Kohno H, Kubo H, Takada A, Mori M, Arias TD. Isoniazid acetylation phenotyping in the Japanese: The molar metabolic ratio INH/AcINH. Am J Ther 1996; 3: 74-8.

  52. Augustynowicz-Kopec E, Zwolska Z. Type of isoniazid (INH) acetylation determined in tuberculosis patients at the Institute of Tuberculosis and Lung Diseases in Warsaw during the years 1990-1997. Pneumonol Alergol Pol 2002; 70: 180-92.

  53. Ait Moussa L, Khassouani CE, Hue B, Jana M, Begaud B, Soulaymani R. Determination of the acetylator phenotype in Moroccan tuberculosis patients using isoniazid as metabolic probe. Int J Clin Pharmacol Ther 2002; 40: 548-53.

  54. Mehiri BR, Zouaoui A, Cherif J, Ourari B, Daghfous R, Oueslati MH, et al. Isoniazid acetylation in a group of Tunisian patients. Report of 620 patients. Tunis Med 2005; 83: 385-9.

  55. Chen B, Zhang WX, Cai WM. The influence of various genotypes on the metabolic activity of NAT2 in a Chinese population. Eur J Clin Pharmacol 2006; 62: 355-9.

  56. Parkin DP, Vandenplas S, Botha FJ, Vandenplas ML, Seifart HI, van Helden PD, et al. Trimodality of isoniazid elimination: phenotype and genotype in patients with tuberculosis. Am J Respir Crit Care Med 1997; 155: 1717-22.

  57. Kita T, Tanigawara Y, Chikazawa S, Hatanaka H, Sakaeda T, Komada F, et al. N-Acetyltransferase2 genotype correlated with isoniazid acetylation in Japanese tuberculous patients. Biol Pharm Bull 2001; 24: 544-9.

  58. Schaaf HS, Parkin DP, Seifart HI, Werely CJ, Hesseling PB, van Helden PD, et al. Isoniazid pharmacokinetics in children treated for respiratory tuberculosis. Arch Dis Child 2005; 90: 614-8.

  59. Kinzig-Schippers M, Tomalik-Scharte D, Jetter A, Scheidel B, Jakob V, Rodamer M, et al. Should we use N-acetyltransferase type 2 genotyping to personalize isoniazid doses? Antimicrob Agents Chemother 2005; 49: 1733-8.

  60. Peloquin CA. Using therapeutic drug monitoring to dose the antimycobacterial drugs. Tuberculosis 1997; 18: 79-87.




2020     |     www.medigraphic.com