[FREE PERFORATION IN ACUTE TERMINAL ILEITIS].
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A 23-year-old man in otherwise good health had diarrhoea for two days during a holiday on Maldives. Two months later he suddenly collapsed and had to be admitted to hospital. Haemoglobin concentration was found to be 76 g/l, with a haematocrit of 0.22, WBC count of 17,800/microliters and platelets of 22%. Massive passage of bright red blood in the stools (none previously) could not be explained by abdominal sonography, oesophagogastroduodenoscopy, coloscopy, technetium scintigraphy or angiography of the superior mesenteric artery. Exploratory laparotomy revealed severe inflammatory changes in the terminal ileum with enlargement of the regional lymph-nodes and spurting bleeding from a branch of the ileocolic artery. Histological examination showed focal necrotizing, ulcerative and haemorrhagic ileitis. After ileocaecal resection and end-to-end anastomosis to the ascending colon the patient quickly recovered. Salmonella Livingstone was isolated from the stool and the infection was treated with ciprofloxacin, 200 mg twice daily intravenously for 5 days. Subsequent stool samples were negative but follow-up continues.
Transabdominal ultrasonography in a female patient hospitalized for acute right lower quadrant pain revealed a nonspecific tubular structure in the region of the right adnexa. Endovaginal ultrasonography clearly showed this structure to be an abnormal loop of small bowel with its "target lesion" appearance and thickened wall. A tentative diagnosis of Crohn's disease was made. This was later confirmed by barium studies and histology.
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BACKGROUND AND AIMS: Intestinal inflammation alters neuronal and enteroendocrine signalling, leading to functional adaptations in the inflamed bowel. Human studies have reported functional alterations at sites distant from active inflammation. Our aims were to determine whether neuronal and enteroendocrine signalling are altered in the uninflamed colon during ileitis. METHODS: We used neurophysiological, immunohistochemical, biochemical and Ussing chamber techniques to examine the effect of 2,4,6-trinitrobenzene sulphonic acid (TNBS)-induced ileitis on the properties of submucosal neurones, enteroendocrine cells and epithelial physiology of the distal colon of guinea pigs. RESULTS: Three days after TNBS administration, when inflammation was restricted to the ileum, the properties of colonic enteric neurones were altered. Submucosal AH neurones were hyperexcitable and had reduced after hyperpolarisations. S neurones received larger fast and slow excitatory postsynaptic potentials, due to an increase in non-cholinergic synaptic transmission. Despite the absence of inflammation in the colon, we found increased colonic prostaglandin E(2) content in animals with ileitis. Ileitis also increased the number of colonic 5-hydroxytryptamine (5-HT)- and GLP-2-immunoreactive enteroendocrine cells. This was accompanied by an increase in stimulated 5-HT release. Functional alterations in epithelial physiology occurred such that basal short circuit current was increased and veratridine-stimulated ion transport was reduced in the colon of animals with ileitis. CONCLUSION: Our data suggest that inflammation at one site in the gut alters the cellular components of enteric reflex circuits in non-inflamed regions in ways similar to those at sites of active inflammation. These changes underlie altered function in non-involved regions during episodes of intestinal inflammation.
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