ABSTRACT
Aluminum phosphide (ALP)-induced cardiotoxicity is a major cause of high mortality rates. As there is no specific antidote, restoring cardiac hemodynamics is the cornerstone for saving patients. Based on oxidative stress theory in acute ALP poisoning, we examined the cardioprotective role of coconut oil and Coenzyme Q10 (COQ10) in ALP poisoning, focusing on their antioxidant capacity. This study was a randomized, controlled, single-blind, phase II clinical trial conducted at Tanta Poison Control Center over 1 year. Eighty-four ALP poisoned patients received supportive treatment and were randomly allocated to three equal groups. Gastric lavage was performed using sodium bicarbonate 8.4% with saline in group I. Alternatively, group II received 50 ml coconut oil, and group III initially received 600 mg CoQ10 dissolved in 50 ml coconut oil; and repeated 12 hours later. In addition to patient characteristics, clinical, laboratory, electrocardiography (ECG), and total antioxidant capacity (TAC) data were recorded and repeated 12 hours later. Patient outcomes were evaluated. There was no significant difference among groups considering patient characteristics, initial cardiotoxicity severity, vital, laboratory data, ECG changes, and TAC. However, 12 hours post-admissions, group III was significantly improved in all clinical, laboratory, and ECG parameters than comparable groups. Significant correlations were observed between elevated TAC in groups II and III with hemodynamic, serum troponin, and ECG variables. Accordingly, the need for intubation, mechanical ventilation, and the total vasopressor dose was significantly decreased in group III compared with other groups. Therefore, coconut oil and COQ10 are promising cardioprotective adjuvant therapy ameliorating the ALP-induced cardiotoxicity.
ABSTRACT
Organophosphorus poisoning is a major global health problem with hundreds of thousands of deaths each year. Research interest in N-acetylcysteine has grown among increasing evidence of the role of oxidative stress in organophosphorus poisoning. We aimed to assess the safety and efficacy of N-acetylcysteine as an adjuvant treatment in patients with acute organophosphorus poisoning. This was a randomized, controlled, parallel-group trial on 30 patients suffering from acute organophosphorus poisoning, who were admitted to the Poison Control Center of Tanta University Emergency Hospital, Tanta, Egypt, between April and September 2014. Interventions included oral N-acetylcysteine (600 mg three times daily for 3 days) as an added treatment to the conventional measures versus only the conventional treatment. Outcome measures included mortality, total dose of atropine administered, duration of hospitalization and the need for ICU admission and/or mechanical ventilation. A total of 46 patients were screened and 30 were randomized. No significant difference was found between both groups regarding demographic characteristics and the nature or severity of baseline clinical manifestations. No major adverse effects to N-acetylcysteine therapy were reported. Malondialdehyde significantly decreased and reduced glutathione significantly increased only in the NAC-treated patients. The patients on NAC therapy required less atropine doses than those who received only the conventional treatment; however, the length of hospital stay showed no significant difference between both groups. The study concluded that the use of N-acetylcysteine as an added treatment was apparently safe, and it reduced atropine requirements in patients with acute organophosphorus pesticide poisoning.
