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M Stolte

Publications and source records attributed to M Stolte.

At least 271 records · Page 15Linked to original sources

What role does Helicobacter pylori eradication play in gastric MALT and gastric MALT lymphoma?

The concept of mucosa-associated lymphoid tissue (MALT) has been introduced to differentiate biological functions from behavior of nonnodal vs. nodal lymphoid tissues. Lymphomas arising from MALT also behave differently than typical nodal lymphomas. In contrast to other tissues, MALT in the stomach is almost exclusively a result of Helicobacter pylori infection. Thus, MALT is part of the host defense against the pathogen H. pylori. Consequently, lymphomas arising from gastric MALT may be a clonal evolution starting from the infection. In low-grade gastric MALT lymphoma, cure of the infection may induce complete histological remission in the majority of patients. Investigators have recently reported that complete remission rate is between 70% and 80%. In an extended analysis, we have treated 84 patients with low-grade gastric MALT lymphoma in stage El, using a dual regimen to eradicate H. pylori. Complete remission was observed in 68 (80%) patients; a partial remission was found in 4 patients. In contrast, 12 patients showed no change and were referred to alternative treatment. In patients in complete remission, a polymerase chain reaction assay for the rearranged immunoglobulin heavy-chain gene remained positive in many cases. Together with data from the literature, these data suggest that the majority of patients with low-grade gastric MALT lymphomas in stage El respond to eradication of H. pylori. Longer follow-up investigations are necessary to determine if remissions indicate a cure from the disease.

Gastric Mucosa↗

Demonstration of Helicobacter pylori-like organisms in the gastric mucosa of captive exotic carnivores.

Samples of gastric tissue from the cardiac, fundic and pyloric region of 30 carnivores comprising 12 tigers (Panthera tigris), 10 lions (Panthera leo), three pumas (Felis concolor), two leopards (Panthera pardus), one serval (Felis serval), one wolf (Canis lupus) and one hyena (Crocuta crocuta) kept at German zoological gardens were subjected to histopathological and immunohistochemical examination. Selected tissue specimens of 12 animals were examined also by electron microscopy. The purpose of this study was to determine the prevalence of Helicobacter-like organisms in carnivores and to record infection rates, degree of colonization and associated histopathological changes. Three morphologically different types of spiral-shaped bacteria were demonstrated. A Helicobacter pylori-like organism (HPLO) was found in 42% of the tigers and 90% of the lions examined. Large Helicobacter-like organisms (HLOs) were identified in three pumas, one serval, one hyena and in three lions (in the latter, in coexistence with HPLOs). A third organism with a spiral periplasmic fibril (Helicobacter felis-like) was demonstrated in a wolf. The most striking histopathological finding associated with HPLO and HLO colonization was the formation of lymphoid follicles in the mucosa. Additional lymphoplasmacytic and neutrophilic infiltrates in the gastric mucosa were found in a number of tigers and lions infected with HPLOs, but none in the other carnivores infected with HLOs. From these results it is concluded that gastric bacteria similar or identical with H. pylori may also be an important cause of chronic gastritis in tigers and lions.

Animals↗

Gastric MALT-lymphoma and Helicobacter pylori infection.

The presence of lymphoid tissue in the gastric mucosa is virtually pathognomonic of Helicobacter pylori infection. This lymphoid tissue has mucosa-associated lymphoid tissue (MALT) characteristics suggesting that H. pylori infection may represent a stimulus for the growth of gastric MALT lymphoma. H. pylori can be detected in more than 90% of patients with low-grade gastric MALT lymphoma supporting the aetiological role of the organism. The strongest evidence for the significance of H. pylori in the pathogenesis of low aetological-grade gastric MALT lymphoma is provided by clinical studies showing that cure of H. pylori infection is followed by a complete regression of these tumours in most patients. This paper reviews the current knowledge about antibacterial treatment of low-grade gastric MALT lymphoma, and immunological and molecular aspects in the pathogenesis of the disease.

Anti-Bacterial Agents↗

H2-receptor antagonists and antacids have an aggravating effect on Helicobacter pylori gastritis in duodenal ulcer patients.

BACKGROUND: Antacids, such as aluminium-magnesium hydroxide (AIMg(OH)3), or H2-receptor antagonists, such as ranitidine, are common drugs used for treating peptic ulcer disease and acid-related symptoms. METHODS: In a prospective double-blind controlled study, 174 patients were randomized to a 4-week course of treatment with either AIMg(OH)3 (acid-binding capacity: 280 mval/day) or ranitidine 300 mg for active Helicobacter pylori-associated duodenal ulcers (as determined by histology and the urease test). Before and after treatment, two biopsy specimens each were obtained from the antrum and corpus, and the grade and activity of gastritis, as well as H. pylori density, were determined using a score ranging from 0 = none to 4 = severe. RESULTS: Pre- and post-treatment histology were available for 138 patients (AIMg(OH)3: 67, ranitidine; 71). Treatment with AIMg(OH)3 significantly increased the activity of corpus gastritis (Wilcoxon signed-rank: P = 0.0014), while ranitidine treatment significantly increased both the grade and activity of corpus gastritis (P = 0.0002 and P = 0.0001 respectively). In the antrum, both regimens provoked a significant increase in the frequency of intestinal metaplasia, but this may be a consequence of sampling error. CONCLUSIONS: Ranitidine and AIMg(OH)3 have an aggravating effect on H. pylori gastritis in duodenal ulcer patients. This should be considered a side-effect of the respective drugs and is more pronounced with ranitidine.

Aluminum Hydroxide↗

Double-blind comparison of an oral Escherichia coli preparation and mesalazine in maintaining remission of ulcerative colitis.

BACKGROUND: Aminosalicylates are used as standard treatment for maintaining remission in ulcerative colitis. As yet, there is no other existing alternative with proven efficacy. In light of the hypothesis that the intestinal environment may contribute to the pathophysiology of ulcerative colitis, a trial was conducted to test the effects of probiotic treatment with an oral preparation of non-pathogenic E. coli. METHODS: A total of 120 patients with inactive ulcerative colitis were included in a double-blind, double-dummy study comparing mesalazine 500 mg t.d.s. to an oral preparation of viable E. coli strain Nissle (Serotype 06: K5: H1) for 12 weeks with regard to their efficacy in preventing a relapse of the disease. Study objectives were to assess the equivalence of the clinical activity index (CAI) under the two treatment modalities and to compare relapse rates, relapse-free times and global assessment. RESULTS: The start and end scores of the CAI demonstrated no significant difference (P = 0.12) between the two treatment groups. Relapse rates were 11.3% under mesalazine and 16.0% under E. coli Nissle 1917 (N.S.). Life table analysis showed a relapse-free time of 103 +/- 4 days for mesalazine and 106 +/- 5 days for E. coli Nissle 1917 (N.S.). Global assessment was similar for both groups. Tolerability to the treatment was excellent and did not differ. No serious adverse events were reported. CONCLUSIONS: From the results of this preliminary study, probiotic treatment appears to offer another option for maintenance therapy of ulcerative colitis. Additional support is provided for the hypothesis of a pathophysiological role for the intestinal environment in ulcerative colitis.

Adult↗

Efficacy and tolerability of a one-week triple therapy consisting of pantoprazole, clarithromycin and amoxycillin for cure of Helicobacter pylori infection in patients with duodenal ulcer.

BACKGROUND: Previous studies have shown that one-week triple therapy consisting of omeprazole, clarithromycin and amoxycillin may cure Helicobacter pylori infection in the vast majority of patients. The present study was designed to test the hypothesis that a triple therapy with pantoprazole, clarithromycin and amoxycillin cures the infection in > or = 80% of duodenal ulcer patients infected with H. pylori. METHODS: In an open two-centre study, 60 duodenal ulcer patients were treated with pantoprazole 40 mg b.d., clarithromycin 500 mg b.d. and amoxycillin 1 g b.d. for 1 week. During the second week patients received pantoprazole 40 mg once in the morning. We assessed H. pylori infection before treatment and 4 weeks after cessation of the study medication by a rapid urease test, histology after Warthin-Starry stain and a 13C-urea breath test. RESULTS: Sixty patients (42 males, mean age 47.4 years) entered the trial. All patients were infected with H. pylori. One patient was withdrawn from the study because of allergy to penicillin and six patients were protocol violators. H. pylori infection was cured in 47 out of 53 patients who completed the trial according to the protocol (89%; 95% CI: 80-97%) and in 49 of 60 patients included in the trial (82%; 95% CI: 72-92%). Four weeks after the last administration of study drugs, 55 out of 60 ulcers had healed (92%). Twenty-nine patients reported 51 adverse events that were mostly mild to moderate. CONCLUSIONS: One-week triple therapy consisting of pantoprazole, clarithromycin and amoxycillin is a simple and effective approach to the cure of H. pylori infection in patients with duodenal ulcer. In those patients who took the drugs as prescribed the H. pylori cure rate was 89%, with the lower 95% confidence limit being 80%.

2-Pyridinylmethylsulfinylbenzimidazoles↗

An increasing dose of omeprazole combined with amoxycillin cures Helicobacter pylori infection more effectively.

BACKGROUND: The combination of omeprazole and amoxycillin has demonstrated effectiveness with very few side-effects in the treatment of H. pylori infection, however cure rates have varied widely. The present study addresses the question as to the extent to which the cure rate of H. pylori infection depends on the size of the daily omeprazole dose, and investigates other patient-related factors that influence treatment success. METHODS: In a randomized, controlled and investigator-blinded trial, 163 hospitalized patients with H. pylori-associated gastritis were treated with 20 mg omeprazole once daily in the morning, 20 mg omeprazole b.d., 40 mg omeprazole b.d. or 60 mg omeprazole b.d. for 14 days. In addition, all patients received 1000 mg amoxycillin b.d. on days 5-14. Endoscopic and histological examinations were performed prior to treatment, at the end of treatment and 4 weeks after completion of treatment. RESULTS: H. pylori infection was cured in 18 of 40 (45%, 95% CI: 29-62%), in 22 of 39 (56.4%, 95% CI: 40-72%), in 25 of 38 (65.8%, 95% CI: 49-80%), and in 33 of 40 (82.5%, 95% CI: 67-93%) patients, respectively, (P < 0.001). Side-effects leading to discontinuation of treatment occurred in only 1.2%. CONCLUSION: The daily dose of omeprazole is an important factor for the success of dual therapy comprising omeprazole and amoxycillin in curing H. pylori infection. Cure of H. pylori infection correlates positively and significantly with the size of the daily omeprazole dose. The combination of high-dose omeprazole and amoxycillin is an effective and well-tolerated regimen for the treatment of H. pylori-associated diseases.

Adolescent↗

Focally enhanced gastritis: a frequent type of gastritis in patients with Crohn's disease.

BACKGROUND & AIMS: Gastric histology is not well studied in patients with Crohn's disease. The aim of this study was to analyze the histological appearance of gastric mucosa in patients with Crohn's disease. METHODS: In a prospective study, biopsy specimens taken from the antrum and body of 75 patients with known Crohn's disease of the large and/or small bowel and 200 Crohn's disease-free controls were evaluated by histology and immunohistochemistry. RESULTS: Helicobacter pylori-associated gastritis was found in 25 patients with Crohn's disease (33.3%) and 78 controls (39%). In H. pylori-negative patients with Crohn's disease, a characteristic type of gastritis was found in antral biopsy specimens of 36 patients (48%) and in body biopsy specimens of 18 patients (24%). It was characterized by a focal infiltration of CD3+ lymphocytes, CD68R+ histiocytes, and, in 80% of cases, of granulocytes. Granulomas were found in 11 patients. Overall, granulomas and/or focally enhanced gastritis were observed in 76% of H. pylori-negative patients with Crohn's disease and in 0.8% of controls. There were no correlations between the occurrence of focally enhanced gastritis and clinical and laboratory findings. CONCLUSIONS: Focally enhanced gastritis is common in Crohn's disease. Its recognition should guide the clinician into further investigations in patients not yet known to have Crohn's disease.

Adolescent↗

Pattern of adhesion molecule expression on vascular endothelium in Helicobacter pylori-associated antral gastritis.

BACKGROUND & AIMS: The inflammatory response in Helicobacter pylori-associated gastritis (HAG) is characterized by an intense infiltrate of granulocytes and lymphocytes. The emigration of white blood cells into sites of inflammation is mediated by receptors on endothelial cells and on blood leukocytes. The aim of this study was to characterize endothelial adhesion molecule expression in HAG leading to leukocyte infiltration. METHODS: Endothelially expressed adhesion molecules were studied in situ by immunohistochemical analysis of antral mucosal biopsy specimens from 20 control patients, 10 of whom had chemical gastritis, 10 normal mucosa, and 44 HAG. Adjacent biopsies were used to evaluate messenger RNA (mRNA) transcripts for the respective adhesion molecule and its inducing cytokines. RESULTS: Constitutive expression of P-selectin was found in all groups. Intercellular adhesion molecule 1 (ICAM-1) was up-regulated in patients with HAG and chemical gastritis in contrast to normal controls. Vascular adhesion molecule 1 (VCAM-1) was only found within lymphoid aggregates present in HAG. Neither mRNA transcripts nor the protein product of E-selectin were detected in normal or inflamed mucosa, although mRNA of the E-selectin-inducing cytokines, tumor necrosis factor alpha and interleukin 1beta, were found. CONCLUSIONS: Data suggest a major role of ICAM-1 and VCAM-1 in leukocyte-endothelial interaction in HAG without E-selectin up-regulation showing a unique pattern within the gastrointestinal tract, in contrast to observations made in inflammatory bowel disease.

Adult↗

Regression of gastric MALT lymphoma after eradication of Helicobacter pylori is predicted by endosonographic staging. MALT Lymphoma Study Group.

BACKGROUND & AIMS: Recent studies suggest that eradication of Helicobacter pylori may result in complete regression of low-grade lymphoma of the gastric mucosa-associated lymphoid tissue (MALT). Which patients benefit from this treatment is unknown. The aim of this study was to prospectively study whether staging by echoendoscopy predicts the outcome of treatment of MALT lymphoma by eradication of H. pylori. METHODS: Twenty-two patients positive for H. pylori with low-grade gastric B-cell MALT lymphoma were examined by echoendoscopy at the time of diagnosis. Treatment for H. pylori consisted of a 2-week course of oral omeprazole and amoxicillin. Patients were followed up by endoscopy and biopsy. RESULTS: H. pylori was eradicated in all patients. Complete regression of MALT lymphoma was observed in 12 patients (54%), partial regression in 5 patients (23%), and no response in 5 patients (23%) during follow-up. Twelve of 14 patients with lymphoma restricted to the mucosa or submucosa (stage E-I1) at echoendoscopy, but none of the 10 patients with higher stage (P < 0.01), showed complete regression of MALT lymphoma. In stage E-I1 patients, the probability of complete regression of lymphoma was 60% at 6, 79% at 12, and reached 100% at 14 months, respectively. CONCLUSIONS: Staging of gastric low-grade MALT lymphomas by endoscopic ultrasonography allows prediction of the response to therapy by eradication of H. pylori.

Adult↗

Clinical impact of routine biopsies of the gastric antrum and body.

Biopsy sampling of gastric mucosa at diagnostic endoscopy provides information that cannot be obtained by other means. The most common indication for gastric biopsy is the need to know whether or not the patient is infected with Helicobacter pylori, and whether the stomach is gastritic or not. Microscopic examination of gastric biopsy specimens, in addition to H. pylori status, provides information about the grade, extent, and topography of gastritis-related and atrophy-related lesions in the stomach. This information provides further opportunities for assessing the risk and likelihood of various gastric disorders. These are: a) The predominance or restriction of the H. pylori-related gastritis in the antrum strongly correlates with an increased risk of peptic ulcer disease, and of duodenal ulcer in particular (the duodenal ulcer phenotype of gastritis). b) The presence of atrophic gastritis (loss of normal glands) in the area of the gastric body indicates a low risk of ulcer and also a reduction in the capacity of the patient to secrete acid. c) The occurrence of advanced atrophic gastritis and intestinal metaplasia multifocally in the stomach (advanced multifocal atrophic gastritis), and in the lesser curvature and angular notch in particular, are features suggestive of an increased risk of gastric neoplasias (the gastric cancer phenotype of gastritis). d) The presence of normal and healthy gastric mucosa indicates, on the other hand, an extremely low risk of both peptic ulcer disease and gastric cancer. In addition to diagnosis of H. pylori-related gastritic lesions, routine gastric biopsies may reveal findings that indicate special forms of gastritis, such as eosinophilic, lymphocytic, reactive, or granulomatous gastritis (e.g., Crohn's gastritis), or Helicobacter heilmannii gastritis. These types of gastritis can be found incidentally in a small percentage of patients who undergo diagnostic gastroscopy for abdominal complaints.

Biopsy↗

Symptoms in patients with giardiasis undergoing upper gastrointestinal endoscopy.

BACKGROUND AND STUDY AIMS: The aim of the study was to compare symptoms of Giardia-positive and -negative patients undergoing upper gastrointestinal endoscopy. PATIENTS AND METHODS: Multi-center questionnaire-based case-control study of 120 Giardia-positive and -negative patients who underwent upper endoscopy. Cases were identified through histological detection of trophozoites of Giardia lamblia in duodenal biopsy specimens. Giardia-negative patients with inconspicuous duodenal histology served as controls. RESULTS: There was a clear male predominance in the Giardia-positive groups, with 75 cases (62.5 %) being male and 45 (37.5 %) female (P < 0.0001). Giardia-positive cases tended to be older than controls (median 60 years vs. 45.2 years, P < 0.009). The main symptom of positive cases were tenderness to palpation (52.1%), abdominal discomfort (43.3 %), sensation of fullness (40.8%), distension (37.5%), epigastralgia (37.5%), nausea and/or vomiting (35.8%), heartburn (26.7%), and diarrhea (25.8%). Only sensation of fullness (P < 0.02), nausea/vomiting (P < 0.02) and heartburn (P < 0.03) were observed significantly more often in positive cases. Foul-smelling stools, considered typical for giardiasis, were observed in 5.8% of cases. Symptoms lasted for less than 1 month in 28.2 % of cases, for 1-6 months in 35.9%, and for more than 12 months in 35.9% (ns to controls). Treatment resulted in symptomatic cure in 60.5 % and in improvement of symptoms in 21.1 % of cases (P < 0.0001 vs controls). CONCLUSION: There are no symptoms that reliably allow the recognition of giardiasis in patients undergoing upper endoscopy.

Adolescent↗

Identifying persons at risk for gastric cancer?

BACKGROUND: Although considerable evidence suggests that Helicobacter pylori infection plays a crucial role in the pathogenesis of gastric carcinoma, a striking difference exists between the number of infected individuals and the proportion of those developing gastric carcinoma. The purpose of this article is to review the available evidence supporting the existence of identifiable risk factors for the development of gastric carcinoma. METHODS: We performed a critical review of the pertinent literature, which forms the basis for this study. RESULTS: In terms of treatment strategies for prevention of gastric carcinoma, cure of H. pylori infection in all infected patients seems unfeasible, mainly for economic reasons. However, the final and definite step to prove that infection with H. pylori is a preneoplastic condition for the development of gastric cancer would be the observation that cure of the infection leads to a significant reduction in gastric cancer incidence rates in comparison with an untreated population. Therefore, in 1997 a multicenter preventive interventional study on gastric carcinoma will be started in Germany. The target group in this study includes patients with a specific pattern of H. pylori gastritis who will be summarized by a "gastric cancer risk index." CONCLUSIONS: It is hoped that long-term follow-up of these patients will reveal whether preventive treatment of H. pylori infection is capable of reducing the risk for development of gastric cancer.

Carcinoma↗

Role of adherence in interleukin-8 induction in Helicobacter pylori-associated gastritis.

Active Helicobacter pylori-associated gastritis is characterized by a dense mucosal infiltration with granulocytes. Since H. pylori is noninvasive, secondary signals must induce the accumulation of granulocytes. Interleukin-8 (IL-8) has been shown to play a key role in this event. Using competitive reverse transcriptase-PCR on mRNA from gastric biopsies, we could show a clear correlation between the amount of IL-8 transcripts and the activity of H. pylori gastritis. Due to the inability of the bacterium to invade host cells, the epithelial layer is a potential candidate as an IL-8 source. To study the mechanism of IL-8 induction, established gastric carcinoma epithelial cell lines (AGS and Kato III) and well-defined H. pylori strains were used in a modified in vitro system. The experimental design enabled us to prevent direct contact of bacteria with epithelial cells by use of a filter membrane which did not block secreted bacterial products crossing the membrane. The data clearly showed that the direct contact of the bacterial cell with the epithelial cell is necessary for optimal IL-8 production because not only live bacteria, but also metabolically inactive bacteria, increased IL-8 secretion. Neither purified lipopolysaccharide nor water-soluble protein fractions of H. pylori NCTC 11637 and Tx30a nor the cytotoxin of H. pylori was able to increase IL-8 production significantly by the epithelial cells used. Furthermore, preparations of total membrane and outer membrane proteins of H. pylori were not able to stimulate IL-8 release in vitro. Accumulatively, these results imply that active metabolism is not necessary for stimulation as long as there is an intact membrane aiding the presentation of a stimulating membrane complex or aggregate on the surface of the bacteria. From these results, we conclude that whole bacteria and their direct contact with epithelial cells may be critical for IL-8 induction in vivo.

Bacterial Adhesion↗

Effect of curing Helicobacter pylori infection on intragastric acidity during treatment with ranitidine in patients with duodenal ulcer.

BACKGROUND: In patients with duodenal ulcer cure of Helicobacter pylori infection resulted in a pronounced decrease in intragastric pH during treatment with omeprazole. AIM: To test the hypothesis that treatment of H pylori adversely affects the pH response to ranitidine. PATIENTS: Eighteen patients with duodenal ulcer who were infected with H pylori were studied. METHODS: Twenty four hour pH recordings were performed during treatment with ranitidine (300 mg) at night before and four to six weeks after cure of H pylori infection. Presence of H pylori was assessed by a rapid urease test, culture, histology, and a 13C urea breath test. Also, the fasting gastrin concentrations were measured before and after treatment for H pylori infection. RESULTS: Cure of H pylori infection resulted in a considerable improvement in both antral and corpus gastritis and a decrease in fasting gastrin concentrations. As a result of the cure the night time intragastric pH during treatment with ranitidine decreased (median pH 6.8 v 5.4; p = 0.007), whereas the acidity during the daytime was not affected. CONCLUSIONS: In patients with duodenal ulcer the intragastric pH during treatment with ranitidine depends on H pylori. However, the loss of effectiveness in altering pH seems to be less pronounced than previously found with omeprazole.

Adult↗

Non-alcoholic duct destructive chronic pancreatitis.

BACKGROUND: The pathology of non-alcoholic chronic pancreatitis has not yet been sufficiently studied. AIMS: To identify the major changes of pancreatic tissue in patients surgically treated for non-alcoholic chronic pancreatitis. PATIENTS: Pancreatectomy specimens from 12 patients with non-alcoholic chronic pancreatitis, including four patients with autoimmune or related diseases (Sjögren's syndrome, primary sclerosing cholangitis, ulcerative colitis, and Crohn's disease), were reviewed. METHODS: Morphological changes were studied histologically and immunohistochemically (to type inflammatory cells) and compared with the pancreatic alterations found in 12 patients with alcoholic chronic pancreatitis. RESULTS: In patients with non-alcoholic chronic pancreatitis, with or without associated autoimmune or related diseases, pancreatic inflammation particularly involved the ducts, commonly resulting in duct obstruction and occasionally duct destruction. None of these features was seen in alcoholic chronic pancreatitis which, however, showed pseudocysts and calcifications. CONCLUSION: The pancreatic changes in patients with non-alcoholic chronic pancreatitis clearly differ from those with alcoholic chronic pancreatitis. The term chronic duct destructive pancreatitis is suggested for this type of pancreatic disease.

Adolescent↗

Is the polymerase chain reaction or cure of Helicobacter pylori infection of help in the differential diagnosis of early gastric mucosa-associated lymphatic tissue lymphoma?

PURPOSE: The differential diagnosis of early gastric mucosa-associated lymphatic tissue (MALT) lymphoma based on Helicobacter pylori gastritis may be difficult when lymphoepithelial lesions are not detected. The aim of the present study was to investigate the question whether the polymerase chain reaction (PCR) or cure of H pylori infection may be of help in this respect. PATIENTS AND METHODS: Twenty patients with suspected low-grade gastric MALT lymphomas were treated in a double-blinded, randomized, crossover trial with 2,250 mg of either amoxicillin or placebo, both in combination with omeprazole, for 14 days with the aim to cure H pylori infection. PCR was performed using primers specific for the CDR3 region to detect monoclonal B cells. RESULTS: In five of 20 patients, MALT lymphomas were finally diagnosed. Three of these five patients went into complete remission, while two were referred to surgery. In the 15 patients with gastritis, complete regression was observed in all cases. With respect to PCR, monoclonal bands were detected in all four of the analyzed lymphoma patients before histology showed lymphoma. In addition, monoclonal bands were found in three patients with gastritis. In the patients with gastritis and monoclonal PCR, complete regression took longer as compared with the remaining 12 patients with polyclonal PCR and gastritis (P = .0209). Successful H pylori eradication was associated with earlier diagnosis of the MALT lymphoma (P = .0237). CONCLUSION: CDR3-PCR may be of help in the differential diagnosis of early gastric MALT lymphoma. Furthermore, H pylori eradication may lead to earlier diagnosis.

Adult↗

Focal inflammatory infiltrations in gastric biopsy specimens are suggestive of Crohn's disease. Crohn's Disease Study Group, Germany.

BACKGROUND: Crohn's disease is a systemic inflammatory disease that may involve all regions of the gut. METHODS: Thirty-six patients with Crohn's disease and 36 age- and sex-matched control patients were prospectively evaluated by upper endoscopy. Biopsy specimens were taken from the oesophagus, duodenum, and 10 locations in the antrum and corpus. RESULTS: Granulomas were found in four patients (11.13%) with Crohn's disease but in none of the control patients (P > 0.5). In 23 of 36 patients (63.9%) with Crohn's disease focal inflammatory infiltrations were found, as compared with 7 of 36 (19.4%) of the controls (P < 0.001). For focal inflammatory infiltrations, an odds ratio of 7.33 (2.55-21.38) was calculated, which increased to 20.04 (4.07-98.45) when only specimens from the angulus were considered. Helicobacter pylori infection was present in 13 of 36 controls (36.1%) and in 3 of 36 patients (8.3%) with Crohn's disease (P = 0.009). CONCLUSION: These data suggest that Crohn's disease is typically associated with focal inflammatory infiltrations of the gastric mucosa.

Adult↗