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Retrospective study of clinical features and prognosis of edaravone in the treatment of paraquat poisoning

机译:依达拉奉治疗百草枯中毒的临床特征及预后的回顾性研究

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摘要

To observe whether edaravone can protect organs and inhibit pulmonary fibrosis in patients with paraquat poisoning and to provide a method for clinical intervention for paraquat poisoning . Forty-four cases of paraquat poisoning were collected from March 2011 to December 2017 in our hospital. Eighteen cases from March 2011 to November 2013 did not receive edaravone treatment and were considered the control group, and 26 cases from January 2014 to December 2017 were treated with edaravone and were considered the observation group. Injuries to the central nervous system, heart, liver, kidney, and digestive system were evaluated on at 24 hours, 3 days, and 7 days after hospitalization. The expression of serum inflammatory factors (interleukin [IL]-6, IL-10, tumor necrosis factor-α [TNF-α]) and oxidative stress correlation (superoxide dismutase [SOD] and malondialdehyde [MDA]) were assayed at 24 hours, 3 days, and 7 days after being hospitalized. After 7, 14, and 30 days, the changes in pathological lung characteristics in the 2 groups were assessed, and survival rates were calculated. Edaravone significantly increased the serum levels of SOD and obviously markedly reduce the serum levels of IL-6, IL-10, TNF-α, and MDA in patients poisoned with paraquat ( P .05). Edaravone significantly protected the liver ( P = .021), cardiovascular ( P = .031), and renal ( P = .028) organs of patients from paraquat poisoning -induced injury after 7 days but had no significant protection or improvement on respiratory and digestive tract damage. Edaravone delayed the occurrence of pulmonary fibrosis and increase the survival time of patients at 7 and 14 days ( P .05). However, the 1-month follow-up found that edaravone did not reduce pulmonary fibrosis (77.8% vs 73.1%, P = .615) and did not increase the survival rate of the patients (61.1% vs 65.3%, P = .853). Edaravone is beneficial for protecting the kidneys and liver from paraquat poisoning through reducing oxidative stress and inhibiting inflammatory response. It can also inhibit the pulmonary fibrosis process and prolong the survival time of the patients. However, no significant improvements were seen in the probability of pulmonary fibrosis and the survival rate.
机译:观察依达拉奉是否可以保护百草枯中毒患者的器官,抑制肺纤维化,为百草枯中毒提供临床干预方法。 2011年3月至2017年12月在我院收治的百草枯中毒病例44例。 2011年3月至2013年11月有18例未接受依达拉奉治疗,被认为是对照组,而2014年1月至2017年12月的26例接受了依达拉奉治疗并被认为是观察组。在住院后24小时,3天和7天评估中枢神经系统,心脏,肝脏,肾脏和消化系统的损伤。 24小时检测血清炎症因子(白介素[IL] -6,IL-10,肿瘤坏死因子-α[TNF-α])的表达和氧化应激相关性(超氧化物歧化酶[SOD]和丙二醛[MDA])的表达。 ,住院后3天和7天。在第7、14和30天后,评估两组病理肺部特征的变化,并计算存活率。百草枯中毒患者中,依达拉奉显着提高了SOD的血清水平,并显着降低了IL-6,IL-10,TNF-α和MDA的血清水平(P <.05)。 7天后,依达拉奉显着保护了百草枯中毒引起的患者的肝脏(P = .021),心血管(P = .031)和肾脏(P = .028)器官,但对呼吸和呼吸系统的保护作用并没有明显的改善。消化道损害。依达拉奉延缓了肺纤维化的发生,并延长了患者在7天和14天的生存时间(P <.05)。然而,在1个月的随访中发现依达拉奉不能减轻肺纤维化(77.8%vs 73.1%,P = .615),也没有增加患者的生存率(61.1%vs 65.3%,P = .853)。 )。依达拉奉可通过减少氧化应激和抑制炎症反应来保护肾脏和肝脏免受百草枯中毒。它还可以抑制肺纤维化过程并延长患者的生存时间。但是,肺纤维化的可能性和存活率均未见明显改善。

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