Esophagogastric polyurethane bezoar complicated by stomach wall microperforation and acute peritonitis: case report.

BACKGROUND: Bezoars are collections of indigestible material in the gastrointestinal tract, mostly described in children. Polyurethane "plastobezoars" consisting of composites used in the construction industry are rarely described bezoars formed in the esophagus and stomach, causing gastrointestinal obstruction, usually necessitating gastrectomy. We describe an unusual presentation of polyurethane bezoar with a volcanic rock consistency, that caused gastrointestinal obstruction and perforation of the stomach wall. CASE PRESENTATION: A 39-year-old man, a construction worker, was referred with signs and symptoms of high gastrointestinal obstruction and abdominal pain. Esophagoscopy revealed a foreign body in the esophagus, 20 cm from the incisor line, causing its obstruction. The attempt to collect the material with forceps failed as the material was too hard. Spiral computed tomography visualized a wide, gas-filled esophagus and a large stomach. The patient with symptoms of acute peritonitis was operated. There were several microperforations of the stomach wall, caused by sharp bezoar fragments that filled the upper one-third of the stomach and lower part of the esophagus. After a longitudinal stomach incision, the bezoar was bluntly dissected from the wall and removed, and the stomach microperforations were closed by wall duplication. After the operation, the patient confessed to drinking, of his own free will, a two-component building foam used to seal pipes. The patient started normal feeding on the 4th day and was discharge home. CONCLUSIONS: Polyurethane bezoars may cause stomach wall perforation and acute peritonitis. Computed tomography has limited usefulness in patients with polyurethane bezoars due to their low specific weight.

Immunosuppressive immunophilin ligands attenuate damage in cultured rat astrocytes depleted of glutathione and exposed to simulated ischemia in vitro. Comparison with N-acetylcysteine.

The aim of the present study was to test the hypothesis that exposure of astrocytes depleted of glutathione (GSH) to simulated ischemia conditions in vitro and treated with immunosuppressant immunophilin ligands (cyclosporin A (CsA) and FK506) can increase intracellular GSH levels and that such mechanism may be responsible, at least in part, for their protective effects. In addition, we also compared the antioxidant properties of these immunosuppressants with N-acetylcysteine (NAC), a precursor of GSH synthesis. GSH depletion was induced by 24 h pretreatment with L-buthionine sulfoximine (BSO). Cultures of rat astrocytes were exposed to CsA (1-50 microM) and FK506 (1-1000 nM) and NAC (100 or 200 microM). We examined the effects of these compounds on apoptosis, cell viability, reactive oxygen species production and GSH content. Our study demonstrated that toxicity of simulated ischemia conditions were enhanced when intracellular GSH was depleted, and immunosuppressants (especially 100 nM FK506 and 10 microM CsA) effectively prevented ischemia toxicity in GSH depleted astrocytes. In addition, we have shown that interfering with the generation of GSH and attenuation, the rise of oxidative stress level by NAC may be a powerful tool for prevention of ischemia-induced glial cell damage.