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M Stolte

Publications and source records attributed to M Stolte.

At least 109 records · Page 6Linked to original sources
PubMed2001

[Precancerous risk markers in Helicobacter pylori gastritis].

Primarily on the basis of epidemiological evidence, Helicobacter pylori was classified as a definite human carcinogen in 1994. Although several pathophysiological consequences of chronic H. pylori gastritis have been identified which may contribute to the development of gastric carcinoma, it is still largely unknown why only a minority of individuals infected with H. pylori (approximately 1/1000) develop this fatal disease. In recent years many studies have examined potential risk factors of H. pylori gastritis to improve our understanding of the early events in gastric carcinogenesis. The present paper summarizes research data supporting the following hypotheses: (a) Some H. pylori possess virulence factors which may contribute to the pathogenicity of the organism and may increase the risk for subsequent severe gastroduodenal diseases such as gastric cancer. However, the associations between these virulence factors and disease is not specific, and may vary considerably among different geographic regions. (b) Chronic H. pylori gastritis induces several pathophysiological alterations which may promote cancer development. In particular, the corpus-dominant phenotype of H. pylori gastritis is strongly associated with gastric cancer. (c) A family history of gastric cancer per se, but also in combination with H. pylori infection, is associated with histopathological and molecular alterations that are considered relevant in gastric carcinogenesis.

Chronic Disease↗
PubMed2001

[Diagnosis of celiac disease and sprue. Recommendations of the German Society for Pathology Task Force on Gastroenterologic Pathology].

The diagnosis of celiac disease (CD) is based upon histological findings in duodenal or jejunal biopsy specimens. In recent years it has been seen that the development of CD lesion in the small bowel is a dynamic process which may present in various histological forms. At one end of the spectrum is a mucosa with normal architecture and an increase in intraepithelial lymphocytes; at the other end is the classical flat mucosa. Histological features supporting the diagnosis of CD are architectural changes of the villi and/or crypts, an increase in lamina propria cell density, and an increase in intraepithelial lymphocytes counts. Exact histological classification of the histological findings is required for diagnostic purposes and for monitoring of CD patients. This has become possible by using a modified Marsh classification. We present both the histological presentation of CD and the modified Marsh classification, and the most important differential diagnoses.

Biopsy↗
PubMed2001

[Lymphocytic gastritis--a rare disorder of the gastric mucosa].

Lymphocytic gastritis, first described by Haot et al. in 1986, is a very rare form of gastritis (0.8-1.6% of cases) with unclear pathogenesis. On endoscopy, lymphocytic gastritis may present either a normal appearance, such as gastritis varioliformis with multiple elevated chronic erosions in the corpus and fundus, or as a giant fold gastritis in the corpus and fundus. This type of gastritis is diagnosed histologically based on an accumulation of intraepithelial lymphocytes (more than 25/100 epithelial cells) in the surface cells of the gastric mucosa. Its etiopathogenesis is currently thought to be a sprue-associated reaction or an atypical reaction to Helicobacter pylori infection. Some studies report the lymphocytic gastritis in almost 45% of cases of sprue, with the gastritis regressing in response to a gluten-free diet, while others report a correlation of lymphocytic gastritis with serologically and/or histologically confirmed H. pylori infection, with the lymphocytic gastritis being cured by H. pylori eradication treatment in a high percentage of the cases. It is possible that a similar abnormal immune reaction to an inflammatory agent underlies both pathological entities, sprue and lymphocytic gastritis--in the one case gluten and in the other H. pylori--which would mean that sprue-induced and H. pylori-induced forms of lymphocytic gastritis exist side by side.

Celiac Disease↗
PubMed2001

[Active pre-atrophic autoimmune gastritis. A practice-oriented concept for diagnosis and treatment].

Helicobacter pylori infection sometimes leads to an antigastric autoimmunity that ultimately develops into complete atrophy of the glands of the gastric mucosal glands. It has been found that the "classical" parietal cell antibody positive and H. pylori induced autoimmune gastritis share common aspects of histomorphology, stages, and pathomechanisms. Healing of H. pylori associated active preatrophic autoimmune gastritis by eradication treatment has been confirmed both in case reports and in prospective and retrospective studies. This leads to a general practice-oriented four-step concept for diagnosis and treatment in daily routine: (a) Histological work-up on the basis of: lymphocytic infiltration of the glands of the corpus and fundic mucosa, focal destruction in individual corpus glands, reactive hypertrophy of the parietal cells, and search for H. pylori. (b) Additional serological work-up if histological evidence of H. pylori is lacking: determination of H. pylori and parietal cell antibodies in the serum. (c) Initiation of an established H. pylori eradication therapy if histology and/or serology is positive for H. pylori. (d) Histological and serological follow-up for 9-12 months to monitor the results of treatment.

Autoimmune Diseases↗
PubMed2001

Tenascin: a sensitive and specific diagnostic marker of minimal collagenous colitis.

Collagenous colitis is a rare cause of chronic watery diarrhea. In this condition, endoscopic findings are usually normal. Currently, the diagnosis relies on the histological presence of thick subepithelial bands of collagen deposits and an inflammatory infiltrate within the mucosa. However, these subepithelial bands may be developed only focally and may be too subtle to allow a definitive diagnosis upon routine hematoxylin and eosin (HE) and van Gieson's stainings. Recently, we and others were able to show a prominent staining of tenascin and type-VI collagen in the subepithelial band-like structures. In this study, we tested the diagnostic value of tenascin staining and type-VI collagen immunolocalization for the identification of collagenous colitis and compared it with conventional histology and histochemical detection of collagens. The analysis was based on 434 biopsy specimens of collagenous colitis, other forms of colitis, and normal mucosa. We were able to show that the immunohistochemical detection of increased amounts of tenascin, selectively in the subepithelial zone, is a specific test for collagenous colitis, with a sensitivity superior to conventional histological and histochemical detection, especially in minimal collagenous colitis (P<0.001). Of note, tenascin staining also allows the diagnosis of collagenous colitis in biopsies obtained only from the rectum and sigmoid colon, thus avoiding the need for colonoscopic investigations. Tenascin immunostaining is a simple and safe tool to complement conventional histological diagnostics in clinically and histopathologically unclear cases of diarrhea.

Adolescent↗
PubMed2001

A comparative study of E-cadherin and stromelysin-3 expression in de novo and ex adenoma carcinoma of the colorectum.

An apparent exception to the colorectal adenoma-carcinoma carcinogenetic pathway is the so-called "de novo" carcinoma which has no evidence of adenoma in its vicinity. Despite the fact that they are often quite small, these lesions appear to be more aggressive (i.e., greater likelihood of lymph-node metastases) than carcinomas that clearly arise from surrounding adenomas exadenoma carcinoma. The purpose of the present comparative immunohistochemical study was to compare rates of cell adhesion molecule (E-cadherin) and protease [stromelysin-3 (ST-3)] expression in groups of de novo (n=64) and ex adenoma (n=42) lesions in order to see whether their more aggressive behavior is associated with decreased cell adhesion and increased protease expression. The rates of extensive ST-3 expression and decreased E-cadherin expression were significantly higher in the de novo group (P=0.014 and 0.005, respectively). Histopathologically, the de novo group also had a significantly higher percentage of cases with an infiltrative invasion pattern. These differences highlight the more aggressive phenotype of the de novo colorectal carcinoma and fit with their greater invasive potential.

Adenoma↗
PubMed2001

Review of histological classifications of gastrointestinal epithelial neoplasia: differences in diagnosis of early carcinomas between Japanese and Western pathologists.

Gastrointestinal lesions considered to be high-grade adenoma/dysplasia by Western pathologists using the conventional Western classification are often diagnosed as carcinoma by Japanese pathologists using the Japanese group classification. To overcome these differences, the Padova classification, the Vienna classification, and a revision of the Vienna classification have recently been proposed. The clinical usefulness of these five classifications needs to be reviewed for early gastric, esophageal, and colorectal neoplasias. In 1998, 31 pathologists from 12 countries individually diagnosed the same 35 gastric, 21 esophageal, and 20 colorectal specimens. Their histological diagnoses can be classified conventionally and according to the newly proposed terminology, and from these data, the extent of agreement between pathologists with Western and Japanese viewpoints can be calculated, using kappa statistics. With the conventional Western, Japanese, Padova, Vienna, and revised classifications, the agreement scores were 37%, 37%, 71%, 71%, and 80%, respectively, for gastric lesions; 14%, 14%, 57%, 62%, and 67% for esophageal lesions; and 45%, 50%, 65%, 65%, and 70% for colorectal lesions. The kappa values were lower than 0.3 with the conventional Western and Japanese classifications, but higher than 0.5 for gastric lesions, higher than 0.3 for esophageal lesions, and higher than 0.4 for colorectal lesions with the newly proposed classifications. When the literature regarding treatment indications for early neoplastic lesions is reviewed, it becomes apparent that the categories of the revised classification would fit best with current clinical treatment considerations. This classification would be particularly useful for endoscopically resected specimens, to determine whether additional surgery with lymph node dissection is required. In conclusion, the use of the newly proposed terminology can, in large part, resolve the intercountry differences in the diagnosis of adenoma/dysplasia and early carcinoma. However, the newly proposed classifications should be used with caution for biopsy specimens, as sampling error may result in an underestimation of the neoplastic grade or depth of invasion. For the choice between endoscopic and surgical treatment, assessment of the depth of invasion by endoscopic inspection and ultrasound or radiography is essential.

Adenoma↗
PubMed2001

Long-term follow-up of gastric MALT lymphoma after H. pylori eradication.

For almost 10 years, we have been familiar with the concept of mucosa-associated lymphoid tissue (MALT)-type lymphoma of the stomach caused by chronic Helicobacter pylori infection. Many epidemiologic, biologic, and molecular genetic studies have implicated H. pylori for its role in lymphoma genesis. Since the first reports on complete remission of gastric MALT lymphomas after cure of bacterial infection, many clinical studies have investigated the effect of eradicating H. pylori on the course of MALT lymphoma, and indeed were able to confirm remission of the lymphoma. To date, more than 650 patients worldwide have been treated for gastric MALT lymphoma with antibiotics, and we have gained many new insights concerning the biologic behavior of this disease, especially from the deepened knowledge of cytogenetics. Furthermore, factors relevant for the prediction of treatment outcome have been identified, which has helped to stratify patients into risk groups.

Follow-Up Studies↗
PubMed2001

Down-regulation of Akt/PKB in senescent cardiac fibroblasts impairs PDGF-induced cell proliferation.

OBJECTIVE: Cardiovascular diseases are the leading cause of death in the Western World, especially in the elder population. One pathophysiological component of cardiovascular disease is myocardial fibrosis, primarily derived from cardiac fibroblasts. Here we investigated the regulation of proliferation of fibroblasts from hearts of adult rats by platelet derived growth factor AA (PDGF-AA). METHODS: Cardiac fibroblasts were isolated from adult Wistar rats. PDGF-induced cell proliferation was analysed by FACS. PDGF-receptor numbers were analysed by receptor binding assays. Using differential display, differentially expressed kinases were identified during ageing in vitro and confirmed by Northern and Western blotting. Transient overexpression of IRES-GFP constructs was used to analyse the role of the akt kinase on proliferation by FACS. RESULTS: During in vitro senescence/aging of primary fibroblasts, the growth response to PDGF-AA was greatly reduced without alterations in its receptor number or affinity and without changes in downstream signalling via the MAP-kinase pathway. By using a differential display strategy selective for protein kinases, we identified reduced expression of Akt-1 kinase (PKB-alpha) in senescent rat cardiac fibroblasts. These findings were supported by data showing reduced expression of Akt-1 in heart samples from old humans. Overexpression of activated Akt-1 almost completely reconstituted PDGF-AA dependent cell proliferation in aged fibroblasts. CONCLUSION: These results support an important role for Akt in senescence and regulation of cardiac fibroblast cell proliferation.

Animals↗
PubMed2001

Atrophy-metaplasia-dysplasia-carcinoma sequence in the stomach: a reality or merely an hypothesis?

The results of recent investigations have suggested that the old hypothesis of an atrophy-metaplasia-dysplasia-carcinoma sequence in the stomach needs to be qualified. The most common cause of intestinal metaplasia is Helicobacter pylori gastritis. The consequence of this intestinal metaplasia is focal atrophy. Helicobacter pylori infection may also trigger an autoimmune gastritis of the corpus mucosa, with atrophy and intestinal metaplasia. Most intestinal metaplasias are only 'paracancerous' but not 'precancerous' lesions. Diffuse gastric carcinomas, such as the signet ring cell carcinoma, arise independently of intestinal metaplasia. Histogenetically, numerous carcinomas of the stomach are primarily of the gastric type, and may secondarily change into the intestinal type.High-grade intra-epithelial neoplasias (dysplasias) detected during the biopsy-based diagnostic work-up appear to be a marker for carcinoma and must, therefore, be removed endoscopically. The detection of intestinal metaplasia in routinely obtained biopsy material is subject to sampling error and is, therefore, not a suitable marker for an increased risk of a gastric carcinoma developing. As an alternative, the concept of gastritis of the carcinoma phenotype, which is more frequently found in early gastric carcinomas and in the relatives of gastric carcinoma patients, has been developed. In this concept, the diffuse parameters of grade and activity of the gastritis in the antrum and corpus, which are independent of sampling error, are subjected to a comparative analysis. A risk gastritis of the carcinoma phenotype is diagnosed when the grade and activity of the gastritis in the corpus are at least equally as pronounced as in the antrum. Currently, this concept is being tested in a prospective ongoing study. Future studies must show whether, and if so which, immunohistochemical or molecular-genetically detectable changes can be applied as risk markers in the diagnostic work-up. Helicobacter pylori eradication probably does not lead to complete regression of the intestinal metaplasia and ensuing focal atrophy. However, eradication of H. pylori does lead to the normalization of changes that can lead to mutations of the stem cells of the gastric mucosa (free radicals, nitric oxide, cell proliferation and vitamin C secretion).

Gastric Mucosa↗
PubMed2001

[Study Group of Gastroenterological Pathology of the German Society of Pathology. Recommendations for celiac disease/sprue diagnosis].

The diagnosis of celiac disease (CD) is based upon histological findings in duodenal or jejunal biopsies. In the past few years it has turned out that the development of CD lesion in the small bowel is a dynamic process which may present in various histological forms. At one end of the spectrum is a mucosa with normal architecture and an increase in intraepithelial lymphocytes (IEL), at the other end is the classical flat mucosa. Histological features supporting the diagnosis of CD are architectural changes of the villi and/or crypts, an increase in lamina propria cell density and an increase in IEL counts. For diagnostic purposes and for monitoring of CD patients an exact histological classification of the histological findings has to be given. This has become possible by using a modified Marsh classification. In the present paper the histological presentation of CD is presented as well as the modified Marsh classification and the most important differential diagnoses.

Biopsy↗
PubMed2001

[Ulcerative esophagitis and colitis as rare manifestations of Adamantiades-Behcet disease].

We report the case of a 39-year-old German women who suffered from chronic inflammatory bowel disease which had not been exactly classified for 6 years. In the course of the disease she developed recurrent iritis, nodular skleritis, oral and genital ulcer, erythema nodosum and axillary folliculitis. For the first time retrosternal pain occurred. Endoscopy of the upper gastrointestinal tract showed mid esophageal ulcer formation. Colonoscopy demonstrated ulcerative colitis with no involvement of rectal mucosa. Histologically a cutaneous vasculitis in the lower limb was seen and diagnosis of Adamantiades-Behçet disease with marked gastrointestinal involvement and rare manifestation in the esophagus was established. A therapy with prednisolone, azathioprine and mesalazine was started. Under this regimen stomatitis, esophagitis and cutaneous vasculitis resolved, while the colitis showed partial remission now for up to one year.

Adult↗
PubMed2001

Improvement in the quality of the endoscopic/bioptic diagnosis of gastric ulcers between 1990 and 1997--an analysis of 1,658 patients.

BACKGROUND: Helicobacter pylori research has greatly improved the diagnosis and treatment of gastric ulcer. The aim of the present study was to investigate the question whether the new perceptions had been incorporated into the daily diagnostic routine of the nineteen-nineties. PATIENTS AND METHODS: Analysis of the biopsy material at the institute of Pathology of the Klinikum Bayreuth obtained from 1,658 patients with gastric ulcers in the months of January and February 1990 (n = 506), 1992 (n = 525), 1994 (n = 532), 1995 (n = 432) and 1997 (n = 400) with the aim of determining the quality of the endoscopic assessment of biological significance, and the number of biopsy specimens obtained from the ulcer, as well as the number of additional biopsies taken from the antrum and corpus. RESULTS: 1,436 (88.9%) of the endoscopically diagnosed ulcers proved to be histologically benign and 222 (11.1%) malignant, of which 192 (86.5%) were carcinomas, 24 (10.8%) MALT lymphomas, 2 (0.9%) sarcomas, and 4 (1.8%) ulcerated metastases. The percentage of false-negative endoscopic assessments of biological significance was 1.8%, that of the false-positive assessments 4.1%, that is, both very low figures. In the case of endoscopically suspicious findings, the histological examination revealed an ulcerated malignant tumor in almost 30% of the cases. The average number of biopsies harvested from the ulcer increased from 5.9 in 1990 to 7.1 in 1997. The frequency of biopsies obtained additionally from antrum and corpus rose statistically significantly from 14.1% of the cases in 1990 to 43.0% in 1997. CONCLUSION: During the course of the nineteen-nineties, the quality of the endoscopic/bioptic diagnosis improved noticeably. In terms of the number of biopsy specimens obtained from the ulcer to identify its biological significance, and the number of additional biopsies from antrum and corpus to identify underlying diseases, there is, however, still room for improvement.

Adolescent↗
PubMed2001

Short-term changes in Helicobacter pylori gastritis and bulbitis during and after 2 weeks of treatment with omeprazole and amoxicillin in duodenal ulcer patients.

OBJECTIVE: To evaluate the dynamics of histological changes in the mucosa of the stomach and duodenal bulb during and after completion of a 14-day course of Hp-eradication dual treatment with high-dose omeprazole and amoxicillin. PATIENTS: 12 patients (mean age 53 +/- 16 years SD, 9 male, 3 female) with an acute Hp-positive duodenal ulcer were included in this open, prospective, single-centre study. METHOD: Patients were given omeprazole 40 mg b.i.d. and amoxicillin 1,500 mg b.i.d. for a period of 14 days. Endoscopic biopsies were obtained on days 3, 7, 14, 28, 42 as well as at following endoscopies performed a mean of 17 months after treatment. RESULTS: The Hp-eradication rate achieved 4 weeks after treatment was 82%. On day 14, 88% of the ulcers were healed. Already on day 7 Hp had almost completely disappeared from the antrum, corpus and duodenal bulb, and the activity of gastritis in the antrum and corpus and the activity of bulbitis in the duodenal bulb was almost nonexistent. The decrease in the grade of gastritis was much lower by day 42. CONCLUSIONS: Our study shows for the first time that in all patients signs of primarily successful Hp-eradication treatment during the first days of treatment are consistently demonstrable and complete already after one week of therapy, irrespective of the subsequent cure or persistence of Hp-infection. In the patients with persistence of Hp-infection Hp-colonization and activity of gastritis quickly increased within 2-4 weeks after cessation of treatment. Checks to evaluate complete eradication or recrudescence of Hp-infection should be carried out not earlier than 28 days after cessation of treatment.

Adult↗
PubMed2001

Red streaks in the oesophagus in patients with reflux disease: is there a histomorphological correlate?

BACKGROUND: The Los Angeles classification of reflux oesophagitis includes sharply demarcated areas of erythema without any associated slough within the definition of reflux-induced mucosal breaks, though there is uncertainty as to whether these "red streaks" actually represent such a mucosal lesion. This study evaluates the histopathology of these red streaks. METHODS: Forty patients with one or more red streaks on the tops of the mucosal folds in the distal oesophagus were included in a multinational, multicentre prospective study. All patients were referred for upper gastrointestinal endoscopy to investigate chronic heartburn and acid regurgitation. Biopsies were taken from the red streaks and from control biopsies from more normal appearing mucosa 1 cm lateral to the red streaks. A two-sided probability test using normal approximation assessed differences in the histological findings at the two biopsy locations. RESULTS: Compared to control biopsies, biopsies of red streaks had a significantly thicker basal cell layer (mean +/- s 41% +/- 32% versus 18% +/- 23% of mucosal thickness, P=0.001) and longer papillae (mean +/- s 71% +/- 19% versus 49% +/- 24% of mucosal thickness, P= 0.001). Of the red streak biopsies, 25% had either newly re-epithelized lesions or granulation tissue beneath squamous epithelium. Only 10% of the control biopsies had moderate or more marked regenerative changes (based on elongation of papillae and basal cell hyperplasia), compared to 65.1% of red streak biopsies. Of the biopsies from the red streak itself, 7% showed no abnormality and 27.9% only slight changes. In comparison, 25% of the biopsies from control biopsies showed no regenerative changes and 62.5% only slight change due to gastro-oesophageal reflux disease. CONCLUSION: The histomorphological counterpart to the endoscopically visible red streaks of the distal oesophagus is marked regenerative changes of the squamous epithelium and/or capillary rich granulation tissue beneath the squamous epithelium. Red streaks are validated as being indicative of acid/peptic mucosal injury, but they do not satisfy a strict definition of a mucosal break.

Biopsy↗
PubMed2001

Acute measles gastric infection.

We describe the case of a 44-year-old man who was referred for gastroscopy because of abdominal pain. During endoscopy, inflammatory changes of the antrum and corpus mucosa were clearly visible, and biopsy samples from the antrum and corpus mucosa were taken. At histology, routine hematoxylin and eosin staining showed characteristics indicative of so-called ex-Helicobacter pylori-gastritis that had developed after antibiotic treatment 2 years ago. Additional large, bizarre inclusion bodies and clusters of multinucleated giant cells were located in the surface epithelium and within the lamina propria. These giant cells had an appearance similar to that of Warthin-Finkeldey cells, which can be found during the prodromal phase of measles infection. Anti-measles virus immunochemistry showed a strong positivity for measles virus antigen within the giant cells. Based on these results, the final diagnosis of morbilliform gastritis was made. To our knowledge, no case of measles gastritis has been described in the literature. Our case report confirms the systemic character of measles virus infection and confirms that measles viral replication can involve the gastric mucosa in addition to the conjunctiva, lung, and intestina.

Acute Disease↗