苯并硝唑治疗巴西亚马逊地区急性恰加斯病患者胰岛素水平降低

IF 1.9
João Marcos Barbosa-Ferreira, Jessica Vanina Ortiz, Fernanda Gallinaro Pessoa, Maria das Graças Vale Barbosa, Jorge Augusto de Oliveira Guerra, Kátia do Nascimento Couceiro, Mônica Regina Hosannah Silva E Silva, Matheus Martins Monteiro, Keila Cardoso Barbosa Fonseca, Felix Alvarez Ramires, Barbara Maria Ianni, Charles Mady, Fábio Fernandes
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引用次数: 0

摘要

背景:在亚马逊地区,急性恰加斯病(ACD)的数量显著增加,导致心电图和超声心动图异常。恰加斯心肌病(CCM)的主要病理生理机制包括微血管功能障碍、自主神经系统(ANS)功能障碍、寄生虫的直接攻击和炎症活动。恰加斯病(Chagas disease, CD)是炎症性心肌病的一个很好的例子,它可能影响代谢参数和ANS的变化,关于ACD患者脂肪细胞因子和胰岛素水平测量的研究很少。目的:评价苯并硝唑治疗ACD前后脂联素、瘦素、胰岛素水平及其与ANS和心功能的相关性。方法:28例患者分为两组:对照组(CG) 15例,ACD组13例。所有受试者均进行了标准的12导联心电图、全面的经胸超声心动图检查,评估了自主神经功能和血清脂联素、胰岛素和瘦素水平。采用显著性水平为5% (p值< 0.05)。结果:ACD组治疗前后胰岛素水平均低于对照组,治疗后胰岛素水平低于治疗前胰岛素水平。各组间脂肪细胞因子、瘦素、脂联素水平无显著差异。结论:ACD组治疗前后胰岛素水平均低于对照组,治疗后胰岛素水平低于治疗前胰岛素水平。脂肪细胞因子和胰岛素水平与心功能和ANS参数无显著相关性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Decreased Insulin Levels in Patients with Acute Chagas Disease from Brazilian Amazon treated with Benznidazole.

Background: In the Amazon region, there has been a significant increase in the number of acute Chagas disease (ACD) leading to electrocardiographic and echocardiographic abnormalities. The main pathophysiological mechanisms involved in Chagas cardiomyopathy (CCM) are microvascular dysfunction, Autonomic Nervous System (ANS) dysfunction, direct parasite aggression, and inflammatory activity. Chagas disease (CD) is a perfect example of inflammatory cardiomyopathy that might influence changes in metabolic parameters and ANS. Studies on the measurement of adipocytokines and insulin levels in humans with ACD are scarce.

Objective: To evaluate adiponectin, leptin and insulin levels before and after the treatment of ACD with benznidazole and to correlate with ANS and cardiac function.

Methods: Twenty-eight subjects were divided into groups: control group (CG), with 15 subjects, and ACD group, with 13 subjects. All subjects underwent a standard 12-lead ECG, comprehensive transthoracic echocardiographic, evaluation of autonomic function and serum adiponectin, insulin and leptin levels. A level of significance of 5% (p-value < 0,05) was used.

Results: Insulin levels were lower in the ACD group both before and after the treatment when compared to the control group and lower in the post-treatment phase when compared to the pre-treatment phase. Adipocytokine, leptin and adiponectin levels showed no differences between groups.

Conclusion: Insulin levels were lower in the ACD group both before and after the treatment when compared to the control group and lower in the post-treatment phase when compared to the pre-treatment phase. There was no significant correlation between adipocytokine and insulin levels with cardiac function and the ANS parameters.

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