RESUMO
Leprosy is a chronic infectious disease caused by Mycobacterium leprae The main clinical manifestations involve the skin and the peripheral nervous system. Several types of nephropathy have been described in leprosy. One frequent form of renal involvement is amyloidosis, especially in patients with lepromatous leprosy. In these patients, end-stage renal disease is an important contributor to morbidity and mortality. Here, we present the case of a patient with nephrotic syndrome caused by secondary amyloidosis, chronic peripheral neuropathy and a history of leprosy. The patient was correctly treated in her youth, which is the best way to avoid renal pathology, but she developed a nephrotic syndrome years later.
Assuntos
Amiloidose/complicações , Hanseníase Virchowiana/complicações , Mycobacterium leprae , Síndrome Nefrótica/microbiologia , Doenças do Sistema Nervoso Periférico/complicações , Amiloidose/microbiologia , Europa (Continente) , Feminino , Humanos , Hanseníase Virchowiana/microbiologia , Pessoa de Meia-Idade , Doenças do Sistema Nervoso Periférico/microbiologia , Fatores de TempoRESUMO
INTRODUCTION: Clinical trials (CT) on triple therapy against HCV infection in HIV-infected patients including TVR plus pegylated interferon and ribavirin (PR) have reported considerably higher response rates than with PR alone. This study was aimed to evaluate the efficacy and safety of triple therapy including TVR in HIV/HCV-coinfected patients in real-life conditions. MATERIALS AND METHODS: HIV/HCV genotype 1 patients seen at four Hospitals in Madrid who received therapy including TVR plus PR for at least two weeks were included. The response was evaluated during treatment, and sustained viral response (SVR) was evaluated 12 and 24 weeks after the end of the treatment. RESULTS: Fifty-eight patients have been included; 79% male, median age 48 y.o.; 38% were IL28B rs12979860 genotype CT or TT, 58.6% of patients presented cirrhosis and 24.1% presented fibrosis F3. Infection with genotype 1a was observed in 53.4% of patients. Median baseline HCV-RNA was 3,282,263 IU/mL (77.5% had >800,000 IU/mL). The most commonly used antiretroviral (ARV) drugs were tenofovir/emtricitabine [36 (62%) patients], etravirine [21 (36%) patients], abacavir/lamivudine [18 (31%) patients], boosted protease inhibitors [16 (27.5%) patients] and raltegravir [12 (20.6%) patients]. Of the 42 (72.4%) patients who had received previous HCV treatment, 13.7% were null responders, 25.8% were partial responders and 31% had relapsed. In an ITT approach, proportions of patients with undetectable HCV RNA were 67.8% (38/56) at TW4, 83.3% (40/48) at TW12, 80% (36/45) at TW24, 79.4% at TW36 (31/39) and 72% (26/36) at TW48. Fifteen (25.8%) patients discontinued HCV therapy [8 (13.8%) because they fulfilled stopping rules, 5 (8.6%) individuals due to adverse events and 2 (3.4%) were lost to follow-up]. Rash associated with TVR (grade 1) was observed in two cases (3.4%) and all the patients showed anaemia at some point of treatment. In an analysis by ITT in the 31 patients who had a 60 week follow-up after starting therapy, SVR-12 was observed in 21 (67.7%) patients. And in the analysis by ITT in 28 patients who had a 72 week follow-up after starting therapy, SVR-24 was observed in 17 (60.7%) patients. CONCLUSIONS: Response to triple therapy with TVR plus PR in HIV/HCV-patients under real-life conditions, and therefore, including a high proportion of difficult to treat patients, is similar to that found in CT. The safety profile of TVR-based therapy is also comparable to that shown in CT, with only a rate of discontinuation of 8.6% of individuals related to toxicity.
RESUMO
OBJECTIVES: The effects of antiretroviral drugs on the response to pegylated interferon plus ribavirin remain uncertain. We evaluated whether antiretroviral drugs affected the response to pegylated interferon plus ribavirin in patients co-infected with HIV and hepatitis C virus (HCV). METHODS: We conducted a retrospective analysis of two cohorts of HIV/HCV-co-infected patients treated with pegylated interferon plus ribavirin between 2001 and 2007 in Spain. The outcome measure was sustained virological response (SVR). Logistic regression models were used to test possible associations between non-response and pre-treatment characteristics, including accompanying antiretroviral drugs. RESULTS: The study sample comprised 1701 patients: 63% were infected with HCV genotype (G) 1 or 4 and 88% were taking highly active antiretroviral therapy (HAART). Factors independently associated with increased odds of SVR were G2 or 3, HVC RNA <500,000 IU/mL and CDC clinical category A or B. When we adjusted for these prognostic factors and dose of ribavirin/kg, the adjusted odds ratio (AOR) of SVR for patients without HAART was 1.31 [95% confidence interval (CI) 0.91-1.88; P = 0.144]. Taking the backbone of tenofovir and lamivudine/emtricitabine as a reference, we found that, with the exception of regimens including zidovudine, the effect of other nucleoside reverse transcriptase inhibitor backbones had little effect on SVR. The AOR of SVR for zidovudine and lamivudine was 0.65 (95% CI 0.46-0.93, P = 0.017). We carried out several sensitivity analyses, the results of which were consistent with the findings of the primary analysis. CONCLUSIONS: Our results suggest that, with the exception of regimens including zidovudine, accompanying antiretroviral drugs have little effect on the virological response to pegylated interferon plus ribavirin in HIV/HCV-co-infected patients.