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These guidelines provide a practical and evidence-based resource for the management of patients with Barrett's oesophagus and related early neoplasia. The Appraisal of Guidelines for Research and Evaluation (AGREE II) instrument was followed to provide a methodological strategy for the guideline development. A systematic review of the literature was performed for English language articles published up until December 2012 in order to address controversial issues in Barrett's oesophagus including definition, screening and diagnosis, surveillance, pathological grading for dysplasia, management of dysplasia, and early cancer including training requirements. The rigour and quality of the studies was evaluated using the SIGN checklist system. Recommendations on each topic were scored by each author using a five-tier system (A+, strong agreement, to D+, strongly disagree). Statements that failed to reach substantial agreement among authors, defined as >80% agreement (A or A+), were revisited and modified until substantial agreement (>80%) was reached. In formulating these guidelines, we took into consideration benefits and risks for the population and national health system, as well as patient perspectives. For the first time, we have suggested stratification of patients according to their estimated cancer risk based on clinical and histopathological criteria. In order to improve communication between clinicians, we recommend the use of minimum datasets for reporting endoscopic and pathological findings. We advocate endoscopic therapy for high-grade dysplasia and early cancer, which should be performed in high-volume centres. We hope that these guidelines will standardise and improve management for patients with Barrett's oesophagus and related neoplasia.

Objective: To determine the ability of selective antibody testing to screen for coeliac disease in the presence of IgA deficiency and to define the sensitivity of a pathway using this method., Method: All IgA and IgG anti-tTG tests performed at our centre between January 2008 and December 2009, using the Immunocap 250 analyser, were retrospectively reviewed. Positive results were correlated with histology. Results were used to validate our diagnostic pathway., Results: 12 289 consecutive serological tests were reviewed. IgA deficient patients gave either an 'error' reading or very low response on the Immunocap 250 analyser. Subsequent testing of this sub-group demonstrated raised IgG anti-tTG antibodies in those with histologically proven coeliac disease., Conclusions: Using our antibody screening pathway, which involves the selective use of IgG anti-tTG, sensitivity increased from 87% to 92% in those with IgA deficiency. Adoption of this pathway for coeliac screening would negate the routine screening of immunoglobulin levels, with resultant cost saving.

Background & Aims: Esophageal adenocarcinoma (EA) is increasingly common among patients with Barrett's esophagus (BE). We aimed to provide consensus recommendations based on the medical literature that clinicians could use to manage patients with BE and low-grade dysplasia, high-grade dysplasia (HGD), or early-stage EA., Methods: We performed an international, multidisciplinary, systematic, evidence-based review of different management strategies for patients with BE and dysplasia or early-stage EA. We used a Delphi process to develop consensus statements. The results of literature searches were screened using a unique, interactive, Web-based data-sifting platform; we used 11,904 papers to inform the choice of statements selected. An a priori threshold of 80% agreement was used to establish consensus for each statement., Results: Eighty-one of the 91 statements achieved consensus despite generally low quality of evidence, including 8 clinical statements: (1) specimens from endoscopic resection are better than biopsies for staging lesions, (2) it is important to carefully map the size of the dysplastic areas, (3) patients that receive ablative or surgical therapy require endoscopic follow-up, (4) high-resolution endoscopy is necessary for accurate diagnosis, (5) endoscopic therapy for HGD is preferred to surveillance, (6) endoscopic therapy for HGD is preferred to surgery, (7) the combination of endoscopic resection and radiofrequency ablation is the most effective therapy, and (8) after endoscopic removal of lesions from patients with HGD, all areas of BE should be ablated., Conclusions: We developed a data-sifting platform and used the Delphi process to create evidence-based consensus statements for the management of patients with BE and early-stage EA. This approach identified important clinical features of the diseases and areas for future studies., (Copyright © 2012 AGA Institute. Published by Elsevier Inc. All rights reserved.)

Background: Endoscopic retrograde cholangiopancreatography (ERCP) relies on the use of ionising radiation but risks to operator and patient associated with radiation exposure are unclear. The aim of this prospective study was to estimate the radiation dose received by personnel performing fluoroscopic endoscopic procedures, mainly ERCP., Methods: Consecutive procedures over a two month period were included. The use of thermoluminescent dosimeters to measure radiation exposure to the abdomen, thyroid gland, and hands of the operator permitted an estimation of the annual whole body effective dose equivalent., Results: During the study period 66 procedures (61 ERCP) were performed and the estimated annual whole body effective dose equivalent received by consultant operators ranged between 3.35 and 5.87 mSv. These values are similar to those received by patients undergoing barium studies and equate to an estimated additional lifetime fatal cancer risk between 1 in 7000 and 1 in 3500. While within legal safety limits for radiation exposure to personnel, these doses are higher than values deemed acceptable for the general public., Conclusions: It is suggested that personnel as well as patients may be exposed to significant values of radiation during ERCP. The study emphasises the need to carefully assess the indication for, and to use measures that minimise radiation exposure during any fluoroscopic procedure.

Background: A key step for success at endoscopic retrograde cholangio-pancreatography (ERCP) is cannulation of the sphincter of Oddi. This prospective randomised controlled study was conducted to assess the effect of glyceryl trinitrate (GTN) on ease of cannulation., Method: Two hundred and fifty four patients undergoing ERCP were randomised into two groups, 126 controls and 128 pre-treated with GTN., Result: There were 29 cannulation failures in the whole group (overall failure rate of 11.4%). Failure was significantly less common in the GTN group, 7.03% (9/128) as compared with 15.8% (20/126) in the control group (p=0.0002). Deep cannulation was desired but not achieved in 45/200 patients (22.5%) Of these, 18.4% (19/103) were in the GTN group versus 26.8% (26/97) in the control group. This pattern of difference applied to both trained and trainee endoscopists. No significant side effects of GTN were noticed., Conclusion: GTN appears to be safe and effective in improving ERCP success rate. We recommend its routine use.

Background and Study Aims: A clean colon is essential for an efficient examination. The aim of this study was to compare a novel low-dose, low volume triple regimen with Fleet Phospho-soda., Methods: A blinded, experienced colonoscopist examined 132 consecutive patients randomly allocated to receive either a triple regimen consisting of senna syrup (sennoside B), Picolax (sodium picosulphate), and Klean Prep (polyethylene glycol 3350), or Fleet Phospho-soda (sodium dihydrogen phosphate and disodium phosphate dodecahydrate). The colonoscopist recorded cleanliness according to a scoring system (1-very clean to 4-solid stools), and time taken to reach the caecum., Results: In the triple regimen group (n = 81), 73% scored 1 or 2 compared with 57% in the Fleet Phospho-soda group (n = 51, p = 0.037 Mann-Whitney U-test). Examination to caecum was achieved in 95% of the triple regimen group and 89% of the Fleet Phospho-soda group. Among those examined as far as the caecum, the time to reach the caecum was 11 minutes (range 5-50) in the triple regimen group compared with 16 minutes (range 5-65) in the Fleet Phospho-soda group (p = 0.08, Mann-Whitney U-test). Patient tolerability was not assessed in this study., Conclusions: This novel triple regimen produces a cleaner colon than Fleet Phospho-soda, is associated with a trend towards a quicker and more efficient colonic examination, and is also 30% cheaper per patient.

Background: The duration of Helicobacter pylori eradication regimens has decreased to 1 week with cure rates of over 90%. This can be attributed to the use of triple drug regimens including potent inhibitors of gastric acid secretion and clarithromycin. There is no theoretical reason why shorter regimens should not be possible., Aim: To compare two 3-day, low-dose, twice daily regimens with 1 week of omeprazole 20 mg b.d., clarithromycin 250 mg b.d., and metronidazole 400 mg b.d. (OCM) METHODS: Outpatients referred for gastroscopy were screened by biopsy urease test. H. pylori-positive patients were randomized to receive either lansoprazole 30 mg b.d., tri-potassium dicitrato bismuthate one tablet b.d., clarithromycin 250 mg b.d., and amoxycillin 1 g b.d. for 3 days (LTdbCA), or ranitidine bismuth citrate 400 mg b.d., clarithromycin 250 mg b.d. and amoxycillin 1 g b.d. for 3 days (RbcCA) or omeprazole 20 mg b.d., clarithromycin 250 mg b.d. and metronidazole 400 mg b.d. for 1 week (OCM). They were not pre-treated with a gastric acid inhibitor. After 8 weeks, H. pylori status was assessed by 13C urea breath test., Results: 974 out of 1114 patients referred for gastroscopy were screened by biopsy urease test. 140 patients were not screened either because they were anticoagulated or for technical reasons. 334 patients were H. pylori-positive: 154 were excluded mostly because of allergy to penicillin and personal reasons but 180 were randomized to treatment All regimens were well tolerated. For LTdbCA (n=60), RbcCA (n=59), and OCM (n=61) the H. pylori cure rates (95% CI) were 23% (12-34), 14% (5-23) and 87% (79-95), respectively, using intention-to-treat analysis and 25% (14-36), 15% (6-24) and 88% (80-96), respectively, if analysed per protocol. OCM was significantly superior to LTdbCA and RbcCA (P < 0.001) but there was no significant difference between regimens LTdbCA and RbcCA., Conclusions: OCM is an extremely effective H. pylori eradication regimen. The 3-day regimens tested both have poor cure rates. Pre-treatment with a proton pump inhibitor, higher doses or more frequent dosing may be necessary to increase the cure rate of short duration regimens. However, this could make them less acceptable than the H. pylori eradication regimens currently available.

Objective: To associate Helicobacter pylori-associated antibodies with clinical disease in groups of patients with duodenal ulcer, gastric adenocarcinoma, oesophageal adenocarcinoma and normal mucosa., Design: Prospective observational sero-epidemiology study. Identification of consecutive in-patients with duodenal ulcer, gastric adenocarcinoma, oesophageal adenocarcinoma and normal mucosa. Analyses of sera for antibodies to whole H. pylori, Cag A and Vac A antigens using ELISA and Western blot. Statistical analyses., Setting: Walsgrave Hospital, Coventry, a district general hospital that serves a population of 350,000., Participants: Consecutive in-patients with an endoscopic diagnosis of duodenal ulcer (n = 31), gastric adenocarcinoma (n = 31), oesophageal adenocarcinoma (n = 40) and normal mucosa (n = 46)., Main Outcome Measures: A profile of antibodies was constructed for each patient group and between-group comparisons were made. A logistic regression model determined the H. pylori-associated antibody that could best predict a patient's diagnosis. A discriminatory power for each antibody was calculated., Results: Whole H. pylori, Cag A and Vac A antibodies are found more commonly in duodenal ulcer patients when compared to oesophageal adenocarcinoma (P < 0.003) and normal mucosa patients (P < 0.015). Similarly, gastric adenocarcinoma patients have antibodies to whole H. pylori, Cag A and Vac A more frequently than oesophageal adenocarcinoma (P< 0.002) and normal mucosa patients (P < 0.006). Vac A antibodies discriminate between duodenal ulcer/gastric adenocarcinoma and oesophageal adenocarcinoma/normal mucosa patients (odds ratio 5.56, log likelihood -90.06, P < 0.001) more effectively than Cag A antibodies (odds ratio 4.17, log likelihood -91.88, P < 0.001)., Conclusions: Similar profiles of H. pylori-associated antibodies are seen in patients with duodenal ulcer and gastric adenocarcinoma, confirming that virulent H. pylori are involved in the pathogenesis of both diseases. Antibodies to Vac A could be used to identify patients at increased risk of developing H. pylori-associated disease.

The traditional definition of coeliac disease is inadequate because it includes only patients with abnormal small intestinal morphology. Gluten sensitivity is a systemic disorder whose common factor is an immune response to gluten in the context of the susceptible 'coeliac' HLA haplotype and possibly environmental triggers. Gluten sensitivity embraces traditional coeliac disease as well as subjects with normal small bowel morphology including latent coeliac disease, dermatitis herpetiformis, and symptomatic gluten intolerance. The diagnosis of gluten sensitivity and coeliac disease are not mutually inclusive. Small intestinal biopsy and clinical criteria are essential in diagnosing classical coeliac disease. IgA endomysial antibody is valuable in identifying gluten sensitivity and has particular value as a screening test. Serology should include total IgA levels to exclude selective IgA deficiency, a potential cause of false negative IgA endomysial antibody. A combination of histology, serology and clinical criteria will identify most cases of coeliac disease and gluten sensitivity.

Background: There are no published comparative studies on the effect of low-dose H2-antagonists on pentagastrin-stimulated gastric acid secretion., Methods: Twenty-four healthy subjects were dosed with either famotidine 10 mg, ranitidine 75 mg or placebo in a balanced three-period cross-over design. The subjects were studied in groups of 12, simultaneously, under identical controlled environmental conditions. Gastric juice was aspirated in 15-min aliquots during sub-maximal (0.6 microgram.h/kg) intravenous pentagastrin stimulation in the third and fourth hours (early period) and the eighth and ninth hours (late period) after oral dosing. The hydrogen ion (H+) content of gastric juice was measured ex vivo, by titrating to pH7 known volumes of gastric aspirate against 0.1 M sodium hydroxide, using a versatile microprocessor-controlled auto-titration unit. Gastric acid output during the period of interest was calculated by adding the hydrogen ion content of 15-min aliquots collected during that period. The geometric mean of the cumulative pentagastrin-stimulated gastric acid output during the early and late periods was determined for the subjects dosed with either famotidine, ranitidine or placebo. Comparisons were performed by ANOVA., Results: During the early period (2-4 h post-dose), When the subjects were given placebo, mean gastric acid output was 46.6 mmol, decreasing by 76% to 11.3 mmol (P < 0.001) when treated with famotidine and by 76% to 11.1 mmol (P < 0.001) when treated with ranitidine. During the late period (7-9 h post-dose), when the subjects were dosed with placebo, mean gastric acid output was 41.2 mmol, decreasing by 38% to 25.7 mmol (P < 0.001) when treated with famotidine and by 27% to 30.0 mmol (P = 0.007) when treated with ranitidine. The difference between the inhibitory effects of famotidine and ranitidine on gastric acid output were non-significant during either period., Conclusions: Low-dose famotidine and ranitidine, intended for over-the-counter use, inhibit stimulated gastric acid secretion profoundly in the third and fourth hours after an oral dose. Modest effects are still detectable up to 9 h after dosing.

Thirty two patients (74 (43-93) years; median, (range)) with dysphagia because of inoperable, unresectable or recurrent oesophagogastric carcinoma were treated by ethanol induced tumour necrosis (ETN). Endoscopic injection of absolute alcohol was performed using a variceal injector needle, with 0.5-1 ml aliquots injected retrogradely from distal to proximal tumour margin. Dilatation to 12 mm was used only if the endoscope would not traverse the stricture. In patients with total occlusion, injection into the proximal tumour was followed by a repeat endoscopy 3-7 days later. Dysphagia was graded from 0 = no dysphagia to 4 = total dysphagia. The significance of changes in the dysphagia grade after ETN were assessed using the Wilcoxon rank sum test. Results (median (range)) were as follows: stricture length = 5.0 cm (1-15). Dysphagia grade before treatment was 3 (2-4) improving after first treatment to 1 (0-3), p < 0.003. Best dysphagia grade achieved was 1 (0-3) and interval between treatments was 28.5 days (4-170). The volume of ethanol injected = 10 ml (1.5-29) and survival after first treatment was 93 days (6-660). The number of treatment sessions required to achieve best grade = 1 (1-3). There were no treatment complications. ETN significantly improves dysphagia. Results of palliation are similar to those of laser therapy, but can be achieved quickly and safely on a day case basis in most patients and at a small proportion of the cost.

Objective: To search for evidence of subclinical neurotoxicity in patients treated with tripotassium dicitrato bismuthate., Design: Prospective, controlled, triplicate study using urinary bismuth concentration, magnetic resonance imaging (MRI), nerve conduction studies, visual evoked response and a battery of 10 neuropsychological screening tests., Setting: Out-patient clinics, Walsgrave Hospital, Coventry, UK., Subjects: Fourteen dyspeptic patients; 8 (treatment group) treated with tripotassium dicitrato bismuthate one tablet q.d.s and 6 (control group) treated with ranitidine 150 mg b.d. for 8 weeks., Main Outcome Measures: Changes in urinary bismuth, MRI, nerve conduction studies, visual evoked response, and neuropsychological tests performed before, immediately after and 8 weeks after the cessation of treatment., Results: In the treatment group the median (range) urinary bismuth concentration was 1 (1-12) ng/ml before treatment, increased to 560 (140-1300) immediately after treatment (P < 0.01, Wilcoxon Rank Sum test) and was still significantly elevated (23 (7-53) ng/ml) 8 weeks after the cessation of treatment. In the patient who recorded the highest urinary bismuth, a high intensity signal appeared in the globus pallidus immediately after treatment and was still present (though diminished in intensity) 8 weeks after the cessation of treatment. This isolated MRI finding was not associated with evidence of subclinical neurotoxicity. No changes in the MRI, nerve conduction studies, visual evoked response and neuropsychological tests were observed among the other patients studied., Conclusions: Bismuth accumulation occurs in patients receiving a conventional course of treatment with tripotassium dicitrato bismuthate but this is not associated with significant changes in the nervous system.

Intestinal pseudo-obstruction is defined as a syndrome in which there are signs and symptoms of intestinal obstruction without an actual obstructing lesion. In many cases it is associated with other disease entities but may be idiopathic. We report a case associated with partial malrotation of the gut which has not been described in the literature before.

To study changes in rectal mucosa that might be attributable to the effects of gluten, rectal biopsy specimens from untreated and treated gluten sensitised subjects were analysed morphometrically and by immunohistochemical techniques and were compared with a series of disease control mucosae. Although morphometry showed increased populations of plasma cells, lymphocytes, and mast cells in the mucosae of untreated patients, which were reduced (except for mast cells) by dietary gluten restriction, immunohistochemical techniques were far more sensitive in defining these changes. There were highly significant increases in CD3+ and gamma delta+ lymphocytes within both the lamina propria and the epithelium while neutrophils (CD15+ cells) were not at all prominent. Activated (CD25+) lymphocytes expressing interleukin (IL)-2 receptors were increased in lamina propria, usually subjacent to basal lamina, although a few IL-2R+ intraepithelial lymphocytes were found: other IL-2R+ cells were deemed to be macrophages (CD68+). These results clearly indicate that in untreated, gluten sensitised subjects the rectal mucosa shows a lymphoplasmacytoid reaction that is responsive to gluten restriction. The absence of neutrophilia suggests that this lesion is not a conventional inflammatory type proctitis, but rather one presumed to be induced by gluten antigen(s) present in the faecal stream--that is, a cell mediated form of response.

The proportion of intra-epithelial lymphocytes (IEL) that utilize the gamma/delta form of the T-cell receptor (TCR) is increased in coeliac disease, but their function remains unexplained. The response of intra-epithelial lymphocytes to rectal gluten challenge in coeliac and control subjects was studied after a rectal challenge of 2 g of Frazer's fraction III. A marked rise in CD3+ IEL occurred after challenge in the coeliac patients, peaking at 6 h and returning to normal by 48 h, with no significant changes in the gamma/delta TCR+ IEL. The IEL did not significantly change after gluten challenge in the controls. Acute gluten challenge induces infiltration of the rectal mucosa by T cells in coeliac patients, which is not accompanied acutely by increased numbers of gamma/delta TCR+ IEL. This study supports the hypothesis that alpha/beta TCR+ T cells may be of importance in the early response of coeliac patients to local gluten challenge.

Percutaneous endoscopic insertion of gastrostomy tubes is a technique becoming more widely used in the UK. It allows insertion of a gastrostomy tube without laparotomy, under local anaesthesia and sedation, and so operative insertion may eventually become a rarity. We report on our successful early experience with a new gastrostomy tube (Bower PEG) which does not require endoscopy if eventual removal is required, and describe the methods of insertion and removal.

A 60-year-old female patient with a 3-year history of nausea underwent oesophagogastroduodenoscopy. Red lesions were found in the cervical oesophagus: one of 2 cm and the other less than 1 cm. These lesions were biopsied and the larger lesion showed typical gastric mucosa. Following 40 mg/day omeprazole for 3 days all symptoms disappeared. Treatment was stopped after the patient remained symptom-free for 4 weeks.

44 patients referred consecutively for jejunal biopsy underwent rectal gluten challenge with 2 g peptic-tryptic digest (Frazer's fraction III; FF3). Rectal biopsy was done before the challenge and 6 h afterwards. Total intraepithelial lymphocytes (IEL) overlying a 10(4) micron 2 test area of muscularis mucosae were quantified by computerised image analysis. The subjects comprised 21 controls with disorders other than coeliac disease and 23 patients (14 treated, 9 untreated) with coeliac disease diagnosed by strict jejunal biopsy gold standard criteria. There was no difference between the groups in IEL numbers before challenge. Coeliac disease patients but not controls responded to FF3 with a rise in mucosal IEL (median 60.5% rise for treated, 63.0% for untreated). There was no response to challenge with beta-lactoglobulin in coeliac disease or control subjects. When a predefined, post-challenge IEL "predictive index" of more than 10% above baseline was used to indicate a diagnosis of coeliac disease, it gave a sensitivity of 90% and specificity of 91% (95% confidence intervals 78-93%). Rectal gluten challenge is a simple, safe, and reliable test of gluten sensitivity, both as a screening test for untreated coeliac disease and as a confirmatory test in patients with treated coeliac disease.

One hundred and sixty-two of 182 patients with coeliac disease provided satisfactory details of family size and the prevalence of coeliac disease and inflammatory bowel disease among their first-degree relatives. Patients ranged in age from 11 months to 79 years with a mean age of 41 (+/- 23) years. Twenty patients had at least one first-degree relative with coeliac disease: a total of 25 of 861 relatives were affected (prevalence = 2904/100,000) compared with an expected 0.9 cases (prevalence = 100/100,000; p less than 0.001). Six relatives had inflammatory bowel disease (prevalence = 697/100,000) compared with an expected 1.3 cases (prevalence = 150/100,000; p less than 0.001). Five of these had ulcerative colitis, and one had Crohn's disease. The relative risk of ulcerative colitis is, therefore, five times greater for first-degree relatives of people with coeliac disease than for the general population (95 per cent confidence interval, 4.7-7.2). There is a clear association between coeliac disease and ulcerative colitis, which may point to factors involved in the aetiology of colitis.

A proportion of epithelial lymphocytes in various mammalian species is characterised by cells containing cytoplasmic granules. We have studied the total number of granular lymphocytes within surface and crypt epithelium of jejunal mucosae (per 10(4) micron2 muscularis mucosae) from six groups of subjects, comprising (i) young healthy volunteers (ii) family relatives of known coeliac patients, patients with gastrointestinal disorders associated with either (iii) normal or (iv) "flat" mucosae, and groups of (v) untreated and (vi) treated patients with coeliac disease. There was no difference in the absolute number of gEL between the three control groups with normal mucosal architecture, the proportion of granular to total EL per unit of tissue varying between 30-40%. In untreated coeliac mucosae, there was a significantly increased population of gEL, compared with the same control groups (p less than 0.001): the ratio of granular to total EL approximated 65%, and did not differ from flat-control mucosae in which the proportion of gEL was 55%. On withdrawal of gluten, the absolute number of gEL fell significantly in comparison with the untreated coeliac group (p less than 0.05). To further evaluate the effect of gluten challenge, granular lymphocytes were monitored during a five-day period in groups of treated coeliac patients orally challenged with increasing doses (500-3000 mg) of a peptic-tryptic digest of gluten. A significant rise in the absolute number of granular lymphocytes occurred at 12 h, but without any deterioration in mucosal architecture.

Oesophageal injury is a well recognized complication of certain oral medications but warfarin has not been implicated previously. We present a case of an oesophageal ulcer occurring in a patient with mitral regurgitation taking warfarin, and demonstrate a delayed oesophageal tablet transit time.

The immunopathologic, structural, and functional changes within rectal mucosa of known celiac sprue subjects were quantitated during local challenge with a peptic-tryptic digest of gluten. In the celiac sprue patients challenged with 2 g of digest, major effects occurred in lamina propria, submucosa, and local microvasculature. The lamina propria swelling was biphasic, starting 1-2 h after challenge with widespread extravascular deposition of fibrinogen, indicative of increased microvascular permeability, receding by 24 h postchallenge. A rapid fall in mast cells together with granule discharge suggested their involvement in this response. The late-phase swelling (48-72 h) was preceded by a rapid influx of neutrophils and basophils, the latter showing evidence of degranulation beyond 72 h. Reestablishment of vessel lumina, a rise in mast cells, and loss of neutrophils indicated tapering of the inflammatory cellular cascade by 96 h. Lymphocytes, first seen to enter the lamina by 2 h postchallenge, increased progressively, thereby resulting in substantial infiltration between 36 and 96 h. A marked rise in epithelial lymphocytes, maximal at 6-8 h, waned by 24 h. Volumes of surface and crypt epithelium remained constant throughout. In another challenge series with 4 g of gluten digest, electrical potential difference across rectal mucosa decreased significantly 12 h postchallenge, but the associated decreases in net sodium and chloride absorptive fluxes were insignificant. It is concluded that rectal mucosa is sensitized to gluten in celiac sprue disease and thus offers a promising and convenient in vivo substrate for investigative and diagnostic purposes.