Demographic and clinical manifestations of patients with <i>T. cruzi</i> infection and neoplastic disease.

a<p>Severe chronic cardiac disease according to Kuschnir classification.</p><p>ND, no data; NA, not accomplished; NR, no reactivations; VC, contact with the vector; VT, mother with <i>T. cruzi</i> infection; IND, indeterminate stage of Chagas disease; CCC, chronic cardiac disease stage; R-MEGACHOP, Rituximab-MEGACHOP; R-ESHAP, Rituximab-ESHAP; IDICE-G, idarubicin, ARA-C, etoposide; MTX, intrathecal methotrexate; Mitox, mitoxantrone; VBCMP or M2, vincristine, carmustine, melphalan, cyclophosphamide, prednisone; LN: lymph node.</p

Patients with Chagas disease and HIV infection: demographic and clinical manifestations related to Chagas disease

a<p>Mild chronic cardiac disease according to Kuschnir classification <a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0001965#pntd.0001965-Kuschnir1" target="_blank">[67]</a>.</p>b<p>Relevant comorbidities: asymptomatic strongyloidosis diagnosed in 2006 treated with albendazole and ivermectin; type 2 diabetes mellitus and high blood pressure, well controlled by oral antidiabetic and antihypertensive drugs; macrocytic anemia due to folic acid deficiency.</p><p>VC, contact with vector; VT, mother with <i>T. cruzi</i> infection; TF, transfusion in endemic area; BZD, benznidazole; CCC, chronic cardiac disease stage; ND, no data; NA, not accomplished.</p

Patients with systemic autoimmune diseases: demographic and clinical manifestations related to autoimmune disease

<p>AM, acid mycophenolic; AZA, azathioprine; CYC, cyclophosphamide; HDX, hydroxychloroquine; MP, methylprednisolone; PDN, prednisone; RA, rheumatoid arthritis; SLE, systemic lupus erythematosus.</p

Patients with systemic autoimmune diseases: demographic and clinical manifestations related to Chagas disease

a<p>Mild chronic cardiac disease according to Kuschnir classification <a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0001965#pntd.0001965-Kuschnir1" target="_blank">[67]</a>.</p>b<p>PCR was negative in nine determinations between 03/18/2008 and 07/02/2010, after treatment with posaconazole.</p><p>VC, contact with the vector; TF, transfusion in endemic area; BZD, Benznidazole; CCC, chronic cardiac disease stage; ND, no data.</p

Patients with Chagas disease and HIV infection: demographic and clinical manifestations related to HIV infection

<p>ND, no data; EFV, efavirenz; EMC, emtricitabine; TDF, tenofovir; ABV, abacavir; 3TC, lamivudine.</p

Altered Hypercoagulability Factors in Patients with Chronic Chagas Disease: Potential Biomarkers of Therapeutic. Response

Thromboembolic events were described in patients with Chagas disease without cardiomyopathy. We aim to confirm if there is a hypercoagulable state in these patients and to determine if there is an early normalization of hemostasis factors after antiparasitic treatment. Ninety-nine individuals from Chagas disease-endemic areas were classified in two groups: G1, with T.cruzi infection (n = 56); G2, healthy individuals (n = 43). Twenty-four hemostasis factors were measured at baseline. G1 patients treated with benznidazole were followed for 36 months, recording clinical parameters and performance of conventional serology, chemiluminescent enzyme-linked immunosorbent assay (trypomastigote-derived glycosylphosphatidylinositol-anchored mucins), quantitative polymerase chain reaction, and hemostasis tests every 6-month visits. Prothrombin fragment 1+2 (F1+2) and endogenous thrombin potential (ETP) were abnormally expressed in 77% and 50% of infected patients at baseline but returned to and remained at normal levels shortly after treatment in 76% and 96% of cases, respectively. Plasmin-antiplasmin complexes (PAP) were altered before treatment in 32% of G1 patients but normalized in 94% of cases several months after treatment. None of the patients with normal F1+2 values during follow-up had a positive qRT-PCR result, but 3/24 patients (13%) with normal ETP values did. In a percentage of chronic T. cruzi infected patients treated with benznidazole, altered coagulation markers returned into normal levels. F1+2, ETP and PAP could be useful markers for assessing sustained response to benznidazole

Altered Hypercoagulability Factors in Patients with Chronic Chagas Disease: Potential Biomarkers of Therapeutic. Response

Thromboembolic events were described in patients with Chagas disease without cardiomyopathy. We aim to confirm if there is a hypercoagulable state in these patients and to determine if there is an early normalization of hemostasis factors after antiparasitic treatment. Ninety-nine individuals from Chagas disease-endemic areas were classified in two groups: G1, with T.cruzi infection (n = 56); G2, healthy individuals (n = 43). Twenty-four hemostasis factors were measured at baseline. G1 patients treated with benznidazole were followed for 36 months, recording clinical parameters and performance of conventional serology, chemiluminescent enzyme-linked immunosorbent assay (trypomastigote-derived glycosylphosphatidylinositol-anchored mucins), quantitative polymerase chain reaction, and hemostasis tests every 6-month visits. Prothrombin fragment 1+2 (F1+2) and endogenous thrombin potential (ETP) were abnormally expressed in 77% and 50% of infected patients at baseline but returned to and remained at normal levels shortly after treatment in 76% and 96% of cases, respectively. Plasmin-antiplasmin complexes (PAP) were altered before treatment in 32% of G1 patients but normalized in 94% of cases several months after treatment. None of the patients with normal F1+2 values during follow-up had a positive qRT-PCR result, but 3/24 patients (13%) with normal ETP values did. In a percentage of chronic T. cruzi infected patients treated with benznidazole, altered coagulation markers returned into normal levels. F1+2, ETP and PAP could be useful markers for assessing sustained response to benznidazole

Identification of Trypanosoma cruzi Discrete Typing Units (DTUs) in Latin-American migrants in Barcelona (Spain)

Trypanosoma cruzi, the causative agent of Chagas disease, is divided into six Discrete Typing Units (DTUs): TcI–TcVI. We aimed to identify T. cruzi DTUs in Latin-American migrants in the Barcelona area (Spain) and to assess different molecular typing approaches for the characterization of T. cruzi genotypes. Seventy-five peripheral blood samples were analyzed by two real-time PCR methods (qPCR) based on satellite DNA (SatDNA) and kinetoplastid DNA (kDNA). The 20 samples testing positive in both methods, all belonging to Bolivian individuals, were submitted to DTU characterization using two PCR-based flowcharts: multiplex qPCR using TaqMan probes (MTq-PCR), and conventional PCR. These samples were also studied by sequencing the SatDNA and classified as type I (TcI/III), type II (TcII/IV) and type I/II hybrid (TcV/VI). Ten out of the 20 samples gave positive results in the flowcharts: TcV (5 samples), TcII/V/VI (3) and mixed infections by TcV plus TcII (1) and TcV plus TcII/VI (1). By SatDNA sequencing, we classified the 20 samples, 19 as type I/II and one as type I. The most frequent DTU identified by both flowcharts, and suggested by SatDNA sequencing in the remaining samples with low parasitic loads, TcV, is common in Bolivia and predominant in peripheral blood. The mixed infection by TcV–TcII was detected for the first time simultaneously in Bolivian migrants. PCR-based flowcharts are very useful to characterize DTUs during acute infection. SatDNA sequence analysis cannot discriminate T. cruzi populations at the level of a single DTU but it enabled us to increase the number of characterized cases in chronically infected patients.Fil: Abras, Alba. Universidad de Barcelona; España. Universidad de Girona; España. Barcelona Centre for International Health Research; EspañaFil: Gállego, Montserrat. Universidad de Barcelona; España. Barcelona Centre for International Health Research; EspañaFil: Muñoz, Cármen. Hospital de la Santa Creu i Sant Pau; España. Universitat Autònoma de Barcelona; EspañaFil: Juiz, Natalia Anahí. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; ArgentinaFil: Ramirez Gomez, Juan Carlos. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; ArgentinaFil: Cura, Carolina Inés. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular “Dr. Héctor N. Torres” ; ArgentinaFil: Tebar, Silvia. Universidad de Barcelona; España. Barcelona Centre for International Health Research; EspañaFil: Fernández Arévalo, Ana. Universidad de Barcelona; España. Barcelona Centre for International Health Research; España. Hospital de la Santa Creu i Sant Pau; EspañaFil: Pinazo, María Jesús. Barcelona Centre for International Health Research; EspañaFil: de la Torre, Leonardo. Barcelona Centre for International Health Research; EspañaFil: Posada, Elizabeth. Barcelona Centre for International Health Research; EspañaFil: Navarro, Ferran. Universitat Autònoma de Barcelona; España. Hospital de la Santa Creu i Sant Pau; EspañaFil: Espinal, Paula. Hospital de la Santa Creu i Sant Pau; EspañaFil: Ballart, Cristina. Universidad de Barcelona; España. Barcelona Centre for International Health Research; EspañaFil: Portús, Montserrat. Universidad de Barcelona; EspañaFil: Gascón, Joaquim. Barcelona Centre for International Health Research; EspañaFil: Schijman, Alejandro Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentin