RESUMO
BACKGROUND: Central venous stenosis and occlusion (CVO) is an increasing problem in the growing hemodialysis population. Sequelae include loss of access, loss of sites suitable for future venous access, and venous hypertension. Endoluminal techniques are often unsuitable to treat long-standing stenoses, and open surgery confers higher morbidity and is not appropriate in many patients. CASE: We present a case of long-standing central venous stenosis with an ipsilateral functioning fistula but with significant symptoms and signs of venous hypertension. The stenosis was not considered appropriate for endoluminal treatment, and the patient was considered to be at too high risk for open surgery. The Hemodialysis Reliable Outflow (HeRO) (Merit Medical Systems, UT) device was used to bypass the fistula to the superior vena cava via the contralateral internal jugular vein. CONCLUSIONS: This case demonstrates the utility of the HeRO device in cases of long-standing CVO necessitating contralateral bypass. This technique confers the benefits of open surgery while minimizing the associated risks.
Assuntos
Derivação Arteriovenosa Cirúrgica , Implante de Prótese Vascular/instrumentação , Prótese Vascular , Pressão Venosa Central , Falência Renal Crônica/terapia , Diálise Renal , Extremidade Superior/irrigação sanguínea , Doenças Vasculares/cirurgia , Grau de Desobstrução Vascular , Cateterismo Venoso Central , Feminino , Humanos , Falência Renal Crônica/diagnóstico , Pessoa de Meia-Idade , Desenho de Prótese , Diálise Renal/efeitos adversos , Resultado do Tratamento , Doenças Vasculares/diagnóstico por imagem , Doenças Vasculares/etiologia , Doenças Vasculares/fisiopatologiaRESUMO
BACKGROUND: Raltegravir is a potential treatment option for virologically suppressed HIV-1 infected patients on enfuvirtide with injection site reactions. OBJECTIVES: To characterize safety and efficacy of an enfuvirtide to raltegravir switch including changes in T-cells, quality of life, and residual viremia. STUDY DESIGN: In patients with viral load <50 copies/mL and injection site reactions, enfuvirtide was switched to raltegravir without additional changes to the antiretroviral regimen. Virologic failure was defined as a viral load >1000 copies/mL or two consecutive viral load measurements between 50 and 1000 copies/mL (low-level viremia). Over the 24 week study, we compared changes in T-cells, injection site reactions, quality of life, and residual viremia, as measured through the single-copy assay which can detect plasma virus down to a single copy, using paired t-tests. RESULTS: Fourteen patients with a median CD4+ T-cell count of 420 cells/microL were enrolled. After the switch, two patients experienced virologic failure due to confirmed low-level viremia. However, both patients subsequently were re-suppressed, one without any changes to his regimen. There was no change in CD4+ T-cell count. Injection site reactions resolved. However, there was little reported change in quality of life. The baseline median level of residual viremia was 6 copies/mL and did not change after the switch to raltegravir. CONCLUSIONS: A switch to raltegravir in virologically suppressed patients on enfuvirtide is effective in maintaining immunologic and virologic control at 24 weeks but did not result in a change in residual viremia.
Assuntos
Proteína gp41 do Envelope de HIV/uso terapêutico , Inibidores da Fusão de HIV/uso terapêutico , Infecções por HIV/tratamento farmacológico , Fragmentos de Peptídeos/uso terapêutico , Pirrolidinonas/uso terapêutico , Viremia/tratamento farmacológico , Contagem de Linfócito CD4 , Enfuvirtida , HIV-1/efeitos dos fármacos , Humanos , Masculino , Pessoa de Meia-Idade , Estudos Prospectivos , Qualidade de Vida , Raltegravir Potássico , Resultado do Tratamento , Carga ViralRESUMO
When fully suppressive regimens are not available, incompletely suppressive regimens also provide immunologic benefits. In this study, with stable background therapy, human immunodeficiency virus (HIV)-infected patients who were randomized to receive atazanavir or boosted atazanavir, compared with those who continued boosted protease inhibitor therapy, maintained similar virologic and immunologic control, resistance-mutation patterns, and replication capacities with reduced use of lipid-lowering medication.
Assuntos
Fármacos Anti-HIV/uso terapêutico , Infecções por HIV/tratamento farmacológico , Infecções por HIV/imunologia , Inibidores da Protease de HIV/uso terapêutico , HIV/efeitos dos fármacos , Viremia , Adulto , Sulfato de Atazanavir , Contagem de Linfócito CD4 , Linfócitos T CD4-Positivos/imunologia , Farmacorresistência Viral , Feminino , Infecções por HIV/virologia , HIV-1/fisiologia , Humanos , Masculino , Pessoa de Meia-Idade , Oligopeptídeos/uso terapêutico , Piridinas/uso terapêutico , Replicação ViralRESUMO
BACKGROUND: We sought to determine the safety of treatment interruption (TI) and to identify parameters that would define patients with human immunodeficiency virus (HIV) for whom TI is safer. METHODS: AIDS Clinical Trials Group 5170 was a multicenter, 96-week-long, prospective study of HIV-infected patients receiving antiretroviral therapy (ART) who had CD4(+) cell counts >350 cells/mm(3) and who underwent TI. RESULTS: A total of 167 patients were enrolled. The median nadir in CD4(+) cell count was 436 cells/mm(3). The initial decrease (i.e., during the first 8 weeks) in CD4(+) cell count after ART interruption was 20 cells/mm(3)/week; the subsequent decrease was 2.0 cells/mm(3)/week until week 96. Both the CD4(+) cell count before enrollment and the increase in CD4(+) cell count during ART predicted early decrease; later decrease was predicted by the level of interleukin-7 at enrollment. A Centers for Disease Control and Prevention (CDC) diagnosis of a category B or C event was made for 2 and 2 patients, respectively (all had CD4(+) cell counts >350 cells/mm(3)). At week 96, 17 patients had CD4(+) cell counts < or =250 cells/mm(3), and 46 patients had resumed ART; 5 patients died (unrelated to HIV or acquired immunodeficiency syndrome). In a multivariate analysis, a higher nadir in CD4(+) cell count (>400 cells/mm(3)), a lower HIV load (<50 copies/mL) at the time of TI, and an HIV load < or =22,000 copies/mL before ART predicted a longer time to the primary end point (CDC category B or C event, death, CD4(+) cell count < or =250 cells/mm(3), or resumption of ART). CONCLUSION: Disease progression after TI was low in this cohort. A higher nadir in CD4(+) cell count, a lower HIV load before ART, and an HIV load < or =50 copies/mL at the time of TI predicted a longer time to the primary end point.