Gastroenterology involves many disciplines, including physicians, surgeons, radiologists, pathologists, nurses, dieticians, clinical scientists and general practitioners, who need to work together closely to deliver the best care. Gastrointestinal and liver disorders are common, but the specialty is poorly understood and has attracted little attention from a policy perspective. Thus, it has no National Service Framework, was not included in the “Quality and Outcome Framework” for general practice and does not attract significant charitable research funding, in comparison with many other disciplines. Yet the burden of disease relating to gastroenterology and hepatology is very considerable. Gastrointestinal disease is the third most common cause of death, and cancer of the gastrointestinal tract is the leading cause of cancer death. Including day case investigations, gastrointestinal disorders account for as many hospital admissions as respiratory illnesses, and both are second only to circulatory disorders. In the past few decades there have been increases in the incidence of most gastrointestinal diseases that have major implications for future healthcare needs. These include hepatitis C, acute and chronic pancreatitis, alcoholic liver disease, gallstone disease, upper gastrointestinal haemorrhage, diverticular disease, Barrett’s oesophagus and oesophageal and colorectal cancers. The impairment of quality of life is substantial in terms of symptoms, activities of daily living and employment. Conditions with a particularly high level of disruption to the lives of sufferers include gastro-oesophageal reflux disease, dyspepsia, irritable bowel syndrome, anorectal disorders, gastrointestinal cancers and chronic liver disease. The evidence underpinning …

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.

Colorectal DiseaseVolume 3, Issue s2 p. 51-53 The natural history of Crohn’s disease: prevalence in Europe and the cancer risk M.D. Hellier, M.D. Hellier Princess Margaret Hospital, Swindon, UKSearch for more papers by this author M.D. Hellier, M.D. Hellier Princess Margaret Hospital, Swindon, UKSearch for more papers by this author First published: 18 July 2008 https://doi.org/10.1111/j.1463-1318.2001.00008.x Hellier Consultant Gastroenterologist, Princess Margaret Hospital, Okus Road, Swindon SN1 4JU, UK. Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Volume3, Issues2September 2001Pages 51-53 RelatedInformation

Editor,—We read with great interest the leading article by Hellier and Morris ( (2000) Gut 47:459–60; ) regarding the future of endoscopic retrograde cholangiopancreatography (ERCP) training in the UK. They discuss the importance of restricting training in ERCP to some trainees and training only in centres that are accredited for training by the Joint Advisory Group (JAG) in Endoscopy. JAG, at the request of the Conference of Royal Colleges, produced endoscopy training guidelines.1 For ERCP training, these state that a centre should be performing a minimum of 250 procedures per annum (with specialist centres performing 500 per annum). They should also have regular meetings to discuss radiological findings with a radiologist with special interest in ERCP. While we certainly agree with the importance of ensuring satisfactory training, we are concerned that the guidelines base competence for training in ERCP solely on the number of procedures carried out in individual centres. We have noted that larger centres often have several practitioners performing ERCP and several trainees learning. To determine the likely impact of the JAG recommendations on ERCP training and whether trainees were likely to have greater individual exposure to procedures in larger units, we performed a questionnaire based study, which was mailed to all acute UK hospitals. A total of 178 of 292 units replied …

It has become increasingly clear that no longer is it appropriate or practical to train all specialist gastroenterology registrars in endoscopic retrograde cholangiopancreatography (ERCP). This realisation has caused much disquiet and uncertainty among trainees, concern among trainers, and debate in the journals.1 At present the implication of the Joint Committee for Higher Medical Training (JCHMT) curriculum for higher specialist training in gastroenterology is that all trainees are expected to become proficient in all areas of endoscopy. In recent months this issue has been extensively discussed by the appropriate bodies—Training Committee of the British Society of Gastroenterology (BSG), Joint Advisory Group on Endoscopy Training (JAG), and in particular the Specialist Advisory Committee in Gastroenterology to the Joint Committee for Higher Medical Training (SAC to JCHMT). It is the JCHMT alone that has the statutory powers to enforce decisions on training. The SAC Gastroenterology, with the approval of the other bodies, has decided that from now, ERCP will no longer be an essential requirement for a certificate of completion of specialist training. Most gastroenterologists would accept the need for full training in oesophago-gastro-duodenoscopy and in colonoscopy. These are areas of endoscopy where demand can be expected to continue to rise, especially with the increasing need for cancer screening. In contrast, despite the recent sharp rise in demand for ERCP coming on the back of laparoscopic cholecystectomy, it is likely that numbers will plateau or even fall as magnetic resonance cholangiopancreography and laparoscopic exploration of the common bile duct become more widespread. Even with the existing numbers of cases it is not possible for all trainees to meet the requirements of JAG and become proficient in ERCP, nor would trainers be able to maintain their expertise. These concerns were very clearly expressed in a recent paper by Wicks et al , with …

Hospitals in the UK have recently seen a marked increase in C. difficile for reasons which are unclear. Reduced standards of hygiene, increasingly elderly patients, greater cephalosporin use and longer hospital stay have been suggested. We retrospectively studied all cases of C. difficile diarrhoea at Princess Margaret Hospital, Swindon, over two years. Cephalosporins, patient age and LOS appeared unrelated to the rise in C. difficile; penicillins and macrolides were related. Our policy of using amoxycillin and clarithromycin for community-acquired pneumonia coincided with this study and may explain the observed rise in C. difficile.

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.

The study was designed to identify patterns of dyspeptic symptoms in patients presenting to General Practitioners and to determine whether a classification based on published symptom sub-groups con be used to predict which patients respond best to treatment with a prokinetic. It was a multicentre study involving symptom assessment before and after four weeks' open treatment with 10mg cisapride tid and after a further four-week period without treatment.Patients presenting with dyspepsia, whom General Practitioners considered suitable for a trial of therapy without prior gastrointestinal investigation, were recruited to the study and their symptoms were recorded. Symptoms were recorded from 9,974 patients, of whom 7,928 completed the treatment phase and 5,125 returned at the end of the follow-up Period. Symptom occurrence and severity were recorded before and after treatment The pattern of symptom presentation was compared with pre-defined symptom sub-groups, and the response rates of different sub-groups to treatment were analysed.Only half the patients (n=4,518) could be categorised according to the predefined dyspepsia sub-groups: 27.9% had ulcer-like, 12.1% dysmotility-like and 4.1% reflux-like dyspeptic symptoms. The other patients had symptoms associated with more than one sub-group. Symptom patterns and sub-group distribution were not related to patients' age or sex and showed no regional variation. After four weeks of treatment with cisopride, 89.9% of patients showed symptom improvement which was sustained for a further four weeks after treatment in most patients (63.3%). Response rates to treatment with cisapride were similar in all sub-groups (range 84-92%). We conclude that symptom sub-groups ore not helpful in predicting response to treatment with a prokinetic.

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.