Localization of infection by the microsporidian Enterocytozoon bieneusi in the gastrointestinal tract of AIDS patients with diarrhea.

OBJECTIVE: We compared the level of Enterocytozoon bieneusi infection at different sites within the small intestine among patients with AIDS. DESIGN: The level of E. bieneusi infection of each patient biopsy was determined and compared using semi-thin plastic section light microscopy and transmission electron microscopy (TEM). PATIENTS, PARTICIPANTS: Nine subjects with chronic diarrhea who had endoscopic biopsies of either proximal (bulb) or distal (fourth portion) duodenum plus proximal jejunum (just past ligament of Treitz), either simultaneously or within a few months of each other were studied. All patients had TEM-confirmed diagnoses of E. bieneusi intestinal microsporidiosis. RESULTS: The intensity of infection was always greater in biopsies taken from the patients' jejunum compared with those taken from the duodenal bulb. In one patient, the duodenal bulb biopsy was negative while the jejunal biopsy, taken at the same time, was positive. The distal duodenum was usually, but not always, equal to the jejunum in terms of parasite burden. Esophageal, gastric, and colorectal biopsies from these and other patients were negative for E. bieneusi. CONCLUSIONS: For the diagnosis of E. bieneusi to evaluate chronic diarrhea in AIDS patients, upper intestinal endoscopy biopsies should be taken at the most distal site possible.     

Patchiness and duodenal-jejunal variation of the mucosal abnormality in coeliac disease and dermatitis herpetiformis.

The incidence and degree of patchiness of mucosal abnormality in both coeliac disease (CD) and dermatitis herpetiformis (DH) is documented. As judged by both stereomicroscopy and subjective histology, patchiness occurred frequently in both CDand DH patients. In most cases the difference of abnormality was of only one grade, but in approximately 25% as assessed by stereomicroscopy and 10% as assessed by histology the difference was of two or more grades. In control subjects with normal small bowel mucosa the variation of the mucosal appearance between the duodenum and proximal jejunum was studied. Contrary to popular belief, no significant difference of villous and crypt measurements or of apparent villous "bridging" and "branching" between these two sites was found, if only well-orientated sections were studied. The stereomicroscopic appearances were also similar at these two sites, although villi tended to be broader in the duodenal biopsies. The duodenal-jejunal variation was also studied in CD and DH patients and although by both stereomicroscopy and subjective histology the appearances were similar in most patients, in approximately 33% the duodenal abnormality was the most severe and, surprisingly, the jejunal abnormality was more severe in approximately 15%. It is concluded that multiple, precisely located biopsies of both the duodenum and proximal jejunum are invaluable in the investigation of small bowel disease and in assessing response to treatment.     

Intestinal disaccharidase deficiency without villous atrophy may represent early celiac disease

BACKGROUND: Intestinal disaccharidase activities are decreased in untreated celiac disease and also in other conditions without villous atrophy. Of 908 patients examined for suspected malabsorption, 37 (4.1%) had generalized disaccharidase deficiency without villous atrophy. The aim was to determine if generalized disaccharidase deficiency without villous atrophy represented latent celiac disease. METHODS: Case notes and histology of the 37 patients were reviewed. History and blood investigations including antigliadin and endomysial antibodies were checked. Where celiac disease was suspected, endoscopic duodenal biopsies for histology and disaccharidase estimation were repeated. RESULTS: Of the initial 37 patients, 6 patients had had repeat endoscopic biopsies; one having celiac disease. A further 18 patients were reviewed. The remainder declined further investigation. Eight had repeat endoscopic duodenal biopsies; one had celiac disease. Two with positive celiac serology also had enteroscopy with jejunal biopsies; both had celiac disease. CONCLUSIONS: At least 11% of patients with generalized disaccharidase deficiency without villous atrophy develop celiac disease. Enteroscopic biopsies from distal duodenum and proximal jejunum should be considered as the next investigation if endomysial or antigliadin antibodies are positive.     

Enteroscopic evaluation of the gastrointestinal tract in symptomatic patients with hereditary hemorrhagic telangiectasia

OBJECTIVES: Hereditary hemorrhagic telangiectasia is an autosomal dominant disease in which 25% to 30% of patients will develop gastrointestinal bleeding from telangiectases. The extent of telangiectases has not been previously evaluated. This cross-sectional study compared the presence, number, and size of telangiectases in the stomach and duodenum to those in the jejunum using enteroscopy. METHODS: At the Yale University Vascular Malformation Center, 30 consecutive, symptomatic adult patients with hereditary hemorrhagic telangiectasia were evaluated using a 220-cm-length enteroscope. The number and size of the telangiectases were documented in the esophagus, proximal and distal stomach, four parts of the duodenum, and every 20 cm in the jejunum. The indication for the procedure was recorded as anemia, gastrointestinal bleeding, or anemia out of proportion to epistaxis. RESULTS: The results of 27 patients were analyzed. A total of 89% of patients had telangiectases in the first 60 cm of the jejunum. In individual patients, there was a strong correlation between the number of telangiectases in the stomach/duodenum when compared with the jejunum. In group analysis, the median number of telangiectases in the stomach and duodenum was significantly higher than in the jejunum (13 vs. 3; Wilcoxon signed rank test, P = 0.001). The presence of large (> or =5 mm) telangiectases in the stomach/duodenum did not necessarily indicate that there would be large telangiectases in the jejunum. CONCLUSIONS: The presence and number of stomach and duodenal telangiectases correlated with the presence and number of jejunal ones. However, the occurrence of large proximal telangiectases was not associated with large distal ones.     

Intestinal Disaccharidase Deficiency Without Villous Atrophy May Represent Early Celiac Disease

Background: Intestinal disaccharidase activities are decreased in untreated celiac disease and also in other conditions without villous atrophy. Of 908 patients examined for suspected malabsorption, 37 (4.1%) had generalized disaccharidase deficiency without villous atrophy. The aim was to determine if generalized disaccharidase deficiency without villous atrophy represented latent celiac disease. Methods: Case notes and histology of the 37 patients were reviewed. History and blood investigations including antigliadin and endomysial antibodies were checked. Where celiac disease was suspected, endoscopic duodenal biopsies for histology and disaccharidase estimation were repeated. Results: Of the initial 37 patients, 6 patients had had repeat endoscopic biopsies; one having celiac disease. A further 18 patients were reviewed. The remainder declined further investigation. Eight had repeat endoscopic duodenal biopsies; one had celiac disease. Two with positive celiac serology also had enteroscopy with jejunal biopsies; both had celiac disease. Conclusions: At least 11% of patients with generalized disaccharidase deficiency without villous atrophy develop celiac disease. Enteroscopic biopsies from distal duodenum and proximal jejunum should be considered as the next investigation if endomysial or antigliadin antibodies are positive.     

Prevalence of celiac disease and its endoscopic markers among patients having routine upper gastrointestinal endoscopy

OBJECTIVE: The aim of this study was to determine the prevalence of duodenal villous atrophy (VA) among patients undergoing routine upper gastrointestinal (GI) endoscopy and the value of endoscopic markers for VA in selecting patients for duodenal biopsy. METHODS: One hundred and fifty adult patients with upper GI symptoms or iron-deficiency anemia had inspection and biopsy of the second part of the duodenum during endoscopy. Endoscopic markers for VA sought were mosaic or nodular mucosa, scalloping of duodenal folds, and reduction in number or absence of duodenal folds. RESULTS: Endoscopic markers were seen in seven patients (5%): scalloped folds with mosaic pattern mucosa (three patients), scalloped folds, reduced in number with mosaic pattern mucosa (three patients), and nodular mucosa with reduction in fold numbers (one patient). All seven patients had partial, subtotal, or total VA. One of 143 patients with no endoscopic abnormality had patchy VA. The prevalence of VA was thus 1:19 (8 of 150). Endoscopic markers had a sensitivity of 87.5% (7 of 8), specificity of 100% (142 of 142), positive predictive value of 100% (7 of 7), and negative predictive value of 99% (142 of 143). Of the eight patients with VA, the indications for endoscopy were upper GI symptoms in seven patients (two with anemia) and anemia without GI symptoms in one. After 6 months of dietary gluten exclusion, improvement by at least one criterion was documented in all eight patients. CONCLUSIONS: Careful inspection of the duodenum during routine upper GI endoscopy allows accurate selection of patients for biopsy but may not detect patchy VA or milder enteropathy. Celiac disease should be considered as a cause of dyspeptic and reflux symptoms, as well as of iron-deficiency anemia.     

Evaluation of gastroduodenal mucosal lesions in patients with Crohn's disease and ulcerative colitis

Background: Patients with Crohn's disease (CD) are reported to suffer from upper gastroduodenal lesions with varying frequency, although concurrent Helicobacter pylori infection is reported to be low. Methods: A prospective study was carried out on patients diagnosed with CD or ulcerative colitis (UC) in order to evaluate the degree of upper gastroduodenal tract involvement and the prevalence of Helicobacter pylori infection. Results: Gastroduodenal lesions were found in 18 (78%) of 23 CD patients, the location being the stomach in 18 (78%), the duodenal bulb in 16 (70%) and the descending duodenum in 16 (70%). Bamboo joint‐like lesions were found in four cases (17%) in gastric body and cardia. In contrast, gastroduodenal lesions were found in 10 (53%) of 19 UC patients, the location being the stomach in nine (47%), the duodenal bulb in six (32%), and the descending duodenum in three (16%). The H. pylori‐positive rate in patients with CD and UC was 0%, and 11%, respectively. Conclusion: Minute upper gastroduodenal lesions are much more common in CD than in UC patients, especially in the descending duodenum. Accordingly, upper gastrointestinal endoscopy would seem to be a useful means with which to obtain a definitive diagnosis in all suspected IBD cases.     

Endoscopic biopsy diagnosis of acute gastrointestinal graft-versus-host disease: rectosigmoid biopsies are more sensitive than upper gastrointestinal biopsies

OBJECTIVES: The diagnosis of gastrointestinal (GI) graft- versus -host disease (GVHD) is based upon histologic findings in endoscopic mucosal biopsy specimens. The portion of the GI tract with the highest diagnostic yield is a topic of debate. Our aim was to evaluate the sensitivity of simultaneous biopsy of the stomach, duodenum, and rectosigmoid in establishing the diagnosis of GI GVHD.
METHODS: We identified 112 patients who had simultaneous endoscopic biopsies of the stomach, duodenum, and rectosigmoid within the first 100 days following allogeneic hematopoietic stem cell transplantation (HSCT). GVHD was defined histologically as the presence of gland apoptosis, not explained by other inflammatory or infectious etiologies. The patient was diagnosed with GI GVHD if at least one biopsy site was positive.
RESULTS: Overall, 81% of the patients had GI GVHD. Of these, 66% had involvement at all three biopsy sites. Rectosigmoid biopsies had the highest sensitivity, specificity, positive predictive value, and negative predictive value for diagnosing GI GVHD, at 95.6%, 100%, 100%, and 84%, respectively. The sensitivities of gastric and duodenal biopsies were 72.5% ( P < 0.0001 vs rectosigmoid) and 79.2% ( P = 0.0018), respectively. The negative predictive values of gastric and duodenal biopsies were 45.6% ( P = 0.0039 vs rectosigmoid) and 52.5% ( P = 0.0205), respectively. Rectosigmoid biopsies had a higher sensitivity and negative predictive value than biopsies at other sites whether the patient presented with diarrhea or nausea/vomiting. No association between the degree of mucosal injury and the presence of GVHD was found at any site.
CONCLUSIONS: Biopsy of the rectosigmoid is the single best test for diagnosing GI GVHD.     

Comparison of duodenal with jejunal biopsy and aspirate in chronic human immunodeficiency virus–related diarrhea

Objectives: In human immunodeficiency virus (HIV)-infected patients with chronic unexplained diarrhea, upper endoscopy with small bowel biopsy and aspirate is often performed to identify treatable pathogens. The purpose of this study was to compare the diagnostic yield of duodenal with jejunal biopsy and aspirate.
Methods: All HIV-infected patients with chronic unexplained diarrhea who were evaluated by upper endoscopy at Bellevue Hospital Center between January 1992 and January 1997 were identified. Data were collected by reviewing patient charts, endoscopy reports, and pathology records.
Results: During the 5-yr study period, 442 patients underwent upper endoscopy with sampling of the duodenum (  N = 173  ) or jejunum (  N = 269  ). A pathogen was identified in 123 patients (27.8%). Microsporidia was the most common organism detected (12.2%). The diagnostic yield of jejunal biopsy and aspirate was significantly higher than that obtained from the duodenum (32.3% vs 20.8%,   p = 0.009  ). Small bowel aspirates detected a pathogen in only 1.8% of patients evaluated, and there was no difference in the yield of duodenal and jejunal aspirates (1.3% vs 2.1%,   p = 0.7  ). Patients with a CD4 count of < 100 cells/mm³ were significantly more likely to have a pathogen identified than those with higher CD4 counts (38.8% vs 7.1%,   p < 0.0001  ).
Conclusions: Upper endoscopy with small bowel biopsy and aspirate identifies a pathogen in 27.8% of individuals with HIV-related chronic unexplained diarrhea. In this patient population, jejunal biopsies acquired by enteroscopy are superior to those obtained from the duodenum. Small bowel aspirates are of little value in the workup of chronic HIV-related diarrhea.     

The Response of Symptomatic Gastrointestinal Kaposi''s Sarcoma to Chemotherapy: A Prospective Evaluation using an Endoscopic Method of Disease Quantification

We used an endoscopic method of quantification to evaluate the response of symptomatic gastrointestinal Kaposi's sarcoma (KS) prospectively in seven patients with acquired immune deficiency syndrome (AIDS) who were participating in chemotherapy trials for extensive cutaneous KS. The sums of the diameters of KS lesions in the esophagus, stomach, duodenum, and distal colon were used as a measure of extent of disease. Intravenous therapy [adriamycin/bleomycin/vincristine (N = 5), adriamycin (N = 1), or bleomycin/vincristine (N = 1)] was given every 2 wk for a mean of six cycles. Five of seven patients (71%) had a cutaneous response, whereas 9/15 (60%) gastrointestinal sites showed a remission. Sites of complete response all had an initial sum of lesion diameters less than or equal to 30 mm. Five of five patients with duodenal KS responded (3/5 complete), whereas just two partial responses were seen in five patients with gastric KS (4/5 with duodenal KS had sums of diameters less than or equal to 20 mm, whereas 4/5 with gastric KS had sums greater than or equal to 150 mm). Symptoms (abdominal pain, nausea/vomiting, hematemesis, diarrhea) resolved in all patients within two cycles of therapy. In summary: 1) the response rate of gastrointestinal KS to chemotherapy is similar to that of cutaneous KS; 2) the best response is seen in patients with less extensive disease and duodenal involvement; and 3) symptoms of gastrointestinal KS respond to chemotherapy even if the KS lesions do not resolve.     

Mucosal cell proliferation in duodenal ulcer and duodenitis.

Mucosal cell proliferation in the first part of the duodenum was studied in 24 patients using a tissue culture technique in which endoscopic biopsies were subjected to autoradiography after exposure to tritiated thymidine. Eight patients had a normal duodenum, eight had duodenal ulcer, and eight had symptomatic chronic non-specific duodenitis. The mean crypt labelling index (LI) in normal duodenum was 8.8 0.4% (SEM). Increased labelling indices of 15.6 +/- 1.7% were found near the edge of duodenal ulcers and 17.8 1.8% in duodenitis. Treatment with cimetidine reduced both the severity of duodenitis and the mean crypt LI. The LI of histologically normal duodenal mucosa distal to ulcer of duodenitis was similar to that of the control subjects' mucosa. The increased mucosal cell proliferation seen in severe duodenitis, either alone or associated with duodenal ulceration, suggested that erosions and ulcers arose when the crypts passed into 'high output failure' and were unable to compensate for further epithelial cell loss. There was no evidence in out study for a generalised failure of mucosal cell proliferation in duodenal ulcer or duodenitis.     

Helicobacter pylori infection, gastric metaplasia in the duodenum and the relationship with ulcer recurrence

OBJECTIVE: To study the prevalence of Helicobacter pylori (H. pylori) infection and gastric metaplasia (GM) in the duodenum a large group of patients with duodenal ulcer was evaluated to determine whether these factors are related to the number of ulcer recurrences. METHODS: Three hundred and seven patients diagnosed by endoscopy as having active duodenal ulcers were studied. At endoscopy, all patients had gastric biopsies taken for histology, the rapid urease test and culture. Three duodenal biopsies were also taken and processed for histology (haematoxylin & eosin, Giemsa, Warthin-Starry, and PAS stain). RESULTS: GM and H. pylori in the duodenum was identified in 73% (68-78%) and 66% (60-71%) of the cases, respectively. All patients with H. pylori in the duodenum also had GM at this location, while areas with GM but without H. pylori were described. The kappa statistic for concordance between GM and H. pylori at the duodenum was 0.82. The prevalence of GM and H. pylori, depending on the number of ulcer recurrences, was: 1st episode, 34% and 27%, respectively; 2nd episode, 84% and 80%; and > or = 3rd episode, 90% and 79% (P < 0.001 when comparing 1st vs 2nd or > or = 3rd episode). In the multivariate analysis, age and number of ulcer recurrences correlated both with GM and with H. pylori in the duodenum. Chronic duodenitis was demonstrated in all duodenal biopsies, 87% being active chronic duodenitis. H. pylori in the duodenum was more frequent in patients with active duodenitis (73%) than in those with inactive duodenitis (13%) (P < 0.001). CONCLUSIONS: Patients with recurrent ulcer disease have a higher prevalence of both GM and H. pylori infection in the duodenum, suggesting that these two factors are related with the chronicity and recurrence of duodenal ulcer disease. H. pylori infection in the duodenum always appears in areas of GM, although GM is not necessarily colonized by the organism. H. pylori infection cannot be excluded based only on the results of duodenal biopsies, as false negative results at this area are frequent.     

Motility of the Roux-en-Y hepaticojejunostomy in asymptomatic patients

OBJECTIVE: The aim of our study was to describe the motility in the limb, the duodenum, and the jejunum distal to the limb after Roux-en-Y hepaticojejunostomy in patients who remained asymptomatic postoperatively. Our objective was to obtain reference manometric recordings for interpretion of recordings in symptomatic patients. METHODS: Manometric recordings were obtained in the Roux-en-Y limb in 13 patients 15.6 +/- 1.1 days postoperatively, using a probe inserted into the limb during surgery and coming out through the abdominal wall. The recording openings were positioned in the limb itself in eight patients, and also in the jejunum immediately distal to the limb in five patients. In four of eight patients, limb manometry was combined with duodenal manometry using a second probe introduced nasally. RESULTS: Phase IIIs were recorded in all 13 patients, either spontaneously or after trimebutine stimulation (100 mg i.v.). Phase IIIs occurred spontaneously in 12 patients. They always migrated throughout the Roux-en-Y limb, and were also most often observed in the distal jejunum; migration stopped in the distal jejunum in three of five patients. Phase IIIs in the limb occurred independently from duodenal phase IIIs. In the limbs, the duration of phase IIIs was longer (p < 0.02), and the migration slower than in the duodenum (p < 0.001) and in controls (p < 0.02). In nine of 13 patients, injection of trimebutine (100 mg i.v.) initiated phase III in the Roux limb or in the distal jejunum within 2 min. During the combined recordings, trimebutine initiated phase III simultaneously in the duodenum and in the limb. The response to meals in the limb was poorer than in controls. Interruption of phase IIIs was shorter, and the area under the postprandial curve was smaller (p < 0.01) for each postprandial half-h. Postprandial motility was poorer in the limb than in the distal small bowel (p < 0.01). CONCLUSIONS: In asymptomatic patients, interdigestive motility is present in the hepaticojejunostomy Roux-en-Y limb, but it is abnormal because of slow migration of phase IIIs. The second abnormality observed in the limb is a response to meals that is both short and of low amplitude.     

Do scattered white spots in the duodenum mark a specific gastrointestinal pathology?

OBJECTIVE: To discover whether scattered white spots (SWS) in the duodenum are related to a specific kind of disease. We also scrutinized other upper endoscopic findings which might be associated with SWS. METHODS: Among the patients who were admitted for upper gastrointestinal system endoscopy, those having the endoscopic appearance of SWS in duodenum were enrolled in this study. In total 107 patients [70 women, 37 men, mean age: 51.6 ± 16.88 years (range: 17–82 years)] were included. At least three duodenal biopsies were taken from each patient and histopathological examinations were done by experienced pathologists. RESULTS: The histopathological examination revealed that 39 (36.4%) patients had intestinal lymphangiectasia (IL), 15 (14%) patients had giardiasis (G) and 30 (28.1%) patients had chronic non‐specific duodenitis (CD). Two patients with IL were also found to have G. Twenty patients had both IL and CD. One had both G and CD. G was the least common etiology for SWS in the duodenum. The most common reasons for SWS in the duodenum in this study group were IL and CD, in order of decreasing frequency. There was no significant relationship with the other upper endoscopic findings in all these patients. CONCLUSION: Histopathological examinations should be provided for each patient with SWS in the duodenum to assess the etiology.     

Duodenal intraepithelial lymphocytes in inflammatory disorders of the esophagus and stomach.

BACKGROUND & AIMS: Duodenal cluster designation 3 positive (CD3+) intraepithelial T lymphocytes (IELs) are increased in gluten-sensitive enteropathy (GSE) and, because of the dispersed nature of the gut immune system, might also be increased in mucosa distant from the duodenum. Conversely, little is known about their frequency in the duodenum during inflammatory conditions of the stomach and esophagus. This study assessed whether CD3+ IELs are increased in duodenal biopsies in patients with esophagitis or gastritis relative to normal control subjects. METHODS: Cases (n=46) with concurrent mucosal biopsies of the duodenum, stomach, and esophagus were divided into 4 groups: I, no inflammation in any site; II, active esophagitis only; III, chronic active gastritis only, with Helicobacter pylori bacteria; IV, chronic gastritis only, without H pylori bacteria. Immunostains against CD3 were performed by using standard techniques, the number of CD3+ cells/100 enterocytes in 3 well-oriented villi was recorded, and the results for the groups were compared statistically. RESULTS: The average number of CD3+ IELs/100 enterocytes for each group was I, 6.7; II, 11.8; III, 7.2; and IV, 9.1. The differences among the groups were not statistically significant. There was no correlation between the number of duodenal IELs and severity of inflammation, patient age or sex, or symptoms. CONCLUSIONS: Duodenal mucosal biopsies from patients with esophagitis and/or gastritis may have a slightly increased number of CD3+ IELs relative to normal control subjects. This finding may reflect an underlying mechanism of diffuse inflammation in the gastrointestinal tract.     

Duodenal involvement of Crohn's disease

PURPOSE: This study was designed to assess clinical and pathologic features of duodenal Crohn's disease (CD) and address its management according to different patterns of disease. METHODS: Twelve cases of duodenal involvement in CD are reported out of 336 patients treated between 1978 and 1993. They represent 3.6 percent of all cases. Three patients had a duodenal fistula, and nine had an intrinsic duodenal lesion. The duodenal fistula was in all cases a manifestation of recurrent CD involving an ileocolic anastomosis and the third portion of the duodenum. RESULTS: Treatment consisted of resection of the fistula's source and primary closure of duodenal breach. Of nine patients with intrinsic CD, five had stenosis and the remaining four had peptic ulcer-like lesions. Duodenal stenosis was treated with strictureplasty in three cases and duodenojejunostomy in two. No patient with ulcer-like lesions underwent surgery. CONCLUSIONS: Differences encountered in intrinsic duodenal lesions apparently reflect two different clinical patterns. Stenosis is not usually associated with multifocal disease and is often the first evidence of disease. Ulcer-like lesions are not specific; they do not evolve into stenosis as do ulcers in other sites of the disease, spontaneously disappear and relapse, and do not require surgery, except for complications. They are always associated with other locations of the disease.     

Disappointing sensitivity of endoscopic markers for villous atrophy in a high-risk population: implications for celiac disease diagnosis during routine endoscopy

OBJECTIVE: Endoscopic markers of duodenal villous atrophy (VA) can facilitate diagnosis of celiac disease during routine upper GI endoscopy. We studied their sensitivity for VA in a large series of patients undergoing GI endoscopy specifically for duodenal biopsy. Poor sensitivity in this setting would have significant and adverse implications for their performance during routine endoscopy. METHODS: All patients with VA on duodenal biopsy performed for positive serum endomysial antibody (EmA) and/or clinical features suggestive of celiac disease were included. The second part of duodenum was inspected carefully for endoscopic markers using videogastroscopes. RESULTS: Of 129 patients studied, 99 (77%) had at least one endoscopic markers. The most commonly seen marker were a mosaic pattern mucosa (68 patients, 53%) and scalloping of duodenal folds (74 patients, 57%). The prevalence of markers was significantly lower for partial VA (15 of 26 patients, 58%) than for subtotal or total VA (84 of 103 patients, 82%) (p < 0.02). CONCLUSIONS: Endoscopic markers have disappointing sensitivity even in a population at high risk of celiac disease, particularly for partial VA. Their performance may be even poorer in an unselected dyspeptic population. Although they may help improve diagnosis rates among patients with nonspecific dyspeptic symptoms, many patients, particularly those with milder enteropathy, will be missed. As celiac disease is an important cause of dyspepsia, consideration should be given to serological screening to further improve diagnosis rates, as few centers will have the resources to routinely biopsy all patients.     

Lymphocytic infiltration and expression of inducible nitric oxide synthase in human duodenal and colonic mucosa is a characteristic feature of ankylosing spondylitis

OBJECTIVE: In patients with ankylosing spondylitis (AS), inflammatory processes have been detected in the ileal and colonic mucosa. The inducible isoform of nitric oxide synthase (iNOS) may be expressed early in the inflammatory process. We investigated iNOS activity and lymphocytic infiltration in the duodenum and colon in patients with AS and ulcerative colitis compared with controls. METHODS: Gastroscopy with duodenal biopsies and/or colonoscopy with biopsies were conducted in 42 patients with AS treated or not treated with nonsteroidal antiinflammatory drugs (NSAID), in 15 with ulcerative colitis, and in 46 controls. Lymphocytic infiltration in the lamina propria and intraepithelial infiltration were quantified by histological score. iNOS expression was assessed by immunohistochemistry with monoclonal antibodies, and iNOS activity was determined by radiochemical assay. RESULTS: Endoscopic examination of the gastroduodenal or colonic mucosa did not reveal macroscopic lesions in the AS patients. In the duodenum, mucosal lymphocytic infiltration was found in 83.3% of the AS group compared to 48.6% of controls (p = 0.02), and was independent of the NSAID intake. Intraepithelial lymphocyte infiltration was increased in both duodenum and colon in AS patients compared to controls. iNOS activity in duodenum and colon and expression of iNOS protein in lamina propria inflammatory cells was increased in AS patients compared to controls. CONCLUSION: Lymphocytic infiltration and iNOS expression and activity were detected in duodenal and colonic mucosa from patients with AS. Such findings may indicate an inflammatory process in the small intestine and colon of patients with AS.