Comments on ‘oxidative stress increases in carbon monoxide poisoning’

Abstract

We read with great interest the article by Kavakli et al. in which the total oxidant and the antioxidant status were investigated in patients with carbon monoxide (CO) poisoning. Although lipid peroxidation has been linked to CO-induced neuropathology for more than two decades, serum levels of oxidative stress markers have not been investigated before. In this study, they measured, in patients with CO poisoning (n 1⁄4 88) and control subjects (n 1⁄4 37), serum levels of total oxidant and antioxidant status and calculated oxidative stress index (1⁄4 total oxidant status/total antioxidant status). They found that total oxidant status and oxidative stress index, but not total antioxidant status significantly increased in patients with CO poisoning when compared with controls. Additionally, they found that carboxyhemoglobin (COHb), total oxidant status and oxidative stress index were significantly reduced after 6 h of treatment. We applaud their efforts to gain insight into the pathophysiology of CO poisoning, which is a frequent cause of morbidity and mortality in Turkey. In the discussion, they conclude that ‘ . . . oxidative stress index may be a useful guide in planning treatment of CO poisoned patients’ and ‘ . . . in decision of hyperbaric oxygen therapy application, oxidative stress index levels should be taken into consideration’. We think that the data presented in this article is not sufficient to support their conclusion that oxidative stress index is a marker of severity and can be used in the selection of patients for hyperbaric oxygen therapy. Oxygen is first-line therapy in CO poisoning. Severely poisoned patients are referred to hyperbaric oxygen therapy. In order to argue that oxidative stress index can discriminate severely poisoned patients, they should have compared oxidative stress index levels in mild, moderate and severely poisoned patients. They could also analyze whether there is a correlation between COHb and oxidative stress markers. If the data is available, the authors could also analyze the correlation between oxidative stress markers and the number of clinical manifestations. Interestingly, in a recent study Garrabou et al. measured serum levels of lipid peroxidation (oxidative stress) in patients with CO poisoning and analyzed its correlation with clinical findings. Although, serum levels of lipid peroxidation were similar in patients with moderate and severe CO poisoning, pretreatment lipid peroxidation level was strongly correlated with the total number of symptoms along the 3 months follow-up. In addition, pretreatment lipid peroxidation was significantly higher in patients who developed late neurological sequel (LNS) compared with those without LNS. Since COHb poorly correlates with severity of CO poisoning, new serum markers are needed to evaluate severity and outcome of patients with CO poisoning. Further studies are needed to elucidate the value of oxidative stress markers in the management of CO poisoning.