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Our purpose was to evaluate the long-term clinical significance of gastric erosions. A series of 117 patients with gastric erosions without peptic ulcer disease, and matched controls were studied in 1974–1979. All available subjects were reinvestigated 17 years later, including detailed clinical history and laboratory analysis. At follow-up, erosions were still more prevalent (39%; 20/50) in the erosion group than in the controls (11; 7/66). In Helicobacter pylori–positive participants, peptic ulcer or a scar was more common in the erosion group (17%; 9/52) than in controls (5%; 3/66). Overall malignancy rate was higher in controls (15%; 17/117) than in erosion group (5%; 6/117; P= .025), but no other differences were seen between the groups or related with current erosion. We conclude that a significant proportion of gastric erosions are chronic or recurrent but mostly without serious complications. However, H. pylori–positive patients with erosions have significant risk to develop a peptic ulcer.Our purpose was to evaluate the long-term clinical significance of gastric erosions. A series of 117 patients with gastric erosions without peptic ulcer disease, and matched controls were studied in 1974–1979. All available subjects were reinvestigated 17 years later, including detailed clinical history and laboratory analysis. At follow-up, erosions were still more prevalent (39%; 20/50) in the erosion group than in the controls (11; 7/66). In Helicobacter pylori–positive participants, peptic ulcer or a scar was more common in the erosion group (17%; 9/52) than in controls (5%; 3/66). Overall malignancy rate was higher in controls (15%; 17/117) than in erosion group (5%; 6/117; P= .025), but no other differences were seen between the groups or related with current erosion. We conclude that a significant proportion of gastric erosions are chronic or recurrent but mostly without serious complications. However, H. pylori–positive patients with erosions have significant risk to develop a peptic ulcer.

Serrated adenoma has been proposed to be a distinct entity among colorectal neoplasms. Progression to frank carcinoma has been suggested in individual cases, but the prevalence of carcinomas originating from serrated adenomas and their clinico‐pathological characteristics are not known. In the present study, a large series of colorectal cancers was analysed for the occurrence of serrated adenoma in association with carcinoma and clinico‐pathological features were compared in cases with and without serrated adenoma. Specimens from 466 colorectal carcinoma patients undergoing operations between 1986 and 1996 were re‐evaluated for the presence of juxtaposed serrated adenoma and carcinoma. Clinico‐pathological features such as location, Dukes' stage, histological grade, mucinous differentiation, and prognosis were evaluated. Twenty‐seven carcinomas (5.8%) were found in association with an adjacent serrated adenoma. Eight of the patients were male and 19 were female. All of these adenocarcinomas showed a serrated appearance resembling that of serrated adenomas. Nine (33%) cases were mucinous and a mucinous component was present in 11 (41%) additional cases. The majority of the tumours were located either in the caecum (14 cases; 51%) or in the rectum (9 cases; 33%). DNA microsatellite instability was more common in carcinomas associated with serrated adenoma (37.5%) than in other carcinomas (11.0%). It is concluded that carcinoma associated with serrated adenoma is a distinct type of colorectal neoplasm, accounting for 5.8% of all colorectal carcinoma cases in this study. Predilection for the caecum and the rectum may reflect their aetiological factors. Female preponderance is contrary to that reported for hyperplastic polyps and serrated adenomas. Copyright © 2000 John Wiley & Sons, Ltd.

We studied the ultrastructural distribution of laminin, type IV collagen, and the amino terminal pro-peptide of type III collagen (type III pN-collagen) in normal human lymph nodes. After fixation with freshly prepared 4% paraformaldehyde mixed with 0.1% glutaraldehyde, cryoultramicrotomy proved to preserve the antigenicity of these proteins better than embedding in Lowicryl K4M. Sections were treated with rabbit antibodies against the 7S domain of human type IV collagen, the fragment P1 of human laminin, and the amino terminal pro-peptide of human type III pro-collagen, followed by anti-rabbit IgG conjugated to 10-nm colloidal gold. Laminin and type IV collagen were seen in the basement membrane structures of the blood vessels and in the walls of sinuses. The amorphous material between the collagenous fibers in locations corresponding to reticular fibers also contained laminin and type IV collagen. The amino terminal pro-peptide of type III pro-collagen was present in the collagenous fibers in reticular fibers and in the walls of blood vessels and sinuses. Therefore, a significant number of the type III collagen molecules in these fibers must have retained their amino terminal pro-peptide. These results indicate that the basement membrane proteins laminin and type IV collagen are genuine components of reticular fibers, as suggested earlier by immunohistochemical studies at the light microscopic level.

Collagenous colitis is a rare clinical andpathological entity characterized by watery diarrhea anddeposition of collagen beneath the surface epithelium ofthe colon. Its etiology is unknown. We present a careful retrospective clinicopathologicalanalysis of six patients with collagenous colitisdiagnosed at our hospital during a three-year period.Three of the patients had had a Yersinia enterocolitica infection, detected by stool culture andelevated serum antibody titers, preceding the diagnosisof collagenous colitis. Four patients had duodenalvillous atrophy, which in two patients was refractory to a gluten-free diet. We propose that Yersiniaenterocolitica infection may be a triggering factor forthe development of collagenous colitis in some cases.Duodenal villous atrophy not responding to gluten withdrawal is common in association withcollagenous colitis.

Background: Helicobacter pylori seems to be the commonest cause of chronic gastritis, but the natural course of H. pylori-associated gastritis is largely obscure. Methods: We present a histologic follow-up of 39 patients with H. pylori-positive gastritis. Gastroscopies with stepwise biopsies were performed in all the patients at an interval of 10 years. Results: Of the patients 87% (34/39) had a persistent infection and showed a significant decrease in the grades of antral gastritis, eosinophilic granulocytes, corpus eosinophilic granulocytes, and foveolar hyperplasia and a significant increase in the grade of corpus neutrophilic granulocytes. The quantities of H. pylori as estimated histologically did not change significantly during the follow-up period inpatients with a persistent infection. In the five other patients (13%) the H. pylori infection had apparently disappeared spontaneously, and this was accompanied by decreases in the amount of inflammatory cells in the gastric mucosa. Conclusions: H. pylori infection in the gastric mucosa is chronic and may be associated with both regressive and progressive histologic changes. Spontaneous healing of H. pylori infection is possible and is associated with partial resolution of the inflammatory changes in the gastric mucosa.

Background: The course of gastric ulcer disease and its relations to certain indicators of inflammation and Helicobacter pylori in the gastric mucosa were examined in a 10-year follow-up. Methods: Thirty-three patients with gastric ulcer were examined endoscopically with biopsies in 1981-82 and invited for re-examination in 1991-92. Twenty-one of them were able to comply with the invitation. A gastroscopy with biopsies was performed on each of these, and the results were compared with those of age- and sex-matched control patients with non-ulcer H. pylori-positive gastritis. Results: All the patients were H. pylori-positive at the first examination and had a persistent infection at the second examination, if they had not undergone a gastric resection. Thirteen patients had a non-operated stomach at the second examination. The grades of gastritis and intestinal metaplasia in the antrum at the second examination were significantly higher in the ulcer patients than in the controls (p = 0.009 and p = 0.04, respectively). Eosinophilic granulocytes in both the antral and the corpus mucosa had decreased significantly in the controls (p = 0.002 and p = 0.04, respectively) but not in the ulcer patients. Conclusions: The results suggest that the course of ulcer-associated H. pylori-positive gastritis is different from that of non-ulcer-associated H. pylori-positive gastritis and that abnormal eosinophilic infiltration persists in patients with gastric ulcer.

Background: We performed a cross-sectional study to estimate the prevalence of duct abnormalities and exocrine pancreatic dysfunction in an unselected group of patients with inflammatory bowel disease (IBD) and to correlate the findings with clinical, endoscopic, and histologic variables. Methods: A total of 237 IBD patients were screened for pancreatic enzymes and with a PABA test. Seventy-one (30%) patients with values more than twice the upper normal limit in biochemical tests or with a PABA test <40% were further evaluated. The pancreatic evaluation included endoscopic retrograde pancreatography, ultrasonography, and a secretin test. The endoscopic and histologic findings were systematically evaluated. Results: The secretin test was completed in 54 patients, and in 10 (19%) it showed a decreased maximal bicarbonate concentration, corresponding to 4% of the whole study group. The pancreatograms of 59 patients were studied. In 20 (34%) patients unequivocal duct abnormalities were found. The prevalence of pancreatic duct abnormalities in IBD was 8.4%. Conclusion: Our results show the presence of pancreatic duct abnormalities and exocrine pancreatic insufficiency in some patients with IBD.

We have examined the relationship of Campylobacter -like organism (CLO) and duodenogastric reflux (DGR) in 107 patients with unoperated stomachs. Neither the extent of externally measured bile reflux nor the concentrations of bile acids or lysolecithin in the gastric fluid differed significantly in the groups with different numbers of CLO in the gastric mucosa. Our results suggest that DGR, in the quantities commonly present in unoperated stomachs, does not effect the presence of C. pyloriin the gastric mucosa.

Background: We studied the mRNA expressions of interferon-gamma (IFN-γ), interleukin-10 (IL-10), and IL-12 in gastric biopsy and blood samples from patients with and without Helicobacter pylori infection, by reverse-transcription polymerase chain reaction (RT-PCR). Methods: RT-PCR was performed on total RNA preparations, and the expressed mRNA were semiquantitated on the basis of band intensities on Southern blots. Results: In gastric mucosa the expression of IFN-γ and IL-10 was found in most patients with and without H. pylori infection, whereas IL-12 was found in most of the infected ones. The level of IFN-γ and IL-10 did not differ between groups, whereas the IL-12 level was significantly higher in those with H. pylori infection. In the blood IFN-γ expression was found in most samples, with higher level in patients with gastritis than in normals. Few blood samples (33%) had IL-12. and none had IL-10. Conclusion: IFN-γ and IL-10 expressions in healthy mucosa may indicate a biologic role in a healthy state. IL-12 expression in mucosa was related to the presence of bacterial stimulant and therefore resembles proinflammatory cytokines.

The relationship between different features of gastric mucosal inflammation, intragastric pH and serum gastrin concentration and the distribution and quantity of Helicobacter pylori was studied in a series of 107 dyspepsia patients. H. pylori was identified in 62 cases (59%), and its presence was associated with increased amounts of mononuclear inflammatory cells and neutrophilic and eosinophilic leucocytes in both the antrum and the corpus. The number of H. pylori in the antral mucosa was significantly associated with the quantity of mononuclear inflammatory cells. It was also associated with glandular atrophy in antral mucosa, so that slight and moderate glandular atrophy were significantly more common in cases with abundant H. pylori. Intragastric pH and serum gastrin concentration were inversely related to the number of H. pylori in both the antral and corpus mucosa. H. pylori positive patients were also divided into groups according to proportions of H. pylori in the antral and corpus mucosa. In 5 of these patients (8%) the bacteria were present only in the corpus, and this group had a significantly more pronounced degree of glandular atrophy in the corpus mucosa, higher intragastric pH and a higher serum gastrin concentration than the other H. pylori positive patients. The other patients with a higher corpus H. pylori than antral H. pylori score (n = 25; 34%) also had a significantly higher intragastric pH and serum gastrin concentration than those with a corpus H. pylori score lower than or equal to the antral score, while the latter had more severe inflammation in the antral mucosa and a lower intragastric pH and serum gastrin concentration. The results suggest that inflammation in the antrum forms a favourable environment for H. pylori, while atrophy of the corpus glands, being connected with increased pH, leads to a diminished amount of H. pylori. They thus support the view that proliferation of H. pylori is dependent on acid produced by the corpus mucosa.

Background: We performed a cross-sectional study to evaluate the prevalence of hepatobiliary disease in unselected patients with inflammatory bowel disease (IBD), to estimate the frequency of coexisting cholangiographic and pancreatographic duct abnormalities, and to correlate the findings with clinical, endoscopic, and histologic variables. Methods: We screened 237 IBD patients for increased liver function values. Further, hepatobiliary evaluation consisted of transabdominal ultrasonography, endoscopic retrograde cholangiopancreatography (ERCP), and a liver biopsy. In addition, we evaluated the ERCP findings of patients with abnormal pancreatic screening tests (pancreatic enzymes or para-aminobenzoic acid excretion). Results: Laboratory signs of hepatobiliary disease were found in 37 (16%) of our IBD patients. Abnormal liver test results were commoner in patients with Crohn's disease (CD) than in patients with ulcerative colitis (UC) (30.4% versus 11.2%, P > 0.05), and a similar trend was observed in the frequency of primary sclerosing cholangitis (PSC) in the respective groups of IBD patients. When the ERCP findings were combined with liver histology, 26 (11% of the whole study group) patients with PSC were found, with small-duct disease included. In 23 (10% of the whole study group) patients, definite cholangiographic changes consistent with PSC were found. Eleven (48%) of these showed coexisting pancreatic duct abnormalities. The prevalence of coexisting cholangiographic and pancreatographic duct changes in the whole study group was 4.6%. Conclusion: Hepatobiliary disease is at least equally common in patients with UC and CD. Coexisting cholangiographic and pancreatographic duct abnormalities in patients with IBD are relatively frequent and are considered extraintestinal manifestations of IBD.

The occurrence of Campyfobacter-like organisms (CLO) was studied in the gastric mucosa of 33 patients with gastric ulcer and 33 age- and sex-matched controls with non-ulcer dyspepsia, and the relation of CLO to the severity of gastritis was determined in both groups. CLO was significantly commoner in the ulcer patients (57.5%) than in the non-ulcer cases (33.3%) (p < 0.05); this was related to a higher frequency of antral atrophic gastritis in the former. It is suggested that CLO may be associated with chronic antral gastritis and hence with gastric ulcer, but the causal relationship remains unclear.

Seven human lymph nodes showing different types of reactive change, were examined for the presence of acid cysteine-proteinase inhibitor (ACPI) by the peroxidase-antiperoxidase method. A clear positive reaction was found in the germinal centres. The staining pattern indicated immunoreactivity of the dendritic reticulum cells, but the possibility that other cells, particularly histiocytic reticulum cells, may also react with antiserum raised against ACPI cannot be excluded.

The amount of postprandial duodenogastric bile reflux was correlated with detailed histologic findings in the stomachs of 107 patients with dyspepsia. The reflux was associated with infiltration of mononuclear leukocytes, neutrophilic granulocytes, and eosinophilic granulocytes and with foveolar hyperplasia in the gastric mucosa. No significant association with intestinal metaplasia emerged. Our results suggest that postprandial duodenogastric bile reflux is characterized by superficial inflammatory changes in the gastric mucosa.