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

Abstract

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.

Renal safety evaluation of aspirin plus edaravone in patients with ischaemic stroke: a retrospective cohort study

“…The mechanisms might involve scavenging free radicals, inhibiting lipid peroxidation, inhibiting inflammatory factors, protecting renal mitochondria, inhibiting cell apoptosis and reducing oxidative stress 13 14 24. Similarly, it has also been found in clinical studies that edaravone might play a protective role in the kidney by exerting antioxidant stress and inhibiting inflammatory levels in patients with paraquat poisoning 25 26. A study found a negative correlation between edaravone use and AKI in 5689 patients with acute ischaemic stroke,26 which was consistent with our results.…”

Mono‐ and bis‐edaravone adducts formed in the presence of vanillin in an aqueous solution

“…Specifically, the use of vanillin has been proposed to reduce kidney damage and cisplatin-induced nephrotoxicity [30]. Similarly, the use of EDA is also envisioned to prevent cisplatin-induced acute kidney injury [31] and as a reno-protective drug in diverse pathological situations [32][33][34]. Both EDA and vanillin can be useful protecting agents to reduce and prevent kidney diseases, but our work strongly suggests that the two compounds shall never be combined and used simultaneously, due to the high risk of adducts formation.…”

Hemodynamic and electromechanical effects of paraquat in rat heart

“…Atorvastatin, a lipid lowering drug, has been recently shown to attenuate PQ-induced cardiotoxicity in a rat model through similar mechanisms [ 42 ]. The results from a retrospective study demonstrated that edaravone, a free radical scavenger with an anti-inflammatory effect, protected the kidneys and liver but did not reduce pulmonary fibrosis and survival rate in patients with paraquat poisoning [ 43 ]. Currently, finding an effective strategy for the treatment of PQ-induced toxicity is attracting the attention of researchers.…”