Ogawa K, Kanemoto K, Shirasaka Y, Kawasaki J, Yamasaki S
Division of Internal Medicine, DainiBiwako-Gakuen Hospital, Shiga, Japan.
Psychiatry Clin Neurosci. 2001 Dec;55(6):619-22. doi: 10.1046/j.1440-1819.2001.00914.x.
Three cases involving a previously unreported association of acute pancreatic damage following convulsive status epilepticus (SE) are presented. A review of literature failed to reveal a similar association between SE and acute pancreatic damage. As possible pathophysiological mechanisms of this so far unknown sequel of SE, increased intraduodenal pressure during SE leading to the reflux of the duodenal contents into the pancreatic duct, along with altered metabolism of oxygen-derived free radicals during a prolonged seizure with hypoxia and ischemia resulting in acinar cell injury are suggested. We believe that SE should be considered as an additional risk factor of acute pancreatitis and that pancreatic enzymes should be monitored in patients who have prolonged seizures.
