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M Stolte

Publications and source records attributed to M Stolte.

At least 145 records · Page 8Linked to original sources

[Esophageal, gastric and colorectal tumors].

The new WHO-classification of the tumours of the digestive System replaces the "blue books", and are now dealt with completely in a single book. In addition to the histological features of the lesions, the new classification also contains information on epidemiology, aetiology, endoscopy, genetic susceptibility, molecular genetics, prognosis and predictive factors. The erstwhile mostly black-and-white histological photographs have at last again been replaced by numerous colour photographs and supplemented by endoscopic and macroscopic pictures. The changes to the individual tumour classifications are only few. The former classification of the malignant lymphomas of the gastrointestinal tract has now been replaced by the classification of these lesions that has long been in use. New additions are the gastrointestinal tract has long been in use. New additions are the gastrointestinal stroma tumours (GIST) and the gastrointestinal autonomic nerve tumour (GANT). To the epithelial tumours of the oesophagus have now been added the basaloid squamous cell tumours of the vermiform appendix and the colorectum have now been added the serrated adenoma and the small-cell carcinoma. The following new chapter have been included: adenocarcinoma of the oesophagogastric junction, secondary carcinomas of the stomach, secondary tumours of the small bowel and colon, the Peutz-Jeghers syndrome, juvenile polyposis, familial adenomatosis coli, and HNPCC. For the first time the intra-epithelial neoplasias in chronic inflammatory bowel disease have been differentiated, i.e. adenomas distinguished from the dysplasias, while the latter term has now been replaced by the term "intra-epithelial neoplasias". In comparison with the former "blue books", the new WHO-classification, prepared by presentatives of numerous disciplines--for the first time including clinicians--has taken on the character of a text book.

Colonic Neoplasms↗

The Helicobacter pylori vacA s1, m1 genotype and cagA is associated with gastric carcinoma in Germany.

BACKGROUND: The H. pylori vacuolating cytotoxin encoded by vacA and the cytotoxin-associated protein encoded by cagA are considered to be important virulence determinants that have been implicated in the development of peptic ulcers and gastric carcinoma. However, conflicting results regarding the association between these virulence factors and clinical disease have been reported from different geographic regions. AIMS: To determine the frequency of vacA genotypes, vacuolating cytotoxin activity, and cagA in H. pylori isolates obtained from patients with gastric cancer in Germany. METHODS: H. pylori isolates were obtained from 34 patients with gastric cancer and from 35 subjects with asymptomatic H. pylori gastritis. vacA genotypes and cagA were identified by PCR. Cytotoxic activity was determined by HeLa cell assays. Gastritis was assessed according to the updated Sydney System. RESULTS: The H. pylori vacA s1,m1 genotype was significantly more frequent in patients with gastric cancer (24/34, 70.6%) as compared with controls (12/35, 34. 3%) (p = 0.005). Cytotoxic activity was detected in 24 (70.6%) and 15 (42.9%) H. pylori isolates from gastric cancer patients and controls, respectively (p = 0.03). The cagA gene was identified in 30 (88.2%) and 21 (60%) H. pylori isolates in the respective groups (p = 0.01). CONCLUSIONS: Our study suggests a significant association between the H. pylori vacA s1,m1 genotype, cytotoxic activity, cagA, and gastric cancer. Detection of H. pylori possessing these virulence determinants may help to identify patients being at an increased risk to develop gastric cancer in our population.

Adenocarcinoma↗

Gastric MALT lymphoma and its relationship to Helicobacter pylori infection: management and pathogenesis of the disease.

Chronic Helicobacter pylori infection is strongly associated with the development of primary gastric B cell lymphoma of MALT-type. Therapeutic decisions in primary gastric MALT lymphomas, e.g., the choice for gastric surgery or stomach-conserving treatments in the form of radio-, chemo-, or eradication therapy, should be based on an accurate histopathological diagnosis, grading and clinical staging. Primary gastric low-grade MALT-NHLs in an early clinical stage associated with H. pylori infection were shown to respond with complete remission in approximately 77% of cases upon successful cure of the infection as only treatment modality. The effect of curing H. pylori infection on the course of a high-grade gastric MALT lymphoma is largely uncertain but preliminary results indicate a possible benefit for patients with high-grade MALT lymphoma upon eradication therapy. Concerning the pathogenetic mechanisms of lymphomagenesis, there are many questions to be addressed in the near future. In general, it is still unclear what the exact mechanisms are which lead to the malignant transformation of a reactive infiltrate. Is there a molecular-genetic or immunological point of no return? What is the biological significance of the immunoglobulin rearrangement detected with PCR? The wave of new data each year about the role of H. pylori in gastric MALT lymphoma might help that many of these questions addressed above might be answered within the next years.

Gastric Mucosa↗

Differences in diagnostic criteria for esophageal squamous cell carcinoma between Japanese and Western pathologists.

BACKGROUND: Large discrepancies have been found between Western and Japanese pathologists in the diagnosis of adenoma/dysplasia versus carcinoma for gastric and colorectal glandular lesions. It is important to determine whether similar differences exist in the diagnosis of esophageal squamous lesions. METHODS: Eleven expert gastrointestinal pathologists from Japan, North America, and Europe individually reviewed a set of microscopic slides containing 21 sections of biopsies and corresponding endoscopic mucosal resection specimens from Japanese patients with superficial esophageal squamous neoplastic lesions. The pathologists indicated the pathologic findings on which they based each diagnosis. RESULTS: Invasion was the most important diagnostic criterion of carcinoma for the Western pathologists whereas nuclear and structural features were more important for the Japanese pathologists. For two sections showing low grade dysplasia according to most Western pathologists, the Japanese pathologists diagnosed suspected carcinoma in one case and definite carcinoma in the other. For nine sections with high grade dysplasia according to the Western pathologists, the Japanese pathologists diagnosed suspected carcinoma in two cases and definite carcinoma in seven cases. For six sections with suspected carcinoma according to most Western pathologists, the Japanese pathologists diagnosed suspected carcinoma in one case and definite carcinoma in five cases. Four sections showed definite carcinoma according to both the Western and Japanese pathologists. Thus, there was agreement among the Western and Japanese pathologists for only 5 of the 21 sections (kappa value, 0.04). However, when high grade dysplasia, noninvasive carcinoma, and suspected carcinoma were grouped together, the agreement was excellent (19 of the 21 sections; kappa value, 0.75). CONCLUSIONS: In Japan, esophageal squamous cell carcinoma is diagnosed mainly based on nuclear criteria, even in cases judged to be noninvasive low grade dysplasia in the West. This difference in diagnostic practice may contribute to the relatively high incidence rate and good prognosis of superficial esophageal carcinoma in Japan. To improve the comparability of research data, the authors recommend that high grade dysplasia, noninvasive carcinoma, and suspected carcinoma be grouped together into one category of "noninvasive high grade neoplasia." [See editorial on pages 969-70, this issue.]

Aged↗

Eradication of Helicobacter pylori and stability of remissions in low-grade gastric B-cell lymphomas of the mucosa-associated lymphoid tissue: results of an ongoing multicenter trial.

The normal human stomach is devoid of any organized lymphatic tissue. Acquisition of mucosa-associated lymphatoid tissue (MALT) in the stomach is considered to be a direct consequence of chronic infection with Helicobacter pylori. Thus, MALT appears to be part of the host defense against the pathogen H. pylori. Consequently, lymphomas arising from gastric MALT may be seen as an end point of a clonal evolution starting from the infection. Cumulative data from several studies show that eradication of H. pylori induces complete histologic remissions in about 70%-80% of the patients. Here we present data of an extended analysis of an ongoing multicenter trial. Eighty-four patients with low-grade gastric MALT lymphoma in stage EI were treated using a dual regimen to eradicate H. pylori. Complete remission was observed in 68 (81%) patients; a partial remission was found in seven (8%) patients. In contrast, nine (11%) patients revealed "no change" and were referred for alternative treatment strategies. The majority of these cases were found to harbor high-grade lymphomas in deeper mucosal areas. Polymerase chain reaction (PCR) performed on the VDJ rearrangements of the immunoglobulin heavy chain yielded monoclonal bands in 50 of 65 analyzed patients (77%) at diagnosis. Interestingly, in patients analyzed during follow up after achieving complete histologic remission, ongoing PCR monoclonality was found in 19 of 39 eligible patients (49%). Several patients who developed local relapse of the lymphoma were found in the group with ongoing PCR monoclonality. Together with data from the literature, these results suggest that the majority of low-grade gastric MALT lymphomas in stage EI respond to eradication of H. pylori. Longer follow-up investigations are necessary to determine whether remissions really indicate a cure from the disease and to elucidate whether PCR monoclonality after complete histological remission is predictive of increased relapse rate.

Anti-Bacterial Agents↗

Gastric polyps: an update of their pathology and biological significance.

Gastric polyps are clinically important lesions that are frequently encountered in routine pathology (2-3% of all gastroscopies). Polyps may occur sporadically or in polyposis syndromes, such as familial adenomatous polyposis coli (FAP), Peutz-Jeghers syndrome, juvenile polyposis, Cowden's disease and Cronkhite-Canada syndrome. In biopsy specimens taken during routine gastroscopic examinations, it is almost always possible to differentiate between neoplastic and non-neoplastic polyps and to type polyps. In this review, we focus on the morphological spectrum of gastric polyps in an attempt to assist the pathologist and the gastroenterologist in recognising the lesion and in treating patients with gastric polyps, respectively. Further, we propose that the World Health Organization (WHO) classification should be modified to include the following categories: non-neoplastic polyps (WHO: tumour-like lesion), hamartomatous polyps/polyps of polyposis syndromes (WHO: tumour-like lesion), heterotopic tissue polyps (WHO: tumour-like lesion), neoplastic polyps (WHO: epithelial, non-epithelial and endocrine tumours) and reactive polypoid lesions.

Biopsy↗

Endoscopic mucosal resection of early cancer and high-grade dysplasia in Barrett's esophagus.

BACKGROUND & AIMS: In view of the mortality and morbidity rates of esophagectomy and the relatively large group of inoperable patients, local therapeutic techniques are required for high-grade dysplasia and early Barrett's cancer. METHODS: A prospective investigation of endoscopic mucosal resection was conducted in 64 patients (mean age, 65 +/- 10 years) who had early carcinoma (61 patients) or high-grade dysplasia (3 patients) in Barrett's esophagus. Thirty-five patients met the criteria for low risk: macroscopic types I, IIa, IIb, and IIc; lesion diameter up to 20 mm; mucosal lesion; and histological grades G1 and G2 and/or high-grade dysplasia (group A). The remaining 29 patients were included in group B (high risk). RESULTS: A total of 120 resections were performed, with no technical problems encountered. The mean number of treatment sessions per patient was 1. 3 +/- 0.6 in group A and 2.8 +/- 2.0 in group B (P < 0.0005). Only one major complication occurred, a case of spurting bleeding, which was managed endoscopically. Complete local remission was achieved significantly earlier (P = 0.008) in group A than in group B. In May 1999, complete remission had been achieved in 97% of the patients in group A and in 59% of those in group B; however, 1 patient in group A and 9 in group B are still undergoing treatment or awaiting the first check-up. During a mean follow-up of 12 +/- 8 months, recurrent or metachronous carcinomas were found in 14%. CONCLUSIONS: Endoscopic mucosal resection of early carcinoma in Barrett's esophagus is associated with promisingly low morbidity and mortality rates. The procedure may offer a new minimally invasive therapeutic alternative to esophagectomy, especially in low-risk situations. Comparisons with surgical results will need to be done when the long-term results of this procedure become available.

Adult↗

Helicobacter heilmannii-associated primary gastric low-grade MALT lymphoma: complete remission after curing the infection.

BACKGROUND & AIMS: Cure of Helicobacter pylori infection may lead to complete remission of associated low-grade mucosa-associated lymphoid tissue (MALT) lymphoma in stage EI. This study investigated whether Helicobacter heilmannii infection-associated primary gastric MALT lymphoma will regress after cure of the infection. METHODS: H. heilmannii-induced gastritis was diagnosed histologically, by a new specific immunoglobulin G enzyme-linked immunosorbent assay, and with 16S ribosomal RNA amplification and sequencing in 5 consecutive patients with primary gastric MALT lymphoma clinical stage EI. Patients received 40 mg omeprazole and 750 mg amoxicillin 3 times per day for 14 days. Polymerase chain reaction (PCR) was used to detect rearrangement of immunoglobulin heavy-chain genes before treatment and during follow-up. RESULTS: Five patients (3 men, 2 women; mean age, 65 years; range, 42-79 years) were studied. H. pylori was not detected by culture, histology, serology, or PCR. Treatment resulted in the cure of H. heilmannii infection in each case and complete histological and endoscopic remission of the tumors. Three of 5 patients showed monoclonal B cells before treatment, 2 of whom remained PCR positive. Within a median follow-up period of 24 months, no relapse of the lymphoma or reinfection with H. heilmannii occurred. CONCLUSIONS: These data suggest that gastric MALT lymphoma may arise in patients with H. heilmannii infection. Cure of this infection may lead to complete remission of the MALT lymphoma.

Adult↗

Malignant tumors of the stomach. Gastric mucosa-associated lymphoid tissue lymphoma and Helicobacter pylori.

With the help of many clinical studies, the diagnosis and therapy of gastric MALT lymphoma have evolved. Major progress has been seen in this area, including improvement of biopsy diagnosis, better histologic classification, new information concerning pathogenesis, and, especially, the start of a revolution in the treatment of low-grade gastric MALT lymphomas by eradicating H. pylori. About 12 clinical studies with almost 400 patients and case reports have shown that cure of H. pylori infection is associated with complete remission in approximately 80% of patients with low-grade MALT lymphoma in an early clinical stage. To establish H. pylori eradication as the primary choice in low-grade gastric MALT lymphoma further, it is necessary to select patients before therapy who are most likely to benefit from this single treatment modality. An excellent histologic workup of obtained biopsy specimens and comprehensive clinical staging are necessary. Because of the supposition that H. pylori-related growth support may play a role only in the early stages of low-grade gastric MALT lymphoma, the importance of determining the depth of lymphoma infiltration in the gastric wall is evident. Examinations by endosonographic ultrasonography have been shown to be the most reliable method to differentiate the layers of the gastric wall and to determine the infiltration depth of lymphomas. Eradication of H. pylori has to be considered as a first-line and single treatment modality in patients with low-grade gastric MALT lymphoma in clinical stage EI1. As a therapy with fewer side effects than radiation, surgery, or chemotherapy and as a stomach-conserving treatment, eradication of H. pylori in patients with low-grade gastric MALT lymphoma should be the treatment of the choice within clinical trials because there are no long-term results available thus far. Besides pretreatment patient selection, careful follow-up with endoscopy, biopsies, and clinical staging including endoscopic ultrasonography is necessary. A 5- to 10-year follow-up is necessary before the definitive value of H. pylori eradication can be established, but long-term results are excellent thus far. There are many questions to be addressed: What are the exact mechanisms that lead to the malignant transformation of a reactive infiltrate? Why do approximately 20% of low-grade MALT lymphomas not regress after H. pylori eradication? Is there a molecular-genetic or immunologic point of no return? What is the biologic significance of the immunoglobulin rearrangement detected with PCR? What will be the 5- and 10-year relapse-free survival rates of patients suffering from low-grade MALT lymphoma treated with H. pylori eradication alone as first and only treatment? The wave of new data each year about the role of H. pylori in gastric MALT lymphoma may help many of these questions to be answered.

Adult↗

Ocular findings in Fryns syndrome.

PURPOSE: To demonstrate the ocular histopathologic findings in Fryns syndrome, a multiple congenital anomaly syndrome, with characteristic features including Dandy-Walker malformation, cleft palate, diaphragmatic hernia, lung hypoplasia, distal limb anomalies and polyhydramnios. The prevalence is about 0.7 per 10,000 births. Reported ocular features include microphthalmus, "cloudy cornea", irregularities of Bowman's layer, thickened posterior lens capsule and retinal dysplasia. METHODS: Case report. The ocular histopathologic and ultrastructural findings in a male fetus with Fryns syndrome who died immediately after his birth at 26th week of gestation are shown. RESULTS: An abnormal Descemet's membrane was found in addition to "cloudy corneae". Electron microscopy demonstrated absence of the banded collagen fibrils in Descemet's membrane, indicating corneal endothelial dysfunction. Otherwise, the eye was morphologically normal for its age; none of the other reported ocular features of Fryns syndrome were found. CONCLUSION: Corneal endothelial dysfunction might cause abnormal composition of anterior Descemet's membrane and could contribute to the "cloudy cornea" known to occur in Fryns syndrome.

Abnormalities, Multiple↗

The effects of omeprazole on healing and appearance of small gastric and duodenal lesions during dosing with diclofenac in healthy subjects.

BACKGROUND: Non-steroidal anti-inflammatory drugs (NSAIDs) are associated with gastrointestinal mucosal damage. Omeprazole prevents the formation, and accelerates the healing, of NSAID-induced ulcers. AIM: To test whether omeprazole accelerates healing of standardized gastroduodenal lesions in the presence of diclofenac. METHODS: In a double-blind, double-dummy, placebo-controlled, crossover study, 12 healthy volunteers received consecutive, 2-week courses of omeprazole (40 mg o.d.) and placebo, in random order, with an intervening, 4-week washout period; diclofenac (50 mg t.d.s.), was given for the second week of each course. Five endoscopies were performed, one at the outset and the others before and after each course of diclofenac. Biopsies were taken from the endoscopically normal mucosa of the corpus, antrum and duodenum and also from any new mucosal lesion that developed after diclofenac. The sites of biopsies taken before each course of diclofenac were evaluated endoscopically after each course to assess the extent of healing according to a predetermined healing score scale. RESULTS: The healing scores observed after administration of placebo/diclofenac (median=0; range 0-6) and after omeprazole/diclofenac (median=0; range 0-6; P=0.17) did not differ. Small gastroduodenal lesions developed de novo in six subjects during placebo/diclofenac and in seven during omeprazole/diclofenac. Focal chemical gastropathy was observed only in close proximity to macroscopic lesions. CONCLUSIONS: In healthy subjects, omeprazole does not accelerate the healing of pre-existing mucosal lesions or prevent the development of small diclofenac-induced mucosal lesions.

Adult↗

Diagnostic criteria for gastrointestinal carcinomas in Japan and Western countries: proposal for a new classification system of gastrointestinal epithelial neoplasia.

BACKGROUND: Large differences have been found between Western and Japanese pathologists in their diagnosis of adenoma/dysplasia and early carcinoma for gastric, colorectal and oesophageal epithelial neoplastic lesions. Common worldwide terminology based on clinical usefulness, that is, on neoplastic severity and depth of invasion, is needed. METHODS: Thirty-one pathologists from 12 countries reviewed 35 gastric, 20 colorectal and 21 oesophageal biopsy and resection specimens. The extent of diagnostic agreement between those with Western and Japanese viewpoints was assessed by kappa statistics. RESULTS: Suspected or definite carcinoma was diagnosed in 17-66% 'of gastric, in 5-40% of colorectal, and in 10-67% of oesophageal slides by pathologists with a Western viewpoint, but in 77-94% of gastric, in 45-75% of colorectal and in 81-100% of oesophageal slides by pathologists with a Japanese viewpoint (from Japan, Germany, Austria and UK). Overall, there was poor agreement between the conventional Western and Japanese diagnoses (kappa values lower than 0.3 for gastric, colorectal and oesophageal lesions). There was much better agreement among the pathologists (kappa values higher than 0.5 for gastric and colorectal lesions) when the original assessments of the slides were regrouped into the five categories of the following classification of GI epithelial neoplasia we hereby propose: C1, negative for neoplasia; C2, indefinite for neoplasia; C3, mucosal low-grade neoplasia (low-grade adenoma/dysplasia); C4, mucosal high-grade neoplasia (high-grade adenoma/dysplasia plus mucosal carcinoma); C5, submucosal invasion of neoplasia. CONCLUSIONS: The intercountry differences in the diagnoses of adenoma/dysplasia and early carcinoma can, in large part, be resolved by adopting terminology based on neoplastic severity and depth of invasion. Problems with defining intramucosal invasion are thus avoided. Moreover, grouping high-grade adenoma/dysplasia and mucosal carcinoma together in one category is clinically useful, as patients with small mucosal neoplastic lesions can be cured by endoscopic local resection.

Adenoma↗

Barrett's mucosa, Barrett's dysplasia and Barrett's carcinoma: diagnostic endoscopy without biopsy-taking does not suffice.

Many gastroenterologists are of the opinion that endoscopic diagnosis of gastro-oesophageal reflux disease (GORD) suffices and that additional biopsies are not necessary. The data obtained from 1068 consecutive patients with histologically confirmed Barrett's oesophagus were analysed retrospectively. In 37.9% of the patients, the histological diagnosis of Barrett's oesophagus was an incidental finding, whereas 32.7% of Barrett's carcinomas were diagnosed only at histology but not during endoscopy. Of the Patients with dysplasia, 92.4% were diagnosed only by the pathologist. Our analysis shows that an endoscopic diagnosis suspicious for Barrett's mucosa is made in 62.1% of the cases, carcinoma in 70%, and dysplasia in only 7.6% of the cases. Also, because neoplasia is detected for the most part at the invasive carcinoma state, but not in the dysplasia stage, the diagnosis of Barrett's oesophagus, with and without dysplasia, needs to be improved by additional biopsies for histopathological investigation.

Aged↗

Expression of transforming growth factor beta-1 in gastric cancer and in the gastric mucosa of first-degree relatives of patients with gastric cancer.

Transforming growth factors beta (TGF-beta) constitute a family of polypeptide growth factors that control cell growth, cell differentiation and migration, as well as the formation of the extracellular matrix. Recent analyses revealed the overexpression of TGF-beta1 in human gastric cancers and demonstrated increased cell proliferation in the stomach of patients with gastric cancer and their first-degree relatives. Using human gastric tissues obtained from patients with gastric cancer (n = 19), biopsies from healthy first-degree relatives of gastric cancer patients (n = 18) and healthy individuals (n = 19), we analysed the expression of TGF-beta1 using the reverse transcriptase polymerase chain reaction (RT-PCR) and immunohistochemistry. Fifteen of 19 patients with gastric cancer expressed TGF-beta1 in the tumour. In 11 of these 15 cases TGF-beta1 mRNA was also detectable in the non-tumourous stomach. Interestingly, all but two individuals with a first-degree relative diagnosed with gastric cancer exhibited TGF-beta1 expression in either the antrum or corpus biopsy or both. In contrast, only one of 19 individuals without a family history of gastric cancer expressed TGF-beta1 in the stomach (P< 0.0001). TGF-beta1 expression is detectable in a large proportion of gastric cancers and in the stomach of healthy first-degree relatives of gastric cancer patients. Since individuals without gastric cancers in their family express TGF-beta1 only in one of 19 cases, the induction of TGF-beta1 expression in first-degree relatives of patients with gastric cancer points to the presence of specific molecular alterations in a subgroup of individuals with an increased risk of developing gastric cancer that may precede the development of gastric cancers.

Adult↗