Week 4 response predicts sustained virological response to all-oral direct-acting antiviral-based therapy in cirrhotic patients with hepatitis C virus genotype 3 infection.

OBJECTIVE: The aim of this study was to determine the predictive capacity of response at treatment week (TW) 4 for the achievement of sustained virological response 12 weeks after the scheduled end of therapy date (SVR12) to treatment against hepatitis C virus (HCV) genotype 3 (GT3) infection with all-oral direct-acting antiviral (DAA) -based regimens. PATIENTS AND METHODS: From a prospective multicohort study, HCV GT3-infected patients who completed a course of currently recommended DAA-based therapy at 33 Spanish hospitals and who had reached the SVR12 evaluation time-point were selected. TW4 HCV-RNA levels were categorized as target-not-detected (TND), below the lower limit of quantification (LLOQTD) and ≥LLOQ. RESULTS: A total of 123 patients were included, 86 (70%) received sofosbuvir/ daclatasvir±ribavirin, 27 (22%) received sofosbuvir/ ledipasvir/ ribavirin and 10 (8.1%) received sofosbuvir/ ribavirin, respectively. In all, 114 (92.7%) of the 123 patients presented SVR12 in an on-treatment approach, but nine (7.3%) patients relapsed, all of them had presented cirrhosis at baseline. In those who achieved TND, LLOQTD and ≥LLOQ, SVR12 was observed in 81/83 (98%; 95% CI 91.5%-99.7%), 24/28 (85.7%; 95% CI 67.3%-96%) and 9/12 (75%; 95% CI 42.8%-94.5%), respectively; p(linear association) 0.001. Corresponding numbers for subjects with cirrhosis were: 52/54 (96.3%; 95% CI 87.3%-95.5%), 14/18 (77.8%; 95% CI 52.4%-93.6%) and 7/10 (70%; 95% CI 34.8%-93.3%); p 0.004. CONCLUSIONS: TW4-response indicates the probability of achieving SVR12 to currently used DAA-based therapy in HCV genotype 3-infected individuals with cirrhosis. This finding may be useful to tailor treatment strategy in this setting.

Regression of AIDS-related Kaposi's sarcoma following ritonavir therapy.

This paper describes a case report of an HIV-infected patient with mucocutaneous Kaposi's sarcoma (KS) with oral involvement, which presented complete clinical resolution of lesions on antiretroviral treatment with ritonavir, an HIV-1 protease inhibitor. Although it has still not been demonstrated that ritonavir has a specific antiviral action against HHV-8, a gamma herpesvirus probably involved in KS aetiopathogenesis, it has been proven that it reduces the HIV load significantly. This affects certain growth factors of KS, such as Tat protein and cytokines, and favours recovery of immune function, which correlates with protection against AIDS-defining conditions.

[Paronychia in patients infected with HIV treated with indinavir]. / Paroniquia en pacientes infectados por el VIH tratados con indinavir.

A retrospective study of cases of paronychia associated with anti-retroviral therapy diagnosed in two general hospitals is here reported. Lesions appeared from 3 and 48 months after institution of therapy. At diagnosis, 84.6% of patients were on indinavir therapy. CD4 values ranged from 120 and 1,332 cells/mm3 and viral load was lower than 200 copies/ml in 92.3 of cases. Conservative therapy was applied in 7 patients and surgery in 6. In all patients indinavir therapy was discontinued, and cure was achieved 16 weeks later. The "retinoid" effect of indinavir is discussed as likely pathogenic explanation for this complications. We advocate for topic therapy and change of anti-retroviral therapy, reserving surgery for patients not responding to therapy. Pain and functional limitation caused by this non uncommon complication (1.6% of our patients treated with anti-retroviral agents) makes its knowledge necessary and an active search by clinicians in patients receiving indinavir therapy.

Paroniquia en pacientes infectados por el VIH tratados con indinavir / Paronychia in HIV-positive patients treated with indinavir

Presentamos un estudio retrospectivo de los casos de paroniquia, asociados a terapia antirretrovírica, diagnosticados en dos hospitales generales. Las lesiones aparecieron entre 3 y 48 meses desde el inicio de la terapia. El 84,6 por ciento de los pacientes se encontraban en tratamiento con indinavir en el momento del diagnóstico. La cifra de CD4 varió entre 120 y 1.332 cél/mm3 y la carga vírica fue inferior a 200 cop/ml en el 92,3 por ciento de los casos. Se realizó terapia médica conservadora en 7 pacientes y en 6 cirugía; en todos los casos se suspendió la terapia con indinavir, con lo que tras 16 semanas se consiguió la curación.Se discute el probable efecto retinoide-like del indinavir como probable explicación patogénica de esta complicación. Se preconiza la realización de terapia tópica y la modificación del tratamiento antirretrovírico, reservando la terapia quirúrgica para los casos refractarios. El dolor y la limitación funcional que produce esta complicación, no infrecuente (1,6 por ciento de nuestros pacientes tratados con antirretrovíricos), hace necesario su conocimiento y búsqueda activa por parte de los clínicos en los pacientes que reciben tratamiento con indinavir (AU)