Biomedical subjects

P Sipponen

Publications and source records attributed to P Sipponen.

At least 73 records · Page 4Linked to original sources

PubMed1999

Evaluation of gastric biopsies for neoplasia: differences between Japanese and Western pathologists.

Cited variations in the evaluation of gastric endoscopic biopsies for neoplasms between pathologists in Japan and those in the United States and Europe (the West) may have stemmed from several causes. The five-tiered group classification of the Japanese Research Society for Gastric Cancer (JRSGC) for interpretation of biopsies is not used in the West. Some differences may also exist in the morphologic criteria to reach a diagnosis of dysplasia or carcinoma. The goals of this study were to test the Western and Japanese classifications of gastric dysplasia and adenocarcinoma and to assess the differences between four Japanese and seven Western pathologists. One hundred biopsies, 20 from each of the five categories of the JRSGC scheme as determined by one observer, were collected. The Japanese observers used the JRSGC system, expressed in Roman numerals, whereas Western pathologists used a five- or six-tiered scheme expressed in diagnostic terms. Pairwise agreement was evaluated using k statistics within both groups. Consensus diagnosis on each biopsy was accepted as the opinion of the majority. The sensitivity and specificity of each reviewer for a certain diagnosis were also assessed. The intragroup agreements were moderate for both the Japanese (mean k = 0.663) and the Westerners (mean k = 0.652). The pairwise agreements between Japanese and Western observers were low (mean k = 0.542). Overall, the sensitivity was low for all Japanese observers for the diagnosis of dysplasia (38.7% vs 92.5%), and the sensitivity for the diagnosis of adenocarcinoma was high in both groups but higher among the Japanese observers (93.9% and 85.2%, respectively). Overall, the Japanese-Western interobserver agreement was moderate. The JRSCG scheme did not translate into higher interobserver agreement among Japanese observers. The sensitivity for the diagnosis of gastric adenocarcinoma was high for both groups, but the specificity was low among the Japanese. The cause seemed to be centered around the diagnosis of dysplasia in the Western system, which was a lesion frequently interpreted as carcinoma in Japan because of the different definitions of carcinoma in each system. Such a discrepancy might be important because it may explain some of the differences in the prevalence and prognosis of early gastric cancer between Japan and the West. An international effort is needed to harmonize morphologic criteria and analyze whether therapeutic consequences may stem from such discrepancies.

Biopsy↗

PubMed1999

Omeprazole, amoxycillin and metronidazole for the cure of Helicobacter pylori infection.

OBJECTIVE: In two studies, different regimens of omeprazole-amoxycillin-metronidazole were assessed for the eradication of Helicobacter pylori. DESIGN: Randomized, international, multicentre studies with parallel groups. SETTING: The studies were performed at centres in Canada, Czech Republic, France, Germany, Hungary, Sweden and UK. PARTICIPANTS AND INTERVENTIONS: H. pylori-positive patients with duodenal ulcer disease (active or in remission) were randomized to 7-day treatment with: omeprazole 40 mg once daily, amoxycillin 500 mg three times daily and metronidazole 400 mg three times daily (OAMtid; n = 242); omeprazole 20 mg twice daily, amoxycillin 1000 mg twice daily and metronidazole 800 mg twice daily (OAM800; n = 247); or omeprazole 20 mg twice daily, amoxycillin 1000 mg twice daily and metronidazole 400 mg twice daily (OAM400; n = 127). MAIN OUTCOME MEASURES: Eradication of H. pylori. RESULTS: Intention-to-treat analysis revealed H. pylori eradication rates of 76% (184/242) with OAMtid, 80% (198/247) with OAM800, and 76% (97/127) with OAM400. There was considerable variation in the levels of primary resistance to metronidazole in different countries. The overall eradication rate in patients infected with metronidazole-sensitive H. pylori strains was 85% (313/370), compared with 60% (56/94) in patients harbouring metronidazole-resistant strains (P<0.001). All regimens were generally well tolerated, with mild adverse events occurring in 4-26% of patients (mainly diarrhoea, reversible increase in liver enzymes and headache). CONCLUSION: The OAM combination is effective in curing H. pylori infection. Primary metronidazole resistance may reduce its effectiveness, but an increased daily dosing of metronidazole may partly overcome this problem.

Amoxicillin↗

PubMed1999

Gastric cellular turnover and the development of atrophy after 31 years of follow-up: a case-control study.

OBJECTIVE: Why only some patients colonized with Helicobacter pylori (H. pylori) develop atrophy, a preneoplastic change, is not known. Because gastric mucosal mass is dependent upon a balance between epithelial proliferation and turnover, we hypothesized that atrophy may develop due to increased apoptosis relative to proliferation. METHODS: Gastric epithelial apoptosis was measured by terminal deoxyuridine nucleotide nick end labeling (TUNEL) assay and proliferation by Ki-67 immunohistochemistry in gastric corpus biopsies in a unique cohort of patients followed for 31 yr (1952-1983). Sixteen patients who developed atrophy over this time were selected (cases), with two matched controls, who did not develop atrophy, for each. Apoptosis and proliferation were measured in the corpus biopsies taken in 1952. RESULTS: Cases (N = 16) and controls (N = 32) were well matched for age, sex, initial histology, and severity of H. pylori infection. In the initial (1952) biopsies, 4.3 +/- 1.7 cells (mean +/- SEM) per gland were Ki-67-positive in the cases, compared with 2.1 +/- 0.4 in controls (p = 0.48). 9.2 +/- 2.3 cells per gland were terminal deoxyuridine nucleotide nick end labeling-positive in cases, compared with 6.3 +/- 0.8 in controls (p = 0.29). Proliferation to apoptosis ratios were similar in both groups (cases, 0.38 +/- 0.16; controls 0.39 +/- 0.08, p = 0.37). CONCLUSIONS: Patients who later developed atrophy, initially had mildly (but not statistically significant) increased gastric epithelial cell proliferation and apoptosis, compared with those patients who did not develop atrophy, suggesting increased cellular turnover in the atrophy group. However, in these patients with gastritis, the ratio of apoptosis to proliferation was not a determinant of risk for development of atrophy decades later.

Adolescent↗

PubMed1999

Chronic inflammation at the gastroesophageal junction (carditis) appears to be a specific finding related to Helicobacter pylori infection and gastroesophageal reflux disease. The Central Finland Endoscopy Study Group.

OBJECTIVE: The clinical significance of chronic inflammation at the gastroesophageal junction (carditis) is unknown: it may be associated with Helicobacter pylori (H. pylori) gastritis or with gastroesophageal reflux disease (GERD). We aimed to examine the association between carditis and H. pylori gastritis and endoscopic erosive esophagitis. METHODS: One thousand and fifty-three patients undergoing gastroscopy were enrolled in the study. Biopsy specimens were obtained from gastric antrum and corpus, immediately distal to normal-appearing squamocolumnar junction and distal esophagus. RESULTS: Chronic inflammation at the gastroesophageal junctional mucosa (carditis) was detected in 790 (75%) of 1053 patients. The male:female ratio of the carditis group was 1:1.5 and of the noncarditis group 1:1.6 (p = 0.6). The mean age of the carditis group was 58.7 yr (95% confidence interval [CI], 57.6-59.9) and of the noncarditis group, 52.6 yr (95% CI, 50.7-54.6, p < 0.001). Of the carditis group (N = 790), 549 (69%) had chronic gastritis (70% H. pylori positive) and 241 (31%) had normal gastric histology. In multivariate analyses, the only risk factor for carditis in subjects with chronic gastritis was H. pylori infection (odds ratio [OR], 2.9; 95% CI, 1.6-5.0), whereas the independent risk factor for carditis in subjects with histologically normal stomach was endoscopic erosive esophagitis (OR, 1.8; 95% CI, 1.1-3.1). The prevalence of complete intestinal metaplasia (IM) in the gastric cardia mucosa was 7% in the noncarditis group, 19% (p < 0.001) in the carditis group with chronic gastritis, and 10% (p = 0.3) in the carditis group with normal stomach. The respective prevalences of incomplete IM were 3%, 12% (p < 0.001), and 12% (p < 0.001). Among carditis patients with normal stomach histologically (N = 241), those with complete and/or incomplete IM (N = 49) were older than those with carditis only (63.6 yr [95% CI, 59.9-67.2] vs 51.4 yr [95% CI, 48.9-53.9]; p < 0.001). CONCLUSIONS: Two dissimilar types of chronic inflammation of the gastric cardia mucosa seem to occur, one existing in conjunction with chronic H. pylori gastritis and the other with normal stomach and erosive GERD. Most cases of chronic gastric cardia inflammation and intestinal metaplasia are detected in patients with chronic H. pylori gastritis.

Adult↗

PubMed1999

Specialized columnar epithelium of the esophagogastric junction: prevalence and associations. The Central Finland Endoscopy Study Group.

OBJECTIVES: In Barrett's esophagus (BE) normal squamous esophageal epithelium is replaced by specialized columnar epithelium (SCE). BE is related to gastroesophageal reflux disease (GERD) and is a risk factor for esophageal adenocarcinoma. SCE is detected also at normal-appearing esophagogastric junction without BE (junctional SCE). The relationships between junctional SCE, GERD, and cardia adenocarcinoma are obscure and controversial. The aims of the present study were to investigate the prevalence and demographics of junctional SCE and to compare these figures with those reported for BE, and esophageal and cardia adenocarcinoma. A further aim was to examine the association between junctional SCE and GERD, Helicobacter pylori infection, and gastritis. METHODS: One thousand one hundred-nineteen consecutive dyspeptic patients underwent gastroscopy and were enrolled into the study. RESULTS: Junctional SCE was detected in 110 patients (10%). The age-specific prevalence of junctional SCE increased with age. The male:female ratio was 1:1.1. In multivariate analysis, junctional SCE was independently and positively related to endoscopic erosive esophagitis (odds ratio [OR], 1.8; 95% confidence interval [CI], 1.1-3.1), cardia inflammation (carditis) (OR, 3.1; 95% CI, 1.4-6.8), and age (OR, 1.4 per decade; 95% CI, 1.2-1.6), but not to corpus H. pylori infection (OR, 1.4; 95% CI, 0.7-2.8), antral (OR, 1.0; 95% CI, 0.5-2.1) or corpus (OR, 0.8; 95% CI, 0.4-1.8) gastritis, or intestinal metaplasia of the antral mucosa in stomach (OR, 1.2; 95% CI, 0.7-2.1). In univariate analysis, junctional SCE was, however, significantly more common in patients with antral-predominant atrophic gastritis (20%), compared with those with normal gastric histology (8%, p < 0.001). CONCLUSIONS: Junctional SCE is age related and may therefore be an acquired lesion. It is associated with cardia inflammation and endoscopic erosive esophagitis, but not with H. pylori infection or gastric intestinal metaplasia. Unlike BE and cardia cancer, junctional SCE occurs with similar frequency in men and women.

Age Factors↗

PubMed1999

Complete and incomplete intestinal metaplasia at the oesophagogastric junction: prevalences and associations with endoscopic erosive oesophagitis and gastritis.

BACKGROUND/AIMS: Intestinal metaplasia (IM) is a common finding at the oesophagogastric junction, but the aetiopathogenesis of the different IM subtypes-that is, incomplete IM (specialised columnar epithelium, SCE) and complete IM- and their associations with gastro-oesophageal reflux disease and Helicobacter pylori gastritis are unclear. METHODS: 1058 consecutive dyspeptic patients undergoing gastroscopy were enrolled. The gastric, oesophagogastric junctional, and oesophageal biopsy specimens obtained were stained with haematoxylin and eosin, alcian blue (pH 2.5)-periodic acid Schiff, and modified Giemsa. RESULTS: Complete junctional IM was detected in 196 (19%) of the 1058 subjects, and in 134 (13%) was the sole IM subtype. Incomplete junctional IM (SCE) was detected in 101 (10%) subjects, of whom 62 (61%) also had the complete IM subtype. Of patients with normal gastric histology (n = 426), 6% had complete IM and 7% junctional SCE. The prevalence of both types of IM increased with age in patients with either normal gastric histology or chronic gastritis (n = 611). Epithelial dysplasia was not detected in any patients with junctional IM. In multivariate analysis, independent risk factors for incomplete junctional IM were age (odds ratio (OR) 1.3 per decade, 95% confidence interval (CI) 1.2 to 1.6), endoscopic erosive oesophagitis (OR 1.9, 95% CI 1.1 to 3.2), and chronic cardia inflammation (OR 2.9, 95% CI 1.3 to 6.2), but not gastric H pylori infection (OR 1.0, 95% CI 0.6 to 1.7). In univariate analysis, junctional incomplete IM was not associated with cardia H pylori infection. Independent risk factors for "pure" complete junctional IM (n = 134) were age (OR 1.2 per decade, 95% CI 1.0 to 1.4), antral predominant non-atrophic gastritis (OR 2.6, 95% CI 1.3 to 5.2), antral predominant atrophic gastritis (OR 2.1, 95% CI 1.1 to 5.2), and multifocal atrophic gastritis (OR 7.1, 95% CI 2.5 to 19.8). In univariate analysis, junctional complete IM was strongly associated with chronic cardia inflammation and cardia H pylori infection (p<0. 001). CONCLUSIONS: Both complete and incomplete junctional IM are independent acquired lesions that increase in prevalence with age. Although IM subtypes often occur simultaneously, they show remarkable differences in their associations with gastritis and erosive oesophagitis: junctional complete IM is a manifestation of multifocal atrophic gastritis, while the incomplete form (SCE) may result from carditis and gastro-oesophageal reflux disease. The frequency of dysplasia in intestinal metaplasia at the oesophagogastric junction appears to be low.

Aged↗

PubMed1998

Differences in the diagnostic criteria used by Japanese and Western pathologists to diagnose colorectal carcinoma.

BACKGROUND: In view of the many studies of early stage colorectal carcinoma from Japan, it is essential to know whether the criteria for the histologic diagnosis of colorectal carcinoma are similar in Japan and Western countries. METHODS: Eight expert pathologists from Japan (4), North America (2), and Europe (2) individually reviewed microscope slides of 20 colorectal lesions from Japanese patients who had undergone endoscopic mucosal resection or surgery because early stage carcinoma and/or adenoma was suspected. The pathologists indicated the pathologic findings on which they based each diagnosis. RESULTS: For 11 slides that showed adenoma according to the Western pathologists with low grade dysplasia according to at least half of them, the Japanese diagnosed definite carcinoma with or without adenoma in 4 cases and adenoma in 5, and in 2 cases they were equally divided between a diagnosis of adenoma and carcinoma. For five slides showing adenoma with high grade dysplasia according to the Western pathologists, the Japanese diagnosed definite carcinoma with adenoma in three cases and adenoma in one, and in one case they were equally divided between a diagnosis of adenoma and carcinoma. For one case in which the Western pathologists were equally divided between a diagnosis of carcinoma and adenoma with high grade dysplasia, all the Japanese pathologists diagnosed definite carcinoma with or without adenoma. Three slides showed definite carcinoma with or without adenoma, according to both the Western and the Japanese pathologists. The presence of invasion was the most important diagnostic criterion of colorectal carcinoma for the Western pathologists, whereas for the Japanese the nuclear features and glandular structures were more important. CONCLUSIONS: In Japan, colorectal carcinoma is diagnosed on the basis of nuclear and structural criteria, even in cases considered by Western pathologists to be noninvasive lesions with low grade dysplasia. This diagnostic practice may contribute to the relatively high incidence of early stage colorectal carcinoma reported in Japan as compared with Western countries.

Adenoma↗

PubMed1998

Follow-up of Helicobacter pylori positive gastritis and argyrophil cells pattern during the natural course of gastric ulcer.

BACKGROUND: A follow-up of argyrophil cell hyperplasia in Helicobacter pylori-positive corpus gastritis in gastric ulcer patients during the natural course of ulcer disease. METHODS: Endoscopic biopsies (4 specimens) were obtained step-wise from the posterior wall of the corpus mucosa in 55 gastric ulcer (GU) patients. The natural course of GU was followed up in 38 patients during more than 10 years (maximum 19 years), and altogether 115 endoscopic examinations were made: 20 patients were re-examined once, 14 twice, and 4 three times. A total of 364 biopsies from 307 biopsy sites were stained by Grimelius' silver, hematoxylin-eosin, and Giemsa method for the analysis of the argyrophil endocrine cells, chronic gastritis, and H. pylori colonization, respectively, according to the Sydney System. RESULTS: Of 307 biopsy sites, 153 (50%) showed some grade of ACH. Focal (linear/micronodular) hyperplasia was found in 118 (77%) of biopsy sites; it was detected in 78 (66%) cases of atrophic corpus mucosa, but was present in only 14 (12%) cases of gastritis without atrophy or in the normal mucosa. In the follow-up patients, ACH evolved in 17 and progressed in 6 cases, and a simultaneous development of atrophic corpus gastritis was found in 20 cases. CONCLUSION: This study demonstrates that ACH evolves during the natural course of GU, alongside the development of chronic atrophic gastritis.

Adult↗

PubMed1998

The risk of gastric carcinoma and carcinoid tumours in patients with pernicious anaemia. A prospective follow-up study.

BACKGROUND: This endoscopic follow-up study was undertaken to evaluate the risk of gastric cancer (GC) and carcinoids in patients with pernicious anaemia (PA) and to analyse whether early detection of GC could be provided by regular endoscopic follow-up. METHODS: Screening gastroscopy was performed in 71 patients with pernicious anaemia, and thereafter they were followed up with gastroscopies at 3-year intervals for a mean time of 5.8 years. Standardized incidence ratios (SIR) were calculated, the expected number being based on incidence rates in the whole Finnish population. RESULTS: Two GCs were found during the follow-up period; one of these patients was asymptomatic and the other had abdominal symptoms. The SIR was 5.0 (95% confidence interval, 0.6-18). Eight carcinoids were detected, and all but one were removed endoscopically, and no metastases were found. The patients who had carcinoid tumours were younger at the diagnosis of PA than those who did not develop carcinoids (mean, 40 versus 55 years). Additionally, the patients with carcinoids had longer duration of PA (mean, 11 versus 5 years). CONCLUSIONS: During the follow-up period the risk of GC was increased. The risk of gastric carcinoids seems to be very high in patients with pernicious anaemia when compared with a normal population, but they are mostly relatively benign tumours. Regular routine gastroscopic follow-up is not indicated in patients with pernicious anaemia.

Adult↗

PubMed1998

Gastric cancer and premalignant lesions in atrophic gastritis: a controlled trial on the effect of supplementation with alpha-tocopherol and beta-carotene. The Helsinki Gastritis Study Group.

BACKGROUND: Vitamin E and beta-carotene are considered to decrease the risk of gastric cancer both in humans and in laboratory animals. We studied the effect of dietary supplementation with alpha-tocopherol and beta-carotene on the end-of-trial prevalence of premalignant and malignant lesions of the stomach in older men with atrophic gastritis. METHODS: The study was carried out within the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (ATBC study) in Finland, in which 29,133 male smokers aged 50-69 years were randomly assigned to receive daily 50 mg alpha-tocopherol, 20 mg beta-carotene, both of these agents, or placebo, for 5-8 years. Serum pepsinogen was determined at base line and after 3 years' supplementation to find men with atrophic gastritis. A low serum pepsinogen I level, indicating atrophic gastritis of the corpus area of the stomach, was found in 2132 men. These men were invited to have upper gastrointestinal endoscopy (gastroscopy), which was performed on 1344 subjects after a median supplementation time of 5.1 years. RESULTS: Neoplastic alterations were found in 63 of the men (4.7%): 42 with definite dysplasias of low grade (moderate dysplasia), 7 with definite dysplasias of high grade (severe dysplasia), 11 with carcinomas (of which 7 were 'early' cancers), and 3 with carcinoid tumors. Neither alpha-tocopherol (relative risk, 0.98; 95% confidence interval, 0.57-1.69) nor beta-carotene (relative risk, 1.13; 95% confidence interval, 0.65-1.95) supplementation had any association with end-of-trial prevalence of gastric neoplasias after adjustment for other possible risk factors. The effect was not modified by base-line serum level or dietary intake of vitamins, prevalence of Helicobacter pylori infection, or other covariates. CONCLUSIONS: We thus conclude that supplementation with alpha-tocopherol or beta-carotene for 5 years has no major impact on the occurrence of neoplastic changes of the stomach in older male smokers with atrophic gastritis.

Aged↗

PubMed1998

Review article: Pathogenesis of the transformation from gastritis to malignancy.

Helicobacter pylori acquisition is the main cause of chronic gastritis in humans. In up to half of the infected subjects, chronic gastritis progresses to atrophic gastritis and intestinal metaplasia. During this course, various mechanisms are triggered that may contribute to the pathogenesis of gastric cancer. Such mechanisms include the inflammation-related cascades of cytokine and free radical reactions, up- and downregulation of growth factors and their receptors, and the atrophy-related impairment of acid output and intraluminal acidity. An array of other factors may also have become significant including overgrowth of bacteria other than H. pylori in the hypochlorhydric or achlorhydric stomach, a high dietary consumption of salt, nitrate, or nitrite, smoking, deficiency of vitamins or micronutrients, influence of sex hormones, or an inherited liability of the dividing epithelial cells to gene errors. These factors may vary in effect between populations and individuals but, if active, may affect the cell genome which may further influence the course and progression of chronic gastritis, and can finally result in overt gastric neoplasia. The molecular biology of gastric cancer has revealed a spectrum of gene errors which vary in type and extent between different histological types of cancer, and between individual cases. There now is evidence that the intestinal metaplasia or the gastric epithelium in atrophic gastritis reveal signs of abnormal expression of various regulatory genes well before the appearance of gastric neoplasia. It is possible that the mechanisms leading to mutation of the genes in epithelial cells are triggered very early in the H. pylori gastritis cascade, and that atrophic gastritis and intestinal metaplasia result from these processes.

Animals↗

PubMed1998

Evaluation of Pyloriset Screen, a rapid whole-blood diagnostic test for Helicobacter pylori infection.

Helicobacter pylori infection can be detected by several invasive tests based on gastroscopy and by noninvasive methods such as serologic assays. Noninvasive tests can be used not only in addition to invasive tests but also by themselves to screen for H. pylori infection in patients who are not in urgent need of endoscopy. Lately, rapid qualitative serologic tests have been developed. In the present study, the accuracy of a novel rapid whole-blood test, Pyloriset Screen, detecting immunoglobulin G (IgG) and IgA antibodies against H. pylori was evaluated. A total of 207 consecutive adult outpatients referred for upper endoscopy were enrolled. Gastric biopsy specimens were taken from the antrum and corpus for histologic examination and rapid urease testing. Cultures were available for 113 patients. Serum samples collected from all patients were tested for H. pylori antibodies by two enzyme immunoassays (EIAs) (Pyloriset EIA and an in-house EIA), a rapid latex agglutination test (Pyloriset Dry), and Pyloriset Screen. Patients were considered H. pylori positive if helicobacters were seen on histologic examination (77 patients) or, if in combination with histologically verified (although helicobacter-negative) gastritis, their IgG antibody titers were elevated in the two EIAs (five patients). The Pyloriset Screen test had a sensitivity of 95%, a specificity of 94%, a positive predictive value of 91%, and a negative predictive value of 97%. Among 63 patients under the age of 45 years, the Pyloriset Screen test did not miss a single H. pylori diagnosis, and only 1 patient had a false-positive result. Pyloriset Screen could be used reliably to screen for H. pylori infection.

Adult↗

PubMed1998

Positive result by serology indicates active Helicobacter pylori infection in patients with atrophic gastritis.

Patients with atrophic corpus gastritis and elevated Helicobacter pylori antibody titers but 13C-urea breath test (13C-UBT) and histology results negative for H. pylori were randomized into eradication therapy or follow-up only. Antibody levels decreased significantly in six out of seven patients in the eradication group, while in the follow-up group, the titers declined in only one out of eight patients. In patients with atrophic corpus gastritis, positive serology results may indicate an ongoing infection in spite of negative 13C-UBT and histology results.

Aged↗

PubMed1998

Natural course of Helicobacter pylori gastric infection.

Helicobacter pylori acquisition induces chronic gastritis that affects antrum, corpus or both. In approximately half of the cases, Helicobacter pylori gastritis slowly (years, decades) develops to atrophic gastritis, thereby resulting in severe abnormalities in the function of the stomach. In humans, the appearance of intestinal metaplasia associates with atrophic gastritis (loss of normal antral and/or oxyntic glands), and intestinal metaplasia linearly increases in grade and extent with increasing age and progression of atrophy. Several mechanisms may play in role in the development of atrophic gastritis and intestinal metaplasia; i.e., including genetic liability of the host to destruction of cells and glands, specific cytotoxic strains of Helicobacter pylori, environmental factors other than the bacterial ones, and some functional properties of the stomach, such as output of acid and intragastric acidity. Atrophic and metaplastic alterations may also result from genotoxic and mutagenic injuries which are triggered by the inflammation, or are exogenous.

Animals↗

PubMed1997

Differences in diagnostic criteria for gastric carcinoma between Japanese and western pathologists.

BACKGROUND: There have been many studies on gastric carcinoma in populations with contrasting cancer risks. We aimed to find out whether the criteria for the histological diagnosis of early gastric carcinoma were comparable in Western countries and Japan. METHODS: Eight pathologists from Japan, North America, and Europe individually reviewed 35 microscope slides: 17 gastric biopsy samples and 18 endoscopic mucosal resections taken from 17 Japanese patients with lesions ranging from early gastric cancer to adenoma, dysplasia, and reactive atypia. The pathologists were given a list of pathological criteria and a form on which they were asked to indicate the criteria on which they based each diagnosis. FINDINGS: For seven slides most Western pathologists diagnosed low-grade adenoma/dysplasia, whereas the Japanese diagnosed definite carcinoma in four slides, suspected carcinoma in one, and adenoma in only two. Of 12 slides with high-grade adenoma/dysplasia according to most Western pathologists the Japanese gave the diagnosis of definite carcinoma in 11 and suspected in one. Of six slides showing high-grade adenoma/dysplasia with suspected carcinoma according to most Western pathologists the Japanese diagnosed definite carcinoma in all. There were no major differences in the diagnoses of three slides showing reactive epithelium and seven slides with clearly invasive carcinoma. When the opinion of the majority of the pathologists was taken as the final diagnosis there was agreement between Western and japanese in 11 of the 35 slides (kappa coefficient 0.15 [95% CI 0.01-0.29]). Presence of invasion was the most important diagnostic criterion for most Western pathologists whereas for the Japanese nuclear features and glandular structures were more important. INTERPRETATION: In Japan, gastric carcinoma is diagnosed on nuclear and structural criteria even when invasion is absent according to the Western viewpoint. This diagnostic practice results in almost no discrepancy between the diagnosis of a superficial biopsy sample and that of the final resection specimen. This may also contribute to the relatively high incidence and good prognosis of gastric carcinoma in Japan when compared with Western countries.

Adenoma↗

PubMed1997

Expression of cyclooxygenase-2 in human gastric carcinoma.

Epidemiological studies suggest that the use of aspirin decreases the incidence of and mortality from gastrointestinal cancers. The best known target of aspirin and other nonsteroidal anti-inflammatory drugs is cyclooxygenase (Cox), the rate-limiting enzyme in the conversion of arachidonic acid to prostanoids. Two Cox genes have been cloned, of which Cox-2 is an inducible immediate-early gene. It is still unknown how nonsteroidal anti-inflammatory drugs act as chemopreventive agents, but they may target Cox-2. Cox-2 mRNA and protein were recently found to be expressed in human colon carcinoma. We have now studied the expression of Cox-2 in human gastric adenocarcinoma tissues which contained significantly higher levels of Cox-2 mRNA when compared with paired gastric mucosal specimens devoid of cancer cells. In contrast, Cox-1 mRNA levels were not elevated in the carcinoma. However, Cox-2 mRNA was not expressed in mucinous ovarian carcinoma samples as detected by Northern blot hybridization. Immunohistological detection of Cox-2 protein showed cytoplasmic staining in the gastric carcinoma cells but not in the surrounding stroma. Some hyperplastic glands showed intense staining, whereas glands of normal morphology were negative. Our data thus suggest that Cox-2 is expressed by human gastric adenocarcinoma.

Adenocarcinoma↗

PubMed1997

Culture of Helicobacter pylori from gastric biopsies transported in biopsy urease test tubes.

Gastric biopsy specimens of 57 consecutively observed dyspeptic patients were studied for the presence of Helicobacter pylori by histological examination, biopsy urease test (BUT) and culture. For culture, biopsy samples were transported in both Stuart media and BUT tubes. All 15 isolates could be cultured from both Stuart and BUT tubes. Thus, if the main reason for culture of Helicobacter pylori is for antimicrobial susceptibility testing, only positive BUT tubes need to be submitted. This would reduce both the expense and the number of biopsies needed.

Adult↗

PubMed1997

Helicobacter pylori gastritis--epidemiology.

The acquisition of Helicobacter pylori is the main cause of chronic gastritis in humans. In Europe, a small proportion (less than 1%) of gastritis cases are caused by H. Heilmannii, and somewhat more (5%) are autoimmune in origin, in which condition H. pylori may not probably play a role. Recent findings on chronic gastritis and H. pylori acquisition in developed countries can be summarized as: (1) H. pylori gastritis is acquired in childhood and adolescence (age less than 20) in more than 50% of cases; (2) the risk and rate of acquisition is highest in early childhood, after which the rate exponentially declines; (3) new infections occur in adulthood but are quite rare (annual incidence 0.4%, on average, in Finland); (4) H. pylori gastritis is a birth cohort-related phenomenon; i.e., different cohorts show a rate and prevalence of H. pylori gastritis that varies between cohorts; (5) the rate and risk of H. pylori infection is high in cohorts born in the beginning of the century, but is much lower in those born later; (6) this decline is due to a decrease in the rate and risk of H. pylori acquisition in childhood in particular. H. pylori gastritis-related complications, such as peptic ulcer diseases and gastric cancer, show epidemiological features similar to H. pylori gastritis. Both peptic ulcer and gastric cancer have declined in incidence over time. Gastric cancer is a birth-cohort phenomenon in the same way as is H. pylori gastritis, and the incidence of gastric cancer shows a positive but exponential relationship with the "birth-cohort-specific" prevalence of gastritis in the general population.

Adolescent↗