[Order in the chaos of classifications of erosions of the gastric mucosa].
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Biomedical subjects
Publications and source records attributed to M Stolte.
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A 42-year-old man developed giant fold gastritis that was associated with massive Helicobacter pylori colonization, highly active, high-grade gastritis and severe hypoproteinemia with gastric protein-loss syndrome. Histology revealed marked focal foveolar hyperplasia of the body and fundic mucosa. Combination treatment with amoxicillin and omeprazole resulted in the eradication of the Helicobacter pylori. Concomitantly, the foveolar hyperplasia, gastritis and the giant folds regressed completely, and the protein loss was arrested. It would appear highly likely that colonization with Helicobacter pylori had led to the formation of the giant folds and to gastric protein loss. The clinical picture described here mimics Ménétrier's disease, the cause of which is still unknown, and possibly represents a subgroup of this heterogeneous clinical entity.
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Seven hundred seventy biopsy specimens obtained from 10 different sites in stomachs of 77 patients were examined for the presence of active chronic gastritis (ACG) and Helicobacter pylori to investigate the characteristics of gastritis in the antrum and body. Forty-eight patients with ACG at one or more sites were all H. pylori positive. H. pylori was not found in 20 patients who had chronic gastritis with no activity or in 9 patients who had histologically normal mucosa. In patients with ACG in at least one biopsy site, a strong positive topographic association between H. pylori colonization and ACG was seen in the Warthin-Starry stain. The frequency of H. pylori colonization was similar in the antrum and body. However, the incidence of ACG declined significantly proximal to the borderline between the antrum and body (P less than 0.001). The average grade of gastritis at the individual biopsy sites was distributed evenly throughout the antrum but decreased markedly in the body (P less than 0.0001). In the same manner, the average grade of H. pylori colonization decreased in the body (P less than 0.0027). The grade of H. pylori colonization in the individual biopsy specimens was closely related to the grade of gastritis (r = 0.51); also, the grade of neutrophil infiltration was related to the grade of gastritis (r = 0.79). A good correlation existed between the grade of H. pylori colonization and the grade of neutrophil infiltration (r = 0.70). The results of this study show a different expression of H. pylori gastritis in the antrum and body, which is the main subtype of chronic type B gastritis. The close topographic and graded association between the presence of H. pylori and the activity and grade of gastritis lend further support to the major pathogenic role of H. pylori in active chronic gastritis. The different expression of gastritis in antrum and body is suggested to be increased reactivity of the antral mucosa to the infection, possibly on the basis of an enhanced immunologic response to H. pylori in this region.
In a case of adenocarcinoma in the anastomosis of a stomach resected by the Billroth II technique osteoplastic bone infiltration and microangiopatic haemolytic anaemia are described as paraneoplastic syndromes. Both phenomena open up a great deal of differential diagnoses for consideration. Even when the extended bone infiltration could already be observed, the primary tumor macroscopically in the stomach was not visible. Even an unremarkable B II anastomosis should be biopsied as a matter of routine.
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Our experience with 66 endoscopic-bioptic diagnosed malignant non-Hodgkin's lymphomas (NHL) showed that in most of them (57 of 66 patients) a tumor stage IE or IIE was present. All 57 primary gastric lymphomas were B-cell-lymphomas arising from the mucosa-associated lymphoid tissue (MALT). After curative primary gastric resection in stage IE and IIE the 5-year survival rate was 81%, and the 5-years lymphoma-related survival rate was 88%. These results are superior to those reported in the literature. The following two points are probably of importance for improving the prognosis: early diagnosis made possible by better knowledge of the infiltrative-flat type of tumor growth (38 out of 57 patients, including 23 cases in which infiltration was limited to mucosa and submucosa = "early lymphoma"), and extensive preoperative staging. The infiltrative-flat type, which is difficult to diagnose endoscopically, usually shows low-grade malignancy on histology (76%; in early lymphoma 83%) and has an excellent prognosis when submitted to surgery. In our experience the question as to whether additional treatment by chemotherapy and/or radiotherapy improves the prognosis of NHL of the stomach remains unanswered and further studies are needed.
To date, autoimmune gastritis has been diagnosed for the most part only when total atrophy of the oxyntic glands is detected. On the basis of 40 patients without total atrophy of the glands, and with parietal cell antibodies in the serum, we show that the diagnosis of type A gastritis is also possible in the pre-atrophic stage. The histological criteria for the diagnosis of active autoimmune gastritis without total atrophy of the glands are 1. usually dense, diffuse locally emphasized lymphocytic infiltration of the lamina propria between the glands in the oxyntic mucosa, 2. focal destruction of individual glands in the corpus of the stomach by lymphocytes, and 3. reactive pseudohypertrophy of the parietal cells. A comparison with a group of patients with autoimmune gastritis and total atrophy of the glands shows that in active autoimmune gastritis, too, women are more frequently affected than men (in both groups, the sex ratio is approximately 3:1). Patients without atrophy of the glands are, on average, about 12 years younger than those with "burnt out" type A gastritis (average age 69.98:57.80 years). While in the case of burnt out type A gastritis, no colonisation with Helicobacter pylori was to be found, such colonisation was demonstrated for the corpus mucosa in 22.5%, and for the antral mucosa in 15.0%. In 27.5% a minimal or low-grade inactive superficial gastritis, as may be seen after eradication of Helicobacter pylori, was additionally diagnosed in the antrum. A knowledge of the histological appearance of the pre-atrophic stage of type A gastritis might be of importance for the possible prevention of pernicious anaemia.(ABSTRACT TRUNCATED AT 250 WORDS)
The etiopathogenesis of chronic erosions of the antral mucosa still remains to be clarified. In order to investigate the question as to whether chronic erosions might be a sequela of Helicobacter pylori-induced gastritis, we submitted biopsy material obtained from 250 patients with chronic erosions of the antral mucosa to a histological evaluation. The grading of Helicobacter pylori colonisation, and gastritis was compared with the results of histological evaluation of the biopsy material obtained from 1,196 patients with Helicobacter pylori gastritis, but no lesions of the gastric mucosa. The results of a histological analysis showed that Helicobacter pylori gastritis was present in 99.1 percent of the patients with chronic erosions of the antral mucosa. A comparison of the histological findings in patients with no lesions of the gastric mucosa revealed, that the density of Helicobacter pylori colonization, the severity of the antral gastritis together with its activity were statistically significantly more pronounced (p < 0.001) in patients with chronic erosions. In contrast, no differences in the morphological parameters were seen in the case of corpus mucosa. On the basis of these results, we conclude that chronic erosions of the antral mucosa represent a sequela of Helicobacter pylori gastritis, and that these Helicobacter pylori-induced chronic erosions should, in future, be differentiated from other erosions.
With the aim of investigated the question as to whether surgery for colorectal carcinoma is being carried out in a standardised tumor-oriented manner, 777 surgical specimens containing colorectal carcinomas obtained from 33 hospitals were analysed. Only 4.76% of these carcinomas were pT 1 early carcinomas, the largest portion of the tumors (63.96%) was classified as pT 3. The pN stages were distributed as follows: pN 0 53.4%, pN 1 22.0%, pN 2 13.77%, pN 3 9.39%, and pN X 1.41%. The surgeons indicated an R-classification in only 24% of the specimens. Measurements of the length of the resected material, the width of the mesocoli or perirectal tissue, the distal margin of clearance, the number of lymph nodes on the vessel trunk, and the number of pericolic or perirectal lymph nodes revealed a considerable degree of fluctuation in the measurements, and thus in the operative methodology applied to colorectal carcinoma surgery. Analysis of the four hospitals with the highest operating rates taking sigmoidorectal specimens as an example, showed that some abdominal surgeons are still not performing this operation in accordance with the oncological rules for tumor-oriented surgery.
Paraffin-embedded and haematoxylin-eosin-stained sections of biopsy material obtained from patients taking omeprazole reveal a characteristic "hypertrophy" of the parietal cells; these are taller than the chief cells, and project, with convexly bulging apical cell membrane, into the lumen of the body glands, producing a serrated internal gland profile. We have found this phenomenon in 92.9% of 198 patients with non-operated stomachs. After Billroth I or II resection, this phenomenon was found in the body mucosa of the stomach remnant in only 35.3% of the cases (n = 17). The specificity of the diagnosis "hypertrophy" of the parietal cells under omeprazole therapy was 89.4%, the sensitivity 91.0%. A comparative morphometric analysis in forceps biopsy material investigated after paraffin and epoxide embedding, showed that this "hypertrophy" was a pseudohypertrophy. Apparently, as a result of an increase in intracytoplasmic secretory canaliculi, the gastrin-stimulated parietal cell shrinks less than the non-stimulated parietal cell. This pseudohypertrophy of the parietal cells can readily be used to monitor the compliance of the patient prescribed omeprazole. A question that has yet to be clarified is how quickly pseudohypertrophy develops, and how long it takes to regress after discontinuation of omeprazole. The phenomenon can also be seen in active autoimmune gastritis with no atrophy of the gland, since the parietal cell antibody also binds selectively to the proton pump of the parietal cell.
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In a retrospective study (1982-1990), 12 adenomas, 35 carcinomas of the papilla of Vater, and 21 duodenal adenomas were examined. All patients had endoscopicbioptic examinations (5-10 forceps biopsies, snare biopsy or forceps-biopsies after endoscopic sphincterotomy). Special attention was paid to malignant transformation of adenomas and of residual adenomatous tissue in surgical resected cancer. Follow-up data were gained by reexamination or questionnaires. In papillary adenomas, an adenocarcinoma was found in 30% at operation or by follow-up. In 41.2% of the operated cases, residual adenomatous tissue was found, more often in well-differentiated adenocarcinomas than in other histological types. A transformation from duodenal adenomas to adenocarcinomas was seen less frequently (9.5%). Therefore, the risk of malignancy in ampullary adenomas is greater than elsewhere in the duodenum. In eight of 11 patients (72.7%) with duodenal adenomas, one or more simultaneously developed colonic adenomas were found (in four cases a Gardner syndrome not known before). We conclude that there is strong evidence that most ampullary and duodenal carcinomas develop in preexisting adenomas, with an adenoma-cancer sequence similar to that accepted for colorectal carcinoma. This has to be kept in mind for diagnostic as well as therapeutic reasons. When either an adenoma of the ampulla or duodenum is diagnosed, colonoscopy is mandatory to find or exclude colonic adenomas. In patients with familiar adenomatosis, the duodenum and the papilla of Vater have to be examined endoscopically.
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Ten cases of the rare solid and cystic pancreatic tumors are presented. All except one occurred in young women (mean age, 25 +/- 9.2 years). The large neoplasms were evenly distributed across the pancreas; in one case, metastasis occurred; all other cases were free from disease after complete resection. Histologic hallmarks of solid and cystic neoplasms were papillary growth, large intracytoplasmic granules, and immunoreactivity with alpha 1-antitrypsin, alpha 1-antichymotrypsin, phospholipase A2, and neuroendocrine markers (neuron-specific enolase [NSE], synaptophysin). This suggests both endocrine as well as exocrine differentiation.
The effects of the water-soluble and delayed-release formulations of a nonsteroidal antiinflammatory drug, diclofenac, on the healing of gastroduodenal mucosal lesions were compared in a double-blind, double cross-over, placebo-controlled endoscopic study conducted in 14 healthy volunteers. Severe endoscopic lesions (petechiae, erosions, ulcers, and esophageal candidiasis) were found only in the group taking the soluble formulation of diclofenac (P less than 0.05 vs placebo). The endoscopic healing of biopsies at one week was delayed by both preparations in comparison to placebo (P less than 0.05 vs placebo). Neither formulation produced significantly more histological inflammation or minor endoscopic lesions (erythema, red striae) than placebo. Both formulations were equally well tolerated and produced no more symptoms than placebo. This study suggests that soluble diclofenac acts topically to delay gastroduodenal healing and produce gastroduodenal injury; it thus provides a model for future studies of the production, perpetuation, and healing of peptic lesions.
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