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A Hackelsberger

Publications and source records attributed to A Hackelsberger.

At least 19 recordsLinked to original sources
PubMed1999

Role of aging in the expression of Helicobacter pylori gastritis in the antrum, corpus, and cardia.

BACKGROUND: Earlier studies identified a pylorocardial expansion of chronic gastritis. We investigated the age-dependent changes in grading and topography of Helicobacter pylori gastritis. METHODS: Antral, corpus, and cardial biopsy specimens from 216 H. pylori-positive patients with no peptic ulcer disease (PUD), malignancy, or Barrett's oesophagus were evaluated with haematoxylin and eosin and modified Giemsa. The patients were separated into four equal-sized age groups (1, < 46 years; II, 46-56 years; III, 57-68 years; IV, > 69 years). Sydney-system gradings of bacterial density and activity and degree of gastritis were used to calculate gastritis sum scores for age- and biopsy site-dependent comparisons. The prevalence of intestinal metaplasia (IM) and atrophy was also compared. RESULTS: Mean antral sum scores decreased slightly in group IV but were higher than those in the corpus or cardia in all groups (P < 0.05 each). In the corpus mean scores increased in groups II-IV versus group I (P < 0.05 each), and aging was associated with a significant increase in bacterial density and active inflammation. The cardia scores remained virtually constant in all groups and exceeded significantly that in the corpus in group I. IM and atrophy increased with age, occurring more frequently and earlier in the antrum and cardia than in the corpus. CONCLUSIONS: Progression of gastritis with age involves the corpus but not the cardia. Antral inflammation decreases slightly in patients of advanced age.

Adult↗
PubMed1998

Increased cell proliferation of the gastric mucosa in first-degree relatives of gastric carcinoma patients.

BACKGROUND: Studies not considering Helicobacter pylori infection have suggested the presence of a hereditary risk for gastric carcinoma. However, other studies have identified intrafamilial clustering of H. pylori infection as a causal factor in gastric carcinogenesis. This prompted the authors to study the effect of H. pylori and hereditary factors on the proliferation of gastric mucosa because hyperproliferation appears to be an early step in carcinogenesis. METHODS: In a total of 39 patients (19 first-degree relatives of patients with gastric carcinoma and 20 dyspeptic controls), 2 biopsy specimens each from the antrum and corpus were examined histologically. In addition, crude nuclei fractions were prepared from other biopsy specimens obtained in the same manner. Nuclei were fixed in 70% ethanol and stained with propidium iodine prior to measurement. A cell cycle analysis was performed using a flow cytometer. For analysis a proliferative index (PI) (percentage of nuclei in the S- and G2/M-phases) was calculated. RESULTS: In comparison with control patients, first-degree relatives of gastric carcinoma patients had increased mucosal proliferation of the antrum (Student's t test, P = 0.017). After excluding patients with H. pylori infection (12 in each group), relatives of gastric carcinoma patients had significantly increased proliferation not only in the antrum (PI: 16.5 vs. 12.1; P = 0.043), but also in the corpus (PI: 17.2 vs. 13.0; P = 0.024). CONCLUSIONS: A family history of gastric carcinoma may increase the risk for developing gastric carcinoma via mucosal hyperproliferation, irrespective of H. pylori infection.

Cell Division↗
PubMed1998

[Percutaneous endoscopic gastrostomy in patients with ENT tumors].

Oral food intake in patients with obstructing pharyngeal and esophageal carcinomas is commonly insufficient because of tumor-induced dysphagia which gives rise to cachexia unless treated. While entailing an unfavorable prognosis, malnutrition is often a therapy-limiting factor. Tube feeding with liquid formula diets currently offers the most efficient and least-risky approach to long-term use and is best adopted even at a pretreatment stage irrespective of the tumor therapy intended. A feeding tube placed by a percutaneous endoscopically controlled gastrostomy (PEG) increasingly offers an alternative to a nasogastric tube. After using diaphanoscopy, the stomach is punctured from outside under local anesthesia and a feeding tube inserted by means of a retrograde thread or a direct puncture method. A modification of the direct puncture method has been preferred at the Magdeburg University E.N.T. Department. The tube is held in place by thermally activated helical winding of a gastric tube end (using a memory-retaining helix). During the 1991-1996 period 415 patients with obstructing carcinomas of the upper digestive tract were treated with a feeding tube. No fatal complications were observed. Severe complications (peritonitis) occurred in three patients. In 160 patients with PEG the following parameters were recorded: weight-to-size index, body mass index, degree of dysphagia, nutrition status, lymphocyte count, total serum protein and patients' compliance to PEG. The enteral nutrition therapy used was indicated in all of the patients treated with advanced carcinomas of the head and neck. In 81% of the patients the compliance to PEG was positive. Findings demonstrated that long-term intestinal nutrition via PEG was a safe and effective form of treatment. Inserting the tube by the direct puncture method was advantageous for patients with carcinomas in the upper digestive tract as only few mechanical alterations take place along tumorous tissues following PEG while contamination with bacteria and neoplastic cells from the tumor region into the abdomen are precluded.

Body Weight↗
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

Performance of a rapid whole blood test for Helicobacter pylori in primary care: a German multicenter study.

BACKGROUND: Serological rapid whole-blood tests for the detection of H. pylori are presently being promoted for use in primary care. We conducted a multi-center study to investigate the diagnostic accuracy of the Boehringer Mannheim Helicobacter pylori test (BM test), which is identical with the Cortecs Helisal test. PATIENTS AND METHODS: A previous diagnosis of H. pylori, a history of peptic ulcer diseases, or proton-pump inhibitor, bismuth or antibiotic use during the preceding month were exclusion criteria. The BM test was performed prior to endoscopy by 7 primary care physicians, 5 practicing gastroenterologists, or a single physician in the university hospital outpatient service. During endoscopy, antral and corpus biopsies were obtained for histology and rapid urease testing (RUT). H. pylori positivity was defined by histology and/or RUT as reference methods. H. pylori IgG-ELISA was performed additionally. RESULTS: Of the 203 patients included, 151 were H. pylori-positive by reference methods (74.4%). The overall accuracy of the BM test was 77.3%. Eight BM tests were indeterminate, and in the other 195 patients the test performed as follows: sensitivity 80.3%, specificity 81.3%, positive predictive value 92.9%, negative predictive value 57.4%. Using IgG-ELISA as reference, the BM test performance was similar. It also did not differ substantially among the three groups of physicians involved. CONCLUSIONS: We found the performance of the BM test to be insufficiently accurate, as both over- and underdiagnosis of H. pylori infection were not infrequent. This test needs to be improved before its use in primary care can be recommended.

Adolescent↗
PubMed1998

Differing patterns of Helicobacter pylori gastritis in patients with duodenal, prepyloric, and gastric ulcer disease.

BACKGROUND: We investigated the risk relationship between histotopographic patterns of Helicobacter pylori gastritis and peptic ulcer site. METHODS: Three hundred and eighty-three infected patients were classified as having duodenal ulcer (n = 79), prepyloric ulcer (n = 39), gastric (angular) ulcer (n = 28), and no ulcer (n = 237). Antral and corpus biopsy specimens were taken. Sydney system-based scores for bacterial density and activity and degree of gastritis were added to antral and corpus sum scores (SS) (range, 0-9). These were used to categorize the phenotype of gastritis. In addition, the presence or absence of mucosal atrophy was taken into account. The relative risk for ulcer association with these conditions was calculated. RESULTS: High-grade antral (SS > 5) associated with mild to moderate corpus (SS > 5) gastritis increased duodenal (RR = 4.9; confidence interval (CI), 2.8-8.5) and prepyloric ulcer risk (RR = 2.99; CI, 1.4-6.2). High-grade gastritis in the antrum (SS > 5) and corpus (SS > 5) increased gastric ulcer risk (RR = 3.7; CI, 1.6-8.3). Antral atrophy and/or intestinal metaplasia is associated with an increased gastric ulcer risk (RR = 3.3; CI, 1.4-7.8). CONCLUSION: The pattern of H. pylori gastritis may define a risk for peptic ulcer at various sites, but additional factors, not reflected in histology, also contribute to this risk.

Atrophy↗
PubMed1998

The prevalence of Helicobacter pylori gastritis in patients with reflux oesophagitis: a case-control study.

OBJECTIVES: To investigate the prevalence of Helicobacter pylori in patients with erosive oesophagitis in comparison with asymptomatic subjects. DESIGN: Hospital based case-control study. METHODS: Two hundred and nineteen consecutive patients with erosive oesophagitis diagnosed over 2 years were studied. Patients with secondary gastro-oesophageal reflux disease, prior H. pylori eradication therapy, PPI or antibiotics were excluded and two case groups were formed: (1) patients with oesophagitis alone (OEA), and (2) patients with oesophagitis and concomitant peptic ulcer disease (OE&PUD). H. pylori was assessed by antral and corpus mucosa histology and the rapid urease test. Age- and sex-matched controls, who underwent voluntary screening for H. pylori by the 13C-urea breath test, had neither symptoms nor a history of upper gastrointestinal disease. RESULTS: The 130 patients in the OEA group had a prevalence of H. pylori of 38.5% compared with 75.6% in the 41 patients in the OE&PUD group and 88.5% in a subgroup of the latter with duodenal ulcer (26 patients). Infected and non-infected cases showed no significant differences in terms of grade of oesophagitis and incidence of Barrett's oesophagus. The prevalence of H. pylori infection in OEA was similar to that found in matched controls. In OE&PUD the relative risk of H. pylori infection was 3.6-fold higher than in controls [P = 0.0069, 95% confidence interval (CI), 1.401-9.195]. CONCLUSION: The prevalence of H. pylori in oesophagitis without PUD is similar to that of the asymptomatic population with no history of upper gastrointestinal disease. When oesophagitis and PUD occur together, the infection rate is within the range found in PUD alone.

Adult↗
PubMed1998

Prevalence of Helicobacter pylori infection and gastric mucosal abnormalities in chronic pancreatitis.

OBJECTIVE: Chronic pancreatitis is often associated with abnormal gastric acid secretion. However, previous studies have taken into consideration neither the potential role of Helicobacter pylori (H. pylori) infection nor histological features of the gastric mucosa in this context. The aim of this study was to analyze the prevalence of H. pylori infection as well as the pattern of gastritis in patients with chronic pancreatitis. METHODS: Forty patients with chronic alcoholic pancreatitis were included in the study: 40 patients with alcoholic liver cirrhosis and normal exocrine pancreatic function and 40 asymptomatic nonalcoholic subjects matched for age and sex used as control subjects. Endoscopy was performed in all patients, and five biopsy specimens from the antrum (three from the gastric body and two from the cardia) were taken for histological grading of gastritis and H. pylori assessment. RESULTS: Prevalence of H. pylori infection was similar in subjects with chronic pancreatitis (38%), asymptomatic subjects (28%) and liver cirrhosis (30%). Topography and expression of H. pylori-associated chronic gastritis was also not different among the three groups of subjects. In H. pylori-negative subjects, the presence of moderate to severe chronic antral gastritis was significantly more common in patients with chronic pancreatitis (40%) than in subjects with liver cirrhosis (18%) and in asymptomatic subjects (14%) (p < 0.05). No difference was found among the three groups of patients with regard to gastritis activity, atrophy, and intestinal metaplasia in the various gastric regions. The chronicity grade of gastritis did not correlate with the severity of pancreatic insufficiency. CONCLUSION: Prevalence of H. pylori infection is not different in patients with chronic pancreatitis as compared with subjects alcoholic liver cirrhosis and asymptomatic subjects. A severe H. pylori-negative chronic gastritis is more common in patients with chronic pancreatitis. This chronic inflammation of the gastric mucosa could contribute to determining the changes in gastric physiology described in patients with chronic pancreatitis.

Adult↗
PubMed1998

Intestinal metaplasia at the gastro-oesophageal junction: Helicobacter pylori gastritis or gastro-oesophageal reflux disease?

BACKGROUND: Intestinal metaplasia, whether in the cardia or the distal oesophagus, has been uniformly defined as specialised columnar epithelium, suggesting a relation with Barrett's oesophagus. It is, however, not clear whether the risk factors associated with intestinal metaplasia are identical at both sites. AIMS: To investigate biopsy specimens obtained below the squamocolumnar junction (SCJ) in relation to endoscopic aspect, gastric histology, and clinical presentation. PATIENTS AND METHODS: In 423 patients investigated the endoscopic aspect of the SCJ was classified as unremarkable (group I, n = 315) or suggestive of Barrett's oesophagus (group II, n = 108). Standardised biopsy specimens from the antrum, corpus, and directly below the SCJ were investigated. RESULTS: Intestinal metaplasia was detected at the SCJ in 13.4% of group I patients, where it was significantly associated with gastric intestinal metaplasia (odds ratio (OR) 6.96; confidence interval (CI) 2.48 to 19.54) and H pylori (OR 7.85; CI 2.82 to 21.85), and in 34.3% of group II patients where it was significantly associated with reflux symptoms (OR 19.98; CI 6.12 to 65.19), erosive oesophagitis (OR 12.16; CI 3.86 to 38.24), and male sex (OR 6.25, CI 2.16 to 18.14), but not with H pylori or gastric intestinal metaplasia. CONCLUSION: This study suggests that the pathogenesis of intestinal metaplasia at the SCJ is not uniform: at an endoscopically unremarkable SCJ it is a sequela of H pylori gastritis, but coexisting with endoscopic features of Barrett's oesophagus it is associated with male sex and gastro-oesophageal reflux disease.

Barrett Esophagus↗
PubMed1998

Age and Helicobacter pylori decrease gastric mucosal surface hydrophobicity independently.

BACKGROUND: Gastric mucosal surface hydrophobicity (GMSH) is an essential component of the mucosal defence system that is decreased by Helicobacter pylori and non-steroidal anti-inflammatory drugs (NSAIDs). Gastric ulcers occur predominantly in elderly subjects, and may thus reflect diminished mucosal resistance. AIMS: To investigate whether aging decreases GMSH. PATIENTS: One hundred and twenty patients without peptic ulcer disease were divided into three age groups: I (41 years or below); II (41-64 years); and III (65 years or above). METHODS: Biopsy specimens were taken from the antrum, corpus, and cardia for histology (Sydney system), urease testing for H pylori, and for contact angle measurement of GMSH with a goniometer. The presence of specific H pylori antibodies was checked by immunoblotting. RESULTS: Fifty two patients (43%) were infected, and 68 were uninfected with H pylori. GMSH at all biopsy sites was lower in H pylori infected subjects (p=0.0001), but also decreased with age independently of infection status (p=0.0001). The most notable decrease in GMSH occurred between age groups I and II in those with, and between age groups II and III in those without, H pylori infection. GMSH was greater in antral than in corpus mucosa in both infected (p=0.0001) and uninfected patients (p=0.0003). CONCLUSIONS: A physiological decrease in GMSH with aging may contribute to the risk of ulcer development in the elderly, and may act synergistically with H pylori and/or NSAIDs on gastric mucosal defence.

Adult↗
PubMed1998

Increased risk for Helicobacter pylori recurrence by continuous acid suppression: a randomized controlled study.

BACKGROUND AND AIMS: Acid hyposecretion may enhance Helicobacter pylori colonization. We tested the hypothesis that maintenance therapy with ranitidine after cure of Helicobacter pylori infection increases the risk of recurrence of infection. PATIENTS AND METHODS: Sixty-six patients with duodenal ulcer and cured Helicobacter pylori infection were randomly assigned to 12 months maintenance treatment with ranitidine 150 mg daily (group A) or no treatment (group B). Follow-up consisted of clinical and endoscopic controls with biopsies for histology and rapid urease test every 4 months. RESULTS: Six patients, 3 in each group, were lost to follow up. Helicobacter pylori recurrence occurred in 9 patients in group A and in 2 patients in group B (30% versus 7%; p < 0.05). Duodenal ulcer recurred in one patient in group A and in 2 in group B, all three patients were reinfected with Helicobacter pylori. A corpus-predominant gastritis was observed in all reinfected patients in group A but in none in group B. CONCLUSIONS: Long-term inhibition of gastric acid secretion after eradication of Helicobacter pylori increases the risk of recurrence of infection. Our data imply that gastric acid not only influences the pattern of Helicobacter pylori localization in gastric mucosa, but also plays a key role in preventing recurrence of infection with Helicobacter pylori.

Adult↗
PubMed1997

Histological diagnosis of Helicobacter pylori gastritis is predictive of a high risk of gastric carcinoma.

Chronic Helicobacter pylori infection has been identified as a major risk factor for the subsequent development of gastric carcinoma On the basis of seroepidemiological studies the relative risk for infected persons was estimated to range between 3 and 6. Our study attempted to determine the relative risk of gastric carcinoma in H. pylori-infected individuals based on the histological evaluation of gastritis in gastric carcinoma patients in the light of a declining prevalence of H. pylori infection in Western countries. We histologically determined the H. pylori infection rate in 215 patients with early gastric carcinoma (tumor stage pT1), and compared it with that of 215 asymptomatic persons matched by age and sex who were tested by the 13C urea breath test. On the basis of these data an odds ratio of 16.7 (CI 9.6-29.1) was calculated for the relative risk of developing gastric carcinoma in H. pylori-infected people. The histological diagnosis of gastritis permits a separate risk assessment for patients with autoimmune gastritis, and by excluding these patients from the analysis we calculated an odds ratio for H. pylori-infected persons of 150 (CI 36.4-622.9). The endoscopic-histological diagnosis of H. pylori infection is associated with an increased risk of the subsequent development of gastric carcinoma of approximately 150-fold compared with H. pylori-negative patients who do not have chronic atrophic corpus gastritis of the autoimmune type (type A gastritis).

Adult↗
PubMed1997

Prevalence and pattern of Helicobacter pylori gastritis in the gastric cardia.

OBJECTIVES: Helicobacter pylori has a predilection for antral colonization. Local acid production is the major determinant of colonization. Because production is low in the antrum and cardia, H. pylori should also colonize the cardia. We therefore investigated the histologic pattern of gastritis and the prevalence of H. pylori in the cardia compared with the antrum and corpus. METHODS: From 135 H. pylori-infected patients with gastritis, ulcer disease, or reflux esophagitis, biopsies were obtained from the antrum, corpus, and cardia. The prevalence, topography, and histologic parameters of gastritis were examined. RESULTS: All 135 patients had active antral H. pylori gastritis: in the cardia, 132 of these patients (97.7%) showed active gastritis, and 124 patients (91.9%) had H. pylori visible on staining. Gastritis of the cardia in most patients resembled antral gastritis, but the density of bacteria and the inflammatory responses were less marked. The most striking finding in the cardia of patients with gastroesophageal reflux was a lower density of bacteria compared with antrum and corpus. Intestinal metaplasia was found in 32 patients in antral mucosa (23.7%) versus 28 patients in the cardia (20.7%), versus 11 patients in the corpus (8.1%), and was multifocal in 17 patients (12.6%). CONCLUSIONS: H. pylori gastritis commonly involves the cardia. The histologic density of the bacteria and inflammatory responses are lower than in the antrum. Intestinal metaplasia in the cardia is a common finding in H. pylori gastritis. The cause of the lower bacterial density in the cardia of patients with reflux esophagitis needs further investigation.

Atrophy↗
PubMed1996

[Epidemiology and pathogenesis of Helicobacter pylori infection].

In 1982 a spiral gram-negative bacterium was first cultured from human gastric mucosa. Helicobacter pylori causes chronic active gastritis, which is the most common chronic infectious disease worldwide. The fact that this bacterial infection is furthermore linked to the majority of all duodenal and gastric ulcers is now commonly accepted after initial scepticism. Some fundamentals of this infectious disease like the extrahuman reservoir of pathogens and the mode of transmission are only partially understood. Some of the bacterial virulence factors allowing mucosal colonization and inflammation have been described. So are some details in the bacterial interaction with the host's immune system. The specific feature of this infection is the inability of the immune system to eliminate H. pylori. Finally no immunity but lifelong chronic infection results. The question, why some individuals infected will have merely gastritis, while others will suffer from peptic ulcer disease, or even gastric carcinoma cannot be answered sufficiently by now. Environmental factors may play a role as well as varying pathogenicity of bacterial strains. Furthermore the age at which infection was acquired and genetic differences in the host's susceptibility to disease are of importance.

Adult↗
PubMed1996

A risk-benefit assessment of drugs used in the eradication of Helicobacter pylori infection.

Helicobacter pylori is the cause of chronic active gastritis and predisposes to peptic ulcer disease (PUD). Furthermore, H. pylori is linked to the pathogenesis of gastric lymphoma and gastric cancer. However, treatment of this infection has proven difficult. In the last decade, many antimicrobial compounds have been studied extensively as monotherapy as well as in combination with bismuth or acid-suppressive drugs. The individual drugs and the most important eradication regimens are discussed with special regard to their risks. In the past, highly complex multidrug regimens, fear of adverse effects and frequent eradication failures have hampered the broad acceptance of H. pylori-eradication therapies. Recently, new 1-week, low-dose combination regimens of 2 antibacterials with a proton pump inhibitor have consistently achieved eradication rates of 90% and more with an acceptably low rate of adverse effects. One week's standard triple therapy [tripotassium dicitrato bismuthate (or bismuth salicylate plus metronidazole plus tetracycline or amoxicillin) has been shown to be highly effective and tolerated better in combination with a proton pump inhibitor. This regimen is, however, more complex and has more adverse effects. Therefore, it is not recommended as first-line therapy. Equipped with these therapies physicians can now be strongly encouraged to use H. pylori eradication as the therapy of choice for patients with PUD and even extend this treatment to other H. pylori-associated disease conditions.

Amoxicillin↗
PubMed1995

Endoscopic polypectomy and management of colorectal adenomas with invasive carcinoma.

BACKGROUND AND STUDY AIMS: Invasive carcinoma is found at histology in 2-5% of colorectal polyps removed under flexible endoscopy. The aim of this study was to confirm that histologically complete endoscopic polypectomy under favorable low-risk conditions is sufficient therapy for pT1 carcinoma, while tumors at or close to the margin of the polypectomy, and histological high-risk criteria, require surgical resection with lymphadenectomy. PATIENTS AND METHODS: Eighty-six patients with 87 pT1 carcinomas underwent polypectomy within a twelve-and-a-half-year period. Further treatment prospectively followed the above guidelines. The follow-up was documented. RESULTS: A local tumor residue was found in 5 of 34 patients who had undergone surgical resection for doubtful or incomplete polypectomy. Two patients were found to have nodal disease in the surgical specimen, only one of them harboring a high-risk carcinoma. Two further patients with high-risk carcinomas had tumor progression, despite postpolypectomy resections without local tumor residue or lymph-node infiltration, and died. One patient had a local tumor recurrence on follow-up endoscopy eight weeks after doubtfully complete polypectomy. He underwent resection, and had no further recurrence. No further manifestations of invasive carcinoma occurred after complete polypectomy of 42 patients with low-risk carcinomas. CONCLUSIONS: This study supports the view that complete endoscopic polypectomy is an adequate therapy for low-risk carcinoma: A modification of the follow-up regimen, with less frequent endoscopic controls, is justified.

Adenoma↗
PubMed1993

[Benign chondroma of the pancreas].

Fragments of a puncture cylinder were obtained from a pancreas tumour, using the ultrasound-guided fine-needle puncture. The tumour appears as an echo-poor, homogeneous structure suggesting good delineation against the adjoining tissue. Histological examination of the punch cylinder revealed a chondroma of the pancreas. Clinical and clinical pathology examinations (lipase, alpha-amylase, glucose, CEA, CA 19-9 in serum) were inconspicuous. Chondroma of the pancreas does not require specific treatment.

Aged↗