Search PubMed⌕ Search

Biomedical subjects

P Sipponen

Publications and source records attributed to P Sipponen.

At least 91 records · Page 5Linked to original sources
PubMed1997

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↗
PubMed1997

Changes in acid secretion over the years. A 30-year longitudinal study.

We studied the effect of aging on gastric acid secretion in 11 physicians who had augmented histamine tests while at medical school in 1962. One of them had a duodenal ulcer at the time. The augmented histamine test was repeated in 1991 and, in addition, upper gastrointestinal endoscopy was done to exclude peptic ulcer and to obtain biopsies for histologic analysis and assessment of Helicobacter pylori status. The mean basal acid output decreased from 7.3 to 1.9 mEq/hr during the 30-year period of follow-up (p < 0.001), and the mean maximum acid output decreased from 29.9 to 20.3 mEq/hr (p < 0.01). The maximum acid output data showed a profound decrease in 4 of the 11 participants, a lesser decrease in 4, and a minimal increase in the remaining 3. Histologic analysis suggested a greater likelihood of atrophic gastritis, H. pylori infection, or both in participants showing a pronounced decrease in acid secretion with aging.

Aging↗
PubMed1997

Frozen-section biopsy in perendoscopic diagnosis of Helicobacter pylori.

BACKGROUND: Our goal was to investigate how reliably Helicobacter pylori infection can be diagnosed from gastric biopsy specimens by frozen-section technique. PATIENTS AND METHODS: The series consisted of 105 consecutive outpatients who underwent diagnostic upper gastrointestinal endoscopy for abdominal complaints at Jorvi Hospital (Espoo, Finland) during the beginning of 1996. Endoscopic biopsies from antrum and corpus were taken for both frozen-section and traditional histology, the latter serving as reference (control) material. In the frozen-section technique, the biopsy specimens were transferred immediately to the pathology laboratory, were prefixed for 30 sec in 10% neutral formalin, were frozen in liquid nitrogen, and were cut into sections with a cryostat. The sections were stained for 10 minutes with 1% toluidine blue. The control biopsy specimens were fixed overnight in 10% neutral formalin and embedded in paraffin, and the sections were stained with the modified Giemsa method. RESULTS: In the diagnosis of H. pylori infection, both the sensitivity and the specificity of the frozen-section technique were 98% compared to the findings in the reference series. One false-negative result occurred among 41 positive cases, and one case erroneously was classified positive among 64 cases that were negative for H. pylori in the ordinary histology. The frozen-section technique slightly underestimated the degree of colonization of the gastric mucosa by H. pylori, compared to the findings in the reference material. In the diagnosis of gastritis (chronic inflammation of any degree), the sensitivity and specificity of frozen sections were 92% and 95%, respectively. In the frozen-section technique, the report of the pathologist of the presence or absence of H. pylori gastritis in biopsy specimens could be given to the gastroenterologist by telephone in approximately 20 minutes. CONCLUSIONS: The frozen-section technique is a reliable and rapid method for the diagnosis of H. pylori and provides possibilities for perendoscopic diagnosis of the infection in the hospitals where the frozen-section service is available.

Adult↗
PubMed1996

The relationships between chronic gastritis and gastric acid secretion.

Helicobacter pylori is the main cause of chronic gastritis in humans. Autoimmune mechanisms and Helicobacter heilmannii infection are other causes, both of which are of minor significance in a worldwide perspective. Atrophic gastritis is a quite common late consequence of H. pylori gastritis and will develop on a multifactorial basis, but not in all infected persons. The evolution of atrophic gastritis is a slow and gradually worsening process leading to subtypes, in which the antrum and corpus are affected to dissimilar extent and degree. The distal part of the stomach is the site where the atrophic sequelae (atrophic gastritis and intestinal metaplasia) of H. pylori infection occur most often. A minority of cases develop corpus-limited, or corpus-predominant atrophic gastritis. Along with the worsening of atrophic gastritis, inflammation and density of colonization of the mucosa by H. pylori tend to decrease in grade. In general, the degree of gastric mucosal inflammation, acute and chronic, is positively related to the degree of colonization of the mucosa by H. pylori. Acid secretion and local acidity are factors which modulate the ecology and density of colonization of H. pylori in the stomach, and may thus also modulate the evolution of chronic gastritis into topographically dissimilar subtypes. Acid secretion varies among individuals, this variation being perhaps caused by hereditary differences in parietal cell mass, or by differences in the sensitivity of parietal cells to hormonal or neural stimuli. It is hypothesized that in genuine hypersecretors, H. pylori colonization and subsequent gastritis with atrophic and metaplastic sequelae may be limited to the antrum, while in hyposecretors gastritis predominates in the corpus. In the latter, atrophic gastritis in the corpus then leads to further impairment of acid output. In these cases, H. pylori infection and gastritis may, finally, heal in the antrum, resulting in hypochlorhydria and atrophic gastritis that is limited to, or predominant in the corpus.

Adolescent↗
PubMed1996

High frequency of helicobacter negative gastritis in patients with Crohn's disease.

The frequency of gastric Crohn's disease has been considered low. This study was undertaken to determine the prevalence of chronic gastritis and Helicobacter pylori infection in patients with Crohn's disease. Oesophagogastroduodenoscopy was performed on 62 consecutive patients suffering from ileocolonic Crohn's disease. Biopsy specimens from the antrum and corpus were processed for both histological and bacteriological examinations. H pylori antibodies of IgG and IgA classes were measured in serum samples by enzyme immunoassay. Six patients (9.7%) were infected with H pylori, as shown by histology, and in five of them the infection was also verified by serology. Twenty one patients (32%) had chronic H pylori negative gastritis (negative by both histology and serology) and one of them also had atrophy in the antrum and corpus. Granulomas were found in four patients. The characteristic appearance of H pylori negative gastritis was focal and mostly mild inflammation resembling the inflammatory changes seen in the gut in Crohn's disease. Patients with H pylori negative chronic gastritis had a significantly more active disease in their gut than those with normal gastric mucosa (p < 0.01). It is concluded that H pylori positive gastritis is rare, while H pylori negative gastritis is relatively common in patients with Crohn's disease. H pylori negative 'Crohn's gastritis' seems to be associated with active Crohn's disease.

Adult↗
PubMed1996

Risk of gastric carcinoma in patients with mucosal dysplasia associated with atrophic gastritis: a follow up study.

AIMS: To assess the risk of gastric carcinoma in patients with histologically verified dysplasia and atrophic gastritis of the stomach. METHODS: One hundred and one patients with mild (n = 84), moderate (n = 14), or severe (n = 3) dysplasia among 359 elderly men who smoked underwent gastroscopy because of low serum pepsinogen. Patients with dysplasia were prospectively followed up for an average of four years with repeated gastroscopies and multiple biopsies. RESULTS: Four of the 84 (4.8%) cases of mild dysplasia had progressed to moderate dysplasia during the follow up. Most of the cases of mild dysplasia had resolved spontaneously. No surgical intervention was required. Three of the 14 (21%) cases of moderate dysplasia had progressed to severe dysplasia, but no carcinomas were observed during follow up. Five moderately dysplastic lesions were removed surgically or endoscopically. In two of these five cases, moderate or severe dysplasia recurred. Two of the three severe dysplasias progressed to carcinoma. CONCLUSIONS: In atrophic gastritis progression of mild and moderate dysplastic lesions seems to be a slow process and is rare in mild dysplasia. However, severe dysplasia is highly predictive of subsequent cancer. It is suggested that a five year follow up interval is sufficient in cases with mild dysplasia and two years in those with moderate dysplasia. Local removal of moderate dysplasia is indicated but does not guarantee that the lesion will not progress. Severe dysplasia requires immediate surgical intervention.

Aged↗
PubMed1996

Prevalence of Helicobacter pylori infection and chronic dyspeptic symptoms among immigrants from developing countries and people born in industrialized countries.

The relationship between Helicobacter pylori infection and chronic dyspepsia is controversial. To determine the effect of H. pylori infection on dyspeptic symptoms, we compared the prevalence of H. pylori infection in immigrants from developing countries and people born in industrialized countries. Upper abdominal symptoms were assessed by a questionnaire and H. pylori infection was determined with a 13C-urea breath test and serology. H. pylori infection was found in 63% of subjects from developing countries and 11% of subjects from industrialized countries. There was no difference in the prevalence of dyspeptic symptoms between the 2 groups. The lack of difference in chronic dyspeptic symptoms between the groups, despite a major difference in the H. pylori prevalence, suggests that H. pylori infection is not a major contributor to chronic dyspepsia.

Adolescent↗
PubMed1996

Helicobacter pylori-negative duodenal and pyloric ulcer: role of NSAIDs.

To investigate the frequency of use of nonsteroidal anti-inflammatory drugs (NSAID) in duodenal or pyloric ulcer patients who do not have Helicobacter pylori gastritis, we retrospectively analyzed the use of these drugs among 16 patients who had an endoscopically diagnosed duodenal or pyloric ulcer but had a histologically normal and noninfected stomach, and compared this frequency of use of NSAIDs with that in three control groups. The 16 patients are a consecutive subgroup (2.3%) from 707 patients who were endoscopically diagnosed as having duodenal or pyloric ulcer in Jorvi Hospital during 1985-1994. In all 16 patients, endoscopical and clinical appearances of the ulcers were seen by the clinician similar to those in ordinary peptic ulcer disease. The ulcers occurred at the same site in the duodenal bulb and pylorus as the ordinary peptic ulcers but tended to bleed more often: endoscopy was done more frequently among the 16 gastritis-negative patients because of ulcer bleeding than among the controls. Thirteen of the 16 patients (81%; CI95: 62-100%) did use NSAIDs. This frequency was higher (p < 0.05) than the corresponding frequency of the use of NSAIDs in any of the three control groups, i.e. (a) H. pylori-positive duodenal or pyloric ulcer patients [16 of 39 (41%)], (b) H. pylori-negative nonulcer patients [11 of 64 (17%)] or (c) H. pylori-positive nonulcer patients [14 of 42 (33%)]. We conclude that the history of use of NSAIDs is more common in duodenal and pyloric ulcer patients who have a normal, noninfected stomach than the history of use of NSAIDs in those in whom the ulcer is associated with H. pylori gastritis.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1996

Rate of Helicobacter pylori acquisition among Finnish adults: a fifteen year follow-up.

BACKGROUND AND METHODS: To investigate the acquisition rate of Helicobacter pylori infection among Finnish adults, we obtained, in 1991, serum samples from 181 subjects who were shown to have histologically normal, noninfected gastric mucosa in 1974-76. RESULTS: During the 15-year follow-up period 12 (6.6%) of the 181 subjects developed H. pylori antibodies (IgG), the overall annual acquisition rate being 0.44%. The acquisition rate correlated somewhat with age. Antibodies developed in 1(4.5%) of the 22 subjects less than 40 years old (in 1991) and in 4 (31%) of 13 subjects who were 70 years old or older. If it is assumed that H. pylori acquisition is a continuous and stable event through the whole life span, and the rate is similar in all birth cohorts, the observed annual acquisition rate of 0.44% or an increase of this rate with age does not explain the current prevalence of chronic gastritis in Finland. Extrapolations of the known and estimated prevalence rates of chronic gastritis in 1974/76 and 1991 indicated rather that the H. pylori acquisition is a birth-cohort-dependent phenomenon and that most of the acquisitions occurred in childhood in every cohort (generation). After being high in childhood (less than 20 years old), the acquisition rate exponentially slowed down with age in all cohorts. CONCLUSIONS: Among adults the acquisition rate of H. pylori infection is low, and the main period of acquisition is childhood. The relationship between the acquisition rate and age is inverse and exponential.

Adult↗
PubMed1996

Long-term course and consequences of Helicobacter pylori gastritis. Results of a 32-year follow-up study.

BACKGROUND: The long-term course of Helicobacter pylori gastritis is not well known because there are few follow-up studies available, and the follow-up time has been short. METHODS: The progression of H. pylori infection and chronic gastritis was retrospectively examined in 102 patients followed up for 32 years. In all patients a blind suction biopsy from the corpus mucosa was taken in 1952, and an endoscopic re-examination with biopsy specimens from the antrum and corpus was performed in 1983. RESULTS: In the first examination 85 patients (83%) were H. pylori-positive as assessed from Giemsa-stained corpus mucosa specimens as compared with 70 H. pylori-positive patients (69%) at the end of the follow-up (1983). Two of the 17 patients who were initially H. pylori-negative became positive in 1983, implying an infection rate of 0.4% per patient-year. On the other hand, 17 of the 85 patients who were initially H. pylori-positive became negative in 1983, representing a disappearance rate of 0.6%. However, the stomach became completely normal in only eight cases, which represents a healing rate of 0.3% per patient-year. All patients with duodenal ulcer disease were H. pylori-positive at the first examination and remained so during the follow-up. In these patients chronic gastritis affected predominantly the antral mucosa, and corpus atrophy did not develop. Parietal cell antibodies appeared during the follow-up in six cases, and five of them were H. pylori-positive at the first examination. In most of these cases gastritis progressed into severe grades of corpus atrophy accompanied by the disappearance of H. pylori infection and normalization of the antral mucosa. CONCLUSIONS: New H. pylori infection and complete healing of infected mucosa may occur in adult life, but this is rare. Duodenal ulcer disease is associated with persistent H. pylori infection and absence of corpus atrophy. The appearance of parietal cell antibodies leads to progression of corpus atrophy and disappearance of H. pylori.

Adult↗
PubMed1996

Gastric inflammation and neutrophil-activating and cytotoxin-producing Helicobacter pylori strains.

BACKGROUND: Some Helicobacter pylori strains activate human neutrophils without opsonins and/or produce vacuolating cytotoxin. METHODS: Human gastric isolates of H. pylori were studied for their ability to nonopsonized induce an oxidative burst in human neutrophils as measured by chemiluminescence and for the production of vacuolating cytotoxin. In all, 80 strains were examined, and the type and grade of inflammation in the gastric biopsy specimens from the antrum and corpus of these patients were assessed in accordance with the Sydney system. RESULTS: CL+ (rapid, strong response in chemiluminescence) strains (p < 0.0001) and Tox+ (cytotoxin-producing) strains (p < 0.0001) were associated with higher acute inflammation scores in gastric ulcer patients. CL+ (p = 0.0002) and Tox+ (p < 0.0001) strains were also associated with higher chronic inflammation scores in gastric ulcer patients. CONCLUSIONS: CL+ and Tox+ strains seem to cause more severe inflammation in the gastric mucosa during H. pylori infection.

Cytotoxins↗
PubMed1996

Helicobacter pylori infection in young patients with gastric carcinoma.

BACKGROUND: Helicobacter pylori infection has been linked with chronic atrophic gastritis and gastric cancer. This case-control study was performed to investigate a possible relationship between H. pylori infection and gastric cancer in young age groups. METHODS: Gastrectomy and/or biopsy samples were collected from 50 consecutive patients 45 years old or younger treated between 1980 and 1994 for noncardiac gastric cancer. The control group consisted of age- and sex-matched dyspeptic patients. The presence of H. pylori infection was assessed by modified Giemsa staining and immunostaining, using antibody against H. pylori. RESULTS: H. pylori was found in 36 (72%; 95% confidence interval 60-84%) cancer patients and in 22 (43%; 30-58%) control patients (p = 0.0023, chi-square test). The odds ratio was 3.27 (1.42-7.52). Nonatrophic (superficial) gastritis was present in 30 (60%) cancer patients and in 19 (38%) (p = 0.028, chi-square test) control cases. CONCLUSIONS: The results of the present study support the hypothesis that H. pylori is a risk factor for gastric cancer also in young age groups and in patients with a diffuse type of gastric cancer.

Adult↗
PubMed1996

H. pylori corpus gastritis--relation to acid output.

H. pylori acquisition is the main cause of chronic gastritis in humans. After acquisition, non-atrophic gastritis appears which develops with time into atrophic gastritis in approximately one third of infected subjects. Gastritis may affect the gastric antrum, both antrum and corpus or, occasionally, corpus alone. Acid secretion and local acidity are factors which are considered to influence the ecology and flourishing of H. pylori infection in the stomach, and can, therefore, also modulate the evolution of gastritis into topographically dissimilar subtypes. In the present study, we analysed whether there occurs an association between the intensity of chronic gastritis (inflammation) of the corpus mucosa and the pentagastrin stimulated peak acid output (PAO) in 94 subjects who had an H. pylori positive, non-atrophic gastritis. It appeared that the mean PAO was significantly higher in subjects who had mild or no chronic corpus gastritis than in those who had severe corpus gastritis. The prevalence of subjects with mild or no gastritis was highest among those with a high PAO ( > or = 30 mmol/hr) and lowest among those with a low PAO ( < 30 mml/hr). Furthermore, the mean score of chronic corpus gastritis was significantly (P < 0.01) lower in those with PAO < or = 19 mmol/hr than among those with PAO > or = 40 mmol/hr. We conclude that the intensity of chronic inflammation (gastritis) in the corpus mucosa is inversely related to PAO. This supports the hypothesis that acid output may affect the course of H. pylori gastritis and can modulate the topographic distribution of gastritis in the stomach.

Female↗
PubMed1996

Alpha 6 beta 4 integrin and newly deposited laminin-1 and laminin-5 form the adhesion mechanism of gastric carcinoma. Continuous expression of laminins but not that of collagen VII is preserved in invasive parts of the carcinomas: implications for acquisition of the invading phenotype.

We studied the expression and distribution of different laminin chains, the alpha 6 beta 4 integrin and type VII collagen, i.e., components of the epithelial adhesion complex, in gastric carcinomas and in suggested preneoplastic stages of this malignancy. Intestinal-type gastric carcinomas showed strong reactivity for laminin alpha 1, alpha 3, beta 1, and beta 3 chains, the components of laminin-1 and -5, at the interface between malignant cells and tumor stroma. The reactivities were continuous throughout the carcinomas, even in structures invading through the smooth muscle layers of the gastric wall. The expression of different laminin chains was accompanied by strong polarized reactivity for the alpha 6 beta 4 integrin, which is a receptor for both laminin-1 and laminin-5. Collagen type VII was only occasionally present at sites showing reactivity for laminin-5 and was totally absent from the cell islands invading through the gastric wall. Intestinalized gastric epithelium showed a similar expression pattern of laminins and the alpha 6 beta 4 integrin as the gastric carcinomas. Our results suggest that gastric carcinomas use the alpha 6 beta 4 integrin and newly deposited laminin-1 and -5, accompanied by the disappearance of type VII collagen, as their mechanism of adhesion during the invasion through surrounding tissues. Unlike in previous studies, the reactivity for the laminin-5 protein was not restricted to the invading cells but surrounded the malignant glandular structures throughout the tumor. Our results also show that both intestinal-type gastric carcinoma, and intestinal metaplasia mimic the gastric surface epithelium in the expression pattern of laminins and the beta 4 integrin subunit. This supports previous studies proposing a pathogenetic sequence from intestinal metaplasia to gastric carcinoma.

Antigens, Surface↗
PubMed1995

Pathophysiological effects of long-term acid suppression in man.

A critical evaluation has been made of the available evidence in man of the effects of prolonged low acid states on the structure and function of the stomach. Various human models have been examined. 1. Ageing does not affect acid output from the normal male stomach, and there may be an increase in women. With progressive atrophy of the corpus mucosa, which is more frequent and rapid in patients with gastric ulcer, there is an associated loss of secretory function. Chronic gastritis and atrophy are the most important age-related changes, which in many cultures are hypothesized to develop via a prior Helicobacter pylori-related gastritis. However, H. pylori colonization of the mucosa decreases with increasing grades of gastric atrophy probably because intestinal metaplasia provides a hostile environment. Atrophy and intestinal metaplasia are associated with precancerous lesions and gastric cancer. Apparent hyperplasia of the gastric argyrophil endocrine cells is a common and spontaneous phenomenon in patients with atrophic gastritis, which in part may be related to the preferential loss of nonendocrine cells. 2. Pernicious anemia is associated with a complete lack of acid production, marked hypergastrinemia, and endocrine cell hyperplasia in the majority of patients. ECL-cell carcinoids and gastric cancer occur with a prevalence of 3-7%, and endoscopic surveillance in routine clinical practice is not warranted. 3. Gastric ECL-cell carcinoids are rare events that have been described in association with two diseases in man, pernicious anemia and Zollinger-Ellison syndrome as part of multiple endocrine neoplasia syndrome type I, and usually relate to marked hypergastrinemia and the presence of chronic atrophic gastritis with gastric antibodies or a genetic defect rather than the presence or absence of acid. Regression or disappearance of ECL-cell carcinoids, either spontaneously or after removal of the gastrin drive, has been recorded. Lymph node, and rarely hepatic, metastases are documented but death in these cases has been anecdotal. 4. Therapy with H2 antagonists may result in up to a twofold rise in serum gastrin levels but in man no endocrine cell hyperplasia has been recorded. However, the data for H2 antagonists on these aspects are very limited. There is no drug-related risk of gastric or esophageal cancer, although the incidence of the latter may be raised. Long-term treatment with omeprazole is associated with a two- to fourfold increase in gastrin levels over baseline values in one third of patients and apparent endocrine cell hyperplasia in 7% of cases overall.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗
PubMed1995

Cure of peptic gastric ulcer associated with eradication of Helicobacter pylori. Finnish Gastric Ulcer Study Group.

The effect of Helicobacter pylori eradication on ulcer healing and the relapse rate were investigated in a multicentre trial of 239 gastric ulcer patients. Patients with H pylori positive gastric ulcer were randomly assigned to one of three groups: (A) 10 days' treatment with metronidazole and eight weeks' treatment with colloidal bismuth subcitrate (CBS) (84 patients); (B) 10 days' treatment with metronidazole placebo and eight weeks with CBS (73 patients); or (C) ranitidine (82 patients). At 12 weeks in 210 patients, gastric ulcer was present in three (9%) of 35 H pylori negative patients, and in 45 (26%) of 175 H pylori positive patients (p < 0.05). Results after one year of follow up were available for 205 patients. Between 12 and 52 weeks, two (7%) ulcer relapses occurred in 29 H pylori negative patients and in 60 (47%) of 128 H pylori positive patients (p < 0.001). After two weeks of open triple therapy (CBS 120 mg four times daily, amoxicillin 500 mg four times daily, and metronidazole 400 mg three times daily), given to the patients with ulcer relapse, only one (an NSAID user) of 55 successfully treated patients had an ulcer relapse during the one year follow up. Healing of gastric ulcer is rapid and recurrence is infrequent after successful H pylori eradication. H pylori eradication changes the natural history of the gastric ulcer disease.

Adult↗
PubMed1995

A 12-year follow-up study of chronic gastritis and Helicobacter pylori in a population-based random sample.

BACKGROUND: The study is a 12-year endoscopic follow-up investigation on the course of chronic gastritis and Helicobacter pylori infection in a sample of 81 Estonian people. METHODS: The series is a subset from a random sample of 227 subjects in whom a gastroduodenal endoscopy had been done. The grade of superficial gastritis (SG), atrophy, and colonization of the mucosa by H. pylori was evaluated in biopsy specimens from both antrum and corpus in accordance with the principles of the Sydney System. RESULTS: The healing rate of the H. pylori and gastritis was 0.3% (3 of 81); H. pylori colonization with gastritis developed in 5 of 81 during the follow-up. The mean prevalence of atrophic gastritis (AG) was three times more common in the corpus than in the antrum on the average. The formation of new cases of AG and the disappearance of AG were quite equal during the follow-up, and the overall changes in the grade of SG and atrophy were slow. The mean life span of corpus AG was nearly three times as long as that of antrum AG. In the antrum the grade of chronic inflammation correlated positively with the grade of H. pylori colonization. In cases of SG a low grade of colonization of H. pylori in the antral mucosa in connection with moderate inflammation predicted a reduction or even a healing of gastritis in the long term. CONCLUSIONS: New H. pylori infections with subsequent gastritis may occur in adulthood; a healing of gastritis occurs but is a quite rare event in the course of the 12-year follow-up. Further, in the present random sample of Estonian people atrophic corpus gastritis did not show an overall progression, in contrast to our earlier findings.

Adult↗