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Plenary session 162–166

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A. Jayaprakash1, P.E. Stevens1, S. Mian2, A.S. McIntyre3, R.F. Logan4, A.F. Muller1. 1The Kent & Canterbury Hospital, Kent;2BSG Research Unit, London;3Wycombe Hospital, Bucks;4University Hospital, Nottingham, UK

Nephrotoxicity is an unusual complication of 5 amino-salicylic acid (5-ASA) therapy in inflammatory bowel disease. The literature documenting its frequency, severity & recovery is limited. This study assessed the retrospective experience of all 1298 names on the British Society of Gastroenterology (BSG) register and 237 Consultant members of the Renal Association (RA).

Each was sent a detailed questionnaire asking for patient demographic details, frequency with which renal function was assessed, time to development of renal impairment, drug(s) thought to be responsible, renal function at diagnosis and recovery, renal biopsy histology & any other relevant information.

Results: See table. 72 BSG respondents measured renal function less than once per year; 27 never measured it. Responsible agents for nephrotoxicity were: [BSG (RA)] Asacol 132(29), Colazide 1(1), Olsalazine 3(1), Pentasa 12(2), Salofalk 1(0), & Sulphasalazine 13(8). *The BSG reported 6 pts needing dialysis & 7 a renal transplant. The RA reported medico-legal action in 4 cases.

Abstract 162

All 5-ASA's may cause severe nephrotoxicity, which at best may only be partially reversible. Most cases occurred with Asacol, many after more than 12 months of therapy. The BSG Research Unit is collecting prospective data that may help in determining associated factors and whether nephrotoxicity can be avoided by frequent monitoring.


P.J. Lamb, J. Wayman, M. Billings, M. Irving, D. Karat, N. Hayes, S.A. Raimes, S.M. Griffin. Northern Oesophago-Gastric Cancer Unit at the Royal Victoria Infirmary, Newcastle upon Tyne & Cumberland Infirmary, Carlisle, UK

Background: Early diagnosis is vital to improve the outcome for patients with oesophago-gastric cancer. The aim of this study was to determine the impact of government referral guidelines on delays in the diagnosis and treatment of these cancers.

Methods: 122 patients (median age 68 (range 48–84), male to female ratio 2:1) with oesophago-gastric cancer initially referred by a general practitioner and treated within this unit from 01/08/99 to 30/09/01 were evaluated. Details of referral, investigation and treatment were obtained by patient interview and cross-referenced with the case notes.

Results: 71 patients (58%) were referred before and 51 patients (42%) after the introduction of referral guidelines. The overall median delay from the onset of symptoms to definitive treatment was 22.0 (IQR 13.0–32.2) weeks comprising patient delay in consulting a doctor (48%), delay in referral (24%), delay in diagnosis (14%), and delay in commencing treatment (14%). After the introduction of guidelines there was a significant decrease in the time from referral to endoscopy, from a median of 2.5 (IQR 2.0–5.5) to 2.0 (IQR 1.0–3.0) weeks (p=0.012). Endoscopy was carried out within 2 weeks of referral in 71% (36/51) of patients compared to only 44% (31/71) before the guidelines (p=0.06). There was a decrease in the number of patients waiting over 6 weeks for endoscopy from 23% (16/71) to 8% (4/51) (p=0.03). No significant reduction in total delay (median 24.0 (IQR 14.0–32.0) vs. 18.0 (IQR 12.0–33.0) weeks, p=0.107) or change in the stage of disease at diagnosis was identified following the introduction of the guidelines.

Conclusion: The introduction of guidelines has resulted in a significant decrease in the time from referral to endoscopy for patients with oesophago-gastric cancer. As the major delay occurs prior to referral this has not translated into a significant reduction in overall delay. To achieve this patient awareness must also be targeted.


D.M. Forton1, M. Prince2, J. Allsop1, N. Patel1, J. Goldblatt2, H.C. Thomas1, M. Bassendine2, D.E.J. Jones2, S.D. Taylor-Robinson1. 1Liver Unit, Imperial College, London;2Centre for Liver Research, University of Newcastle, UK

Fatigue is the commonest symptom in primary biliary cirrhosis (PBC), affecting individuals at all stages of the disease. We examine the hypothesis that a CNS abnormality related to cholestasis, rather than cirrhosis per se, underlies this symptom. Globus pallidus (PAL) hyperintensity on T1-weighted MRI has been reported in biliary atresia, cirrhosis, parenteral nutrition induced cholestasis and in manganese workers.

Methods: 18 women with PBC (14 stage I-II [mean bilirubin 11], 4 stage III-IV [32]) and 8 age-matched healthy women underwent cerebral MRI and proton spectroscopy (1H MRS). Magnetisation transfer ratios (MTR) for white matter (WM) and 4 subcortical structures were calculated and 1H MR spectra (TE 135ms) were obtained from 8cm3 voxels in the basal ganglia (BG) and frontal WM. The patients completed the Fisk Fatigue Severity Score (FSSS) and a battery of neuropsychological tests.

Results: There were no differences between the stage I-II patients and controls in the WM or subcortical MTRs or in the 1H MRS. However, the PAL/WM MTR ratio was significantly reduced in the stage I-II PBC patients (p<0.02), with no similar changes in the thalamus, putamen or caudate. The 4 stage III-IV patients also had reduced PAL/WM ratios, although they were not statistically different from the stage I-II patients. When the pre-cirrhotic patients were divided into 2 equal groups on the basis of the FSSS score, the fatigued patients had a significantly lower PAL/WM than the non-fatigued patients (p=0.05). There was no similar relationship between cognitive performance and PAL/WM.

Conclusion: We demonstrate a highly localised abnormality in the PAL in pre-cirrhotic PBC patients, which was more pronounced in the fatigued patients. It is unlikely to be due to hepatic encephalopathy as these non-cirrhotic patients had normal MRS. We postulate that a failure of biliary excretion results in the accumulation of heavy metals in the PAL, which underlies the reported fatigue.


N.I. Church1, H.J. Dallal1, J. Masson2, A. Fraser2, N.A.G. Mowat2, D.A. Johnston3, G. Fullarton4, E. Radin5, M. Turner5, R. Prescott6, J. Plevris7, K.R. Palmer1. 1Western General Hospital, Edinburgh;2Aberdeen Royal Infirmary;3Ninewells Hospital, Dundee;4Gartnavel General Hospital, Glasgow;5Scottish National Blood Transfusion Service;6University of Edinburgh Medical School;7Royal Infirmary, Edinburgh, UK

Introduction: Ulcer haemostasis is attempted in many centres using a combination of injection and thermal application, but there is little evidence that combination therapy is better than use of a single agent. Furthermore previous studies of endoscopic therapy have not included a placebo arm. In this large multicentre, double blind, randomised, placebo controlled trial we examined the hypothesis that combined haemostatic treatment using the heater probe plus best injection (using thrombin) is superior to the heater probe plus placebo injection.

Method: 247 patients presenting with major peptic ulcer bleeding were randomised to heater probe plus thrombin (group 1) or heater probe plus placebo (group 2). The two groups were well matched for all risk categories including age, endoscopic stigmata, shock and severity of comorbid diseases. Endoscopic therapy was applied using 150 joules on average of the heater probe followed by injection of 3.5ml of thrombin or placebo.

Results: Successful primary haemostasis was achieved in 97% of both groups. Rebleeding developed in 19 (15%) of group 1 patients and 17 (15%) of group 2 patients; surgery was necessary in 16 and 13 of these respectively. Median blood transfusion (3; range 0–32 versus 2; 0–35 units) and median duration of hospital admission (5; 2–82 versus 5; 1–120 days) were similar in both groups. Adverse events occurred in 8 group 1 patients and 4 group 2 patients. Mortality at 30 days was 8 (6%) of group 1 patients versus 14 (12%) of group 2 patients.

Conclusion: Combination of thrombin or placebo injection with the heater probe is a safe and effective haemostatic therapy for bleeding peptic ulcer. The combination of thrombin with the heater probe does not confer an additional benefit over heater probe and placebo, and thrombin injection can not be recommended in preference to any other injection as adjunctive endoscopic therapy for bleeding peptic ulcer in patients receiving heater probe therapy.


D. Gillen, A. Wirz, K.E.L. McColl. University Dept of Medicine & Therapeutics, Western Infirmary, Glasgow G11 6NT, UK

Introduction: There is marked rebound acid hypersecretion after omeprazole in H.pylori -ve but not +ve subjects. Oxyntic gastritis probably prevents it in the latter.

Aim: To determine the effect of H.pylori eradication on rebound acid hypersecretion after omeprazole.

Methods: 17 healthy H.pylori +ve subjects had acid secretion studies prior to commencing omeprazole 40mg/day for 8 weeks. During the last week of omeprazole, they were randomised to a 1 week course of amoxycillin/clarithromycin or placebo. Further acid secretion studies were performed at 1,2,4,6&8 weeks after treatment. A further breath test was performed at 8 weeks to determine H.pylori status after treatment.

Results: Marked rebound hypersecretion to physiological levels of gastrin was observed in the subjects who had their infection eradicated but not in those with persisting infection (table). A similar trend was seen with respect to supraphysiological gastrin stimulation.

Abstract 166

Summary: Eradication of H.pylori infection at time of stopping PPI therapy unleashes marked rebound acid hypersecretion which persists for at least 6 weeks. Rebound acid hypersecretion following PPI is not seen in those remaining H.pylori positive.

Conclusion: This acid hypersecretion induced by H.pylori eradication in patients previously receiving PPI therapy may explain the relation between H.pylori eradication and development of GERD.