Background: Adults with chronic Trypanosoma cruzi exhibit a poorly functional T cell compartment, characterized by monofunctional (IFN-γ-only secreting) parasite-specific T cells and increased levels of terminally differentiated T cells. It is possible that persistent infection and/or sustained exposure to parasites antigens may lead to a progressive loss of function of the immune T cells.
Methodology/principal Findings: To test this hypothesis, the quality and magnitude of T.
Background: The main criterion for treatment effectiveness in Chagas Disease has been the seronegative conversion, achieved many years post-treatment. One of the main limitations in evaluating treatment for chronic Chagas disease is the lack of reliable tests to ensure parasite clearance and to examine the effects of treatment. However, declines in conventional serological titers and a new multiplex assay can be useful tools to monitor early the treatment impact.
View Article and Find Full Text PDFIntroduction And Objectives: The extent to which a patient's socioeconomic conditions determine the persistence or control of chronic Chagas disease has not been previously investigated. The aim of this study was to evaluate the effect of socioeconomic conditions on clinical and serologic measures of disease progression.
Methods: Data on the following socioeconomic variables were obtained by questioning as part of medical history taking at admission: birth in a rural area, time of residence in endemic and urban areas (in years), overcrowding index (i.
Background: As many as 20 million people are living with Trypanosoma cruzi infection in Latin American, yet few receive any treatment. The major limitation in developing and evaluating potential new drugs for their efficacy is the lack of reliable tests to assess parasite burden and elimination.
Methods: Adults volunteers with chronic T.
Chagas disease is caused by a parasite, Trypanosoma cruzi, transmitted primarily by a triatomine insect and affects approximately 8 million people in Latin American countries. The principal aim of the management of the disease is to avoid the development of cardiomyopathy and transmission by blood transfusion, congenital and organ transplants. Currently, benznidazole is the only etiological treatment commercially available for the disease until new and better drugs can be developed and tested.
View Article and Find Full Text PDFBackground: Previously, we identified a set of HLA-A020.1-restricted trans-sialidase peptides as targets of CD8+ T cell responses in HLA-A0201+ individuals chronically infected by T. cruzi.
View Article and Find Full Text PDFIntroduction And Objectives: The development of asymptomatic left ventricular dysfunction signifies a worsening of chronic chagasic cardiomyopathy. Our objective was to identify factors that predict the development of heart failure and all-cause mortality.
Methods: The study included 95 patients with an echocardiographic diagnosis of asymptomatic left ventricular dysfunction.
Background: Benznidazole is effective for treating acute-stage Chagas disease, but its effectiveness for treating indeterminate and chronic stages remains uncertain.
Objective: To compare long-term outcomes of patients with nonacute Chagas disease treated with benznidazole versus outcomes of those who did not receive treatment.
Design: Clinical trial with unblinded, nonrandom assignment of patients to intervention or control groups.
Introduction And Objectives: Previous prognostic studies of Chagas' disease have focused on mortality associated with end-stage cardiopathy (i.e., heart failure).
View Article and Find Full Text PDFMedicina (B Aires)
September 2004
A multicenter, randomized, triple blind and controlled trial was designed to determine whether the combination with thioctic acid (TA), an antioxidant agent, can reduce the intolerance rate to Benznidazol (BZ) in patients infected with Trypanosoma cruzi. Four regimens were assigned randomly for 3 age intervals, administrating placebo or TA orally at daily doses of 50 to 100 mg in association with BZ at a dose of 5 mg/k/day for 30 days. In some, medication was given during a run-in period.
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