Irritable bowel syndrome, for instance, was recently reported to be largely a manifestation of food intolerance.7 Despite this, and the extravagant claims recently made for food allergy notwithstanding, it is likely that food allergy is an underdiagnosed condition.8 This may, however, be obscured by the exaggerated impression of prevalence gained from studies involving highly selected population samples. Without previous regard to the mechanism involved, we therefore proposed to seek specific food intolerance among patients with unexplained gastrointestinal symptoms.One of the reasons for the scepticism surrounding the subject of food intolerance is the absence of simple and reliable tests for diagnosis. Double blind food challenges are required to establish diagnosis and a number of techniques using this approach are available. In view of the recognition that food induced symptoms may be delayed9 10 and to ensure, therefore, that chronic food intolerance sufferers with late onset of symptoms were not missed, we used food challenges over one week periods, repeated as necessary if more than one food was suspected. The challenges were double blind and placebo controlled.

SUMMARY The effects of different types of adrenoreceptor blocking agents on portal venous pressure were studied in patients with cirrhosis and portal hypertension. Oral atenolol (selective P1 blocker), propranolol (non-selective 13I and 12 blocker), and prazosin (aX blocker) were compared in three groups of eight patients. Haemodynamic measurements were made before and after two or three and eight weeks of therapy. The dose of beta blockers was sufficient to reduce the exercise heart rate by more than 25%. Propranolol and prazosin produced a sustained reduction in the mean portohepatic venous pressure gradient of the order of 25% and 18% respectively. The cardiac index was significantly reduced by propranolol but not altered by prazosin. Atenolol produced an early reduction in portohepatic venous pressure which, although not sustained, showed a good correlation with reduction in cardiac index. No such relationship was found with propranolol. All three drugs were well tolerated by these patients with advanced cirrhosis. Therefore propranolol and prazosin have proved to be effective agents for the reduction of portal venous pressure.Lebrec and colleagues have suggested that propranolol can be used in patients with cirrhosis to lower portal venous pressure and thereby reduce the incidence of further variceal haemorrhage.1 2 Portal venous pressure is determined by the product of the outflow resistance and the portal venous blood flow. Outflow resistance is increased in cirrhosis because of the mechanical compression of portal venous radicles and thereafter somewhat reduced by the development of portal-systemic collateral venous flow. Animal studies have shown that the portal vein contains a adrenoreceptors only and no ,3 receptors and its tone is partly maintained by adrenoreceptor stimulation.3 Normally the portal vein shows a linear pressure-blood flow relationship with no evidence of autoregulation, such as is seen in the heart or kidney, whereby blood flow is maintained over a range of pressure changes.3 Propranolol is thought to act by a 1,3 blocking effect reducing cardiac output, hence reducing splanchnic blood

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GlasgowSUMMARY In a study of patients attending a rheumatology clinic 230 unselected patients, 185 with rheumatoid arthritis (RA) and 45 with other rheumatic disorders (non-RA), were examined by endoscopy and a detailed history of symptoms referable to the gastrointestinal tract was taken. A peptic ulcer was found in 67 (36%) of the patients and in 13 (29%) of the non-RA group. Gastric ulceration was more common in the group with RA (32 patients (17%) compared with three patients (7%) in the non-RA group); 17/32 (53%) patients with RA and gastric ulcer were asymptomatic. In the group with RA, of those with gastric ulcer 20/32 (63%) were smokers, compared with only 40/118 (34%) of the non-ulcer group. There was no difference in the duration of rheumatic disease or non-steroidal anti-inflammatory drug (NSAID) treatment between the ulcer and non-ulcer groups. Treatment with H2 receptor antagonist and maintenance of NSAID treatment resulted in healing in 26 out of 29 (90%) patients with gastric ulcer and 23 out of 27 (85%) patients with duodenal ulcer.Key words: non-steroidal anti-inflammatory drugs, H2 antagonists, arthritis.There has been much recent interest in the association between peptic ulceration, non-steroidal antiinflammatory drugs (NSAIDs), and rheumatoid arthritis (RA).' The Committee on Safety of Medicines has drawn attention to the risks of gastrointestinal haemorrhage in elderly patients receiving NSAIDs,2 3 and several reports have confirmed this association.4 Iron deficiency anaemia is a common feature of RA and is often caused by an asymptomatic peptic ulcer. The aetiology of peptic ulceration in RA is controversial, and it is not clear whether the apparent increase in peptic ulceration in this condition is due to the disease itself or to the drugs commonly used in treatment. We have, therefore, studied the prevalence of peptic ulceration in our patients with RA attending a rheumatology clinic, and compared them with subjects with other rheumatic diseases.

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