Estudo longitudinal do eletrocardiograma na doença de Chagas desde a fase aguda

Rc, Pedrosa; Cançado,; Decache, W

doi:10.1590/s0037-86821993000300006

Cited by 7 publications

(8 citation statements)

References 16 publications

(2 reference statements)

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“…After infection, the individual goes through an acute phase, in which nonspecific symptoms are usually presented [2]. The disease progresses for 20 years or more, wherein the symptoms become chronic and more severe, and, when left untreated, leads to death of the individual [3, 4].…”

Section: Introductionmentioning

confidence: 99%

Cardiac Chagas Disease: MMPs, TIMPs, Galectins, and TGF-βas Tissue Remodelling Players

et al. 2019

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A century after the discovery of Chagas disease, studies are still needed to establish the complex pathophysiology of this disease. However, it is known that several proteins and molecules are related to the establishment of this disease, its evolution, and the appearance of its different clinical forms. Metalloproteinases and their tissue inhibitors, galectins, and TGF-β are involved in the process of infection and consequently the development of myocarditis, tissue remodeling, and fibrosis upon infection with Trypanosoma cruzi. Thus, considering that the heart is one of the main target organs in Chagas disease, knowledge regarding the mechanisms of action of these molecules is essential to understand how they interact and trigger local and systemic reactions and, consequently, determine whether they contribute to the development of Chagas' heart disease. In this sense, it is believed that the inflammatory microenvironment caused by the infection alters the expression of these proteins favoring progression of the host-parasite cycle and thereby stimulating cardiac tissue remodeling mechanisms and fibrosis. The aim of this review was to gather information on metalloproteinases and their tissue inhibitors, galectins, and TGF-β and discuss how these molecules and their different interrelationships contribute to the development of Chagas' heart disease.

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Section: Introductionmentioning

confidence: 99%

Cardiac Chagas Disease: MMPs, TIMPs, Galectins, and TGF-βas Tissue Remodelling Players

et al. 2019

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“…The current available drugs are effective in the acute phase of the disease and act against amastigotes of some strains of T. cruzi in late acute, indeterminate, and chronic phases of Chagas disease. But they do not exhibit activity against the Y strain of T. cruzi during the later phases . So, the purpose of this work was to evaluate the effect of NFOH in several tissues (heart, colon, liver, kidney, spleen, brain and skeletal muscle) during the indeterminate form of the disease, induced by the Y strain of T. cruzi in BALB/c male mice.…”

Section: Introductionmentioning

confidence: 99%

“…But they do not exhibit activity against the Y strain of T. cruzi during the later phases. [25][26][27][28][29][30][31][32][33][34][35] So, the purpose of this work was to evaluate the effect of NFOH in several tissues (heart, colon, liver, kidney, spleen, brain and skeletal muscle) during the indeterminate form of the disease, induced by the Y strain of T. cruzi in BALB/c male mice.…”

Section: Introductionmentioning

confidence: 99%

Hydroxymethylnitrofurazone treatment in indeterminate form of chronic Chagas disease: Reduced intensity of tissue parasitism and inflammation—A histopathological study

Scarim

Andrade

Rosa

et al. 2018

Int J Experimental Path

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Summary Hydroxymethylnitrofurazone (NFOH) is a nitrofurazone prodrug effective in vivo during acute infections, and it has less hepatotoxicity effect than the standard drug benznidazole (BZN) which has been used during short‐ and long‐term treatment. In the present study, we induced the indeterminate form of Chagas disease in mice with a Y strain of Trypanosoma cruzi and analysed the histopathological data about the effects of NFOH and BZN on different tissues, including the heart, skeletal muscle, liver, kidney, colon, spleen and brain. After infection, BALB/c mice were treated with NFOH (150 mg/kg) and BZN (60 mg/kg) for 60 days and then submitted to immunosuppression using dexamethasone (5 mg/kg) for 14 days. Two trained analysts, as part of a blind evaluation, examined the results using serial sections of 3 mm diameter in two different moments. The results showed reactivation of the disease only in the infected nontreated group (POS). After treatment, amastigote nests were found in the heart, colon, liver and skeletal muscle in the POS group and in the heart and liver of the BZN group. Interestingly, amastigote nests were not found in the NFOH and NEG groups. The histopathological analysis showed fewer tissue lesions and parasite infiltrates in the NFOH group when compared with the BZN and POS groups. We have not observed any increase in the levels of hepatocellular injury biomarkers (AST/ALT) in the NFOH group. These in vivo studies show the potential for NFOH as an effective and safe compound useful as an anti‐T. cruzi agent.

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“…The acute phase is characterized by an active infection, inflammation and myocardial damage [2,3]. Myocarditis is characterized by tachycardia, prolongation of the PR interval, low-voltage QRS complexes, nonspecific T wave changes, cardiomegaly and heart failure [4,5]. This phase also features the presence of parasites in the circulating blood and several other tissues, including myocardium, and usually results in the appearance of antibodies [6].…”

Section: Introductionmentioning

confidence: 99%