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27 mars 2020 5 27 /03 /mars /2020 06:30

La hidroxicloroquina es un principio activo antimalárico o antipalúdico que se vende con los nombres comerciales Plaquenil, Axemal (en la India), Dolquine, Ilinol, y Quensyl. También, se utiliza para reducir la inflamación en el tratamiento de la artritis reumatoide y del lupus. Se diferencia de la cloroquina por la presencia de un grupo hidroxilo en el extremo de la cadena lateral. Está disponible para administración oral como sulfato de hidroxicloroquina (Plaquenil), de los cuales 200 mg contienen 155 mg de base en forma quiral. La hidroxicloroquina tiene una farmacocinética similar a la cloroquina, con rápida absorción gastrointestinal, y se elimina por el riñón.Luego de su administración por vía oral, empieza la absorción en el tracto digestivo, alcanzando niveles pico de 2 a 4.5 h con una media de 3.2 horas.

Las concentraciones plasmáticas máximas de la droga luego de la dosis oral estuvieron entre 34 y 79 ng/ml. La hidroxicloroquina tiene una gran avidez por los tejidos, especialmente aquellos que contienen melanina, fijándose fuertemente a los mismos. Tiene un gran volumen de distribución.[1]

La hidroxicloroquina posee acciones antimaláricas y también ejerce un efecto benéfico en el lupus eritematoso (sistémico y discoide) y en la artritis reumatoide. El mecanismo de acción no se conoce precisamente, pero parece estar ligado a la elevación del pH intracitoplasmático, lo cual altera el ensamble de las cadenas α y ß de las moléculas de la clase II del complejo mayor de histocompatibilidad, y así estaría interfiriendo con el procesamiento antigénico y, por tanto, disminuyendo el estímulo autoinmune de las células CD4+.[2][3][

La hidroxicloroquina posee acciones antimaláricas y también ejerce un efecto benéfico en el lupus eritematoso (sistémico y discoide) y en la artritis reumatoide. El mecanismo de acción no se conoce precisamente, pero parece estar ligado a la elevación del pH intracitoplasmático, lo cual altera el ensamble de las cadenas α y ß de las moléculas de la clase II del complejo mayor de histocompatibilidad, y así estaría interfiriendo con el procesamiento antigénico y, por tanto, disminuyendo el estímulo autoinmune de las células CD4+.[2][3][4][5]

 

  1. CDC. Health information for international travel 2001-2002. Atlanta, Georgia: U.S. Department of Health and Human Services, Public Health Service, 2001.
  2.  Plowe CV. Antimalarial drug resistance in Africa: strategies for monitoring and deterrence. Curr Top Microbiol Immunol.2005;295:55-79.
  3.  Uhlemann AC, Krishna S. Antimalarial multi-drug resistance in Asia: mechanisms and assessment. Curr Top Microbiol Immunol. 2005;295:39-53.
  4.  Savarino A, Lucia MB, Giordano F, Cauda R. Risks and benefits of chloroquine use in anticancer strategies. Lancet Oncol. 2006 Oct;7(10):792-3.
  5.  Sotelo J, Briceno E, Lopez-Gonzalez MA. Adding chloroquine to conventional treatment for glioblastoma multiforme: a randomized, double-blind, placebo-controlled trial. Ann Intern Med. 2006 Mar 7;144(5):337-43. Summary for patients in: Ann Intern Med. 2006 Mar 7;144(5):I31.
  6.  Yam JC, Kwok AK. Ocular toxicity of hydroxychloroquine. Hong Kong Med J. agosto de 2006; 12(4):294-304.
  7.  «numericalexample.com - Determine the safe dose of medicins: Chloroquine and Hydroxychloroquine (Plaquenil)». Archivado desde el original el 26 de enero de 2008. Consultado el 21 de febrero de 2008.
  8.  Davidson, R. J., I. Davis, et al. (2008). "Antimalarial therapy selection for quiniolone resistance among Escherichia coli in the absence of quinolone exposure, in tropical South America." PLoS One 3
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