Estado protrombótico en estadios tempranos de la enfermedad de Chagas crónica

Herrera, Ramón N.; Díaz, Elba; Pérez, Rossana Cortiza; Chain, Sergio; Sant-Yacumo, Roque; Rodríguez, Eduardo; Bianchi, Jorge; Coviello, Alfredo; Miotti, Julio; Flores, Isolina; Serna, Fernando de la; Muntaner, Juan; Berman, Steve; Luciardi, Héctor

doi:10.1016/s0300-8932(03)76881-x

Cited by 20 publications

(9 citation statements)

References 11 publications

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“…The presence of procoagulation/prothrombotic phase in early stages of CD has been evidenced by elevated plasma levels of prothrombin fragment F1+2, D-dimer (fibrin degradation product), and the antithrombin enzyme complex in seropositive patients. 58,61 However, Melo et al did not find higher prothrombotic states among heart-failure patients with CD compared to that noted in non-CD patients. 62 Echeverria et al 63 performed a metaanalysis of studies evaluating the pathophysiological aspects of hypercoagulation in CD patients in Argentina, Brazil, and Spain during 1996-2016.…”

Section: Role Of Hypercoagulation In Induction Of Thrombosis In Early...mentioning

confidence: 93%

“…Further, euglobulin lysis time (measures fibrinolysis) in patients with chronic CD differed significantly from the values obtained in the control group, suggesting an occurrence of active thrombosis with decreased fibrinolysis. 56,58 Subsequently, strokes were found to occur at a higher rate in chronic CD patients when compared to patients with heart disease of other etiologies. 46 A history of stroke/transient ischemic attack, atrial fibrillation, and CD-positive serology were strongly associated with the occurrence of ischemic stroke in CD.…”

Section: Thromboembolism and Stroke In CDmentioning

confidence: 99%

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Platelets, Macrophages, and Thromboinflammation in Chagas Disease

Choudhuri¹,

Garg²

2022

JIR

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Chagas disease (CD) is a major health problem in the Americas and an emerging health problem in Europe and other nonendemic countries. Several studies have documented persistence of the protozoan parasite Trypanosoma cruzi , and oxidative and inflammatory stress are major pathogenic factor. Mural and cardiac thrombi, cardiac arrhythmias, and cardiomyopathy are major clinical features of CD. During T. cruzi infection, parasite-released factors induce endothelial dysfunction along with platelet (PLT) and immune-cell activation. PLTs have a fundamental role in maintaining hemostasis and preventing bleeding after vascular injury. Excessive activation of PLTs and coagulation cascade can result in thrombosis and thromboembolic events, which are recognized to occur in seropositive individuals in early stages of CD when clinically symptomatic heart disease is not apparent. Several host and parasite factors have been identified to signal hypercoagulability and increase the risk of ischemic stroke in early phases of CD. Further, PLT interaction with immune cells and their role in host defense against pathogens and inflammatory processes have only recently been recognized and evolving. In the context of parasitic diseases, PLTs function in directly responding to T. cruzi infection, and PLT interactions with immune cells in shaping the proinflammatory or immunoregulatory function of monocytes, macrophages, and neutrophils remains elusive. How T. cruzi infection alters systemic microenvironment conditions to influence PLT and immune-cell interactions is not understood. In this review, we discuss the current literature, and extrapolate the mechanistic situations to explain how PLT and innate immune cell (especially monocytes and macrophages) interactions might be sustaining hypercoagulability and thromboinflammation in chronic CD.

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Section: Role Of Hypercoagulation In Induction Of Thrombosis In Early...mentioning

confidence: 93%

Section: Thromboembolism and Stroke In CDmentioning

confidence: 99%

Platelets, Macrophages, and Thromboinflammation in Chagas Disease

Choudhuri¹,

Garg²

2022

JIR

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“…A hypercoagulable state is defined as the presence, in certain individuals, of thrombotic potentialities that activate the endothelium and the formative elements of the blood (mainly, platelets) that favors plasma kinetics that lead to the formation of thrombin, which disturbs fibrinolytic activity and produces hemorheological changes with turbulence phenomena that predispose to thrombogenesis. [ 18 ]…”

Section: Methodsmentioning

confidence: 99%

“…Besides, although whether or not chronic Chagas disease is an independent vascular risk factor remains to be confirmed. [ 17 , 18 ]…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2016

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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.

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“… 19 Silent brain infarcts have also been described by another author. 10 It is speculated that inflammation 18 and thrombogenic factors 20 play a role in this mechanism, but these need to be further clarified.…”

Section: Introductionmentioning

confidence: 99%

Clinical assessment, neuroimaging and immunomarkers in Chagas disease study (CLINICS): rationale, study design and preliminary findings

Oliveira‐Filho

Dias

Jesus

et al. 2012

Dement. neuropsychol.

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Chagas disease (CD) is an important cause of cardiomyopathy and stroke in Brazil. Brain infarcts and atrophy seem to occur independently of cardiomyopathy severity and cognitive impairment is understudied.ObjectiveCompare the prevalence of brain magnetic resonance imaging abnormalities between patients with or without CD; determine if inflammatory biomarkers are increased in CD; and determine the efficacy of aspirin in reducing the rate of microembolization in these patients.Methods500 consecutive patients with heart failure will undergo a structured cognitive evaluation, biomarker collection and search for microembolic signals on transcranial Doppler. The first 90 patients are described, evaluated with cognitive tests and brain magnetic resonance imaging to measure N-acetyl aspartate (NAA), choline (Cho), myo-inositol (MI) and creatine (Cr).ResultsMean age was 55±11 years, 51% female, 38 (42%) with CD. Mean NAA/Cr ratio was lower in patients with CD as compared to other cardiomyopathies. Long-term memory and clock-drawing test were also significantly worse in CD patients. In the multivariable analysis correcting for ejection fraction, age, sex and educational level, reduced NAA/Cr (p=0.006) and cognitive dysfunction (long-term memory, p=0.023; clock-drawing test, p=0.015) remained associated with CD.ConclusionIn this preliminary sample, CD was associated with cognitive impairment and decreased NAA/Cr independently of cardiac function or educational level.

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Estado protrombótico en estadios tempranos de la enfermedad de Chagas crónica

Cited by 20 publications

References 11 publications

Platelets, Macrophages, and Thromboinflammation in Chagas Disease

Platelets, Macrophages, and Thromboinflammation in Chagas Disease

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

Clinical assessment, neuroimaging and immunomarkers in Chagas disease study (CLINICS): rationale, study design and preliminary findings

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