SUMMARY This paper reports the incidence and natural history of macroscopic gastritis in a series of 127 consecutive patients with portal hypertension of various aetiologies. Gastritis was observed endoscopically in 65 patients (51%) and was of two main types. Twenty eight patients had severe or persistent gastritis which caused clinically significant bleeding on 80 occasions and accounted for 25% of the bleeds from all sources. The remainder had mild gastritis. The presence of gastritis seemed to be independent of the severity of liver disease or the degree of rise of wedged hepatic venous pressure and there was no difference in age, sex, or drugs prescribed in patients with or without gastritis. The mean follow up period and the mean number of sclerotherapy treatments was significantly greater (p<0.005) in patients with gastritis. Full thickness gastric biopsies in seven surgical patients and 11 autopsy specimens showed dilated and tortuous submucosal veins. Endoscopic biopsies in 14 patients showed vascular ectasia in the mucosal layer which was in excess of the degree of inflammatory infiltrate. Gastritis occurred in patients with portal hypertension of all common aetiologies and the clinical and pathological evidence supports the contention that it reflects a congested gastric mucosa and should be renamed congestive gastropathy. As injection sclerotherapy improves survival from variceal bleeding congestive gastropathy may become more common. The response to conventional ('anti-erosive') therapy is poor and measures aimed at reducing the gastric portal pressure may be the only effective means of treating this condition.

Obesity as measured by BMI is not associated with the development of incident UC or CD. Alternative measures of obesity are required to further investigate the role of obesity in the development of incident IBD.

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Background/Aims: The causes of ulcerative colitis are unknown, although it is plausible that dietary factors are involved. Case-control studies of diet and ulcerative colitis are subject to recall biases. The aim of this study was to examine the prospective relationship between the intake of nutrients and the development of ulcerative colitis in a cohort study. Methods: The study population was 260,686 men and women aged 20–80 years, participating in a large European prospective cohort study (EPIC). Participants were residents in the UK, Sweden, Denmark, Germany or Italy. Information on diet was supplied and the subjects were followed up for the development of ulcerative colitis. Each incident case was matched with four controls and dietary variables were divided into quartiles. Results: A total of 139 subjects with incident ulcerative colitis were identified. No dietary associations were detected, apart from a marginally significant positive association with an increasing percentage intake of energy from total polyunsaturated fatty acids (trend across quartiles OR = 1.19 (95% CI = 0.99–1.43) p = 0.07). Conclusions: No associations between ulcerative colitis and diet were detected, apart from a possible increased risk with a higher total polyunsaturated fatty acid intake. A biological mechanism exists in that polyunsaturated fatty acids are metabolised to pro-inflammatory mediators.

-This paper discusses the annual incidence of liver disease and resource costs in providing a hepatology service for all new outpatient referrals to a secondary care setting. In a retrospective study, we found that 200 patients (1 in 1,000 of the West Suffolk population) with a mean age of 52 years were referred per year. One-third of patients had cirrhosis (almost half due to alcohol). Annual incidence (per 100,000 population) were as follows: non-alcoholic fatty liver disease (29: of which 23.5 non-cirrhotic and 5.5 cirrhotic), hepatitis C (25), hepatitis B (3), alcohol-related cirrhosis (12.5), primary biliary cirrhosis (3.5), autoimmune hepatitis (3), primary sclerosing cholangitis (2), haemochromatosis (2), hepatocellular carcinoma (1.5) and oesophageal variceal haemorrhage (6.5). Using national indicative tariffs, the total annual hepatology budget was £130K (£58K for resources and £72K for clinic attendances). The greatest resource expenditure was on endoscopy (almost half for oesophageal varices) and radiological imaging (one-third of the total budget). These findings will help inform commissioners in hepatology service funding. IntroductionPurchasing of NHS secondary healthcare resources was implemented at primary care level through practice-based commissioning at the end of 2006. 1,2 Important issues to be addressed, for provision of secondary care hepatology outpatient services, include identifying the local healthcare demands (based upon the local aetiology and epidemiology of liver disease) and the resources required to meet these demands with their associated cost implications. This paper addresses these issues and provides findings from a retrospective study, over a one year period, in a secondary care setting. Methods Local demographicsThe West Suffolk hepatology catchment area serves a population of about 200,000 people, is largely rural with low unemployment rates (about 2%), and 98% of the population is white. The Office for National Statistics (ONS) 3 recently reported that Moreton Hall, a council ward of Bury St Edmunds, has the longest average life expectancy from birth of all council wards in England and Wales -at 93.4 years. Parameters analysedParameters analysed in our study included:• number of annual new patient referrals and patient demographics• number of derived follow-ups • causation, incidence and stage of liver disease • resources (investigations and procedures) required from support services (including laboratory blood tests, liver imaging, liver biopsy, paracentesis of ascites, and endoscopy for screening or management of oesophageal varices)• costs of outpatient clinic attendances and resources used. Inclusion criteriaIndications for referral to the hepatology clinic included patients with decompensated liver disease, alcohol-induced liver disease, viral hepatitis, autoimmune liver disease, haemochromatosis and, more commonly, patients with persistent (more than 3-6 months) elevation of serum liver function tests (LFTs), especially alanine aminotransferase (ALT), des...

Heavy diffuse bleeding from congested gastric mucosa (congestive gastropathy) was treated by propranolol (dose = 24 to 480 mg per day) in 14 consecutive patients with portal hypertension. Thirteen patients (93%) stopped bleeding within 3 days. Gastric mucosal cherry red spots (a sign of severe gastropathy) were unchanged in 5 patients, became less obvious in 4 and appearances returned to normal in 5. Propranolol was discontinued electively in seven patients after 2 to 6 months; four of these patients rebled from the same lesion and stopped bleeding when propranolol was recommenced. No patient has rebled from congestive gastropathy while receiving propranolol during follow-up of 12 to 42 (median = 23) months. A further 24 patients with nonbleeding congestive gastropathy received 160 mg long-acting propranolol per day in a double-blind placebo controlled cross-over trial. Twenty-two patients completed the study; in nine patients, endoscopic grading of congestive gastropathy improved after propranolol compared to three after placebo (p less than 0.05). Although the mechanism of action is not understood, propranolol appears to have a clinically significant role in the management of nonvariceal gastric bleeding in portal hypertension.

Perforated colonic diverticular disease results in considerable mortality and morbidity. This review appraises existing evidence on the epidemiology and mechanisms of perforation, highlights areas of further study, and suggests an epidemiological approach towards preventing the condition. Computerised searches were used to identify published articles relating to the epidemiology, pathophysiology, and clinical features of perforated colonic diverticular disease. Several drug and dietary exposures have potential biological mechanisms for causing perforation. Of these only non-steroidal anti-inflammatory drugs have been consistently identified as risk factors in aetiological studies. The causes of perforated colonic diverticular disease remain largely unknown. Further aetiological studies, looking specifically at perforation, are required to investigate whether cause-effect relationships exist for both drug and dietary exposures. The identification of risk factors for perforation would allow primary public health prevention, secondary risk factor modification, and early prophylactic surgery to be aimed at people at high risk.