Biomedical subjects

M Stolte

Publications and source records attributed to M Stolte.

At least 55 records · Page 3Linked to original sources

PubMed2001

[Insufficient validity of a rapid blood test for diagnosis of Helicobacter pylori infection].

BACKGROUND AND AIM: Rapid blood tests for diagnosis of Helicobacter (H.) pylori infection enable to detect antibodies against H. pylori instantly without laboratory equipment. Primary aim: to validate the Helisal Rapid Whole Blood Test (HRBT) with endoscopic bioptic methods as reference. Secondary aim: to compare the HRBT with ELISA IgG serology. PATIENTS AND METHODS: The HRBT was performed in 145 consecutive dyspeptic patients (median age 59 years) before undergoing esophagogastroduodenoscopy including biopsies from gastric antrum and corpus. A positive H. pylori status was defined by a positive culture or the combination of a positive rapid urease test and a positive histology. Serum for ELISA IgG testing was available from 92 patients. RESULTS: The H. pylori status was positive in 66% of the patients. The sensitivity of the HRBT resulted at 80%, the specificity at 82%. The sensitivity of the HRBT for a positive ELISA test amounted to 87%, the specificity to 96%. CONCLUSIONS: The diagnostic validity of the HRBT is insufficient for clinical application. False test results add up by the general discrepancy between serological and bioptic methods and by diminished sensitivity compared to ELISA serology.

Adult↗

PubMed2001

Are lymphocytic monoclonality and immunoglobulin heavy chain (IgH) rearrangement premalignant conditions in chronic gastritis?

Normal gastric mucosa is devoid of lymphoid cells. Any increase of lymphocytes suggests chronic inflammation. Infection with Helicobacter pylori (Hp) is the major cause for nonautoimmune chronic gastritis and induces a mixed cellular response resulting in an acquired lymphoid tissue, or MALT (mucosa-associated lymphoid tissue). Hp has also been implicated in the genesis of gastric MALT-lymphoma. Polymerase chain reaction-based assays to detect the expansion of monoclonal B-cells have also been used to corroborate the diagnosis. In a considerable number of cases monoclonal B-cells remain detectable in follow-up biopsies, with the lymphoma being in complete histological remission. The clinical relevance of this finding is not clear yet. However, there also exist different reports that monoclonal B-cells can be found in gastric biopsies of patients with neither a histological sign nor a present or past history of lymphoma. In the light of these findings we address the question whether B-cell monoclonality can be seen as a premalignant condition in chronic gastritis and conclude that as of now the relevance of the finding of B-cell monoclonality remains unclear. As of now the only and gold standard for the diagnosis of gastric MALT-lymphoma is histopathology.

B-Lymphocytes↗

PubMed2001

Complete remission of primary high-grade B-cell gastric lymphoma after cure of Helicobacter pylori infection.

PURPOSE: Treatment of low-grade gastric mucosa-associated lymphoid tissue lymphoma by eradication of Helicobacter pylori is reported to result in complete lymphoma remission in approximately 75% of cases. The effect that cure of the infection has on the course of a primary high-grade gastric lymphoma is largely uncertain. The aim of this study was to report the effect of cure of H pylori infection exerted in patients with high-grade B-cell gastric lymphoma. PATIENTS AND METHODS: Eight patients (4 males and 4 females; age range, 26 to 85 years) with H pylori infection and high-grade lymphoma received eradication therapy before planned treatment. The effect of H pylori eradication on the course of high-grade lymphoma was assessed by analysis of surgical specimens (n = 2) or endoscopic biopsies (n = 6). RESULTS: H pylori eradication was successful in all patients and led to complete remission of the lymphoma in seven patients. One patient has experienced partial remission. Two patients were referred to surgery, one of whom (stage II(1E)) had lymph node involvement, and the histologic work-up of the resected stomach revealed residual infiltrates of a low-grade lymphoma, which prompted consolidation chemotherapy. In one patient (initially stage I(1E)), abdominal lymphoma developed 6 months after eradication therapy, which regressed completely after chemotherapy. In four patients, no further treatment was given. Six patients continue in complete remission (range, 6 to 66 months). CONCLUSION: Primary high-grade B-cell gastric lymphoma in stages I(E) through II(E1) associated with H pylori may regress completely after successful cure of the infection. Prospective trials are needed to investigate this treatment in larger numbers of patients.

Adult↗

PubMed2001

Long-term persistence of monoclonal B cells after cure of Helicobacter pylori infection and complete histologic remission in gastric mucosa-associated lymphoid tissue B-cell lymphoma.

PURPOSE: Cure of Helicobacter pylori infection is associated with remission induction in the majority of patients with low-grade gastric mucosa associated lymphoid tissue (MALT) lymphoma in localized stages; however, limited data exist as to whether these patients may be cured of their lymphoma. The present study was performed to investigate whether the polymerase chain reaction (PCR) for the rearranged immunoglobulin heavy chain region may be used to define "molecular" remission. PATIENTS AND METHODS: Ninety-seven patients who suffered from low-grade gastric MALT lymphoma stage I(E) were observed with central pathology and molecular biology after cure of H pylori infection. PCR was performed with the use of consensus primers for the framework regions 1, 2, and 3 and monoclonality was corroborated by sequence analysis. In selected cases, microdissection was performed to study the origin of the monoclonal B cells. RESULTS: Of the 97 patients, 77 obtained complete endoscopic and histologic remission (CR). Twenty of 44 patients with PCR monoclonality at diagnosis and with sufficient molecular follow-up displayed monoclonal bands for a median time of 20.5 months after CR (range, 0 to 50.4 months). These B cells were related to the original lymphoma clone by sequence analysis. Microdissection analysis identified basal lymphoid aggregates as the source of these monoclonal B cells. Local relapse occurred in and was observed by PCR in four patients. All four patients displayed monoclonal PCR before relapse, and three of these four showed ongoing PCR monoclonality throughout their course, indicating the persistence of malignant cells. CONCLUSION: Half of all patients with gastric MALT lymphoma show long-term PCR monoclonality up to several years after cure of H pylori infection and CR. Patients with monoclonal PCR should be observed closely, whereas long-term PCR negativity may indicate cure of the disease.

Adult↗

PubMed2001

Helicobacter pylori eradication therapy in gastric high grade non Hodgkin's lymphoma (NHL).

BACKGROUND: Primary gastric low-grade lymphoma of the mucosa associated lymphoid tissue (MALT) develops on the background of a chronic Helicobacter pylori (H. pylori) infection. Stable remissions can be induced by H. pylori eradication therapy as shown in clinical trials. In 8 cases of high-grade gastric lymphomas remissions after H. pylori eradication were observed retrospectively. AIM: We started a pilot-trial to investigate the value of H. pylori eradication therapy in early gastric high-grade B-cell lymphoma prospectively. PATIENTS AND METHODS: So far, two H. pylori positive patients with high-grade B-cell lymphoma of the stomach stage Ann Arbor I E are included. They received a triple eradication-therapy (Clarithromycin 500 mg/d, Metronidazol 800 mg/d and Omeprazol 40 mg/d) for 7 days. Endoscopic controls are preformed every 4 weeks. RESULTS: Both patients became H. pylori negative after eradication therapy. One patient achieved complete remission (CR) 38 days after eradication. The continuous complete remission lasts now for 170 days. The second patient received only a partial remission (PR) 4 weeks after eradication and showed a slight progress 4 weeks later. He presently receives chemotherapy (CHOP). CONCLUSIONS: Patients with early high-grade gastric B-cell lymphomas should receive H. pylori eradication only within clinical trials. It seems to be possible to induce remissions of early high-grade gastric B-cell lymphomas with exclusive H. pylori eradication therapy. The stability of remission remains to be unclear and should be evaluated by following up the patients closely.

Aged↗

PubMed2001

[Difficult diagnosis: acute appendicitis and appendiceal/cecal carcinoma].

INTRODUCTION: Primary carcinoma of the appendix vermiformis/caecum is very rare. The diagnosis can often be ascertained only postoperatively by histopathological means. Preoperative diagnosis is unusual. METHOD AND RESULTS: We report on five patients with an adenocarcinoma of the appendix/base of caecom, all operated on between July 1998 and October 1999. CONCLUSION: A hemicolectomy "en principe" is not necessary. However, ileocaecal resection should have been performed during the first operation and there should be no positive lymph nodes. Postoperative diagnosis of a carcinoma after simple appendectomy necessitates Reoperation with right hemicolectomy.

Acute Disease↗

PubMed2001

[The new "Vienna Classification" for epithelial neoplasia of the gastrointestinal tract. Pros or cons?].

A number of seminars have shown considerable differences between Japanese and Western pathologists in the the diagnostic differentiation of regenerative changes, dysplasia, and well differentiated adenocarcinoma in gastroenterological biopsy material. Lesions which most Western pathologists identify as "dysplasia" are often considered adenocarcinomas in Japan. A comparison of the biopsy-based diagnoses with those established in resected mucosa, however, reveals appreciable diagnostic inexperience on the part of Western pathologists, with significant discrepancies between their diagnoses based on biopsies and those based on resected material. Against this background, a new classification of epithelial neoplasias of the gastrointestinal tract was drafted on the occasion of the World Congress of Gastroenterology in Vienna in 1998. By collapsing the diagnoses "high-grade adenoma/dysplasia, noninvasive carcinoma (carcinoma in situ), and suspected invasive carcinoma" into a single category ("noninvasive high-grade neoplasia," category 4), this scheme should largely eliminate the diagnostic discrepancies between Western and Japanese pathologists. As with every classification, the Vienna classification has its advantages and disadvantages; these are discussed here. The most important advantage of the Vienna classification is that the various categories are associated with different recommendations for further diagnostic and therapeutic measures. This applies particularly to category 4, with the recommendation for only local treatment initially (endoscopic mucosal resection or surgical excision). Since the introduction of the Vienna classification the new WHO classification of neoplasias of the gastrointestinal tract has recently been published, in which the term dysplasia has been replaced by "intraepithelial neoplasia." This means that the Vienna classification needs to be modified accordingly.

Carcinoma, Squamous Cell↗

PubMed2001

[Extent, topography and symptoms of Helicobacter pylori gastrtitis. Phenotyping for accurate diagnosis and therapy?].

Helicobacter pylori gastritis, a very common condition, may lead to serious sequelae such as peptic ulcer, gastric carcinoma, and mucosa-associated lymphoid tissue lymphoma. Histological grading of the various gastritis parameters can help to identify the risk of these sequelae and thus improve the indication for prophylactic treatment of the H. pylori infection. This applies in particular to two types of "risk gastritis": gastritis of the duodenal ulcer phenotype and gastritis of the carcinoma phenotype. In the former the antrum shows pronounced inflammatory changes while only low-grade gastritis is seen in the corpus. In the latter, by contrast, the gastritis in the corpus is at least equally as severe as that in the antrum; in addition, intestinal metaplasia and focal atrophy is also frequently found in this phenotype. By establishing topographic grading of the gastritis in antrum and corpus the pathologist can therefore play the role of a "litmus test" for prophylactic H. pylori eradication treatment.

Diagnosis, Differential↗

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↗