Opportunity costs of gastrointestinal endoscopic training in Canada.

BACKGROUND: No data exist to define the opportunity costs related to instruction in endoscopic procedures in Royal College of Physicians and Surgeons of Canada-accredited teaching centres. Academic and institutional administrators expect staff to achieve acceptable performance standards. There is a need to measure some of the effects of training activity in the establishment of such standards. OBJECTIVE: To measure the effect of resident training in colonoscopy on real procedure times and, as a secondary goal, to estimate procedural losses related to the process of training. METHODS: Real procedure times for ambulatory colonoscopy in a single academic, hospital-based endoscopy unit were documented. Times for certified endoscopy instructors functioning solo were compared with times for procedures involving trainees at several levels of colonoscopic experience. Procedural reductions associated with resident training were estimated based on the parameters derived from the results. The analysis was executed retrospectively using prospectively collected data. RESULTS: Resident training prolonged procedure times for ambulatory colonoscopy by 50%. The trainee effect was consistent, although variable in degree, among a variety of endoscopy instructors. Such increased procedure times have the potential to reduce case throughput and endoscopist remuneration. CONCLUSIONS: Resident training in colonoscopy in a Canadian certified training program has significant negative effects on case throughput and endoscopist billings. These factors should be considered in any assessment of performance in similar training environments.

Fatal hemorrhage from a gastroaortic fistula secondary to gastric ulceration associated with Nissen fundoplication and nonsteroidal anti-inflammatory drug use.

Acute gastrointestinal hemorrhage from a gastroaortic fistula in the gastric fundoplication pouch is a rare complication of Nissen fundoplication. The present case reports a gastroaortic fistula secondary to gastric ulceration associated with prior Nissen fundoplication and nonsteroidal anti-inflammatory drug use. A 55-year-old man presented with massive hematemesis and died of exsanguination during emergency laparotomy. Recognition of factors that predispose a patient to gastric ulceration after fundoplication, including nonsteroidal anti-inflammatory drug use, is critical to arouse the high index of suspicion required to diagnose and manage this life-threatening complication.

Canadian research fellowship training programs in digestive sciences: achievements and challenges.

BACKGROUND: The Canadian Association of Gastroenterology (CAG) is committed to fostering the development of future Canadian investigators. Up to 1986, research fellowship support was obtained from the Medical Research Council (MRC) of Canada. Since that time, several peer-reviewed, industry-sponsored, CAG-supported research fellowships and a variety of independently funded awards have augmented this effort. In the same period, peer-reviewed operating grants (OGs) from the MRC and other agencies have been constrained. The aim of this study was to determine the success of CAG, MRC or any other Canadian research fellowships in the development of career investigators in digestive sciences and to identify factors influencing the outcomes of such training. METHODS: MRC records and the minutes of CAG annual meetings were reviewed to identify research fellowship support. Canadian program directors were requested to list research fellows affiliated with their groups between 1986 and 1997. Only fellowships providing at least 1 year of training were included. A 7-page questionnaire detailing biographic characteristics, the site and duration, and specific issues related to the quality of research training was sent to identified trainees. Significant associations between success in achieving an academic appointment or OG support and several variables of training were identified. RESULTS: Eighty-six research fellows were trained. Responses were obtained from 43 of them. The demographic characteristics of the whole group and the respondents were similar. Of the respondents, 81% of trainees obtained academic appointments. Fellowships longer than 1 year were associated with higher rates of academic posting, and MRC-funded fellows had greater success rates of academic appointments. Of eligible trainees 63% have obtained OG support. None of the other variables examined predicted success. Of the trainees responding, 85% valued the fellowship very highly. CONCLUSIONS: The establishment of the additional research fellowships has fostered the development of career investigators in digestive sciences. The high success rate of former trainees in obtaining academic appointments and OG support suggests that the fellowship programs are effective and appropriately oriented. The structure of the current programs does not require substantial revision. OG support for new investigators appears now to lag substantially.

Ulcerative colitis of the appendix ('ulcerative appendicitis') mimicking acute appendicitis.

Appendiceal involvement in ulcerative colitis may occur in the setting of either diffuse or distal disease, and is usually diagnosed incidentally at the time of proctocolectomy. The present patient had a rare case of 'ulcerative appendicitis' occurring on a background of clinically quiescent ulcerative colitis, and presented with the signs and symptoms of acute appendicitis.

Upper gastrointestinal toxicity of alendronate.

OBJECTIVE: Alendronate is rapidly gaining widespread use in the treatment of osteoporosis. However, recent postmarketing surveys and endoscopic studies suggest that its use may be associated with significant predictable esophageal and gastric mucosal toxicity, similar to that of aspirin and nonsteroidal anti-inflammatory drugs. Because treatment of osteoporosis may be needed in as many as 30% of all postmenopausal women, and considering that alendronate could be used in all postmenopausal women as prevention, definition of potential mucosal toxicity is crucial. Our aim was to study the upper gastrointestinal toxicity of alendronate in an age-appropriate female population using a clinically applicable dose (10 mg/day) to determine whether it causes predictable damage in the proximal gastrointestinal mucosa in a fashion similar to that seen with aspirin and nonsteroidal anti-inflammatory drugs. METHODS: We conducted a double-blind, randomized, placebo-controlled trial in 32 healthy female volunteers between the ages of 40 and 65 yr recruited by newspaper advertisement. Endoscopic mucosal abnormalities in the esophagus, stomach, and duodenum both before and after 1 month of treatment were scored and compared using validated endoscopic grading systems. Symptom scores before and after treatment were determined. Noninvasive measurements of gastrointestinal permeability were obtained before, during, and after treatment using sucrose and mannitol/lactulose urinary excretions. RESULTS: Endoscopic scores before and after treatment with alendronate were not significantly different. Similarly, mean symptom scores in the alendronate group did not change significantly after treatment. There were no significant mucosal permeability changes in the stomach or small intestine after treatment. CONCLUSION: Alendronate does not cause predictable esophageal, gastric, or duodenal mucosal damage when used as directed.

Predictive value of the Rome criteria for diagnosing the irritable bowel syndrome.

OBJECTIVE: Our aim was to examine the predictive value of the Rome criteria and absence of so-called "red flags" of clinical practice for diagnosing irritable bowel syndrome. Red flags were relevant abnormalities on physical examination, documented weight loss, nocturnal symptoms, blood in stools, history of antibiotic use, and family history of colon cancer. METHODS: In retrospective studies, 98 patients who had one or more Rome criteria and lacked red flags were identified by chart review of a 1-yr period. In prospective studies, 95 patients were identified who met the Rome criteria and lacked red flags. Sensitivity, specificity, predictive value of Rome criteria, and absence of red flags were determined. Consultant's final diagnosis was the gold standard. Investigations before and after referral were recorded and reason for referral was determined in prospective studies. RESULTS: In the retrospective series, the Rome criteria and absence of red flags had a sensitivity of 65%, specificity of 100%, and positive predictive value of 100%. None of these patients required revision of their diagnosis during a 2-yr follow-up. In the prospective study, the positive predictive value was 98%. More than 50% of the patients in this group had been referred because of diagnostic uncertainty and 24% had had an abdominal ultrasound; 66% of those <45 yr old underwent at least partial colonic evaluation. CONCLUSIONS: These findings suggest that the Rome criteria combined with a lack of red flags have a very high predictive value for diagnosing irritable bowel syndrome. Application of these diagnostic criteria has the potential to alter utilization of health care resources.

Primary adenocarcinoma in an enterocutaneous fistula associated with Crohn's disease.

Increasing numbers of intestinal adenocarcinomas in patients with Crohn's disease have been reported, but the strength of this association still needs to be elucidated. Adenocarcinoma has also been documented in different types of fistulous tracts associated with Crohn's disease. The first case of well-differentiated mucinous adenocarcinoma involving only enterocutaneous fistulae is reported in a patient with long-standing Crohn's disease complicated by persistent abdominal wall fistulous tracts. The malignant lesion arose from neoplastic transformation of columnar epithelium lining portions of the fistulae occurring as a result of either re-epithelialization of these inflammatory tracts or mural implantation of mucosal tissue secondary to prior ulceration. The patient has remained disease-free eight years after surgical resection of the tumour. Even though intestinal carcinoma is not as strongly associated with Crohn's disease as with ulcerative colitis, intestinal carcinoma should be considered in the setting of long-standing disease, previous intestinal exclusion surgeries and complications such as enterocutaneous or other types of fistulous tracts. The prognosis of such patients may be excellent with early diagnosis and treatment.

Synthesis of 1,2,3-tri-O-beta-lactosyl-D-threitol and 1-O-benzyl-2,3,4-tri-O-beta-lactosyl-D-threitol.

The coupling of 2,3,6,2',3',4',6-hepta-O-acetyl-alpha-lactosyl bromide with 1,4-di-O-benzyl-D-threitol using mercury(II) cyanide as a promoter, with subsequent deprotection of one or both of the benzyl groups, further glycosylation, and deacetylation afforded the title compounds. This class of compound is useful in the assessment of binding properties of D-galactopyranose to human and rabbit hepatocytes.

Binding of D-galactose-terminated ligands to rabbit asialoglycoprotein receptor.

The binding affinities of a series of D-galactose-terminated glycerol glycosides and oligosaccharides for the asialoglycoprotein receptor isolated from rabbit liver were determined in vitro using a radioreceptor-inhibition assay with 125I-asialoorosomucoid. The relative affinities of the synthetic ligands increased with the number of exposed D-galactose termini. Of the compounds examined, 1,2,3-tri-O-beta-lactosylglycerol associated with the greatest affinity (estimated Kd = 7.97 x 10(-5) M). Examination of the affinities of the synthetic series indicated that both the number and propinquity of the D-galactose termini influenced the strength of the binding interactions.

Evidence for T lymphocyte reactivity to the 65 kilodalton heat shock protein of mycobacterium in active Crohn's disease.

The role of mycobacterial heat shock proteins (Hsp) of the 65 kilodalton Hsp family as a possible factor governing cell-mediated immune responses, leading to chronic mucosal inflammation, was examined. Purified peripheral blood mononuclear cells (PBMC) from patients with CD and ulcerative colitis (UC), and from healthy and disease controls were stimulated in culture with a highly purified, recombinant 65 kilodalton Hsp (rHsp65) of M. bovis BCG for 5 d. Cultures were then pulsed with 3H-thymidine for 24 h and uptake determined by liquid scintillation. We found that PBMC from patients with active CD exhibited a significant proliferative response to the soluble rHsp65 as compared with normal controls. In contrast, the proliferative responses of PBMC from patients with inactive CD, inactive and active UC, pancreatitis and cecal carcinoma were found to be not different from controls. Purified T cells or non-T cells of PBMC in the absence of antigen-presenting cells from active CD patients exhibited a lack of proliferative responses to the rHsp65 stimulation in culture. The data indicate an aberrant sensitization of T cells to the 65 kilodalton mycobacterial Hsp in a specific type of IBD, and thus may provide an important clue for the etiopathogenesis of Crohn's disease.

Synthesis and characterization of 6-O-beta-lactosyl-alpha,beta-lactoses, 1-O-(6-O-beta-lactosyl-beta-lactosyl)-(R,S)-glycerols, and 4,6-di-O-beta-D-galactopyranosyl-alpha,beta-D-glucoses.

1,2,3,2',3',4',6'-Hepta-O-acetyl-beta-lactose (4) was coupled with 2,3,6,2',3',4',6'-hepta-O-acetyl-alpha-lactosyl bromide (7) in the presence of Hg(CN)2 to afford 1,2,3,2',3',4',6'-hepta-O-acetyl-6-O-(2,3,6,2',3',4',6'-hepta-O-acetyl-b eta- lactosyl)-beta-lactose (11) which, upon O-deacetylation, gave 6-O-beta-lactosyl-alpha,beta-lactoses (64% from 4). In contrast, the reaction of 7 with benzyl 2,3,2',3',4',6'-hexa-O-acetyl-beta-lactoside in the presence of Hg(CN)2 produced 3,6,2',3',4',6'-hexa-O-acetyl-1,2-O- (2,3,2',3',4',6'-hexa-O-acetyl-1-O-benzyl-beta-lactos-6-yl orthoacetyl)-alpha-lactose (63%) and 3,6,2',3',4',6'-hexa-O-acetyl-1,2-O-(1- cyanoethylidene)-alpha-lactose (27%). The glycosidation of 4 using 2,3,4,6-tetra-O-acetyl-alpha-D-galactopyranosyl bromide in the presence of Hg(CN)2 afforded, after deprotection, 4,6-di-O-beta-D-galactopyranosyl-alpha,beta-D-glucoses (66%). The reaction of 11 with 1,2-di-O-benzyl-(R,S)-glycerols and trimethylsilyl trifluoromethanesulfonate yielded, after deprotection, 1-O-(6-O-beta-lactosyl-beta-lactosyl)-(R,S)-glycerols (18%). Under the same coupling conditions 11 reacted with 2-O-benzylglycerol to form 3-O-acetyl-2-O-benzyl-1-O-[2',3',4',6'-hexa-O-acetyl-6-O-(2,3,6,2',3',4' ,6'- hepta-O-acetyl-beta-lactosyl)-beta-lactosyl]-(R,S)-glycerols (16%).

Analysis of direct tissue isoelectric focused protein profiles of resected intestinal mucosa and endoscopic biopsies from patients with inflammatory bowel disease.

Direct tissue isoelectric focusing was used as a procedure to analyze differences in soluble tissue protein profiles of resected intestinal segments and endoscopic biopsies from patients with ulcerative colitis, Crohn's disease, and colonic cancer. Extraction of tissue proteins was accomplished by electrophoresis of mucosal cryostat sections on agarose gels across a broad pH gradient. The inflamed colonic mucosa from Crohn's disease patients showed similar isoelectric focusing protein patterns. Small bowel mucosa from a patient with both colonic diverticular disease and Crohn's disease showed protein patterns identical with that of the mucosa from a patient with only Crohn's disease. The inflamed mucosae from ulcerative colitis patients revealed identical protein patterns but were distinct from those of non-inflamed ulcerative colitis mucosa and from the inflamed mucosae from Crohn's disease patients. Non-inflamed small bowel mucosae from cancer, ulcerative colitis, and Crohn's disease patients showed distinct protein patterns which were absent in the non-inflamed large bowel mucosae. The inflamed resected ileum of a Crohn's disease patient exhibited protein patterns similar to those of the biopsy of an inflamed mid-transverse large bowel. Mucosal biopsies from inflamed sigmoid colon of a Crohn's disease patient showed different protein patterns than those in biopsies from the inflamed mid-transverse colon. Thus, distinctive isoelectric focusing protein patterns may be useful in differentiating Crohn's colitis and ulcerative colitis when granulomata are absent, and in resolving indeterminant colitis to one of these classic inflammatory bowel diseases.

Synthesis and characterization of 6-O-beta-lactosyl-alpha,beta-D-mannopyranoses and 2,6-di-O-beta-lactosyl-alpha,beta-D-mannopyranoses.

The reaction of 2,3,6,2',3',4',6'-hepta-O-acetyl-alpha-lactosyl bromide (4) and benzyl 3,4-di-O-benzyl-alpha-D-mannopyranoside (3) in the presence of mercury(II) cyanide in benzene-nitromethane produced benzyl 3,4-di-O-benzyl-2,6-bis-O-(2,3,6,2',3',4',6'-hepta-O-acetyl-beta-lact osy l)-alph a D-mannopyranoside (5) and benzyl 3,4-di-O-benzyl-6-O-(2,3,6,2',3',4',6'-hepta-O-acetyl-beta-lactosyl)-alp ha-D- mannopyranoside (6), as part of a complex mixture. Column chromatography, followed by acetylation of the fraction containing 5 and 6, gave a sample of 5 and benzyl 2-O-acetyl-3,4-di-O-benzyl-6-O (2,3,6,2',3',4',6'-hepta-O-acetyl-beta-lactosyl)-alpha-D-mannopyranoside (7) in approximately 35% and 17% yields (based on 4), respectively. Deprotection of 5 and 7 afforded the target compounds, namely 2,6-di-O-beta-lactosyl-alpha,beta-D-mannopyranoses and 6-O-beta-lactosyl-alpha,beta-D-mannopyranoses, respectively. If the coupling of 4 with 3 were performed in the presence of silver trifluoromethanesulfonate and 2,4,6-trimethylpyridine, only a mixture of 3,6,2',3',4',6'-hexa-O-acetyl- alpha-lactose-1,2-[( 3,6,2',3',4',6'-hexa-O-acetyl-alpha-lactose 1,2-(benzyl 3,4-di-O-benzyl-alpha-D-mannopyranosid-6-yl orthoacetyl)-2-yl]orthoacetate) and 3,6,2',3',4',6'-hexa-O-acetyl-alpha-lactose 1,2-(benzyl 3,4-di-O-benzyl-alpha-D-mannopyranosid-6-yl orthoacetate) was obtained. The orthoacetates were characterized by n.m.r. spectroscopy. The two target materials are useful in the assessment of the binding properties of galactose-terminated ligands to the asialoglycoprotein receptor of normal rabbit and human hepatocytes.

Synthesis and characterization of 2-O-beta-lactosylglycerol, 1,2-di-O-beta-lactosyl-(R,S)-glycerols, and 1,2,3,-tri-O-beta-lactosylglycerol.

The reaction of 2,3,6,2',3',4',6'-hepta-O-acetyl-alpha-lactosyl bromide (5) and 1,3-di-O-benzylglycerol in the presence of mercury(II) cyanide in benzene-nitromethane afforded 1,3-di-O-benzyl-2-O-(2,3,6,2',3',4',6'-hepta-O-acetyl-beta-lactosyl)glyc erol (70%), which was converted into 2-O-beta-lactosylglycerol. 1,2-Di-O-beta-lactosyl-(R,S)-glycerols were obtained by way of the coupling of 5 to either 1-O-benzyl-(R,S)-glycerol or 1-O-benzyl-2-O-(2,3,6,2',3',4',6'-hepta-O-acetyl-beta-lactosyl)-(R,S)-gl ycerols. The most efficient route to 1,2, 3-tri-O-beta-lactosylglycerol (17) involved treatment of 2-O-(2,3,6,2',3',4',6'-hepta-O-acetyl-beta-lactosyl)glycerol with 3 mol. equiv. of 5 followed by removal of the blocking groups, to give 17 (47%).

Hapten-induced model of chronic inflammation and ulceration in the rat colon.

We have developed a simple and reproducible rat model of chronic colonic inflammation by the intraluminal instillation of a solution containing a "barrier breaker" and a hapten. Administration of the hapten 2,4,6-trinitrobenzenesulfonic acid (5-30 mg) in 0.25 ml of 50% ethanol as the "barrier breaker" produced dose-dependent colonic ulceration and inflammation. At a dose of 30 mg, trinitrobenzenesulfonic acid/ethanol-induced ulceration and marked thickening of the bowel wall persisted for at least 8 wk. Histologically, the inflammatory response included mucosal and submucosal infiltration by polymorphonuclear leukocytes, macrophages, lymphocytes, connective tissue mast cells, and fibroblasts. Granulomas were observed in 57% of the rats killed 3 wk after induction of inflammation. Langhan's-type giant cells were also observed. Segmental ulceration and inflammation were common. The characteristics and relatively long duration of inflammation and ulceration induced in this model afford an opportunity to study the pathophysiology of colonic inflammatory disease in a specifically controlled fashion, and to evaluate new treatments potentially applicable to inflammatory bowel disease in humans.

T-cell immunoregulation in patients with inflammatory bowel disease. I. Differential helper T-cell function in ulcerative colitis and Crohn's disease.

The role of helper T-cells in patients with ulcerative colitis (UC) and Crohn's disease (CD) was investigated. Peripheral blood B- and T-cells with or without monocytes were obtained from patients and normal adults of the same age and sex, and co-cultured for 10 days with pokeweed mitogen (PWM). Immunoglobulins (Ig) M, G and A were measured in the culture supernatants using a sensitive enzyme-linked immunosorbent assay. The quantity of Ig present in the culture supernatants was determined from a standard curve. Immunoglobulins M, G and A synthesis and secretion by B-cells in the presence of T-cells required monocytes and PWM. The data indicate that co-cultures of heterologous normal adult T-cells and B-cells with PWM did not significantly affect Ig synthesis as compared with autologous cultures. Autologous cultures of CD patients' B- and T-cells were found not to be significantly different from normals in their capacity to synthesize Ig. In contrast, autologous UC patients' B- and T-cells were found to be significantly less effective as compared with normal adults' co-cultures in the synthesis Ig. When CD patients' T-cells were in co-culture with normal adults' B-cells, Ig synthesis was maintained. However, a marked diminution in Ig synthesis was seen when UC patients' T-cells were used in co-culture with normal adults' B-cells. The degree of inhibition of immunoglobulin synthesis did not correlate with disease activity, duration of illness, location of disease, or corticosteroid treatment. These results suggest that patients with ulcerative colitis have an altered helper T-cell population while CD patients' T-cells are either normal or hyperactive in the capacity to provide helper function in PWM-induced immunoglobulin secretion by peripheral blood B-cells.

T-cell immunoregulation in patients with inflammatory bowel disease. II. Enhanced suppressor T-cell activity in ulcerative colitis.

In a recent study, we have shown that peripheral blood B cells from patients with ulcerative colitis (UC) synthesized less immunoglobulin (Ig) in co-culture with autologous T cells than normal adults' B cells. When UC patients' T cells were co-cultured with normal adults' B cells, Ig synthesis was significantly decreased as compared with normal controls. In contrast, Crohn's disease (CD) patients' B and T cells functioned normally. In the present study, the activity of suppressor T cells in patients with UC and CD was determined. Peripheral blood B and T cells with monocytes were obtained from patients and normal adults of the same age and sex, and co-cultured for 10 days with pokeweed mitogen (PWM). Suppressor T-cell function was measured in mixed co-culture assays in which graded numbers of normal or patient's T cells were added to normal adults' B and T cells with PWM. Immunoglobulins (Ig) M, G and A were measured in culture supernatants using a sensitive enzyme-linked immunosorbent assay. The quantity of Ig present in the culture supernatants was determined from a standard curve. T cells from UC patients significantly decreased immunoglobulin production by control B and T cells (IgM and IgA, p = 0.02; IgG, p = 0.01). In contrast, addition of T cells from CD patients produced no significant differences. Complement mediated, monoclonal OKT8 antibody directed cell lysis revealed that the inhibition observed with UC patients' T cells in co-culture was due to a T8+ suppressor T cell. The degree of inhibition of immunoglobulin synthesis did not correlate with disease activity, duration of illness, location of disease, or corticosteroid treatment. Thus, patients with ulcerative colitis display enhanced suppressor T-cell activity in peripheral blood while patients with CD show normal helper and suppressor T-cell functions. These results provide evidence supporting a role for altered immunoregulatory activity in the pathogenesis of ulcerative colitis.

Spontaneous intramural esophageal hematoma. Diagnosis by CT scanning.

We describe a patient who suffered a spontaneous intramural esophageal hematoma while taking aspirin and dipyridamole. The diagnosis was initially made at endoscopy, with confirmation by computed tomography (CT). CT scanning was particularly valuable in both the diagnosis and in the follow-up of this lesion. As the prognosis for a spontaneous intramural esophageal hematoma is good with conservative management, its specific definition by computed tomography should facilitate proper management decisions.

Isotretinoin-associated proctosigmoiditis.

A 17-yr-old boy developed acute proctosigmoiditis after the institution of isotretinoin for the treatment of cystic acne vulgaris. Painless diarrhea, accompanied by mucus and eventually blood, began within days of commencing treatment and persisted while the drug was administered. At sigmoidoscopy patchy mucosal inflammation associated with numerous discrete aphthous ulcers was seen, apparently restricted to the rectosigmoid. Histologic examination of the affected mucosa revealed an acute focal superficial inflammatory infiltrate. Withdrawal of the drug resulted in prompt resolution of symptoms and a reduction in the severity of the inflammation. Rechallenge with isotretinoin induced a second, almost identical, attack of proctosigmoiditis. Withdrawal was again followed by disappearance of symptoms, and a subsequent sigmoidoscopy and mucosal biopsy were normal. The patient has remained clinically well for 16 mo after his initial presentation. Although the pathogenesis of the colonic mucosal inflammation remains unknown, the relationship of the bouts of proctosigmoiditis to the administration of isotretinoin strongly suggests that the drug was directly responsible.

Indium-111-labeled autologous leukocyte imaging and fecal excretion. Comparison with conventional methods of assessment of inflammatory bowel disease.

This study was designed to evaluate the role of 111In-labeled leukocyte imaging and fecal excretion in the assessment of inflammatory bowel disease. We compared these tests to various indices of disease activity in Crohn's disease, to Truelove's grading in ulcerative colitis, and to endoscopy, x-ray, and pathology in both diseases. Eleven controls, 16 patients with Crohn's disease, 13 with ulcerative colitis, and 3 with other types of acute bowel inflammation were studied (positive controls). Indium scanning was performed at 1, 4, and 24 hr. Fourteen of 16 patients with active Crohn's disease had positive scans but in only five was localization accurate. One patient had inactive ulcerative colitis, and the scan was negative. Of 12 patients with active ulcerative colitis, 10 had positive scans but disease localization was accurate in only four. Disease extent was correctly defined in 1 of the 3 Positive Controls. There was no significant difference in the accuracy of scanning at 1, 4, or 24 hr. 111In fecal excretion was significantly higher in patients with inflammatory bowel disease than in controls, and there was correlation between 111In fecal excretion and most of the indices of disease activity in Crohn's disease. In ulcerative colitis, 111In fecal excretion did not correlate with Truelove's grading but reflected colonoscopic assessment of severity. In conclusion, 111In-labeled leukocyte scanning lacks sensitivity with respect to disease extent, but fecal excretion of 111In correlates well with disease severity as determined by other methods.