BACKGROUND: Recent studies presented evidence that activation of oxygen derived free radicals occurs in patients with acute pancreatitis. The purpose of this study was to evaluate the effect of sodium selenite as a possible antioxidant therapy in acute pancreatitis. PATIENTS AND METHOD: 16 patients with moderate form of acute pancreatitis received a high dose of sodium selenite. Selenium in serum and whole blood, zinc, copper, manganese, superoxid dismutase (SOD), glutathione peroxidase (Gpx) and malondialdehyde (MDA) were determined (before selenium substitution, 3 days later, 8 days later, before demission). No selenium deficiency could be detected before selenium substitution. RESULT: The selenium therapy caused a significant increase in selenium, a moderate increase in activity of Gpx, a significant decrease in activity of MDA, whereas SOD remained unchanged. CONCLUSION: Concerning the particular point of view of "deficiency management", there is no need of selenium substitution in patients with a moderate form of acute pancreatitis in our region. The highly normal selenium concentration we established by our therapy is possibly connected with a decrease of the oxidative stress in acute pancreatitis. More clinical follow-up studies with more patients, who have different grades of severity of the acute pancreatitis, and besides that a control group of patients without selenium substitution, are necessary for evaluating the clinical relevance of our results.
BACKGROUND: Recent studies presented evidence that activation of oxygen derived free radicals occurs in patients with acute pancreatitis. The purpose of this study was to evaluate the effect of sodium selenite as a possible antioxidant therapy in acute pancreatitis. PATIENTS AND METHOD: 16 patients with moderate form of acute pancreatitis received a high dose of sodium selenite. Selenium in serum and whole blood, zinc, copper, manganese, superoxid dismutase (SOD), glutathione peroxidase (Gpx) and malondialdehyde (MDA) were determined (before selenium substitution, 3 days later, 8 days later, before demission). No selenium deficiency could be detected before selenium substitution. RESULT: The selenium therapy caused a significant increase in selenium, a moderate increase in activity of Gpx, a significant decrease in activity of MDA, whereas SOD remained unchanged. CONCLUSION: Concerning the particular point of view of "deficiency management", there is no need of selenium substitution in patients with a moderate form of acute pancreatitis in our region. The highly normal selenium concentration we established by our therapy is possibly connected with a decrease of the oxidative stress in acute pancreatitis. More clinical follow-up studies with more patients, who have different grades of severity of the acute pancreatitis, and besides that a control group of patients without selenium substitution, are necessary for evaluating the clinical relevance of our results.
Authors: Ajith K Siriwardena; James M Mason; Srinivasan Balachandra; Anil Bagul; Simon Galloway; Laura Formela; Jonathan G Hardman; Saurabh Jamdar Journal: Gut Date: 2007-03-13 Impact factor: 23.059