诊断和治疗无明显病理的恰加斯病慢性期的新建议

L. Giménez, J. Mitelman
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摘要

心肌病发生的病理生理干预因素急性期和慢性期的心肌损伤是由于:a)直接寄生作用。b)免疫紊乱。c)神经损伤。2. 由宿主免疫反应引起的疾病。3.自动神经系统的改变4. 微血管病变伴微循环改变和随后的肌细胞溶解我们的研究小组提出了一系列临床结果,通过验证的研究和早期亚临床病变(自主神经、内皮解剖)的治疗建议,以预防恰加斯心肌病的发展。综合评分的目的是在未证实病理的慢性患者中发现可能导致心脏并发症发展的早期改变。风险分析使用工具和诊断测试的方法得到充分验证,并根据它们之间的关联,决定对最忠实的患者进行随访,并根据发现的损害使用不同的治疗方法。值得注意的是,其他研究可能用于检测亚临床病变,这些研究具有相同的推荐和该评分中使用的相同水平的证据。我们认为,在疾病发病机制的发展中,寄生虫在受感染生物体中的持续存在并不是唯一具有决定性作用的机制,因此,即使成功的病因学治疗也无法避免以疾病为特征的终末病变的发展(表1)
本文章由计算机程序翻译,如有差异,请以英文原文为准。
New proposals for diagnosis and treatment of the chronic period without demonstrable pathology of Chagas disease
Introduction Pathophysiology Intervening factors in the development of cardiomyopathy 1. Intrensic myocardial damage during the acute and chronic phase because of: a) Direct parasitic action. b) Immunological disturbances. c) Neurological damage. 2. Induced disorders due to the host immune response. 3. Alterations in the automatic nervous system. 4. Microvascular lesions with alterations in the microcirculation and subsequent myocytolysis.1 Our research group proposes a score of clinical outcomes, with validated studies and proposed treatment for subclinical lesions (autonomic, endothelial anatomical) early to prevent the development of Chagas cardiomyopathy. Integrated Score is to detect early alterations that would lead to the development of cardiac complications in chronic patients without proven pathology. Risk analysis With the approach of the disease using tools and diagnostic tests sufficiently validated and according to the association between them, it is determined to follow up the most committed patients and use different therapies according to the damage found. It is important to note that other studies may be used to detect subclinical lesions that have the same kind of recommendation and the same level of evidence used in this score. We believe that the persistence of the parasite in the infected organism would not be the only mechanism that would have a determinate role in the development of the pathogenesis of the illness and consequently even a successful etiological treatment would not be able to avoid the development of the terminal lesions characterized by the disease (Table 1).2,3
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