Abstract Background Oxidative stress has a significant role in the pathophysiology of snake envenomation. Despite that, antivenom, the mainstay treatment, does not protect against envenomation-induced oxidative stress. This therapeutic gap highlights the need for adjunctive therapy targeting oxidative stress. The current study aimed to determine the role of oxidative stress in the pathophysiology of viper snake envenomation and assess the role of N-acetylcysteine (NAC) as a co-adjuvant therapy in mitigating toxicity. A clinical pilot study was conducted on 30 Egyptian patients admitted to Alexandria Poison Centre within 24 h after bite by viperid snakes. The patients were categorized into two groups: Antivenom (ASV) group and Antivenom plus N-acetylcysteine (ASV + NAC) group. Oxidative stress biomarkers and severity grading were assessed on admission and after 24 h. Results After 24 h, there was a statistically significant improvement in the severity grading among the ASV + NAC group ( P = 0.031). The ASV + NAC group showed a significant decrease in Malondialdehyde (MDA) levels (50.0%, P = 0.011) compared to the ASV group. The ASV + NAC group had a statistically significant shorter hospital stay (Median = 3.60 days, P = 0.016) compared to the ASV group (Median = 6.52 days). Conclusion The findings of this pilot study support the role of oxidative stress in the pathophysiology of viper envenomation. NAC, when used as an adjunct to antivenom, may help mitigate oxidative stress and may contribute to improved clinical recovery. However, larger multicentre clinical studies are required to confirm these preliminary findings before modifications to current treatment protocols can be recommended.
Elgendy et al. (Fri,) studied this question.