During 1977, 5279 male and 4616 female visits (9895 in all) for acute abdominal conditions were made to the emergency room at the Department of Surgery in Malmö, Sweden. Twice as many patients were seen on Mondays and Tuesdays as on Saturdays. More than 50% of the visits were classified as non-specific abdominal pain or gastritis. The highest incidence of these two conditions was found in the 20-29-year age group and 2-3 times as many patients in this age group were seen on Mondays as on Saturdays and Sundays. It is concluded that studies on the age- and sex-specific incidence rates of different abdominal disorders should be of great value for proper planning of diagnostic and therapeutic resources and further of importance for the planning of the education and training of the general surgeon. Differences in the age- and sex-specific incidence rates as well as differences in the incidence rates from one time period to another illustrate the value of retrospective studies as a basis for future prospective studies regarding cause and potential for prevention of acute abdominal diseases.
Age of gastric cancer patients and susceptibility to chronic gastritis in their relatives. A mathematical approach using Poisson's process and scoring of gastritis state.
Indigenous communities across the circumpolar north have elevated H. pylori (Hp) prevalence and stomach cancer incidence. We aimed to describe the Hp-associated disease burden among western Canadian Arctic participants in community-driven projects that address concerns about health risks from Hp infection.
During 2008-2013, participants underwent Hp screening by urea breath test and gastroscopy with gastric biopsies. We estimated Hp prevalence and prevalence by Hp status of endoscopic and histopathologic diagnoses.
Among 878 participants with Hp status data, Hp prevalence was: 62% overall; 66% in 740 Indigenous participants; 22% in 77 non-Indigenous participants (61 participants did not disclose ethnicity); 45% at 0-14?years old, 69% at 15-34?years old, and 61% at 35-96?years old. Among 309 participants examined endoscopically, visible mucosal lesions were more frequent in the stomach than the duodenum: the gastric to duodenal ratio was 2 for inflammation, 8 for erosions, and 3 for ulcers. Pathological examination in 308 participants with gastric biopsies revealed normal gastric mucosa in 1 of 224 Hp-positive participants and 77% (65/84) of Hp-negative participants with sharp contrasts in the prevalence of abnormalities between Hp-positive and Hp-negative participants, respectively: moderate-severe active gastritis in 50 and 0%; moderate-severe chronic gastritis in 91 and 1%; atrophic gastritis in 43 and 0%; intestinal metaplasia in 17 and 5%.
The observed pattern of disease is consistent with increased risk of stomach cancer and reflects substantial inequity in the Hp-associated disease burden in western Arctic Canadian hamlets relative to most North American settings. This research adds to evidence that demonstrates the need for interventions aimed at reducing health risks from Hp infection in Indigenous Arctic communities.
Many individuals are infected with the bacterium Helicobacter pylori. Some develop ulcers or mucosal atrophy.
To correlate the histological characteristics of the H. pylori -induced gastritis to the immunoblot pattern of the H. pylori infection and to compare the presence of H. pylori bacteria in tissue specimens with ELISA serology and immunoblot analysis.
One hundred and sixty-six consecutive patients were referred to gastroscopy. Forty patients were excluded for various reasons and 126 were included in the study.
Twenty-three patients had ulcerations and 25 erosions. Ninety-two (73%) had a chronic gastritis and in 90 (71%) it involved both the antrum and corpus. Ninety-one (72%), of whom 96% had a chronic gastritis, had visible bacteria in the tissue specimens, used as the 'gold standard' for the detection of infection. In patients with chronic gastritis 65 (70%) had positive H. pylori ELISA serology, 27 (30%) had negative H. pylori ELISA, while 76 (83%) had a positive immunoblot pattern. The ELISA positive patients had more advanced chronic gastritis but a lower frequency of metaplasia and atrophy. Acute inflammatory activity in the chronic gastritis had a high immunoreactivity to 120 kDa (CagA) protein and was significantly correlated to antibody reactivity to proteins in the 53-65 kDa range (heat shock proteins) and to a 43 kDa subunit. Metaplasia and atrophy in antrum was associated with a 62 kDa protein band.
Almost all H. pylori-infected patients had a pangastritis, visible in both antrum and corpus. Acute inflammatory activity in the chronic gastritis and the presence of metaplasia and atrophy in antrum were associated with a specific immunoblot pattern, indicating infection with more virulent strains. Immunoblot analysis had a better sensitivity than ELISA H. pylori serology.
All the risk factors of peptic ulcer disease are not thoroughly understood.
To assess duodenal gastric metaplasia (DGM) in relation to Helicobacter pylori status and endoscopy findings with special reference to the effects of highly selective vagotomy.
The study population consisted of 1056 adult patients and an additional 154 patients who had had a highly selective vagotomy. Their clinical and endoscopy records as well as the histology of gastric and duodenal biopsies were evaluated retrospectively. H. pylori infection had been determined by serology and culture.
Widespread (more than 20%) DGM was strongly associated with H. pylori positive duodenal ulcer disease (in 59.7% of patients). The prevalence of DGM diminished progressively the more proximally the ulcer was located in the stomach, and was 2.5% in proximal gastric ulcers patients. In vagotomized patients, the prevalence of widespread DGM (8.4% of patients, median 14 years after operation and the majority still H. pylori positive) was close to that of patients with H. pylori gastritis without peptic ulcer disease (4.5%).
Widespread DGM is an indicator for an increased risk of duodenal ulcer among H. pylori positive patients and it could be used to select patients for eradication therapy.
We studied the dynamics of morbidity of the digestive apparatus including peptic ulcer, gastritis, duodenitis and mortality in the Udmurt Republic from 1992 to 2002. We revealed the decrease of morbidity of the digestive apparatus and stable data for peptic ulcer but the increase of mortality from the digestive apparatus pathologies on the whole and from complications of peptic ulcer. The mortality from the digestive apparatus diseases and peptic ulcer is forecasted to increase in the next years if the same social and economic conditions are preserved and there are no changes in the health-care system.
In this population-based endoscopic survey we found erosive prepyloric changes (EPC) in 38.5% of dyspeptics and 35.1% of non-dyspeptics. EPC were observed more frequently in men than in women in both groups. Occurrence of Helicobacter pylori was not associated with EPC. No common gastrointestinal symptoms were found to be associated with EPC. Endoscopic duodenitis of the duodenal bulb was found more frequently in subjects with EPC of the two highest grades than in subjects without EPC. Only the highest grade of EPC was associated with chronic gastritis. EPC were associated with cigarette smoking and, among women, also use of alcohol. We conclude that EPC constitute an endoscopic finding without relation to specific symptoms. These changes therefore do not represent a clinical entity, and it is doubtful whether this finding will give the clinician a better understanding of dyspepsia.
Gastric erosions are mainly associated with Helicobacter pylori infection and non-steroidal anti-inflammatory drugs (NSAIDs), but there has been no information available on the long-term evolution of gastritis in subjects with erosions.
A series of 117 patients with gastric erosions without peptic ulcer disease and matched controls without erosions or ulcers were studied. Available subjects underwent endoscopy and biopsy 17 years later. Parietal cell antibodies were analysed at the first visit.
Fifty-two patients and 67 controls were available for follow-up. Since H. pylori was a major determinant of gastritis, only subjects with unchanged H. pylori status were included in the evaluation of gastritis progression. At the follow-up visit, gastric erosions were present in 38% (16/42) of the patients and 11% (5/46) of the controls (p=0.005). In H. pylori-negative subjects, no evolution of histological changes was seen. In H. pylori-positive subjects, body gastritis was initially less active in the erosion group. With time, antral gastritis worsened only in the erosion group. Parietal cell antibodies were more common in the control group (23%; erosion patients 0%; p=0.01), which also showed worsening of gastritis (p=0.003) and aggravation of atrophy (p=0.002) in the body mucosa.
Gastritis in H. pylori-positive subjects with gastric erosions shows evolution of antral predominance, body predominance including development of atrophic changes being rare. Accordingly, patients with erosions share the characteristics of gastritis of the duodenal ulcer phenotype. These findings support the importance of H. pylori and acid in the pathogenesis of gastric erosions in H. pylori-positive patients.
To investigate whether the occurrence of chronic gastritis (and Helicobacter pylori acquisition) has changed in Finland in the past 15 years, the prevalence rates of chronic gastritis in biopsy specimens in consecutive series of outpatients (aged 20 or more) who had undergone diagnostic upper gastrointestinal endoscopy in 1977 (702 patients), 1985 (1309 patients), or 1992 (1447 patients) were compared. The prevalences of gastritis in these series were also compared with that in a random sample (438 subjects) of people who underwent endoscopy in 1974-76. It seemed that the prevalence of gastritis was significantly lower in the outpatients in 1992 than in the random endoscopy sample in 1974-76. The reduction was most noticeable in young age groups (20-49 years) in which the decline was 38% (drop from 66% to 41%). In addition, it seemed that the prevalence of gastritis was very dissimilar in different birth cohorts. The prevalence was high (70-80%) in 1977, 1985, and 1992 in the cohorts born at the beginning of the century and lower (40-50%) in those born during later decades. The prevalence rates had remained unchanged in the same cohorts over the 15 years (from 1977 to 1992) suggesting that the people had mainly been infected with H pylori and contracted gastritis before the age of 20. In conclusion, gastritis is a cohort phenomenon and its prevalence has fallen in Finland in the last 15 years. This decrease is caused by a decline of the rate of H pylori acquisition in birth cohorts, particularly in childhood and adolescence (below age of 20).
