ABSTRACT
OBJECTIVE: To assess causes of suspension of hepatitis C treatment in patients receiving triple antiviral therapy (peginterferon+ ribavirin + protease inhibitor). METHODS: Retrospective observational study of patients who received triple antiretroviral therapy against hepatitis C between January 2012 - March 2013 and discontinued their treatment. RESULTS: Of 156 patients who initiated therapy, 41 discontinued treatment: Nineteen due to adverse events, being dermatological events in seven patients ( 36.8 %), intolerance in six(31.6%) and hematologic toxicity in four (15.8%) . Sixteen patients discontinued treatment for being ineffectiveness.Patients with higher inefficacy failure rate were "null-responders"(32.3% ) while the group of "relapsers" were the one with the highest rate of toxicity suspensions (15.6%). Two patients died during treatment for pneumonia. CONCLUSIONS: Triple therapy with boceprevir and telaprevir is associated with a significant number of treatment failures due to toxicity and ineffectiveness.
Objetivo: Evaluar las causas de suspensión de tratamientofrente a Hepatitis C que reciben triple terapia antiviral (peginterferon+ ribavirina + inhibidor de proteasa).Métodos: Estudio observacional retrospectivo de pacientes queiniciaron triple terapia antiviral entre enero 2012 - marzo 2013y suspendieron el tratamiento antes de completar el mismo.Resultados: De 156 pacientes que iniciaron triple terapia, 41interrumpieron el tratamiento: Diecinueve por toxicidad, siendodermatológica en siete pacientes (36,8%), intolerancia en seis(31,6%) y hematológica en cuatro (15,8%). Dieciséis pacientessuspendieron todo el tratamiento por ineficacia. El grupo depacientes con mayor porcentaje de fracasos por ineficacia fueronlos "no respondedores" (32,3%) mientras que el grupo depacientes "recidivantes" fueron el grupo con mayor porcentajede suspensiones por toxicidad (15,6%). Dos pacientes fallecierondurante el tratamiento por neumonía.Conclusiones: La triple terapia frente a VHC está asociada a unnúmero importante de fracasos terapéuticos tanto por toxicidadcomo por ineficacia.
Subject(s)
Antiviral Agents/adverse effects , Hepatitis C/drug therapy , Withholding Treatment , Adult , Aged , Antiviral Agents/therapeutic use , Drug Combinations , Female , Humans , Male , Middle Aged , Recurrence , Retrospective Studies , Treatment FailureABSTRACT
Objetivo: Evaluar las causas de suspensión de tratamient of rente a Hepatitis C que reciben triple terapia antiviral (pegin-terferon + ribavirina + inhibidor de proteasa).Métodos: Estudio observacional retrospectivo de pacientes que iniciaron triple terapia antiviral entre enero 2012 - marzo 2013y suspendieron el tratamiento antes de completar el mismo. Resultados: De 156 pacientes que iniciaron triple terapia, 41interrumpieron el tratamiento: Diecinueve por toxicidad, siendo dermatológica en siete pacientes (36,8%), intolerancia en seis(31,6%) y hematológica en cuatro (15,8%). Dieciséis pacientes suspendieron todo el tratamiento por ineficacia. El grupo de pacientes con mayor porcentaje de fracasos por ineficacia fueron los "no respondedores" (32,3%) mientras que el grupo de pacientes "recidivantes" fueron el grupo con mayor porcentaje de suspensiones por toxicidad (15,6%). Dos pacientes fallecieron durante el tratamiento por neumonía. Conclusiones: La triple terapia frente a VHC está asociada a un número importante de fracasos terapéuticos tanto por toxicidad como por ineficacia
Objective: To assess causes of suspension of hepatitis C treatment in patients receiving triple antiviral therapy (peginterferon+ ribavirin + protease inhibitor).Methods: Retrospective observational study of patients who recived triple antiretroviral therapy agaisnst hepatitis C between January 2012 - March 2013 and discontinued their treatment. Results: Of 156 patients who initiated therapy, 41 discontinued treatment: Nineteen due to adverse events, being dermatological events in seven patients ( 36.8 %), intolerance in six(31.6%) and hematologic toxicity in four (15.8%) . Sixteen patients discontinued treatment for beeing ineffectiveness. Patients with higher inefficacy failure rate were "null-responders" (32.3% ) while the group of "relapsers" were the one with the highest rate of toxicity suspensions (15.6%). Two patients died during treatment for pneumonia. Conclusions: Triple therapy with boceprevir and telaprevir is associated with a significant number of treatment failures due to toxicity and ineffectiveness (AU)
Subject(s)
Humans , Hepatitis C, Chronic/drug therapy , Antiviral Agents/administration & dosage , Withholding Treatment , /prevention & control , Interferon-alpha/administration & dosage , Ribavirin/administration & dosage , Protease Inhibitors/administration & dosageABSTRACT
BACKGROUND AND PURPOSE: Dersalazine sodium (DS) is a new chemical entity formed by combining, through an azo bond, a potent platelet activating factor (PAF) antagonist (UR-12715) with 5-aminosalicylic acid (5-ASA). DS has been demonstrated to have anti-inflammatory effects on trinitrobenzene sulphonic acid (TNBS)-induced colitis in rats and recently in UC patients in phase II PoC. There is Increasing evidence that Th17 cells have an important role in the pathogenesis of inflammatory bowel disease (IBD). The aim of this study was to further characterize the anti-inflammatory effects of DS. EXPERIMENTAL APPROACH: Effect of DS (10 or 30 mg·kg(-1) b.i.d.) on TNBS-induced colitis in rats was studied after 2 and 7 days with special focus on inflammatory mediators. Additionally, its anti-inflammatory properties were analysed in two different models of dextran sodium sulphate (DSS)-induced colitis, BALB/c and C57BL/6 mice, the latter being dependent on IL-17. KEY RESULTS: DS, when administered for 7 days, showed intestinal anti-inflammatory effects in TNBS-induced colitis; these effects were observed both macroscopically and through the profile of inflammatory mediators (TNF, IL-1ß, IL-6 and IL-17). Although the 2 day treatment with DS did not induce intestinal anti-inflammatory effects, it was sufficient to reduce the enhanced IL-17 expression. DS showed beneficial effects on DSS-induced colitis in C57BL/6 mice and reduced colonic pro-inflammatory cytokines IL-1ß, IL-6 and IL-17. In contrast, it did not exert intestinal anti-inflammatory effects on DSS-induced colitis in BALB/c mice. CONCLUSIONS AND IMPLICATIONS: DS exerts intestinal anti-inflammatory activity in different rodent models of colitis through down-regulation of IL-17 expression.
