Summary:The case of a patient with Crohn's disease complicated by progressive and irreversible encephalopathy, who had been on long-term total parenteral nutrition due to short bowel syndrome, is described. He initially experienced a disturbance ofhis vision, which was followed by various neurological symptoms during the next 3 years. These symptoms rapidly progressed until he finally developed consciousness disturbance. He also manifested erythrocytic macrocytosis, a low serum level of tri-iodothyronine and a high level of thyroxine. His blood levels of various trace minerals and vitamins were normal, except for selenium, which showed extremely low values. In addition, impaired plasma glutathion peroxidase activity was confirmed. After intravenous supplementation of selenium, macrocytosis, tri-iodothyronine and thyroxine values, and glutathione peroxidase activity all became normalized, yet he improved little neurologically.Our case suggests that long-term selenium deficiency may cause progressive and irreversible encephalopathy, and that careful monitoring of this mineral is necessary when an excessive period of total parenteral nutrition is being considered in the clinical setting.
Liquid diet (LD) is known to be protective against indomethacin-induced enteropathy, which is thought to be associated with ischemic change. We tested the hypothesis that the solid component of diet modulates small intestinal blood flow (SIBF) following indomethacin administration. In the first experiment, male Wistar rats were divided into 18-hr-fasted and normal diet groups. Indomethacin (20 mg/kg) or vehicle was administered intracolonically. SIBF was measured on both the mesenteric and antimesenteric sides of the intestine, using the hydrogen gas clearance method. In the second experiment, rats were given LD alone or LD with increasing concentration of soluble/insoluble fiber for seven days. The baseline SIBF was significantly higher in the groups with normal diet and LD with fiber than in the fasting and LD groups. Following indomethacin administration, SIBF gradually decreased in the groups with normal diet and LD with insoluble fiber, while neither liquid diet nor fasting reduced SIBF. There was no difference in SIBF between the mesenteric and antimesenteric sides of the intestine in any group. Our findings suggest that solid components of diet increase basal SIBF and decrease SIBF following indomethacin administration.
Background-Recent clinical studies suggest that ischaemic colitis is caused by a microcirculatory disturbance that involves thrombosis of the colon. Aim-To establish a new model of photochemically induced ischaemic colitis in rats. Methods-Thirty male Wistar rats were anaesthetised with amobarbital, the femoral veins were cannulated and laparotomies were performed. The serosal surface of the proximal colon was irradiated by using a krypton laser (wavelength 568 nm, 20 mW) for four minutes. An intravenous infusion of a photosensitising dye, rose bengal (20 mg/kg body weight), was administered over 90 seconds, beginning at the start of irradiation. Rats were killed immediately (n=4), 12 hours (n=2), 24 hours (n=10), three days (n=4), seven days (n=4), 14 days (n=2), or 28 days (n=2) after irradiation. Two control rats received laser irradiation without dye infusion. Specimens of the irradiated sites were examined by using histopathology. Results-Localised ulcers of the colon were present in rats killed at 12 hours, 24 hours, three days, and seven days after irradiation. Microscopy findings were consistent with the features of human ischaemic colitis. Reproducible ulcerative lesions were produced by photothrombosis of microvessels in the colon. Conclusion-This model may be useful for further investigation of the pathophysiology of ischaemic colitis.
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