OBJECTIVES: Recent epidemiological studies suggest that mortality rates for inflammatory bowel disease (IBD) are similar to those of the general population. However, most of this work has been done in referred populations or larger urban centers. We intended to estimate mortality rates for ulcerative colitis (UC) and Crohn's disease (CD) in three British district general hospital practices in Wolverhampton, Salisbury, and Swindon. METHODS: Consecutive patients with CD or UC were identified from 1978 to 1986 and followed prospectively. Demographic data, date and cause of death or health status at December 31, 1993 were used to estimate standardized mortality ratios (SMRs) and 95% confidence intervals. RESULTS: Sixty-four deaths occurred in 552 patients (UC 41 of 356; CD 23 of 196). The overall SMRs were 103 [95% confidence interval (CI): 79–140] for UC and 94 (95% CI: 59–140) for CD. The respective SMRs were higher only in the first year after diagnosis at 223 (95% CI: 99–439; p = 0.02) and 229 (74–535; p = 0.056), and even then, most subjects died from non-IBD causes (5 of 13). Nonsurvivors were significantly older than survivors in both UC and CD (p < 0.01). The SMR was also significantly greater during a severe first attack of UC at 310 (95% CI: 84–793; p = 0.04). Patients with perianal or colonic CD had an increased SMR [396 (95% CI: 108–335; p = 0.02) and 164 (95% CI: 82–335; p = 0.02)] respectively, partly related to the older mean age (52 vs 32 yr, p < 0.001). CONCLUSIONS: Mortality rates are not increased in IBD compared with the general population. However, older patients may be at increased risk of dying from other causes early in the disease clinical course.

The alimentary tract, perhaps more than any other system, reflects the feeling of well-being, or otherwise, of an individual. Indigestion, dyspepsia, abdominal pain, vomiting and diarrhea can arise as the result of almost any functional or organic disease of the digestive system including the liver, biliary system and pancreas; even ischemic heart disease may give rise to symptoms akin to indigestion. When indigestion is reported in a medical history the examiner should attempt to interpret its meaning, otherwise its significance to the life underwriter may be far from clear.

AIM:To study the influence of sulphasalazine treatment on the mucosa-associated bacterial flora of rectal biopsy tissue specimens in patients with ulcerative colitis.PATIENTS:Twenty-four patients had newly diagnosed active ulcerative colitis; 20 patients had acute relapse of ulcerative colitis (10 not taking maintenance sulphasalazine); (40 patients had quiescent ulcerative colitis; 21 not taking maintenance sulphasalazine). The influence of 3 weeks of sulphasalazine treatment on the mucosa-associated flora was studied in the patients presenting with active disease.RESULTS:Comparison of patients according to sulphasalazine usage revealed few differences in the mucosal flora. In patients with quiescent ulcerative colitis, Escherichia coli was found at lower counts in patients taking maintenance sulphasalazine; however, this effect was not evident in patients with active disease. Inconsistent changes in other facultatives were seen between the two active disease groups, particularly for a miscellaneous group of unidentified Gram-positive rods. Three patients, all receiving sulphasalazine, were colonized with Clostridium difficile, but this did not appear to influence their disease.CONCLUSION:Sulphasalazine treatment in ulcerative colitis causes only minor disturbance to the populations of bacteria colonizing the colorectal mucosa.

To test the hypothesis that Crohn's disease is caused by delayed exposure to enteric infections, we did a case-control study. We compared 133 patients who have Crohn's disease and 231 with ulcerative colitis who have controls selected from the general population and matched for age and sex. Crohn's disease was more common in subjects whose first houses had a hot-water tap (odds ratio 5.0, 95% CI 1.4-17.3) and separate bathroom (3.3, 1.3-8.3). Ulcerative colitis showed no clear relation to household amenities in infancy. These findings may explain why the incidence of Crohn's disease has increased in developed countries over the past 50 years.

The adherent properties and hydrophobicity of Escherichia coli isolates have been compared from the rectal mucosa of patients with active and inactive ulcerative colitis and from a control patient group. Patients with active colitis were colonised less frequently and with lower numbers of E coli than were control patients. Mannose resistant adhesion to HEp-2 cells was determined for 124 isolates of E coli and surface hydrophobicity was estimated by salt agglutination in 96 of these isolates. There was no significant difference in the distribution of adherent strains between the colitis patient groups or with disease activity. E coli from the control patients were marginally less adhesive than those from colitics. The hydrophobicity of isolates did not differ significantly between colitic and control groups nor were there significant differences correlated with disease activity. Furthermore, for these mucosal E coli isolates, hydrophobicity and mannose resistant adhesion were unrelated characteristics.

Microbial pathogens were sought in faeces of patients with active ulcerative colitis and again after 3 months treatment. 64 patients were examined during their first episode of ulcerative colitis and 30 with relapse of chronic disease. At presentation, bacterial pathogens were not found; 1 patient had cryptosporidiosis. In 10 patients treatment appeared to result in some loss of colonisation resistance as evidenced by colonisation with beta-haemolytic streptococci, Staphylococcus aureus, candida and Clostridium difficile. Unidentified cytotoxic activity was present in the faeces of 4 patients at presentation and 2 patients during or after treatment. We conclude that enteric infection is an uncommon finding in patients with active ulcerative colitis.

There is broad agreement that microbes play an important role in the aetiology and pathogenesis of ulcerative colitis (UC), probably via an abnormal local immune response to one or several microbial antigens or metabolites; this is clearly in addition to their role in local tissue invasion and microabscess formation. However, numerous investigations have failed to identify either an aetiological agent or a consistent alteration in the composition or balance of the complex faecal microflora.

The rectal mucosa-associated flora (MAF) of patients with ulcerative colitis has been studied in 25 patients with newly diagnosed disease, 20 with relapse of existing disease, and 44 who were in remission. Patients with active disease were re-examined twice during treatment. The MAF was simpler and less dense than the microflora of faeces. Obligate anaerobes usually predominated in the MAF although the ratio of obligate anaerobes to facultative species was lower than that found in faeces. Viable counts of the total flora and of its constituent genera varied considerably between patients. Counts of the total flora, of obligate anaerobes (including bifidobacteria, eubacteria and clostridia), and facultative organisms and micro-aerobes (enterobacteria and lactobacilli) were reduced in patients with active disease compared with those with inactive disease; corresponding carriage rates were also lower. Counts and carriage rates increased during treatment and approached those found in quiescent disease. The alterations in the MAF were especially marked in patients experiencing their first attack of ulcerative colitis. The relationship between these alterations and the aetiology and pathogenesis of this disease remains unclear.

The effect of cimetidine and pirenzepine on the maintenance of healing in duodenal ulceration has been compared in a multi-centre, controlled study. One hundred and sixty-six patients with endoscopically proven duodenal ulceration have been randomised to receive either cimetidine 200 mg t.i.d. and 400 mg nocte, or pirenzepine 50 mg b.i.d. for 6 weeks. Patients in each group were well matched for age, sex, weight and cigarette, alcohol and antacid consumption. After 6 weeks significantly more cimetidine-treated patients had healed ulcers: cimetidine showed 8 unhealed out of 79, and pirenzepine 19 out of 74 (p = 0.01). The follow-up phase lasted for 52 weeks or until patient withdrawal or ulcer relapse. During the follow-up phase 77.6% of cimetidine-treated and 68.8% of pirenzepine-treated patients relapsed. This difference in relapse rates is not statistically significant (p = 0.23).

A double blind multicentre study comparing sodium cromoglycate (600 mg/100 ml) by enema with prednisolone (20 mg/100 ml) by enema is reported. The study was conducted over a nine week period in the treatment of 70 patients with ulcerative colitis. Analysis of symptoms showed significant decreases in scores for patients in both groups, both at four and eight weeks; the only difference between the two groups was a significantly greater improvement in the reduction of rectal bleeding after four weeks in the prednisolone group. On sigmoidoscopy, both treatment groups showed a highly significant improvement after four and eight weeks with no significant differences being seen between the groups. Histology of the rectal biopsies showed a significant improvement in the inflammation of the mucosa for both treatment groups after four and eight weeks with no differences being observed between the groups. There were no significant changes in eosinophils from baseline and no difference between the groups at four and eight weeks.