Monitoring omalizumab treatment efficacy in chronic urticaria by the basophil activation test

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Tasa de mutaciones genotípicas y resistencia a antirretrovirales en un hospital general / Rate of Genotypic Mutations and Resistance to Antiretroviral Drugs in a General Hospital

Objetivo El objetivo es describir la tasa de mutaciones de resistencia en los genes de la proteasa y la transcriptasa inversa y la sensibilidad de los diferentes antirretrovirales en nuestro medio. Métodos Estudio observacional, descriptivo en el cual se estudiaron las muestras remitidas al laboratorio de inmunología clínica desde abril de 2004 hasta abril de 2009. Se analizaron tanto los test de resistencias, como el análisis de sensibilidad a los diferentes fármacos de pacientes en fracaso terapéutico mediante Trugene Hiv-1 Genotyping Kit®. Resultados Se registraron las muestras de 242 pacientes, en 61 de ellos no se detectaron resistencias. Las mutaciones más prevalentes según familia de fármacos fueron: para los inhibidores de la transcriptasa inversa análogos nucleosídicos T215a/C/D/F/L/N/S/Y (24,10%), M184g/I/V/W (14,66%), M41j/L/R/T/W (11,24%) y K219e/G/H/N/R/T/W (10,24%). La estavudina y la lamivudina/emtricitabina fueron los que más resistencias presentaron, y el tenofovir es el que tiene menos resistencias en nuestro medio. En cuanto a los no análogos fueron K103N/R (23,98%), V179d/E/I/M/T (10,82%), A98e/G/S (10,53%) y K101e/P/Q/R (9,06%). Nevirapina presentó más resistencias que efavirenz. Respecto a los inhibidores de la proteasa fueron L10F/I/V (15,95%), M36I/L (13,81%), A71I/T/V (13,10%) y I54l/S/V (7,38%). La combinación darunavir/ritonavir fue la que menos resistencias presentó junto con tipranavir/ritonavir, en contraposición lopinavir/ritonavir fue el que más resistencias obtuvo. Conclusión La resistencia y sensibilidad al tratamiento antirretroviral en nuestro medio fueron similares a las de otros estudios realizados en nuestro país, pero difiere y destaca un alto grado de resistencia a lamivudina/emtricitabina y lopinavir/ritonavir (AU)

Objectives The objective is to describe the resistance mutation rate in protease and reverse transcriptase genes and sensitivity to different antiretrovirals in our environment. Methods We performed an observational descriptive study in which we examined the samples provided at the Clinical Immunology Laboratory between April 2004 and April 2009. We analysed both the resistance tests and the sensitivity to different drugs in patients with therapeutic failure using Trugene HIV-1 Genotyping Kits®. Results We registered samples from 242 patients, 61 of which had no detectable resistance. The most prevalent mutations according to drug families were: for nucleoside analog reverse transcriptase inhibitors T215A/C/D/F/L/N/S/Y (24.10%), M184G/I/V/W (14.66%), M41J/L/R/T/W (11.24%) and K219E/G/H/N/R/T/W (10.24%). The highest levels of resistance corresponded to stavudine and lamivudine/emtricitabine, and tenofovir produced the least resistance in our environment. The non-analogues were K103N/R (23.98%), V179D/E/I/M/T (10.82%), A98E/G/S (10.53%) and K101E/P/Q/R (9.06%). Nevirapine presented greater resistance than efavirenz. Protease inhibitors were L10F/I/V (15.95%), M36I/L (13.81%), A71I/T/V (13.10%) and 154L/S/V (7.38%). The darunavir/ritonavir combination was that which presented the least resistance, and tipranavir/ritonavir and lopinavir/ritonavir the most resistance. Conclusions Antiretroviral resistance and sensitivity to retroviral treatment in our environment was similar to results from other studies in Spain, but differed in the high level of resistance to lamivudine/emtricitabine and lopinavir/ritonavir (AU)

[Rate of genotypic mutations and resistance to antiretroviral drugs in a general hospital]. / Tasa de mutaciones genotípicas y resistencia a antirretrovirales en un hospital general.

OBJECTIVES: The objective is to describe the resistance mutation rate in protease and reverse transcriptase genes and sensitivity to different antiretrovirals in our environment. METHODS: We performed an observational descriptive study in which we examined the samples provided at the clinical immunology laboratory between April 2004 and April 2009. We analysed both the resistance tests and the sensitivity to different drugs in patients with therapeutic failure using trugene hiv01 genotyping kits(®). RESULTS: We registered samples from 242 patients, 61 of which had no detectable resistance. The most prevalent mutations according to drug families were: for nucleoside analog reverse transcriptase inhibitors T215A/C/D/F/L/N/S/Y (24.10%), M184G/I/V/W (14.66%), M41J/L/R/T/W (11.24%) and K219E/G/H/N/R/T/W (10.24%). The highest levels of resistance corresponded to stavudine and lamivudine/emtricitabine, and tenofovir produced the least resistance in our environment. The non-analogues were K103N/R (23.98%), V179D/E/I/M/T (10.82%), A98E/G/S (10.53%) y K101E/P/Q/R (9.06%). Nevirapine presented greater resistance than efavirenz. Protease inhibitors were L10F/I/V (15.95%), M36I/L (13.81%), A71I/T/V (13.10%) and 154L/S/V (7.38%). The combination darunavir/ritonavir combination was that which presented the least resistance, and tipranavir/ritonavir and lopinavir/ritonavir the most resistance. CONCLUSIONS: Antiretroviral resistance and sensitivity to retroviral treatment in our environment was similar to results from other studies in Spain, but differed in the high level of resistance to lamivudine/emtricitabine and lopinavir/ritonavir.