Biomedical subjects

M Stolte

Publications and source records attributed to M Stolte.

At least 235 records · Page 13Linked to original sources

PubMed1998

Loss of heterozygosity and microsatellite instability in de novo versus ex-adenoma carcinomas of the colorectum.

Small adenocarcinomas of the colorectum showing no evidence of origin from an adenoma have been called de novo carcinomas, a name that implies an origin via a different molecular genetic mechanism than the usual colorectal carcinoma which develops from an adenoma. Using microsatellite analysis, 35 early (pT1) de novo and 36 pT1 ex-adenoma carcinomas were compared using 8 microsatellite loci at 6 different chromosomal loci (1p, 2p, 8p, 5q, 17p, and 18q) known or hypothesized to be important for colorectal carcinogenesis. The rate of loss of heterozygosity (LOH) at the 17p locus (near the p53 gene) was significantly higher in the de novo than in the ex-adenoma group (73 vs. 37%, P = 0.004). The rates of LOH at the other loci (including the APC and DCC genes) and the rate of MSI were not significantly different in the two groups. These results indicate that de novo carcinomas of the colorectum develop via a similar carcinogenetic pathway as conventional ex-adenoma carcinomas; however, their higher rate of LOH at 17p is evidence for a biologically more advanced lesion with more frequent p53 mutations, consistent with clinicopathological data indicating that de novo carcinomas are more aggressive than ex-adenoma carcinomas.

Adenocarcinoma↗

PubMed1998

Photodynamic ablation of high-grade dysplasia and early cancer in Barrett's esophagus by means of 5-aminolevulinic acid.

BACKGROUND & AIMS: The first therapeutic experiences with the conventional photosensitizer dihematoporphyrinester in the treatment of Barrett's esophagus show the curative potential of photodynamic therapy (PDT). The aim of this study was to test 5-aminolevulinic acid (5-ALA)-induced protoporphyrin IX, a photosensitizer with a high mucosa specificity without phototoxic side effects on the skin, as a new form of PDT. METHODS: Thirty-two patients (mean age, 68.5 years) with histologically proven high-grade dysplasia (n = 10) and mucosal cancer (n = 22) in Barrett's esophagus were treated. Four to 6 hours after oral ingestion of 5-ALA (dose, 60 mg/kg body wt), irradiation was conducted with a dye laser system (635 nm) with a light dose of 150 J/cm2. The patients received 20-80 mg omeprazole daily after PDT. RESULTS: High-grade dysplasia was eradicated in all patients (10 of 10), and mucosal cancer was eliminated in 17 of 22 patients (77%) at a mean follow-up of 9.9 months (range, 1-30 months). All tumors < or = 2 mm in thickness were completely ablated (17 of 17). The method-related mortality and morbidity was 0%. CONCLUSIONS: Severe dysplasia and thin (< or = 2 mm) mucosal cancer of Barrett's esophagus can be completely ablated. PDT might offer a minimally invasive treatment modality as an alternative to esophagectomy.

Adult↗

PubMed1998

Sarcocystis kirmsei in the brain of a hill mynah (Gracula religiosa).

Cysts of Sarcocystis kirmsei were found in the brain of an exotic bird. The morphological appearance of this protozoon and the changes in the brain tissue are described. This is the second report of S. kirmsei in the brain of a hill mynah, and the third report of this parasite in the avian brain. The affiliation of S. kirmsei to the genus Sarcocystis was confirmed. On the basis of our findings, the genus Frenkelia, which comprises two species affecting the brain of small mammals, becomes synonymous with Sarcocystis.

Animals↗

PubMed1998

Chronic gastritis in tigers associated with Helicobacter acinonyx.

Helicobacter pylori-like organisms (HPLOs) were isolated from the gastric mucosa of two Sumatran tigers and identified by polymerase chain reaction analysis as Helicobacter acinonyx. At histological examination, both tigers revealed a chronic gastritis associated with HPLOs as demonstrated by immunolabelling and electron microscopy. This is the first isolation of H. acinonyx from tigers, in which, as previously reported in cheetahs, it may be a cause of gastritis.

Animals↗

PubMed1998

Loss of heterozygosity of the von Hippel Lindau gene locus in polypoid dysplasia but not flat dysplasia in ulcerative colitis or sporadic adenomas.

Carcinoma in ulcerative colitis (UC) develops from dysplastic precursor lesions, which include flat dysplasia (FD) and polypoid dysplasias (PD). PD may present as single or multiple polypoid structures or as plaque-like lesions that, independent of histological grade, are an indication for colectomy. PDs are histologically similar to adenomas and may not be readily distinguished by light microscopy. It is not known whether FD and PD are different entities, or whether they represent etiologically similar lesions with different morphological expression. We microdissected 25 cases of UC with PD and 19 samples of FD with surrounding chronic colitis (CC) in UC. Loss of heterozygosity (LOH) at the von Hippel Lindau (vHL) gene locus and the putative tumor suppressor genes APC, INK4A (9p16), and p53 was studied. LOH of the vHL gene, INK4A (9p16), and APC was also studied in 11 sporadic adenomas of the colon. LOH at the vHL locus was present in 50% of the samples of PD and in 12% of the samples of FD. LOH was seen in CC close to PD and FD in 26% and 12% of cases, respectively. No adenoma showed LOH of the vHL gene markers studied. LOH in p53 was seen in PD in 16% cases and in FD in 42% cases and in CC close to PD and FD in 0% and 14% cases, respectively. LOH patterns between PD and FD of the markers for APC and 9p16 were not different. LOH in APC was seen in two of five cases of adenoma. We conclude that PD and FD share genetic alterations in APC and 9p16 genes. More frequent involvement of the VHL gene in PD and surrounding CC and involvement of p53 in HGD and CC in FD may represent genetic differences between the development of PD and FD and may be the cause of the different morphology. The infrequency of LOH at the vHL locus in adenomas versus PD may serve as a discriminator between adenomas and PD in diagnostically problematic cases.

Adenoma↗

PubMed1998

Significant improvement of atrophy after eradication therapy in atrophic body gastritis.

Chronic atrophic body gastritis may be induced by H. pylori. Results on the effect of H. pylori eradication therapy have been conflicting. Here, we report on the effect of eradication therapy on both body atrophy and inflammation in 7 patients. They presented with severe or moderate atrophy of the oxyntic mucosa and positive H. pylori histology (Warthin-Starry) and/or serology. Eradication was performed with a standard double or triple therapy regimen. At least 6 weeks after successful eradication therapy, patients underwent rebiopsy and histopathological evaluation of the gastric body. In all 7 patients, the grade of body gastritis improved significantly. Among the patients with severe atrophy before H. pylori eradication, 2 had normal mucosa, 3 low-grade atrophy, and one moderate atrophy after treatment. The one case with moderate atrophy before treatment had normal mucosa after H. pylori eradication. In addition, inflammatory infiltration of the mucosa cleared up in 6 cases and improved from severe to mild in one case after treatment. From these results, we conclude that in patients with histologically demonstrated H. pylori and/or positive H. pylori serology atrophic body mucosa can recover after successful eradication therapy.

Adult↗

PubMed1998

Severe expression of corpus gastritis is characteristic in gastric cancer patients infected with Helicobacter pylori.

In 50 Helicobacter pylori-infected gastric carcinoma patients the corpus gastritis was significantly higher than in matched H. pylori-positive control subjects (P < 0.01). Atrophy and intestinal metaplasia (IM) occurred significantly more often in the antrum of carcinoma patients (P < 0.01). The odds ratio for gastric carcinoma was 8.85 for high-grade corpus gastritis and 8.04 when atrophy in the antrum was present.

Female↗

PubMed1998

Changes in Helicobacter pylori-induced gastritis in the antrum and corpus during 12 months of treatment with omeprazole and lansoprazole in patients with gastro-oesophageal reflux disease.

BACKGROUND: Several studies have shown that treatment with omeprazole leads to aggravation of Helicobacter pylori gastritis in the corpus. Whether this also applies to lansoprazole, and whether, in comparison with omeprazole, there are differences in therapy-induced gastritis parameter changes remains unclear. METHODS: In 111 patients infected with H. pylori and with gastro-oesophageal reflux disease we investigated the gastritis parameters in antral and corpus mucosa before and after 2, 6 and 12 months of treatment with 15 or 30 mg lansoprazole or 20 mg omeprazole/day. RESULTS: In all groups the different treatments had a similar effect: in both regions of the stomach, suppression or partial elimination of H. pylori was seen. However, improvement in the inflammation was observed only in the antrum, while in the corpus most gastritis parameters worsened significantly. There was no increase in intestinal metaplasia or atrophy. CONCLUSION: In common with omeprazole, lansoprazole aggravates the gastritis parameters in the corpus but improves them in the antrum. Treatment with proton pump inhibitors does not result in any increase in the incidence of atrophy/intestinal metaplasia. However, as gastritis predominating in the corpus seems to be associated with an elevated carcinogenic risk, consideration should be given to prophylactic H. pylori eradication therapy before initiating proton pump inhibitor treatment.

2-Pyridinylmethylsulfinylbenzimidazoles↗

PubMed1998

Changes in Helicobacter pylori-induced gastritis in the antrum and corpus during and after 12 months of treatment with ranitidine and lansoprazole in patients with duodenal ulcer disease.

BACKGROUND: Several studies have shown that acid-suppressing treatment leads to aggravation of Helicobacter pylori gastritis in the corpus. It remains unclear whether this augmentation of the inflammation reverts to baseline after termination of treatment. METHODS: In 114 H. pylori-infected duodenal ulcer patients we investigated the gastritis parameters in antral and corpus mucosa before treatment, after 6 and 12 months of therapy, and 6 months after termination of treatment with 15 mg lansoprazole or 150 mg ranitidine/day. RESULTS: Lansoprazole and ranitidine led to a significant aggravation of gastritis in the corpus after 6 and 12 months of treatment. However, while there was no change in gastritis in the antrum with ranitidine, treatment with lansoprazole led to partial elimination of H. pylori with improvement of the inflammation in this part of the stomach. Following termination of therapy, the observed changes reverted to baseline. No increase in intestinal metaplasia and/or atrophy in the antrum or corpus was observed. CONCLUSION: Both substances are associated with an aggravation of H. pylori gastritis in the corpus. However, only lansoprazole leads to a partial elimination of H. pylori with improvement of the inflammation in the antrum. The changes provoked by acid-suppressing treatment revert to baseline after termination of therapy.

2-Pyridinylmethylsulfinylbenzimidazoles↗

PubMed1998

Double-blind trial of omeprazole and amoxicillin in the cure of Helicobacter pylori infection in gastric ulcer patients. The Ulcer Study Group, Germany.

BACKGROUND: Our aim was to investigate the efficacy of omeprazole and amoxicillin in curing Helicobacter pylori infection in gastric ulcer patients. METHODS: In a double-blind trial 185 H. pylori-positive gastric ulcer patients were prospectively randomized to receive 40 mg omeprazole twice daily and either 750 mg amoxicillin three times daily or 750 mg amoxicillin placebo three times daily on days 1-14, followed by 20 mg omeprazole daily on days 15-56. RESULTS: Twenty-seven patients were excluded because of lack of compliance or missed follow-up examinations; one patient receiving amoxicillin discontinued treatment owing to side effects. On an intention-to-treat basis, omeprazole/amoxicillin led to cure of H. pylori infection in 67.1% (47 of 70) of patients not using non-steroidal anti-inflammatory drugs (NSAIDs)/aspirin (ASA) and in 46.7% (14 of 30) of those taking NSAIDs/ASA (P < 0.05). With the omeprazole/placebo regimen, H. pylori infection was cured in 8.8% (no NSAIDs), and 0% (NSAIDs). CONCLUSIONS: The use of NSAIDs/ASA may limit the efficacy of omeprazole/amoxicillin in curing H. pylori infection in gastric ulcer patients.

Adolescent↗

PubMed1998

Animal reservoirs in the transmission of Helicobacter heilmannii. Results of a questionnaire-based study.

BACKGROUND: Infection with either Helicobacter heilmannii or H. pylori causes gastritis in humans. Whereas the route of transmission of H. pylori appears to be human-human, it has been suggested that H. heilmannii is transmitted by animals. METHODS: Two hundred and two patients with histologically confirmed H. heilmannii gastritis and 600 randomly selected patients with H. pylori gastritis were sent a questionnaire, in which they were asked whether they had had or still have regular contact with dogs, cats, rodents, horses, birds, cattle, pigs, or wild animals. RESULTS: The questionnaires of 177 patients with H. heilmannii and 485 with H. pylori infection were evaluated. In comparison with H. pylori, H. heilmanii infection was strongly associated with contact with dogs, cats, cattle, or pigs. Logistic regression analysis showed that contact with pigs, cats, and dogs leads to a significant risk of H. heilmannii infection (odds, 4.990, 1.710. and 1.462). CONCLUSION: Pigs, cats, and dogs appear to be reservoirs in the transmission of H. heilmannii.

Adult↗

PubMed1998

A primary osteosarcoma of the heart as a cause of recurrent peripheral arterial emboli.

The case of a 66-year-old woman with a primary cardiac osteosarcoma is described. These distinctly rare malignant tumors arise preferentially in the left atrium. Clinically, they often present symptoms of both, intramural and intracavitary neoplasm in addition to general weakness, recurrent breast pain, and dyspnea. As shown in the present case, with growing intracavitary tumor masses the risk for peripheral arterial including cerebral embolism increases. Consequently, in most patients with symptoms of systemic arterial embolism of unknown origin performance of transesophageal echocardiography seems advisible, which is presently the most convenient noninvasive imaging method to exclude or to identify intracardiac sources of emboli, irrespective of their type.

Aged↗

PubMed1998

High proportion of granzyme B-positive (activated) intraepithelial and lamina propria lymphocytes in lymphocytic gastritis.

Intraepithelial lymphocytes (IELs) and lamina propria lymphocytes (LpLs) have not been well studied in gastric mucosa, particularly in lymphocytic gastritis. Therefore, they were immunohistologically characterized with antibodies recognizing CD3, CD8, CD57, T cell-restricted intracellular antigen (TIA-1), and granzyme B (GrB). The TIA-1 labels cytotoxic granules of resting and activated T-cells, whereas GrB decorates activated cytotoxic T cells. Thirty patients with celiac disease, including 20 taking gluten and 10 on a gluten-free diet, 15 patients with nonceliac disease-associated lymphocytic gastritis, and 20 controls were studied. Stained cells were counted and results were given as IELs/100 epithelial cells or percentage of lamina propria cells. Sixty percent to 90% of CD3+ IELs and up to 12% of lamina propria cells contained TIA-1-positive cytotoxic granules. The number of GrB+ IELs and LpLs was increased in Helicobacter pylori-positive controls (p < 0.03 vs. H pylori-negative controls) and celiac disease patients taking gluten (p < 0.05 vs. controls). The highest number of GrB+ IELs and LpLs was found in nonceliac disease-associated lymphocytic gastritis (p < 0.009 vs. controls, p < 0.05 vs. celiac disease). This study shows that a high proportion of gastric IELs and LpLs is potentially cytotoxic in nature. Through stimuli not yet identified, a proportion of them becomes activated after H pylori infestation and in lymphocytic gastritis.

Adolescent↗

PubMed1998

Frequency of vacA genotypes and cytotoxin activity in Helicobacter pylori associated with low-grade gastric mucosa-associated lymphoid tissue lymphoma.

The vacA genotypes s1,m1 and s1,m2 were detected in 44 and 30% of Helicobacter pylori isolates, respectively, from patients with gastric mucosa-associated lymphoid tissue lymphoma, compared to 26 and 56% of isolates, respectively, from individuals with gastritis. The vacA s1 genotype was significantly associated with, but not predictive of, the presence of vacuolating cytotoxin activity.

Bacterial Proteins↗

PubMed1998

Photodynamic ablation of early cancers of the stomach by means of mTHPC and laser irradiation: preliminary clinical experience.

BACKGROUND: Radical surgical treatment has been the first choice for early gastric cancer, but high resolution endosonography allows in situ diagnosis with a high sensitivity and specificity and in consequence the option of local endoscopic treatment. AIMS: To evaluate photodynamic therapy (PDT) using meso-tetrahydroxyphenyl-chlorin (mTHPC) as the photosensitiser in superficial gastric cancer. METHODS: Twenty two patients with superficial early gastric cancer received mTHPC (0.075 mg/kg intravenously) and were treated 96 hours later with red light at 652 nm (20 J/cm2). Tumour response was assessed by endoscopy and extensive biopsy. RESULTS: Endoscopies performed two to three days after PDT showed a haemorrhagic fibrinoid necrosis of the mucosal layer. Complete remission was achieved in 16/22 (73%) patients: 13/16 (80%) with intestinal type cancer and 3/6 (50%) with a diffuse Lauren's carcinoma. The mean follow up period was 12 months and 20 months, respectively. An average of 1.8 treatment sessions was required. Severe side effects were not observed. Seven patients had mild to moderate skin photo-sensivity reactions; 12 had local pain after PDT for 1-10 days. CONCLUSION: PDT using mTHPC as the photosensitiser represents a safe and efficient method for topical treatment of early gastric cancer, especially of Lauren's intestinal carcinoma. If the preliminary results can be verified in larger patient series and during long term follow up, local treatment of early cancers of the stomach by PDT could be considered as a therapeutic option for selected patients.

Adult↗

PubMed1998

Ongoing somatic mutations and clonal expansions after cure of Helicobacter pylori infection in gastric mucosa-associated lymphoid tissue B-cell lymphoma.

PURPOSE: Although most patients with primary gastric low-grade mucosa-associated lymphoid tissue (MALT) B-cell lymphoma experience complete endoscopic and histologic remission after the cure of Helicobacter pylori infection, in many patients, the polymerase chain reaction (PCR) still detects monoclonal B cells in the gastric mucosa. The present study asked whether the lymphoma immunoglobulin VH (IgVH) sequences remained stable in patients with gastric MALT lymphoma after H pylori eradication. PATIENTS AND METHODS: Eight patients with stage EI disease treated with H pylori eradication were analyzed before and at different time points after the cure of the infection. After the amplification of IgVH genes from DNA extracted from gastric biopsy specimens, monoclonal PCR products were cloned and multiple clones (43 to 105) were sequenced per patient. RESULTS: Mutations were detected in all lymphoma VH sequences, which suggested germinal center or postgerminal center origin of the lymphoma B cells. In five of the eight patients, clonal heterogeneity was observed at diagnosis or during follow-up. Genealogical analysis of shared and unshared mutations showed that the process of somatic mutations was ongoing after H pylori eradication in four of the five patients who showed clonal instability. Ongoing mutations were observed in three of the four patients who completely responded to H pylori eradication, but in only one of the four patients who did not respond or who partially responded. CONCLUSION: In low-grade gastric MALT lymphomas, an ongoing process of somatic hypermutation and antigen selection can be detected after the therapeutic removal of the underlying stimulus H pylori. These data point to the relevance of yet unknown antigens that drive this disease. In addition, they challenge the view that these lymphomas may be cured solely by the eradication of H pylori.

Adult↗

PubMed1998

Helicobacter pylori and Gastric Cancer.

Gastritis caused by infection with Helicobacter pylori (H. pylori) is one of the most common infectious diseases worldwide. There are data on the epidemiology, pathophysiology, and histology of this disease that show that H. pylori gastritis has an important role in gastric carcinogenesis. However, it has to be considered that only very few of those infected with H. pylori will develop gastric cancer. Hence, it will be a main target of future research to identify individuals who carry a greater risk for developing gastric cancer, and therefore may benefit from eradication of H. pylori in terms of gastric cancer prevention.

Journal Article↗

PubMed1998

[Cryptosporidiosis in adders (Pituiophis melanoleucus sayi)].

Infection of snakes with cryptosporidia is known to occur as hypertrophic gastritis associated with postprandial regurgitation. This is a report of a severe and fatal intestinal cryptosporidiosis in a group of snakes (Pituophis melanoleucus sayi) kept at a zoological garden. The clinical and pathological findings are described and discussed in this paper. Pathohistologically fibrinous, diphtheroid and necrotizing enteritides were diagnosed. Histological examination was completed by electron microscopy. Transmission electron microscopic examination revealed numerous cryptosporidia in close contact to the luminal surface of the intestinal epithelial cells. Different cryptosporidial stages developing in parasitophorous vacuoles occurred. By scanning electron microscopy the superficial localisation of the cryptosporidia in the damaged brush border of the intestinal epithelial cells was demonstrated. In addition, the ultrastructural examination of the small intestine of three animals revealed adenovirus-like particles.

Animals↗