One-hundred-and-thirteen rectal biopsies and 17 total colectomy specimens from 50 patients with ulcerative proctocolitis were examined. These patients had been followed for periods up to 220 months, mean 70 months. The histological changes were compared with the clinical features of the disease. Patients with relatively benign disease which responded to treatment had significantly raised eosinophil counts in the mucosa examined, compared with patients who had aggressive disease which failed to respond to medical treatment (P less than 0.001). Tissue eosinophilia in the rectal mucosa may provide a simple method for predicting the clinical course of patients with ulcerative proctocolitis.
Background/Aims: The normal intestinal epithelium is increasingly being recognised as an important component of the mucosal innate protection against microorganisms.Human neutrophil defensins 1-3 (HNP 1-3) and lysozyme are components of the systemic innate immunity.The aim of this study was to investigate the expression of HNP 1-3 and lysozyme in normal and active inflammatory bowel disease (IBD) mucosa.Methods: Mucosal tissue sections were studied by immunohistochemistry using antibodies to neutrophil defensins 1-3 and lysozyme.Extracts of purified intestinal epithelial cells were used for immunoblotting studies and antimicrobial activity against the phoP negative strain of Salmonella typhimurium.Results: Surface epithelial cells strongly immunoreactive for neutrophil defensins and lysozyme were seen in active ulcerative colitis and Crohn's disease (but not normal or inactive IBD) mucosal samples.Many of these cells coexpressed both of the antimicrobial proteins.Immunoblotting studies confirmed the expression of neutrophil defensins in extracts of purified ulcerative colitis epithelial cells, which also demonstrated antimicrobial activity.Conclusion: HNP 1-3 and lysozyme are expressed in surface enterocytes of mucosa with active IBD and they may play an important role in intestinal host defence against luminal microorganisms.
Two cases of chronic giardiasis of the stomach diagnosed from gastric mucosal biopsy specimens are reported. The first case was associated with an acute-on-chronic gastritis and Helicobacter-like organisms, and the second with an adenocarcinoma of the stomach. In both cases the trophozoites had been missed in earlier biopsy specimens. As far as is known this is the first report of giardiasis of the stomach.
Vagal function in 28 patients with gastro-oesophageal reflux was examined by determining gastric secretory response to insulin-induced hypoglycaemia and pulse-rate variation with respiration. Gastric secretory studies were also performed on 13 patients with duodenal ulcer who had not undergone operations. In all patients the presence and degree of oesophagitis were determined endoscopically and mucosal biopsy and oesophageal manometry were performed. Seven of the 28 patients with gastro-oesophageal reflux showed evidence of impaired vagal efferent function in the upper alimentary tract. No such impairment was found in those patients who showed manometric evidence of oesophageal spasm secondary to gastro-oesophageal reflux. Low pulse-rate variation with respiration was found in 12 of 27 patients with gastro-oesophageal reflux, suggesting dysfunction of cardiac vagal fibres. Impairment of efferent vagal supply may be a causative factor in some patients with gastr-oesophageal reflux but does not seem to be important in oesophageal spasm secondary to gastro-oesophageal reflux.
In a 15 year prospective study of endoscopic surveillance of columnar lined oesophagus, 102 patients with a mean follow up of 54 (12.5) months and total follow up of 462 years have been evaluated. Of all the sets of biopsies taken, 59 in 21 patients were found to exhibit dysplasia or carcinoma. Four male patients had carcinoma of the oesophagus, indicating a 30 times increased risk of development of adenocarcinoma in columnar lined oesophagus. The length of columnar lined oesophagus in subjects with dysplasia was significantly longer as compared with the whole group (p = 0.01) and when compared with the patients without dysplasia (p = 0.005). None of the patients with dysplasia had a columnar lined oesophagus of less than 8 cm. Length of columnar lined oesophagus therefore seems to be a significant risk factor in the development of dysplasia and subsequent carcinoma and intensive follow up of patients with columnar lined oesophagus greater than 8 cm in length is recommended.
Autonomic nervous function in reflux oesophagitis was assessed by measuring the response of the lower oesophageal sphincter to abdominal compression, gastric secretory response to insulininduced hypoglycaemia and pulse rate variability with respiration. Rise in intra-abdominal pressure normally causes an increase in lower oesophageal sphincter pressure through a vagally mediated mechanism. In 59 of 83 patients with reflux oesophagitis the sphincter response was subnormal, and this was commoner in older patients but was unrelated to the presence of a hiatal hernia. During oesophageal acid perfusion, the onset of pain, but not that of disordered motility, was delayed in those with an abnormal sphincter response suggesting impairment of afferent autonomic function. Effcrent gastric vagal function, assessed by the gastric secretory response to insulin induced hypoglycaemia and expressed as a ratio of the maximal acid output after pentagastrin, was subnormal in 15 of 27 patients with reflux oesophagitis. Pulse rate variability with deep respiration, an indicator of one aspect of non-alimentary vagal function, was subnormal in 18 of 62 patients with reflux oesophagitis. There was no correlation between abnormalities in these three tests of vagal function or with the severity of oesophagitis. These findings suggest that vagal impairment is common in reflux oesophagitis. As impairment of vagal function is not confined to the alimentary system it is unlikely to be simply a consequence of reflux oesophagitis and may be important in the pathogenesis of gastro-oesophageal reflux.
There is no satisfactory biomarker yet available for predicting the likelihood of premalignant changes or carcinoma developing in Barrett9s or columnar lined oesophagus. In this study we have evaluated the proliferation of squamous epithelium, columnar epithelium from columnar lined oesophagus and gastric columnar epithelium from 23 Barrett9s patients using positive immunoreactivity with the mouse monoclonal antibody Ki67 (which recognises an antigen associated with proliferative cells) with a view to using this parameter as a biomarker. Squamous epithelium had significantly higher Ki67 immunostaining as compared with columnar epithelium from columnar lined oesophagus (when examining the tissue with greater than 15% cells staining positive for Ki67, Fisher9s exact test p = 0.004) but there was no difference found between the epithelium from the columnar lined oesophagus and gastric columnar epithelium. There was no correlation between histological inflammation and Ki67 immunoreactivity of Barrett9s mucosa, and the Ki67 immunostaining of two patients with dysplasia was no different from the rest of the group. There was, however, a significant correlation between the Ki67 immunoreactivity of columnar epithelium from columnar lined oesophagus and columnar epithelium from the stomach (correlation coefficient = 0.44, p = 0.03) suggesting that epithelium from columnar lined oesophagus behaves in a similar fashion to gastric epithelium.
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