Search PubMed⌕ Search

Biomedical subjects

M Stolte

Publications and source records attributed to M Stolte.

At least 181 records · Page 10Linked to original sources
PubMed1999

Photodynamic destruction of high grade dysplasia and early carcinoma of the esophagus after the oral administration of 5-aminolevulinic acid.

BACKGROUND: Photodynamic therapy (PDT) is a new local, endoscopically controlled therapeutic concept based on the selective sensitization of malignant and precancerous lesions prior to light-induced tissue destruction. 5-aminolevulinic acid (5-ALA) appears to be a promising alternative photosensitizer with a high mucosa specificity without phototoxic side effects on the skin. The authors report on their experiences with this new form of PDT in 27 patients. METHODS: Twenty-seven patients (6 females and 21 males; ages 47-79 years) with histologically proven high grade dysplasia (n = 9) and early carcinoma (normal endoultrasonography or classified as uT1N0M0; n = 19; 1 patient had 2 lesions) of the esophagus were included in this study. Approximately 4-6 hours after oral ingestion of 5-ALA in a dosage of 60 mg/kg of body weight, laser light irradiation was conducted with a dye laser system with a wavelength of 635 nanometers at a light dose of 150 J/cm(2). RESULTS: The length of the segment of the esophagus with severe dysplasia or carcinoma of the mucosa varied between 0.5-9.0 cm (mean length, 2.5 cm). High grade dysplasia was eradicated in all patients. In addition, 19 mucosal tumors in 18 patients were treated successfully in 10 of 19 cases with an average of 1.7 treatment sessions and a mean follow-up of 16.9 months (range, 3-37 months). Method-related morbidity and mortality were not observed. CONCLUSIONS: Severe dysplasia and superficial (</=2 mm) mucosal carcinoma of the esophagus can be ablated completely by 5-ALA-PDT. PDT with 5-ALA has few side effects and might offer an alternative to esophagectomy or radiochemotherapy.

Aged↗
PubMed1999

[Helicobacter pylori screening in a general practice].

BACKGROUND AND OBJECTIVE: The significance of Helicobacter pylori (Hp) infection in asymptomatic persons is largely unknown. This prospective study was undertaken to evaluate the diagnostic and, if appropriate, therapeutic relevance of a noninvasive screening for Hp. In addition, the practicality and validity of a simple serological test on whole blood was elucidated. PATIENTS AND METHODS: 100 consecutive patients (29 males, 71 females, median age 46 [18-79] years) of a general medical practice, seen in November of 1997, were included. Three patients had to be subsequently excluded, because they had been treated for Hp infection. All patients were given a standard interview after which a serological whole-blood test (BM-Test Helicobacter pylori; Boehringer Mannheim) and a 13C-urea breath test were performed as noninvasive reference. Endoscopy of the upper gastrointestinal tract was offered if the serology and/or the breath test were gative. RESULTS: The Hp prevalence was 40%, rising significantly with age. The rapid serology test, when related to the breath test, had a negative and positive predictive value of < 80%. 44 of the 47 patients with a positive serological or breath test agreed to endoscopy. Eleven of them had a clinically significant abnormality macroscopically or histologically: four of them were found to have an Hp infection. CONCLUSIONS: Asymptomatic Hp-positive persons frequently have clinically abnormal findings in the upper gastrointestinal tract. These data point to the need for a large multi-centre study with cost-effect analysis to evaluate a noninvasive Hp screening test in nonsymptomatic persons as a public health measure. The 13C-urea breath test would be suitable as such a screening method.

Adult↗
PubMed1999

Peutz-Jeghers syndrome: four novel inactivating germline mutations in the STK11 gene. Mutations in brief no. 227. Online.

The diagnosis of Peutz-Jeghers syndrome is based on the occurrence of hamartomatous gastrointestinal polyps and perioral pigment spots. In view of the development of hamartomatous polyps in several syndromes and the variability of pigment spots in Peutz-Jeghers patients, identification of affected individuals is difficult. Recently, germline mutations in the STK11 gene have been reported as a molecular cause of Peutz-Jeghers syndrome. We present four novel inactivating mutations identified by direct sequencing of all 9 exons of the STK11 gene in 4 patients suggestive of Peutz-Jeghers syndrome: three frameshift mutations (125-137del; 474-480del; 516-517insT) and one nonsense mutation (Q220X). Our data obtained in these patients and in those reported previously emphasize the diagnostic value of histological discrimination between different types of hamartomatous polyps and of molecular analysis, particularly in cases with no family history of the disease.

AMP-Activated Protein Kinase Kinases↗
PubMed1999

[Preoperative classification of malignant stomach tumors].

Based on the case report of a 51 year-old patient presenting with a lymphoepithelioma like gastric cancer, we discuss the diagnostic challenge to differentiate this entity from gastric non-Hodgkin lymphoma. Since high-level lymphoid stromal reactions are rarely associated with gastric adenocarcinoma, misinterpretation can occur easily. In addition to the lymphoepithelioma like gastric cancer that is often associated with a demonstrable EBV association of the tumor cells, synchronous development of gastric carcinoma and lymphoma must be considered. Establishment of a correct diagnosis requires multiple, deep and multifocally sampled gastric biopsies, and immunohistochemical and molecular techniques to supplement conventional histology. Only through this procedure are correct characterization and classification of these unusual gastric neoplasms possible.

Adenocarcinoma↗
PubMed1999

[Operation technique determines frequency of recurrence of colorectal carcinoma].

INTRODUCTION: In order to investigate whether operative technique determines the 5-year recurrence and survival rates, we analysed the results obtained by two surgical departments using two different operative techniques. Department A: Removal of the tumour and a number of lymph nodes; department B: En-bloc resection in accordance with the requirements of standardised tumour surgery. PATIENTS AND METHODS: The surgical results obtained with all patients with colorectal carcinoma operated on between 1984 and 1988 (department A: 152 colon and 53 rectal carcinomas; department B: 124 colon and 177 rectal carcinomas). RESULTS: The local recurrence rate achieved by department A was significantly higher (colon carcinoma: department A 25 %; department B 10 %; rectal carcinoma: department A 54 %; department B 16 %). The 5-year survival rate for colon carcinoma was 65 % in department A, and 66 % in department B, the corresponding figures for rectal carcinoma being 49 % and 72 %, respectively. CONCLUSION: The results indicate that carcinoma of the colorectum should be operated on only at an institution that complies with the standards required for surgery of colorectal carcinoma.

Adult↗
PubMed1999

Eradication of Helicobacter pylori heals atrophic corpus gastritis caused by long-term treatment with omeprazole.

Long-term treatment with proton pump inhibitors in patients with Helicobacter pylori gastritis can lead to atrophic changes in the corpus mucosa. What is still unclear, however, is whether this atrophy can regress in response to Helicobacter pylori eradication. We report on a male patient with Helicobacter pylori gastritis receiving long-term treatment (4 years) with omeprazole for gastrooesophageal reflux disease, who developed autoaggressive gastritis with progressive atrophy, hypochlorhydria, hypergastrinaemia and nodular ECL-cell hyperplasia. To determine whether these changes might be induced to regress, Helicobacter pylori eradication therapy was administered. Ten months after Helicobacter pylori eradication autoaggressive lymphocytic infiltrates were no longer detectable, and the glands in the corpus mucosa had normalised despite continued treatment with omeprazole - a finding that was confirmed at two further follow-up surveys performed at 6-month intervals. This case report shows that atrophy of the corpus mucosa developing under long-term treatment with a proton pump inhibitor can be cured by eradicating Helicobacter pylori.

Adult↗
PubMed1999

'Pyloric gland-type adenoma' arising in heterotopic gastric mucosa of the duodenum, with dysplastic progression of the gastric type.

'Pyloric gland-type adenoma' is a recently described and very rare entity. We report a case of a pedunculated polyp of the duodenal bulb showing the features of pyloric gland-type adenoma. Heterotopic gastric mucosa was found adjacent to the tumour. Immunohistochemically, the tumour cells at the surface of the polyp showed foveolar-type mucin (M1) while most other tumour cells showed deep gastric mucin (M2), displaying a pattern of differentiation similar to the normal gastric mucosa. The polyp also showed villous or papillary structures with disorganization of gastric differentiation and marked increase of proliferating in foci cells. This is the first case of pyloric gland-type adenoma found to arise in heterotopic gastric mucosa of the duodenum, showing dysplastic progression of the gastric type.

Adenoma↗
PubMed1999

Oral immunization with urease and Escherichia coli heat-labile enterotoxin is safe and immunogenic in Helicobacter pylori-infected adults.

BACKGROUND & AIMS: Oral immunization with Helicobacter pylori urease can cure Helicobacter infection in animals. As a step toward therapeutic immunization in humans, the safety and immunogenicity of oral immunization with recombinant H. pylori urease were tested in H. pylori-infected adults. METHODS: Twenty-six H. pylori-infected volunteers were randomized in a double-blind study to four weekly oral doses of 180, 60, or 20 mg of urease with 5 microg heat-labile enterotoxin of Escherichia coli (LT), LT alone, or placebo. Side effects and immune responses were evaluated weekly after immunization, and gastric biopsy specimens were obtained after 1 month and 6 months for histology and quantitative cultures. RESULTS: Diarrhea was noted in 16 of 24 (66%) of the volunteers who completed the study. Antiurease serum immunoglobulin A titers increased 1. 58-fold +/- 0.37-fold and 3.66-fold +/- 1.5-fold (mean +/- SEM) after immunization with 60 and 180 mg urease, respectively, whereas no change occurred in the placebo +/- LT groups (P = 0.005). Circulating antiurease immunoglobulin A-producing cells increased in volunteers exposed to urease compared with placebo (38.9 +/- 13. 6/10(6) vs. 5.4 +/- 3.1; P = 0.018). Eradication of H. pylori infection was not observed, but urease immunization induced a significant decrease in gastric H. pylori density. CONCLUSIONS: H. pylori urease with LT is well tolerated and immunogenic in H. pylori-infected individuals. An improved vaccine formulation may induce curative immunity.

Administration, Oral↗
PubMed1999

ECL cell tumor and poorly differentiated endocrine carcinoma of the stomach: prognostic evaluation by pathological analysis.

BACKGROUND & AIMS: Gastric endocrine tumors show a wide spectrum of clinical behavior, and prognostic assessement of individual tumors is difficult. The aims of this work were to identify predictors of tumor malignancy and patient outcome and to provide a rationale for treatment guidelines. METHODS: Gastric endocrine tumors (86 enterochromaffin-like cell carcinoids and 16 poorly differentiated carcinomas) were investigated for 15 clinicopathologic variables and for expression of Ki67, P53, and BCL-2 proteins. Data were analyzed by univariate and multivariate statistics for evidence of tumor malignancy and patient survival. RESULTS: Histological grades 2 and 3, size >/=3 cm, 9 or more mitoses, or >/=300 Ki67-positive cells per 10 high-power fields identified 26 of 33 (79%) malignant (metastatic or deeply invasive) tumors, and size <1 cm and/or growth restricted to the mucosa characterized 46 of 69 (67%) tumors with benign behavior during a median follow-up of 39 months. Malignancy-predictive models were developed using angioinvasion, size, clinicopathologic type, mitotic index, and Ki67 index. The same variables, in addition to deep gastric wall invasion and histological grade, predicted patient outcome. CONCLUSIONS: Criteria for the assessment of malignancy risk and patient outcome were developed for the different tumors, providing a basis for treatment guidelines.

Analysis of Variance↗
PubMed1999

KTP laser destruction of dysplasia and early cancer in columnar-lined Barrett's esophagus.

BACKGROUND: The rising incidence of esophageal adenocarcinoma in western countries requires a new strategy in the management of dysplasia in Barrett's esophagus. Esophagectomy, which has high morbidity and mortality rates, has been recommended to treat patients with severe dysplasia. Strictly superficial laser coagulation with tissue ablation therefore is a desirable option for the management of dysplasia in Barrett's esophagus because the tissue to be ablated is only about 2 mm thick. Potassium-titanyl-phosphate (KTP) laser light with a wavelength of 532 nm is preferentially absorbed by hemoglobin and therefore combines excellent coagulation with limited tissue penetration. We report first clinical results with KTP laser superficial vaporization of dysplasia and early cancer in Barrett's esophagus. METHODS: Eight men and 2 women 43 to 84 years of age with short segments of Barrett's esophagus or traditional Barrett's esophagus and histologically proved low-grade (n = 4) and high-grade (n = 4) dysplasia or early adenocarcinoma (n = 2) were selected for this pilot study. For all patients thermal endoscopic destruction was conducted with a frequency-doubled neodymium:yttrium-aluminum-garnet (Nd:YAG) KTP laser system. Laser therapy was performed by means of the free-beam method with coaxial insufflation of gas. An average of 2.4 sessions per patient were required for ablation of the Barrett's mucosa. RESULTS: Two to three days after laser treatment the response of the ablated mucosa was assessed with endoscopy and biopsy. Samples taken showed fibrinoid necrosis of the mucosal layer. A complete response was obtained for all 10 patients. Replacement by normal squamous cell epithelium was induced in combination with acid suppression therapy of up to 80 mg omeprazole daily. No complications occurred. In two patients biopsy showed specialized mucosa beneath the restored squamous cell epithelial layer. Follow-up times were as long as 15 months (mean value 10.6 months). CONCLUSIONS: KTP laser destruction of Barrett's esophagus induced mucosal regeneration with normal squamous cell epithelium in combination with acid suppression. Limitation of the depth of thermal destruction in Barrett's esophagus minimizes risk for perforation or stricture formation. KTP laser ablation of Barrett's esophagus seems to be feasible and safe in short segments of Barrett's esophagus with dysplasia or early cancer.

Adenocarcinoma↗
PubMed1999

The differentiation of true adenomas from colitis-associated dysplasia in ulcerative colitis: a comparative immunohistochemical study.

Adenomas in areas involved by ulcerative colitis (UCA) are difficult to identify because of their morphological similarity to ulcerative colitis-associated dysplasia (UCD) and have an uncertain biology. Recently, a set of morphopathologic criteria were published for the diagnosis of UCA versus UCD. As a first step to analyze these criteria, we studied p53 and bcl-2 expression in groups of UCA and UCD along with a sporadic adenoma control group. Ninety lesions from UC areas (62 patients) were examined, including 24 UCA without high-grade dysplasia (HGD) and 66 UCD consisting of 43 polypoid and 23 flat dysplastic lesions (29 with HGD). Immunohistochemical p53 and bcl-2 expression were evaluated semiquantitatively. P53-positive cases were significantly less frequent in the UCA (4%) versus the UCD group (30%, P = .01) and the polypoid UCD subgroup (35%, P = .005). Moderate or strong bcl-2 expression was significantly more frequent in the UCA than in the UCD group (96% v 70%, P = .01) and in the UCA versus both polypoid and flat UCD subgroups. Comparison of UCA with low-grade dysplastic polypoid UCD cases alone showed a difference just below significance for p53 (P = .07). p53 and bcl-2 expression rates were very similar in the UCA group and the sporadic adenoma (n = 25) control group. These results show that UCA has phenotypic features more similar to sporadic adenomas than UCD and supports the concept that adenomas in UC have a biology different from UC-associated dysplasia.

Adenoma↗
PubMed1999

Can NSAID/ASA-induced erosions of the gastric mucosa be identified at histology?

Studies in animals have shown that NSAID/ASA-induced erosions have an ischaemic pathogenesis. We therefore studied the question of whether such erosions in human gastric biopsy material can be identified on the basis of the ischaemic necrosis. Histological sections prepared from forceps biopsy material obtained from 122 patients with erosions (at least three biopsy specimens from the erosion and two from antrum and corpus each) were classified by a pathologist blinded to the endoscopic findings and the medication used by the patients. NSAID/ASA erosions were diagnosed when a homogeneous eosinophilic ischaemic necrosis blending into the adjoining lamina propria presented. Helicobacter pylori (Hp)-induced erosions were diagnosed when, in the presence of Hp gastritis, erosive defects were covered with a non-homogeneous fibrinoid necrosis containing granulocytes and cell debris. Finally, the histological classification was compared with data on medication usage. The histological diagnosis was Hp-induced erosions in 59 patients, NSAID/ASA-induced erosions with no Hp gastritis in 23, and NSAID/ASA-induced erosions with concomitant Hp gastritis in 40. A comparison of this histological classification with the data provided by the referring physicians on patient medication revealed that 70% of the patients with histological diagnosis of NSAID/ASA-induced erosions in the absence of Hp gastritis, and 65% of those diagnosed to have NSAID/ASA-induced erosions and concomitant Hp gastritis, had been taking such drugs. Among the erosions diagnosed as H. pylori-induced, 81% of the patients were reported not to take such medication. The sensitivity of the diagnosis of NSAID/ASA-induced erosions was 72.9%, and specificity 79.6%. The results of the present study show that a high percentage of the NSAID/ASA-induced erosions of the gastric mucosa can indeed be correctly diagnosed at histology.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1999

Effects of pumaprazole (BY841), a novel reversible proton pump antagonist, and of omeprazole, on intragastric acidity before and after cure of Helicobacter pylori infection.

BACKGROUND: Omeprazole produces a higher intragastric pH in the presence of Helicobacter pylori infection than after cure. AIM: To investigate whether this effect also occurs with pumaprazole (BY841), a reversible proton pump antagonist which, in contrast to omeprazole, does not require activation in the acid compartment of the parietal cell. METHODS: In a randomized, crossover, double-blind study, 24-h intragastric pH was measured in 13 H. pylori-positive subjects before and after a 1-week course of omeprazole (20 mg o.d.) or of pumaprazole (100 mg b.d.). The studies were repeated after the infection was cured. RESULTS: In the absence of drug administration, the median 24-h pH values before cure (median 2.0, 90% CI: 1.2-3.2) did not differ from those after cure (median 1.5, 90% CI: 1.3-2.2; P = 0.115). The 24-h pH values were higher before cure of the infection than after during both pumaprazole (6.0, 4.8-6.7 vs. 4.3, 2.6-5.7; P = 0.002) and omeprazole (5.8, 4.0-6.2 vs. 3.6, 2.8-5; P = 0.004). Both before and after cure, there were no significant differences between the two drugs with respect to acid inhibition over the 24-h period. The median decrease in acid inhibition after cure of the infection (calculated as the difference in H+ activity in mmol/L) during pumaprazole (median 0.05, 90% CI: 6 x 10-4- 2.3) was no different from that during omeprazole (median 0.2, 90% CI: 3 x 10-3-1.5; P = 0.6). CONCLUSIONS: Both before and after cure of H. pylori infection, pumaprazole raised the intragastric pH over a 24-h period to a similar degree as omeprazole. H. pylori infection similarly augments the pH-increasing effect of both drugs. This effect is related to H. pylori infection and not to an increased activation of acid inhibitory agents in the parietal cell compartment.

Adult↗