Abstract
The pathogenesis of celiac disease (CD) is complex and has not been fully elucidated. It has been postulated that oxidative stress, because of an increase in the concentration of reactive oxygen species and antioxidant capacity reduction, is one of the processes possibly involved in gliadin toxicity. Oxidative imbalance induced by gliadin peptides in enterocytes leads to the activation of the transcription of proinflammatory cytokines and enzymes, such as inducible nitric oxide synthase (iNOS), which in turn causes an increased production of nitric oxide (NO) metabolites favoring oxidative stress. Based on the our previous study, we hypothesized that persistent nitrosative stress despite gluten-free diet (GFD) may be responsible for persistent histopathologic changes and that GFD is only partially able to improve oxidative imbalance. Hence, serum NO levels seem to be useful as a marker of treatment efficacy, and alterations in these levels could indicate CD activity. It is possible that oral antioxidant supplementation may decrease the toxic effects of peptides. In the current study, we aimed to evaluate the effect of treatment with oral vitamin E on oxidative imbalance in adult patients with CD on GFD. For that purpose, we assessed the fasting plasma levels of nitrate as a marker of endogenous NO production and oxidative stress. Moreover, we monitored the individual components of antioxidant capacity. To the best of our knowledge, this is the first study evaluating the effects of oral vitamin E supplementation on oxidative imbalance in patients with CD.