Biomedical subjects

Michael Vieth

Publications and source records attributed to Michael Vieth.

At least 55 records · Page 3Linked to original sources

PubMed2005

Detection of non-pylori Helicobacter species in "Helicobacter heilmannii"-infected humans.

BACKGROUND: A small proportion of patients suffering from chronic active gastritis are diagnosed with gastric Helicobacter species other than Helicobacter pylori. Circumstantial evidence has suggested that these bacteria, also referred to as "Helicobacter heilmannii"-like organisms (HHLO), may be transmitted through animals. The isolation of a Helicobacter bizzozeronii strain from a human patient confirmed this hypothesis. It was the aim of the present study to assess the presence of animal Helicobacter species and H. pylori in humans infected with HHLO, as diagnosed by histology. METHODS: Paraffin-embedded gastric biopsy specimens of 108 HHLO-infected patients (42 women and 66 men) from three clinical centers were screened for the presence of animal gastric Helicobacter species by polymerase chain reaction (PCR), using assays targeting the 16S rDNA region of the three known canine and feline helicobacters (H. bizzozeronii, H. salomonis and H. felis), "Candidatus H. suis", and "Candidatus H. bovis". In addition, the presence of H. pylori was evaluated by multiplex PCR analysis. RESULTS: In 63.4% of the stomachs (64/101) classification of the Helicobacter infection into the above mentioned groups was achieved. Non-pylori Helicobacter species commonly colonizing the stomachs of cats and dogs were found in 48.5% (49/101) of the patients. Fourteen (13.9%) samples tested positive for "Candidatus H. suis", and "Candidatus H. bovis" was demonstrated in 1 (0.9%) patient. The presence of H. pylori was established in 13 patients (12.9%). Eleven stomachs (10.9%) were infected with at least two different Helicobacter species. CONCLUSIONS: This study identifies animal Helicobacter species in the stomach of a large series of HHLO-infected patients, which may have clinical implications in a subset of patients with gastric disease.

Adolescent↗

PubMed2005

Small-bowel metaplasia arising in the remnant esophagus after esophagojejunostomy--a [corrected] prospective study in patients with a history of total gastrectomy.

OBJECTIVES: The pathogenesis of Barrett's mucosa is incompletely understood. Acidic gastro-esophageal reflux is considered an essential causative factor. The aim of this study was to detect esophageal columnar metaplasia after total gastrectomy with esophagojejunostomy, a condition of enteric, but nonacidic reflux. METHODS: In a prospective study, patients with a history of total gastrectomy and esophagojejunostomy were investigated for the presence of columnar metaplasia in the remnant esophagus. Patients with such history, who were now referred for esophagogastroduodenoscopy, were included during a 2-yr period. Biopsies for histopathology were taken from the anastomosis and any columnar metaplasia of the esophagus. RESULTS: In 8 of 25 patients (32%) with a history of gastrectomy, columnar metaplasia was found in the remnant esophagus, mostly in shape of tongues, partly associated with erosive reflux esophagitis. Histopathology showed a typical small-bowel mucosa, but with some villous atrophy. In a resection specimen, a double-layered muscularis mucosa was present, which proved the metaplastic nature of the intestinal mucosa. Length of the columnar metaplasia correlated with the time interval since surgery. CONCLUSIONS: Esophageal mucosa, if exposed long term to an enteric, but nongastric refluxate, can evolve into a highly differentiated intestinal metaplasia, which resembles small-bowel mucosa. This proves that complete-type intestinal metaplasia may arise not only in the stomach, but also in the esophagus. Esophageal intestinalization seems to reflect adaptation to enteric reflux.

Aged↗

PubMed2005

Hypermethylation and loss of expression of glutathione peroxidase-3 in Barrett's tumorigenesis.

Chronic gastroesophageal reflux disease is a known risk factor for Barrett's esophagus (BE), which induces oxidative mucosal damage. Glutathione peroxidase-3 (GPx3) is a secretory protein with potent extracellular antioxidant activity. In this study, we have investigated the mRNA and protein expression of GPx3, and explored promoter hypermethylation as an epigenetic mechanism for GPx3 gene inactivation during Barrett's carcinogenesis. Quantitative real-time reverse transcription polymerase chain reaction on 42 Barrett's adenocarcinomas (BAs) revealed consistently reduced levels of GPx3 mRNA in 91% of tumor samples. GPx3 promoter hypermethylation was detected in 62% of Barrett's metaplasia, 82% of dysplasia, and 88% of BA samples. Hypermethylation of both alleles of GPx3 was most frequently seen in BAs (P = .001). Immunohistochemical staining of GPx3 in matching tissue sections (normal, BE, Barrett's dysplasia, and BA) revealed strong immunostaining for GPx3 in normal esophageal and gastric tissues. However, weak to absent GPx3 staining was observed in Barrett's dysplasia and adenocarcinoma samples where the promoter was hypermethylated. The degree of loss of immunohistochemistry correlated with the hypermethylation pattern (monoallelic versus biallelic). The observed high frequency of promoter hypermethylation and progressive loss of GPx3 expression in BA and its associated lesions, together with its known function as a potent antioxidant, suggest that epigenetic inactivation and regulation of glutathione pathway may be critical in the development and progression of BE.

Adenocarcinoma↗

PubMed2004

Inhibition of p38 MAP kinase- and RICK/NF-kappaB-signaling suppresses inflammatory bowel disease.

Ulcerative colitis and Crohn's disease are the two entities of chronic inflammatory bowel diseases (IBD). One of the main pathogenic mechanisms is probably a dysregulated immune response triggered by products of the enteric bacterial flora. The goal of this study was to evaluate the effects of the p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580 on inflammatory responses using the DSS-induced experimental colitis model in mice reflecting human IBD. We found that SB203580 improved the clinical score, ameliorates the histological alterations, and reduces the mRNA levels of proinflammatory cytokines. In addition to p38 kinase activity, the "classical" and the "alternative" NF-kappaB pathways were also strongly activated during colitis induction. All three pathways were drastically down-regulated by SB203580 treatment. An analysis of the molecular basis of NF-kappaB activation revealed that Rip-like interacting caspase-like apoptosis-regulatory protein kinase (RICK), a key component of a pathway leading to NF-kappaB induction, is also strongly inhibited by SB203580. Since RICK is an effector kinase of NOD2, an intracellular receptor of bacterial peptidoglycan, these results support the notion that NOD signaling could play a pivotal role in the IBD pathogenesis. Thus, RICK could represent a novel target for future therapies in human IBD.

Animals↗

PubMed2004

INK4a-ARF alterations in Barrett's epithelium, intraepithelial neoplasia and Barrett's adenocarcinoma.

INTRODUCTION: The INK4a-ARF [CDKN2A]- locus on chromosome 9p21 encodes for two tumour suppressor proteins, p16INK4a and p14ARF, which act as upstream regulators of the Rb-CDK4 and p53 pathways. To study the contribution of each pathway to the carcinogenesis of Barrett's adenocarcinoma, we analysed the alterations of p14ARF and p16INK4a in preneoplastic and neoplastic lesions of this disease. MATERIALS AND METHODS: After microdissection, DNA of 15 Barrett's adenocarcinomas, 40 Barrett's intraepithelial neoplasms (n=20 low- and n=20 high-grade) and 15 Barrett's mucosa without neoplasia was analysed for INK4-ARF inactivation using DNA sequence and loss of heterozygosity (LOH) analysis, methylation-specific polymerase chain reaction, restriction-enzyme-related polymerase chain reaction and immunohistochemistry. RESULTS: We detected 9p21 LOH, p16INK4a methylation and p16INK4a mutations in Barrett's adenocarcinomas in 5 of 15 (33%), 8 of 15 (53%) and 1 of 15 (7%) patients, respectively. P14ARF was methylated in 3 of 15 (20%) adenocarcinomas. In Barrett's intraepithelial neoplasia, p16INK4a was altered in 12 of 20 (60%) high-grade and in 4 of 20 (20%) low-grade intraepithelial neoplasms. In Barrett's mucosa without intraepithelial neoplasia p16(INK4a) was methylated in one case (7%). P14ARF was intact in Barrett's mucosa without intraepithelial neoplasia. CONCLUSIONS: We conclude that most Barrett's intraepithelial neoplasms contain genetic and/or epigenetic INK4a-ARF alterations. Methylation of p16INK4a appears to be the most frequent epigenetic defect in the neoplastic progression of Barrett's tumourigenesis.

Barrett Esophagus↗

PubMed2004

A gradient of TFF3 (trefoil factor family 3) peptide synthesis within the normal human gastric mucosa.

TFF3 is a member of the trefoil factor family (TFF) peptides, which enhance the surface integrity of mucous epithelia, and is typically secreted by intestinal goblet cells together with the mucin MUC2. Reports of the expression of TFF3 within the normal human stomach are contradictory and the precise localisation of TFF3 is unknown. We have mapped the human gastric mucosa by reverse transcription/polymerase chain reaction and Western blot analysis and by immunohistochemistry. Small amounts of TFF3 were detectable in the oxyntic mucosa of the corpus, whereas TFF3 synthesis increased sharply distal to the corpus-antrum transitional zone. TFF3 secretion was demonstrated in the antrum, the pyloric region and the proximal duodenum. High TFF1 levels were present in all regions of the gastric mucosa including the corpus, whereas the proximal duodenum was nearly devoid of TFF1. Immunohistochemistry localised TFF3 to antral and pyloric surface mucous cells. In the antrum, an increasing concentration gradient was found towards cells deeper in the isthmus. TFF1 was confined to superficial pit cells in the antrum. TFF3 was also present in specific layers of the laminated mucous gel of the antral and pyloric regions and variable concentrations of TFF3 (2-62 nmol/l) were measured in gastric juice. Here, a probably N-terminally shortened variant is present that forms disulphide-linked dimers. Thus, TFF3 is a typical secretory peptide of the normal human antral and pyloric gastric mucosa and has a gastric expression pattern different from that of TFF1 and TFF2. TFF3 might therefore have important physiological functions in the stomach, e.g. as a luminal surveillance peptide maintaining particularly the integrity of the antral and pyloric mucosa.

Gastric Juice↗

PubMed2004

Mutations of BRAF and KRAS2 in the development of Barrett's adenocarcinoma.

Activation of the Raf/MEK/ERK (MAPK) signal transduction cascade by RAS mutations has been found in a variety of human cancers. Mutations of BRAF provide an alternative route for activation of this signalling pathway. To determine the role of mutations in BRAF and KRAS2 in the neoplastic progression of Barrett's adenocarcinoma, we analysed both genes for common mutations. After microdissection, DNA of 19 Barrett's adenocarcinomas, 56 Barrett's intraepithelial neoplasias (n=29 low-grade intraepithelial neoplasia (LGIN) and n=27 high-grade intraepithelial neoplasia (HGIN)), 30 Barrett's mucosa without neoplasia and normal squamous, as well as gastric epithelium, were analysed for BRAF and KRAS2 mutation. Activating BRAF mutations were identified in 2/19 Barrett's adenocarcinomas (11%) and in 1/27 HGIN (4%). KRAS2 mutations were found in four out of 19 (21%) Barrett's adenocarcinomas examined and in three cases of HGIN (11%). In LGIN as well as in normal gastric or oesophageal mucosa, neither BRAF nor KRAS2 mutations were detected. All lesions with KRAS2 mutations had an intact BRAF gene. The status of mismatch-repair proteins was neither related to BRAF nor KRAS2 mutations. These data indicate that RAS or BRAF mutations are detected in about 32% of all Barrett's adenocarcinomas. We conclude that the disruption of the Raf/MEK/ERK (MAPK) kinase pathway is a frequent but also early event in the development of Barrett's adenocarcinoma.

Adenocarcinoma↗

PubMed2004

TFF3 expression at the esophagogastric junction is increased in gastro-esophageal reflux disease (GERD).

At the gastric cardia, the molecular mechanisms of inflammation and metaplasia are incompletely understood. Thus, the aim of this study was to determine the expression of TFF1, TFF2 and TFF3 at this site and correlate these data with Helicobacter pylori infection or gastro-esophageal reflux disease (GERD). In 27 patients without intestinal metaplasia at the cardia, endoscopic biopsies were obtained for histology and RT-PCR. TFF1 and TFF2 were expressed in all cardia samples. TFF3 expression was significantly more frequent at the cardia (n = 15/24) than in the corpus (n = 2/26). TFF3 expression at the cardia was mainly observed in GERD patients, and there was a clear tendency towards higher interleukin-8 (IL-8) transcription levels; whereas TFF3 expression was not correlated with the H. pylori status or to tumor necrosis factor-alpha (TNF-alpha) expression. The expression of TFF3 at the cardia may represent an adaptation to GERD and precede the development of Barrett's esophagus.

Barrett Esophagus↗

PubMed2004

Cardia-type metaplasia arising in the remnant esophagus after cardia resection.

BACKGROUND: Specialized intestinalized metaplasia in the distal esophagus (Barrett's esophagus) is a recognized precursor of esophageal adenocarcinoma, but its pathogenesis is incompletely understood. The aim of this study was to investigate the mucosal effects of esophagogastrostomy, an artificial interface between esophageal squamous and gastric oxyntic epithelium. METHODS: EGD was performed in 14 consecutive patients (median age 63 years, range 26-71 years) who had undergone esophagogastrostomy from 3 to 88 months earlier. Biopsy specimens were obtained in 13 patients from the anastomosis and, when present, columnar epithelium in the remnant esophagus. RESULTS: In 10 patients, EGD demonstrated tongue-shaped segments of columnar epithelium extending from 0.3 to 7 cm into the remnant esophagus. Biopsy specimens revealed cardia-type mucosa in all patients, whether at the anastomosis or proximally in esophageal segments of columnar epithelium. Magnification endoscopy of cardia-type mucosa visualized a long-oval, tubular, or ridged surface pattern. In 3 cases, complete intestinal metaplasia was observed within the cardia-type mucosa. CONCLUSIONS: The frequent transformation of squamous epithelium into cardia-type mucosa in the distal remnant esophagus after esophagogastrostomy supports the concept that cardia-type mucosa is a reflux-induced metaplasia that may give rise to the subsequent development of specialized intestinalized metaplasia.

Adult↗

PubMed2004

Reliable detection of macrolide-resistant Helicobacter pylori via fluorescence in situ hybridization in formalin-fixed tissue.

Macrolide-resistant Helicobacter (H.) pylori represent an increasing therapeutic problem. Macrolide resistance is usually determined phenotypically in vitro with methods such as E-test or agar dilution test. A prerequisite for those tests, however, is bacterial culture that is not routinely set up in the course of gastroscopy. In contrast, formalin-fixed, paraffin-embedded biopsies are regularly available from patients who have undergone gastroscopy. In such biopsies macrolide-resistant H. pylori can be detected by the genotype-based technique of fluorescence in situ hybridization (FISH). Experience gained by this new method, however, is still extremely limited, especially in formalin-fixed tissue. Therefore, we retrospectively investigated formalin-fixed, paraffin-embedded biopsy specimens by FISH in 104 patients suffering from therapy-resistant H. pylori gastritis. To test the accuracy of FISH, we initially examined specimens from 53 patients for whom results of the E-test were available. Next we analyzed biopsies from another 51 patients that had been selected since phenotypical resistance testing had failed despite documented culturing attempts. In all 104 patients, H. pylori was detected by FISH and could thus be investigated for macrolide resistance. Overall, macrolide-resistant bacteria were found in 71 patients (68.3%). In 49 of 53 patients (92.4%), FISH and E-test returned identical results (no significant discordance according to McNemar's chi(2)-test). Taken together, our study demonstrates that FISH is a highly sensitive and reliable method for detecting macrolide-resistant H. pylori in formalin-fixed, paraffin-embedded biopsy specimens, which represents the routine method of processing tissue obtained upon gastroscopy.

Anti-Bacterial Agents↗

PubMed2004

Confocal laser endoscopy for diagnosing intraepithelial neoplasias and colorectal cancer in vivo.

BACKGROUND & AIMS: A confocal laser endoscopy system has recently been developed that may allow subsurface imaging of living cells in colonic tissue in vivo. The aim of the present study was to assess its potential for prediction of histology during screening colonoscopy for colorectal cancer. METHODS: Twenty-seven patients underwent colonoscopy with the confocal endoscope using acriflavine hydrochloride or fluorescein sodium with blue laser illumination. Furthermore, 42 patients underwent colonoscopy with this system using fluorescein sodium. Standardized locations and circumscript lesions were examined by confocal imaging before taking biopsy specimens. Confocal images were graded according to cellular and vascular changes and correlated with conventional histology in a prospective and blinded fashion. RESULTS: Acriflavine hydrochloride and fluorescein sodium both yielded high-quality images. Whereas acriflavine hydrochloride strongly labeled the superficial epithelial cells, fluorescein sodium offered deeper imaging into the lamina propria. Fluorescein sodium was thus used for the prospective component of the study in which 13,020 confocal images from 390 different locations were compared with histologic data from 1038 biopsy specimens. Subsurface analysis during confocal laser endoscopy allowed detailed analysis of cellular structures. The presence of neoplastic changes could be predicted with high accuracy (sensitivity, 97.4%; specificity, 99.4%; accuracy, 99.2%). CONCLUSIONS: Confocal laser endoscopy is a novel diagnostic tool to analyze living cells during colonoscopy, thereby enabling virtual histology of neoplastic changes with high accuracy. These newly discovered diagnostic possibilities may be of crucial importance in clinical practice and lead to an optimized rapid diagnosis of neoplastic changes during ongoing colonoscopy.

Acriflavine↗

PubMed2004

Endoscopic resection of superficial esophageal squamous-cell carcinomas: Western experience.

OBJECTIVES: Endoscopic resection of esophageal squamous-cell neoplasia with curative intent appears to be an alternative treatment to radical surgery when the malignant neoplasia is intraepithelial or limited to the mucosal layer, since the risk for lymph-node metastases is very low. In contrast to Japan, there has so far been only limited experience in Europe and the United States with endoscopic resection in such cases. In the present observational study, we report on the largest prospective series so far in Western countries of patients with early squamous-cell cancer or carcinoma in situ, who were treated using endoscopic resection therapy. METHODS: Between December 1997 and November 2001, 115 patients with a suspicion of early squamous cancer were referred for local endoscopic therapy. A total of 39 patients (mean age 61.4 +/- 10.2 yr) with early esophageal carcinoma (n = 29) and carcinoma in situ (Cis) (n = 10) fulfilled the criteria for local endoscopic therapy and were treated using endoscopic resection. Ten patients had Cis (group A), 19 had mucosal cancer (group B), and 10 had submucosal cancer (group C). All patients in group C were inoperable or had refused surgery. RESULTS: A total of 94 resections were performed. Nine of the 10 patients in group A (90%), 19 of the 19 in group B (100%), and 8 of the 10 in group C (80%) achieved a complete response during a mean follow-up period of 29.7 +/- 14.3 months. Tumor-related deaths occurred in three patients (one in group B, who was inoperable; two in group C, who refused surgery). No major complications such as perforation or bleeding requiring blood transfusion occurred. Minor complications were seen in six patients (15%)-three with minor bleeding after endoscopic resection and three with esophageal stenoses, who were successfully treated using injection therapy or dilatation. Calculated 5-yr survival was 90% in group A, 89% in group B, and 0% in group C. CONCLUSIONS: Endoscopic resection appears to be an effective and safe method of curative treatment in patients with Cis and mucosal squamous-cell carcinomas of the esophagus. The preferred method in patients with submucosal cancer should be esophagectomy or chemoradiotherapy, whenever possible.

Carcinoma, Squamous Cell↗

PubMed2004

Helicobacter pylori-mediated gastritis induces local downregulation of secretory leukocyte protease inhibitor in the antrum.

Helicobacter pylori-infected subjects exhibited a strong decline in antral secretory leukocyte protease inhibitor (SLPI) levels compared to H. pylori-negative subjects and subjects from whom H. pylori had been eradicated (P = 0.002). This reduction was specific for the antrum, whereas SLPI expression in corpus and duodenum was not affected. Antral SLPI levels were inversely correlated with inflammatory scores of antrum-predominant gastritis.

Adult↗

PubMed2004

Cathepsins K, L, B, X and W are differentially expressed in normal and chronically inflamed gastric mucosa.

The expression of cathepsins K, L, B, X and W was studied by quantitative RT-PCR in normal and inflamed gastric mucosa (antrum, corpus, cardia). Cathepsins B, L, K and X were expressed ubiquitously. In contrast, cathepsin W was expressed at very low levels. Infection by Helicobacter pylori caused a significant induction of cathepsin X (p<0.008), whereas the other cathepsins were not or only locally affected by H. pylori infection or reflux disease. Immunohistochemistry revealed specific expression of cathepsin X (macrophages), cathepsin K (parietal cells) and cathepsin W (lymphocytes), whereas cathepsins B and L were predominantly expressed in epithelial cells.

Cathepsin B↗

PubMed2003

A prospective, randomized study of quadruple therapy and high-dose dual therapy for treatment of Helicobacter pylori resistant to both metronidazole and clarithromycin.

BACKGROUND AND AIM: Failure of primary anti-H. pylori therapy results in a high rate of antimicrobial resistance. Here, we investigated the efficacy of high-dose dual therapy and quadruple therapy as salvage treatments for eradication of H. pylori resistant to both metronidazole and clarithromycin. PATIENTS AND METHODS: Patients with at least one treatment failure and infected with H. pylori resistant to both metronidazole and clarithromycin, were randomized to receive either omeprazole 4 x 40 mg and amoxicillin 4 x 750 mg; or omeprazole 2 x 20 mg, bismuthcitrate 4 x 107 mg, metronidazole 4 x 500 mg and tetracycline 4 x 500 mg. Both regimens were given for 14 days. In cases of persistent infection, a cross-over therapy was performed. RESULTS: Eighty-four patients were randomized. Cure of H. pylori infection was achieved in 31 patients after dual therapy and in 35 patients after quadruple therapy (per protocol: 83.8% (95% CI, 67.9-93.8) and 92.1% (95% CI, 78.6-98.3), respectively (p=0.71); intention to treat: 75.6% (95% CI: 59.7-87.6) and 81.4% (95% CI: 66.6-91.6), respectively (p=0.60)). Cross-over therapy was performed in six of nine patients, four of whom were cured of the infection. CONCLUSION: Both high-dose dual therapy and quadruple therapy are effective in curing H. pylori infection resistant to both metronidazole and clarithromycin in patients who experienced previous treatment failures.

Adult↗

PubMed2003

The optimal dose of 5-aminosalicylic acid in active ulcerative colitis: a dose-finding study with newly developed mesalamine.

BACKGROUND AND AIMS: 5-Aminosalicylate is the gold standard for inducing remission in patients with mildly to moderately active ulcerative colitis. The optimal dose is as yet not defined. Despite some recent developments, the ideal formulation for 5-aminosalicylic acid is still awaited. A new pellet preparation was designed combining slow and delayed release properties. Aims of the study were to find the optimal dose and to test efficacy and safety of a new 5-aminosalicylic acid formulation. METHODS: Three hundred twenty-one patients were included in a double-blind multicenter trial. Inclusion criteria were active ulcerative colitis (Clinical Activity Index [CAI] and Endoscopic Index [EI] according to Rachmilewitz, CAI 6-12; EI >/=4). Three different doses of 5-aminosalicylic acid (0.5 g 3 times a day, 1.0 g 3 times a day, and 1.5 g 3 times a day) were studied for 8 weeks. RESULTS: Clinical remission rate (CAI </=4) was highest in the 1.0 g 3 times a day group (66 %), 50% in the 0.5 g 3 times a day group, and 55% in the 1.5 g 3 times a day group. Hierarchical testing showed no significance, indicating a lack of dose response across the 3 mesalamine doses. In addition, times to first clinical response were similar: 26.5 days (1.0 g 3 times a day), 27.5 days (0.5 g 3 times a day), and 21.5 days (1.5 g 3 times a day). Endoscopic improvement was better with 1.0 g mesalamine 3 times a day than with 0.5 g 3 times a day, but overall endoscopic and histologic improvement was not different between treatment groups. Baseline activity, duration, and localization of ulcerative colitis did have some influence on the therapeutic activity, but there was no significant interaction with the dose of the study drug. Safety, with special focus on kidney function, was excellent in all 3 groups. CONCLUSIONS: There is no significant dose response between mesalamine 1.5 g/day, 3.0 g/day, and 4.5 g/day. The optimal dose to induce remission of ulcerative colitis is 0.5 g 5-aminosalicylic acid 3 times a day. Patients failing with this dose may benefit from an increase of the dose up to 1.0 g 3 times a day, but should also be considered for alternative treatment. A newly developed pellet formulation of 5-aminosalicylic acid has promising efficacy and excellent safety.

Adult↗

PubMed2003

A prospective randomized trial of two different endoscopic resection techniques for early stage cancer of the esophagus.

BACKGROUND: A variety of different endoscopic resection techniques for early stage cancer of the upper GI tract have been described that are more effective than strip biopsy. However, there is no report of a prospective randomized comparison of different techniques. METHODS: In a prospective randomized study, 100 consecutive endoscopic resections were performed in 72 patients with early stage esophageal cancer. Fifty endoscopic resections were performed with a "suck-and-ligate" device without prior submucosa injection and 50 with the cap technique with prior submucosa injection of a dilute saline solution of epinephrine. The main assessment criteria were maximum diameter of the resection specimen and of the resection area, and the complication rate. RESULTS: No significant differences were observed between the two groups with regard to the maximum diameters and calculated area of the resected specimens (ligation group: 16.4 [4.0] x 11 [3.1] mm/185 [84] mm(2) vs. cap group: 15.5 [4.1] x 10.7 [2.7] mm/168 [83] mm(2)), or the maximum diameters and calculated area of the endoscopic resection ulcers after 24 hours (ligation group: 20.6 [4.8] x 14.3 [4.5] mm/314 [160] mm(2) vs. cap group: 18.9 [5.1] x 12.9 [3.8] mm/260 [145] mm(2)). There was only a slight advantage (greater diameter of resection specimens) for the ligation group in patients who had prior endoscopic treatment. There was one minor episode of bleeding in each group; there was no severe complication. In 41 of 72 patients (57%), further endoscopic therapy after endoscopic resection was necessary because of residual neoplasia at the first follow-up endoscopy after resection (61 of 100 resection specimens [61%] had lateral margins that could not be evaluated because of coagulation artifact or contained malignancy but with the base of the lesion free of tumor). CONCLUSIONS: The cap technique with submucosa injection and the ligation technique without submucosa injection are similar with respect to efficacy and safety for endoscopic resection of early stage esophageal cancers.

Esophageal Neoplasms↗

PubMed2003

High-grade dysplasia in sporadic fundic gland polyps: clinically relevant or not?

Sporadic fundic gland polyps (FGPs) are the most frequent gastric polyps. These FGPs develop almost exclusively in a normal corpus mucosa without Helicobacter pylori infection. This means that they represent an absolutely benign disease (no ulcers, almost no gastric carcinoma and mucosa associated lymphoid tissue (MALT) lymphoma). Most probably there exists a statistically accumulated coincidence rate of sporadic FGPs with colorectal epithelial neoplasias, so it is recommended to consider preventive colonoscopy. In familial adenomatous polyposis (FAP), FGPs are present in up to 80-93% of patients. In such patients, low-grade dysplasia and/or foveolar microadenomas may be present in 44-54% of cases. To date, only three case reports on early gastric carcinoma have been published. In this issue, to the best of our knowledge the first case of a high-grade dysplasia (intraepithelial neoplasia) in a sporadic FGP is reported. Recently, it has been shown that beta-catenin mutations might have led to FGP. Therefore, in the future, patients showing nuclear beta-catenin expression must undergo examination to discover whether this expression may lead to neoplasia. According to the data available at present, such a constellation must be regarded as an extremely rare event.

Adenoma↗