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Enterocolic lymphocytic phlebitis (ELP) is a recently described disease characterized by phlebitis in the wall and mesentery of the colon and small bowel. Unlike other systemic or localized vasculitic diseases that can have similar gastrointestinal manifestations, there is no involvement of the arterial system or evidence of systemic vasculitis. The lymphocytic phlebitis affects not only the grossly involved intestinal segment but also the apparently healthy bowel. The diagnosis of ELP is histologic, and other systemic vasculitis must be ruled out. Surgical resection of the bowel not only provides the diagnostic tissue but also leads to resolution of the symptoms. In the literature, ELP has most commonly been reported to present as an acute abdomen. We describe a case of ELP presenting as a large abdominal mass, without evidence of an acute abdomen. This mass was actually diffusely thickened colonic serosa, caused by extensive organizing fat necrosis and marked edema of the serosa and bowel wall.

Objective: Crohn's disease (CD) and ulcerative colitis (UC) may both affect the colon. However, in approximately 10-20% of these cases, it is impossible to distinguish between these two entities either clinically or histologically, and a diagnosis of indeterminate colitis (IC) is made. Correct diagnosis is important because surgical treatment and long-term prognosis differ for UC and CD. The purpose of this study was to determine the extent of interobserver agreement among board-certified pathologists and a specialist gastrointestinal (GI) pathologist regarding the histological diagnosis of colonic inflammatory bowel disease (IBD)., Methods: A total of 24 university medical center pathologists from eight institutions evaluated 84 colectomy specimens and 35 sets of biopsy specimens from 119 consecutive patients with colonic IBD. A specialist GI pathologist subsequently reviewed all cases without knowledge of clinical data and prior diagnosis., Results: The GI pathologist's diagnoses differed from the initial diagnoses in 45% of surgical specimens and 54% of biopsy specimens. Of 70 cases initially diagnosed as UC, 30 (43%) were changed to CD or IC, whereas 4 of 23 cases (17%) initially diagnosed as CD were changed to UC or IC. The kappa coefficient for the overall agreement of initial diagnoses with the specialist GI pathologist's diagnoses was -0.01 (p = 0.98)., Conclusions: There is significant interobserver variation in the histological diagnosis of colonic IBD. This may have a profound effect on clinical patient care and, especially, on the choice of operation. More accurate diagnostic criteria are needed to facilitate patient care and to optimize treatment outcome.

Lymphocytic colitis (LC) is classically described as a triad of chronic nonbloody, watery diarrhea, normal or nearly normal endoscopy findings, and colonic epithelial lymphocytosis without a thickened subepithelial collagen table (SECT). It is unknown how often patients with colonic epithelial lymphocytosis without a thickened SECT actually present with this classic triad. Cases diagnosed histologically as lymphocytic or microscopic colitis were reviewed. Criteria for inclusion were the presence of at least 15 surface lymphocytes per 100 epithelial cells and the absence of a thickened SECT (<12 microm). Clinical features and course were recorded by chart review and telephone follow-up. Forty patients met the inclusion criteria, including 25 women and 15 men with a mean age of 63.2 years (range, 25-83 years). Twenty-eight patients had the classic triad and were designated as having classic LC. The other 12 patients fulfilled the histologic criteria but not the clinical or endoscopic criteria for classic LC and were classified as having atypical LC (constipation, five patients; macroscopic colitis at endoscopy, five patients; hematochezia, one patient; and incidental finding, one patient). Clinically, patients with classic LC were predominantly women and had a higher incidence of autoimmune disease (p = 0.03) than did those with atypical LC. Histologically, surface eosinophilia was significantly greater in patients with classic LC (p = 0.04). Twenty patients were using nonsteroidal antiinflammatory drugs at the time of their colonic biopsy. Surface epithelial lymphocyte counts were higher in these patients, particularly in the distal sigmoid colon (p = 0.02). Fourteen patients had associated autoimmune disease, including three patients with sprue diagnosed by small bowel biopsy, all of whom responded to gluten withdrawal. Diarrhea present in 25 patients, without documented evidence of celiac sprue, was self-limited in five, resolved with treatment in three, required intermittent treatment in eight, daily treatment in five, and was refractory to treatment in four. All eight patients who experienced spontaneous or treatment-related symptom resolution had classic LC. No histologic feature correlated with clinical course. In conclusion, our study shows that colonic epithelial lymphocytosis without a thickened SECT is a histologic finding seen in a heterogeneous group of patients. Within this heterogeneous group is a distinct subset of patients who have the classic clinicopathologic triad of LC. This subset of patients has striking similarities to patients with collagenous colitis, lending further support to a close relationship between these two entities. Atypical LC comprises a heterogeneous group and includes patients with idiopathic constipation, coexisting LC and inflammatory bowel disease, and possibly infectious colitides. Because of the clinical heterogeneity among our study population, the descriptive term colonic epithelial lymphocytosis may be a more prudent diagnosis than lymphocytic colitis in the absence of adequate clinical information.

Objectives: To determine what structures fluoresce and to what extent in normal colon and colonic adenomas to fully exploit laser-induced fluorescence spectroscopy as a tool for the diagnosis of dysplasia at endoscopy., Methods: Unstained frozen sections of normal colon and colonic adenomas were studied by fluorescence microscopy under 351-364-nm argon ion laser excitation. Tissue fluorescence was observed and compared to morphology in serial sections stained with hematoxylin and eosin (H&E), Movat pentachrome, mucicarmine, and oil red O., Results: In normal colon, fluorescence correlated morphologically with connective tissue fibers (principally collagen) in all layers of the bowel wall and with cytoplasmic granules within eosinophils present between the crypts in the lamina propria of the mucosa. Fluorescence of absorptive cells in normal crypts was very faint, and Goblet cells did not fluoresce. However, marked fluorescence was observed in the cytoplasms of dysplastic epithelial cells in the crypts of colonic adenomas. Fewer fluorescent connective tissue fibers were present in the lamina propria of colonic adenomas resulting in decreased fluorescence intensity as compared to that of normal colon. Fluorescent eosinophil granules were present in larger numbers in adenomas as compared with normal colon., Conclusion: Laser-induced fluorescence in normal colon and colonic adenomas correlates with morphology. Previous reported differences in laser-induced fluorescence emission spectra of normal colon and colonic adenomas obtained in vitro and in vivo may be due to differences in the cytoplasmic fluorescence between the dysplastic epithelium in colonic adenomas and normal colonic epithelium. Laser-induced fluorescence spectroscopy may be useful in studying other forms of epithelial dysplasia such as that which occurs in ulcerative colitis.

Vasoactive intestinal peptide is a neuropeptide with potent modulatory activity on intestinal immunity and may be implicated in the pathogenesis of inflammatory bowel disease (IBD). Previous studies have reported abnormal morphology of vasoactive intestinal peptide-stained enteric nerves, in addition to increased, normal or decreased levels of extractable peptide in Crohn's disease (CD) and ulcerative colitis (UC) tissues. These observations have not been correlated with the amount of enteric nerve fibers or the degree of mucosal inflammation. The investigation was intended to determine whether abnormalities of vasoactive intestinal peptide in IBD are related to quantitative changes of enteric nerve fibers or mucosal inflammation, and whether they are specific for CD or UC. To do this, digitized morphometric analysis was applied to a large number of IBD and control colonic surgical specimens that were immunostained for vasoactive intestinal peptide and S100 protein and scored for severity of inflammation. The results showed that, as compared with controls, there is a marked decrease of vasoactive intestinal peptide-immunoreactive nerve fibers in the lamina propria and submucosa (P less than 0.0001), and of S100-immunoreactive nerve fibers in the lamina propria (P less than 0.0001) of patients with IBD. In the lamina propria but not the submucosa, the variation of decrease is significantly associated with the severity (P less than 0.0001) but not the type (P greater than 0.9) of IBD because it is detected in both CD and UC. We conclude that in IBD there is loss of mucosal neuropeptidic innervation that is intimately associated with inflammation. This loss probably represents a nonspecific event subsequent to damage to enteric nerve fibers but may contribute to disruption of local immunoregulation.

The relationship between histologic changes at resection margins and anastomotic recurrence was evaluated in patients with Crohn's disease. Pathology and medical records from 1960 to 1977 identified 100 patients who met the following criteria: 1) no prior surgery for Crohn's disease, 2) small bowel or small bowel and colonic resection with anastomosis done for Crohn's disease at the Cleveland Clinic, and 3) resection margins available for microscopic analysis. The following histologic features of the margins were evaluated: edema, inflammation, lymphoid aggregates, pyloric metaplasia, fibrosis, cryptitis and crypt abscesses, ulcers, granulomas, villous shortening, mucin depletion, neuronal hyperplasia, and transmural inflammation. Additionally, margins were categorized as histologically normal, showing nonspecific changes, showing changes suggestive of Crohn's disease, and showing changes diagnostic for Crohn's disease. Anastomotic recurrence occurred in 50 patients after an average follow-up period of 11.5 years. Cumulative recurrence-free rates for the four margin categories were not significantly different. Anastomotic recurrence was not associated with any clinical or histologic feature or combination of features.

We have developed a method for defining diagnostic algorithms for pathologic conditions based on fluorescence spectroscopy. We apply this method to human colon tissue and show that fluorescence can be used to diagnose the presence or absence of colonic adenoma. This method uses fluorescence excitation-emission matrices (EEM) to identify optimal excitation regions for obtaining fluorescence emission spectra which can be used to differentiate normal and pathologic tissues. In the case of normal and adenomatous colon tissue, these were found to be: 330, 370, and 430 nm +/- 10 nm. At these excitation wavelengths, emission wavelengths for use in diagnostic algorithms are identified from average difference and ratio of the spectra from normal and pathologic tissues. In colon tissue, at 370 nm excitation, 404, 480, and 680 nm were found to be useful emission wavelengths for diagnosing the presence of adenoma in vitro. The basis of colon tissue autofluorescence was investigated using EEM of pure molecules and relevant excitation-emission maxima in the literature.

Hemorrhagic colitis is characterized by abdominal cramps, bloody diarrhea, and no or low-grade fever. Most cases are caused by the Shiga-like toxin-producing bacteria, Escherichia coli O157:H7. Nineteen colonic biopsy specimens and one resection specimen were reviewed from 11 patients with E. coli O157:H7-associated colitis to determine whether histologic features could be useful in diagnosis or in suggesting pathogenesis. All specimens showed hemorrhage and edema in the lamina propria. Specimens from nine patients were focally necrotic and showed hemorrhage and acute inflammation in the superficial mucosa with preservation of the deep crypts, similar to the pattern of injury associated with acute ischemic colitis. Specimens from five patients showed neutrophils focally infiltrating the lamina propria and crypts, resembling the pattern of injury seen in infectious colitis. One or both of these histologic patterns were observed in specimens from all but one patient. Specimens from four patients had poorly formed inflammatory pseudomembranes. It is concluded that the histologic features of E. coli O157:H7-associated colitis resemble a combination of ischemic and infectious injuries similar to those described in toxin-mediated Clostridium difficile-associated colitis. This suggests that the toxin(s) produced by these E. coliplay a role in the colonic injury. Infection with E. coli O157:H7 should be considered in the differential diagnosis of ischemic and infectious colitis.

Late diagnosis contributes significantly to the mortality and morbidity of mesenteric ischemia. Although flexible endoscopy permits noninvasive assessment of the colon, ischemic colitis is often difficult to differentiate from nonspecific proctitis/colitis or mucosal changes seen in inflammatory bowel diseases. Intravenously administered fluorescein sodium (FSC) has long been used intraoperatively to assess bowel viability because its uptake is inversely proportional to the degree of intestinal ischemia. The authors wished to determine if FSC could be used to augment conventional endoscopy in an attempt to identify and monitor ischemic areas of the bowel within reach of the endoscope. Segmental mesenteric ligation of canine rectum was performed, and serial transanal biopsies obtained. Endoscopy was performed after intravenous FSC administration, using a rigid proctoscope, with a long-wave ultraviolet light source inserted into the lumen of the scope. Areas of nonspecific-appearing proctitis did not take up FSC and were easily differentiated from well-perfused areas by their failure to fluoresce. Ischemic areas were monitored in this manner over a 28-day period. Complete resolution of ischemic mucosal changes occurred with late stricture formation. In humans, the sigmoid and left colon are the areas most frequently affected by ischemic colitis. Because long-wave ultraviolet light is not transmitted through glass fibers, a different light source was needed for potential clinical application. To this end, a single fiber of an argon laser was inserted through the instrument channel of a colonoscope, resulting in greater fluorescence than seen with the ultraviolet light. FSC endoscopy appears to be a sensitive and accurate method of detecting and monitoring ischemic colitis and has many potential clinical applications.