No abstract

Objectives: Clostridium difficile associated diarrhoea (CDAD) is a hospital acquired infection in which optimal methods for diagnosis and the scale of the problem in the community remain to be determined. In hospitalised patients with CDAD, we aimed to (i) study patients in whom the onset of diarrhoea was in the community and (ii) investigate the role of bedside flexible sigmoidoscopy in diagnosis. Methods: Patients with CDAD (onset in hospital or community) were studied prospectively. In those with diarrhoea of unknown aetiology, flexible sigmoidoscopy was compared with stool assay for C difficile cytotoxin. Results: Of 136 patients with CDAD (which was associated with antibiotic exposure in 96%), diarrhoea started in the community in 38 (28%; majority in own home) and while an inpatient in 98 (72%). The majority with CDAD onset in the community had been hospitalised over the preceding 12 months (86.8% v 57.1% in the hospital onset group; p,0.001). In 56 patients with pseudomembranous colitis at sigmoidoscopy, the stool C difficile cytotoxin test was negative in 29 (52%) but toxigenic C difficile was isolated from all of nine stool samples cultured. Of patients with pseudomembranous colitis, 30.4% relapsed over the subsequent 57.7(4.2) days. Conclusions: In a significant proportion of hospitalised patients with CDAD, diarrhoea started in the community. However, the majority of these had been hospital inpatients previously when they may have acquired C difficile, with the subsequent onset of diarrhoea in the community following exposure to antibiotics. Flexible sigmoidoscopy is superior to the stool C difficile cytotoxin test in a subgroup of patients with pseudomembranous colitis. Sigmoidoscopy should therefore be considered in all hospitalised patients with diarrhoea in whom the stool test for C difficile cytotoxin and enteric pathogens is negative.

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.

Fifty-six patients with Barrett's oesophagus diagnosed between 1977 and 1986 were prospectively studied by 6-monthly endoscopic surveillance and biopsy. During follow-up to-date, four patients have developed high-grade dysplasia and three have adenocarcinoma of the oesophagus. Two of the adenocarcinomas were preceded by progressively severe dysplastic changes but in the third no dysplasia had been previously detected. The incidence of adenocarcinoma was 1 per 56 patient-years of follow-up. Changes in symptomatology or gross endoscopic appearances were usually absent, even after adenocarcinoma had developed, indicating that biopsy is essential for early diagnosis. The high risk of malignant change makes endoscopic surveillance advisable in all patients with Barrett's oesophagus.

Three cases of adenoid cystic carcinoma have been identified in a 10-year review of 2686 cases of breast carcinoma. The criteria necessary for diagnosis have been reviewed with particular reference to cribriform intraduct carcinoma and adenocarcinoma of the breast with small, dark, 'basaloid'-cell pattern. The most important single diagnostic criterion of adenoid cystic carcinoma is a biphasic cellular pattern which may be aded by the demonstration of two types of mucin stromal acid mucopolysaccharide and ductal neutral mucopolysaccharide. This tumour most frequently presents as a painful or tender mass near the areola, and it carries a uniquely favourable prognosis when compared with similar tumours elsewhere in the body. Actomyosin has been demonstrated in all three tumours by an immunofluorescent method, and this supports a predominantly myoepithelial origin.