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Biomedical subjects

P Sipponen

Publications and source records attributed to P Sipponen.

At least 109 records · Page 6Linked to original sources
PubMed1995

Incidence of gastric cancer and prevalence of chronic gastritis in outpatients: comparison between two geographical areas in Finland.

We present some evidence that there exists a positive relationship between the incidence of gastric cancer and the prevalence rate of chronic gastritis, regarding the time trends and geography of these diseases in Finland. Both gastric cancer and chronic gastritis have declined in occurrence during the last 15 years, and there exists a similar geographic distribution of these diseases in Finland on the north-south axis: both are more prevalent in Lapland than in Southern Finland. The distribution of the socioeconomic conditions in Finland also shows a north-south axis: the proportion of people with low social class, number of children (birth rate) per household is higher, and the yearly income on average is lower in Lapland than in Southern Finland. We conclude that the epidemiology of chronic gastritis and gastric cancer show similar epidemiological features, regarding at least the time trends and geography of these diseases in Finland.

Adult↗
PubMed1995

Helicobacter pylori: a cohort phenomenon.

Helicobacter pylori infection is an etiopathogenetic cause of chronic gastritis in more than 90% of the cases. In a proportion of infected subjects, gastritis slowly (over years or decades) progresses, for unknown reasons, into atrophic gastritis that affects antral or corpus mucosa, or both (multifocal atrophic gastritis). Some recent improvements have been made in studies of H. pylori gastritis. H. pylori gastritis has shown to associate strongly with peptic ulcer diseases and gastric cancer. The risk for ulcer (excluding the nonsteroidal anti-inflammatory drug-related ulcers) is highest in the nonatrophic forms of gastritis and the risk for gastric cancer in the severe forms of atrophic (metaplastic) gastritis. For routine histopathologic practice, the Sydney System has been developed to describe and grade the histopathologic appearances of gastritis, i.e., chronic and acute ("activity") inflammation, atrophy (loss of normal mucosal glands), intestinal metaplasia, and H. pylori in endoscopic biopsy specimens from antrum and corpus. Different phenotypes of H. pylori gastritis can be reliably described and the risks for various gastric diseases reasonably well predicted by the System. Most recent studies from developed countries have indicated that H. pylori acquisition occurs mainly during childhood and that the infection risk is quite low in adulthood. In addition, the acquisition rate has declined in these countries during the past few decades. The observations suggest that H. pylori gastritis is a birth cohort-related phenomenon. The acquisition rate has been high and the subsequent chronic gastritis is a common disease in the cohorts (generations) born in the beginning of this century but both are much less common in cohorts born more recently.

Adult↗
PubMed1995

Helicobacter pylori infection and chronological extension of atrophic gastritis.

OBJECTIVES: To determine the relationship between Helicobacter pylori infection and chronological extension of atrophic gastritis. PATIENTS AND METHODS: We studied 137 non-ulcer patients. The extent of atrophic gastritis was assessed endoscopically and scored on a scale of 1-6 (endoscopic score) using the atrophic pattern system. H. pylori infection was assessed by enzyme-linked immunosorbent assay with serum anti-H. pylori immunoglobulin G. The correlation between patient age and endoscopic score was determined for H. pylori-positive and -negative patients. RESULTS: A positive correlation between age and extent of atrophic gastritis was found in both H. pylori-positive and -negative patients. In groups of patients aged 20-29 and 30-39 years, those with H. pylori had more extensive atrophic gastritis than those without H. pylori. CONCLUSIONS: Chronological extension of atrophic gastritis was found in patients with and without H. pylori infection.

Adolescent↗
PubMed1994

Tenascin expression in inflammatory, dysplastic and neoplastic lesions of the human stomach.

We studied the expression of tenascin (Tn) in human stomach. In the normal mucosa of the antrum and body, Tn reaction was only seen in the muscularis mucosae, in the region of the pyloric sphincter and in the duodenum, a Tn-immunoreactive rim was seen underlying surface epithelial cells. Antral gastritis, irrespective of the degree of inflammation, showed a rim-like Tn expression under the surface epithelial cells but no Tn reaction was seen in mild chronic gastritis of the body. In some moderate and severe examples of chronic gastritis a delicate Tn-reactive line was seen to underline the surface epithelium focally and the neck regions of gastric pits. Discontinuous Tn immunoreactivity was sometimes seen beneath hyperplastic epithelium in both parts of the stomach. A Tn-immunoreactive line was seldom seen surrounding glands showing intestinal metaplasia. In both benign and malignant ulcers prominent Tn immunoreaction was seen at the base of ulcers extending deep into the underlying muscularis. Only severely dysplastic lesions displayed Tn in the lamina propria, in close association with capillaries. In early forms of diffuse gastric cancer (DGCA) raggedly increased Tn staining was seen in the lamina propria underlying affected surface epithelial cells. In advanced forms of DGCA consistent Tn expression was seen in the tumour stroma. A distinct Tn reaction was seen surrounding invasive tumour cell nests of intestinal type gastric cancer (IGCA) in the submucosa, whereas in early forms of the tumour enhanced Tn reaction was noted predominantly in the upper part of the lamina propria in the vicinity of dysplastic elements. Notably, while most invading DGCA tumour cell nests showed no Tn in the submucosa and muscle cell layer, invading IGCA islets showed prominent expression of Tn. The most conspicuous Tn enhancement in the stomach is seen in invasive tumours and in ulcers suggesting that Tn is an important stromal component in malignant growth and in lesions undergoing active repair and remodelling.

Biomarkers, Tumor↗
PubMed1994

Budesonide enema in active haemorrhagic proctitis--a controlled trial against hydrocortisone foam enema.

BACKGROUND: The aim was to compare budesonide enema, 2 mg/100 mL (Entocort) and hydrocortisone acetate foam enema, 125 mg (Colifoam) in patients with active haemorrhagic proctitis. METHODS: The trial was a controlled, randomized, investigator-blind study with two parallel groups. Endoscopy, histology and diary cards were used to assess the response to therapy. Safety was assessed by laboratory tests and adverse event recording. RESULTS: Seventy-two patients were included. Investigations were made before treatment and after 2 and 4 weeks. Both treatment groups showed statistically significant improvement in endoscopic scores but significant differences between the groups were not found. In the hydrocortisone group, plasma cortisol was significantly lowered after 4 weeks compared with budesonide. Bowel habits and quality of life variables did not differ between the treatments. The recorded adverse events were mild or moderate and may have been due to the proctitis. CONCLUSIONS: These results suggest that budesonide enema is as effective as hydrocortisone foam enema, but without the potential for side-effects associated with suppression of plasma cortisol.

Adult↗
PubMed1994

Fall in the prevalence of chronic gastritis over 15 years: analysis of outpatient series in Finland from 1977, 1985, and 1992.

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).

Age Factors↗
PubMed1994

Helicobacter pylori in functional dyspepsia and normal controls.

BACKGROUND: The aim of this study was to examine whether Helicobacter pylori status can identify a specific subset of patients with functional dyspepsia (FD) and erosive prepyloric changes (EPC). METHODS: Anamnestic, somatic, and psychologic data were collected from 87 patients with functional dyspepsia and 77 normal control persons. Presence of H. pylori infection was assessed by the 14C-urea breath test. RESULTS: H. pylori infection increased with age. Thirty-four per cent of the patients were H. pylori-positive, compared with 36% of the control persons. The patients had higher scores than the normal control persons on psychologic measures regardless of H. pylori status. Of 27 variables analyzed, age was the only factor that discriminated between H. pylori-positive and -negative patients. CONCLUSIONS: For most patients with FD and EPC the presence of H. pylori infection is probably a consequence of age, and it does not seem to help us in the search for factors that can identify a subset of patients within our group of FD patients.

Adolescent↗
PubMed1994

Risk of recurrence of gastric ulcer, chronic gastritis, and grade of Helicobacter pylori colonization. A long-term follow-up study of 25 patients.

BACKGROUND: We describe here our observations on colonization of the gastric mucosa by Helicobacter pylori in a long-term follow-up of 25 patients with gastric ulcer (GU). METHODS: All patients were followed-up endoscopically for more than 10 years (mean, 16 years) and endoscopically verified to have GU in the angular or corpus area of the stomach. None had received treatment with H2 blockers or omeprazole or had undergone any maintenance therapy or surgery. On the basis of the endoscopic findings on the activity of GU at follow-up endoscopies, the patients were divided into a group of subjects with 'low risk' of recurrence (15 patients who either had no (7 patients) or only a single recurrence (8 patients) at the first follow-up endoscopy but not thereafter) and into those with a 'high risk' of recurrence (10 patients who had at least 2 episodes of recurrence at follow-up endoscopies). RESULTS: A severe bilateral (antrum and corpus) colonization of the gastric mucosa by H. pylori at the first re-examination (1-6 years after the initial diagnosis of GU) was the most important characteristic feature in the patients with high risk of recurrence as compared with those with low risk. In the course of the follow-up, colonization of the corpus mucosa by H. pylori remained rather unchanged in both high- and low-risk subjects but decreased in grade in antrum particularly in those with low risk (no bacteria at the last endoscopy in 13 of 16 low-risk patients and in 2 of 8 high-risk patients). In both low- and high-risk groups corpus gastritis developed progressively into atrophic gastritis (11 of 25 patients had severe corpus atrophy at the last endoscopy). On the other hand, antral gastritis showed a tendency to heal (13 of 24 patients had normal or only slightly gastric antrum at the last endoscopy). CONCLUSIONS: The observations indicate that the H. pylori plays a role in and associates closely with the long-term course of angular or corpus GU disease and is related to the tendency of these ulcers to recur.

Adult↗
PubMed1994

Chronic nonatropic ('superficial') gastritis increases the risk of gastric carcinoma. A case-control study.

Atrophic gastritis is a well-known risk condition for gastric carcinoma (GCA). Less is known about the risk of GCA in subjects with nonatrophic ('superficial') gastritis. To investigate this, we estimated the risk of GCA in patients with nonatrophic gastritis as compared with that in subjects with normal, nongastritic mucosa. Two hundred and forty-three consecutive GCA patients and 1408 non-GCA outpatients (controls), for whom histologic data (endoscopic biopsy) of gastric mucosa was available, were included in the study. To estimate the relative risk (RR) of GCA, the odds ratio of gastritis was calculated in patients and controls by adjusting for age and sex. The RR (95% confidence interval) of GCA in patients with nonatrophic antral gastritis and with nonatrophic pangastritis was 1.8 (1.2-2.7) and 2.5 (1.4-4.3), respectively. Correspondingly, the risks of GCA were 9.1 (5.4-15.5) in patients with atrophic antral gastritis or pangastritis (atrophy of any degree) and 4.4 (1.9-10) in those with severe atrophic corpus gastritis (severe corpus limited atrophy of 'A type'). In nonatrophic gastritis the risk of diffuse-type GCA was emphasized, whereas the risk of intestinal-type GCA was emphasized in patients with atrophic gastritis. These results indicate that an increased risk of GCA is not confined to subjects with atrophic gastritis but is also slightly but significantly increased in patients with chronic nonatrophic gastritis.

Adult↗
PubMed1994

Intestinal metaplasia, atrophic gastritis and stomach cancer: trends over time.

BACKGROUND: The pathogenetic association of chronic atrophic gastritis and intestinal metaplasia with gastric cancer implies that the trends seen in these disorders over time should be similar. Both should similarly decrease in incidence with time, and a time-related relationship should occur between the incidence of gastric cancer and the rate of development of atrophic gastritis in the stomach of Helicobacter pylori-infected subjects. AIMS AND METHODS: We reviewed some recent studies from Finland on the time trends seen in chronic gastritis, atrophic gastritis (and intestinal metaplasia) and gastric cancer over a period of 15 years (1977-1992). In addition, using results from earlier studies from Japan and Finland, we formed hypotheses on how the time-dependent evolution and extension of atrophic gastritis may accord with the occurrence of gastric cancer in the stomach. RESULTS: Our investigations showed that the incidence of gastric cancer and the prevalence of H. pylori-associated gastritis, atrophic gastritis and intestinal metaplasia have decreased similarly in outpatient series during the last 15 years. Correspondingly, gastric cancer, atrophic gastritis and intestinal metaplasia are cohort phenomena in the population, and the prevalence rate of atrophic gastritis is correlated with the cohort-specific incidence of gastric cancer; both are high in cohorts born near the beginning of the century but are quite low in those born in recent decades. Since antral and angular areas of the stomach are primary sites for gastric cancer tumours, the earlier investigations indicate that the time-dependent progression of gastritis in grade (development of atrophic gastritis and intestinal metaplasia) and extent (spreading of gastritis by pylorocardial extension) is well correlated with the rate and predisposition of gastric cancer tumours in the distal and angular stomach. CONCLUSIONS: We conclude that atrophic gastritis (or intestinal metaplasia) and gastric cancer are very much alike in time trends and in course. This parallelism favours suggestions that H. pylori-associated gastritis with atrophic and metaplastic sequelae (atrophic gastritis) contribute to the pathogenesis of gastric cancer.

Finland↗
PubMed1994

Gastric cancer--a long-term consequence of Helicobacter pylori infection?

Chronic gastritis and chronic atrophic gastritis in particular are risk factors for gastric cancer. In Western societies, for example Finland, up to 70% of gastric cancer cases are associated with Helicobacter pylori-positive chronic non-atrophic or atrophic gastritis, approximately 15% appear in conjunction with autoimmune chronic corpus-limited H. pylori-negative atrophic gastritis, and 15% develop in individuals with a histologically normal stomach. The role of H. pylori infection in chronic gastritis has led to the hypothesis that this infection could be involved in the pathogenesis of gastric cancer. There are three main factors in support of this hypothesis: (i) H. pylori infection is the single causal aetiological agent in more than 80% of cases with chronic gastritis; (ii) H. pylori-positive chronic gastritis will develop into mucosal atrophy (atrophic gastritis) and intestinal metaplasia in a large proportion of affected individuals; (iii) the risk of gastric cancer is known to be high in people with chronic gastritis, and particularly in those with atrophic gastritis. In addition, there exists some correlation between the rates of H. pylori infection and gastric cancer mortality worldwide, and H. pylori infection relates to socioeconomic conditions known to associate with gastric cancer. Although H. pylori-positive gastritis cannot be considered a single and direct cause of gastric cancer, it is strongly associated with it and may trigger a cascade of events in the gastric mucosa that results in the development of gastric cancer in some patients.

Chronic Disease↗
PubMed1993

Gastroscopic follow up of pernicious anaemia patients.

To assess the value of gastroscopic cancer surveillance of patients with pernicious anaemia, 56 patients were re-endoscoped and biopsied after three years. In addition, changes in the density of fundic mucosal endocrine cells were evaluated morphometrically. Two cases (3.6%) of early gastric cancer and two cases of small gastric carcinoid tumours (3.6%) were detected in addition to the five carcinoids that had been found at the initial endoscopic screening. Nodular argyrophil cell hyperplasia and morphometric density of argyrophil cells were not stable phenomena: nodular hyperplasias regressed in five patients, remained similar in six, and progressed to a small carcinoid tumour in one. Serum gastrin concentrations did not correlate well with changes in the endocrine cell density. Regular endoscopic surveillance for gastric cancer may be beneficial and realistic in young patients with pernicious anaemia while the importance of fundic endocrine cell hyperplasia and that of small gastric carcinoids need further study.

Adenocarcinoma↗
PubMed1993

Role of Helicobacter pylori in the pathogenesis of gastritis, peptic ulcer and gastric cancer.

Helicobacter pylori is the major causal factor in chronic gastritis. Its acquisition leads to a chronic, usually lifelong, inflammation of the gastric mucosa, which may gradually progress to atrophy (with intestinal metaplasia) in a significant proportion of infected individuals. This progression is probably multifactorial, being influenced by genetic or environmental factors in addition to H. pylori infection. The pathogenesis of peptic ulcer and gastric cancer is closely associated with H. pylori gastritis and its subsequent atrophic sequelae (atrophic gastritis). H. pylori-induced gastritis is an important risk factor in the multifactorial aetiology of these diseases. It causes a cascade of reactions that damage the gastric mucosa and epithelium in various ways. The specific mechanisms involved are largely unknown. Some are probably bacterium-related reactions, which are influenced by various virulence factors, and others are consequences of the mucosal inflammation and atrophy. The risk of peptic ulcer and gastric cancer in patients with H. pylori gastritis can be summarized as follows: i) the risk of both peptic ulcer and gastric cancer is low in individuals with a normal stomach; ii) the risk of peptic ulcer is approximately ten times higher and the risk of gastric cancer approximately twice as high in patients with non-atrophic H. pylori-positive gastritis as in those with a normal stomach; iii) these risks are further increased (twofold to threefold) when there is antral atrophy; whereas iv) in the presence of corpus atrophy the risk of gastric cancer remains high, but that of peptic ulcer decreases gradually to zero with increasing severity of corpus atrophy.

Chronic Disease↗
PubMed1992

Diagnostic value of decreasing IgG, IgA, and IgM antibody titres after eradication of Helicobacter pylori.

Titres of antibody to Helicobacter pylori are known to fall with eradication of bacteria. To find out what degree of fall would reliably indicate eradication, 144 patients with Helicobacter pylori infection were given antimicrobial therapy for 2 weeks and then followed up at 6 weeks, 6 months, and 12 months with serological tests, bacterial cultures, and histological studies of gastric specimens. 6 weeks after treatment IgG titres had fallen by 20-30% irrespective of the success of bacterial eradication. In the 121 bacteria-negative patients the decrease continued. 6 and 12 months after treatment the titre was 50% or less of pretreatment value in 97% of these patients. In the 23 patients who remained infected, the initial drop of IgG titres, if any, was followed by unchanged or slightly rising titres. IgA and IgM titres, initially raised in 64% and 4% of the patients, respectively, showed similar trends. The high sensitivity (97%) of the IgG antibody tests and a consistent fall within 6 months after eradication of H pylori infection made IgG the most useful immunoglobulin class for follow-up of antimicrobial therapy in individual patients. IgA antibodies were valuable in the 2% patients who had raised titres in this immunoglobulin class only. The few patients (5.5%) who had raised IgM titres also had high IgG titres. Serological tests thus are a cheap and reliable means of monitoring success of eradication of H pylori.

Adult↗
PubMed1992

Helicobacter pylori infection and chronic gastritis in gastric cancer.

AIMS: To investigate the prevalence of Helicobacter pylori associated chronic gastritis in patients with gastric cancer. METHODS: Serum IgG antibodies for H pylori were determined in 54 consecutive patients with gastric carcinoma. The prevalence of H pylori in gastric mucosa was also examined histologically (modified Giemsa) in 32 patients from whom adequate biopsy specimens of the antrum and corpus were available. Thirty five patients with gastrointestinal tumours outside the stomach and 48 with non-gastrointestinal malignancies served as controls. RESULTS: Of the 54 patients, 38 (70%) had H pylori antibodies (IgG) in their serum (three additional patients had H pylori antibodies IgA, class specific but not IgG specific). This prevalence was significantly higher (p less than 0.05) than that (49%) in the 35 controls. No differences in prevalence of H pylori antibodies were found between gastric cancer cases of intestinal (IGCA) or diffuse (DGCA) type, both these types showing H pylori antibodies (IgG) in 71% of the patients. In the subgroup of 32 subjects, five patients had normal gastric mucosa and four showed corpus limited atrophy ("pernicious anaemia type" atrophy of type A). All of these nine patients had no evidence of current or previous H pylori infection in serum (no IgG antibodies) or in tissue sections (negative Giemsa staining). The remaining 23 patients had antral or pangastritis, and all had evidence of current or previous H pylori infection. CONCLUSIONS: H pylori associated chronic gastritis was the associated disease in 75% of the patients with gastric cancer occurring equally often in both IGCA and DGCA groups. About 25% of cases seem to have a normal stomach or severe corpus limited atrophy, neither of which showed evidence of concomitant H pylori infection.

Adult↗
PubMed1992

Natural history of gastritis and its relationship to peptic ulcer disease.

Chronic gastritis is a common inflammatory disease. In a number of patients, the inflamed gastric mucosa shows a gradual tendency to become atrophic (atrophic gastritis). Gastritis tends to be lifelong, and spontaneous healing is rare. With very few exceptions (e.g. in patients with autoimmune chronic corpus gastritis), gastritis is associated with the presence of the bacterium Helicobacter pylori. Inflammation and atrophy of the gastric mucosa result in impairment of gastric secretory functions (e.g. secretion of gastric acid, pepsin and gastrin). Such impairment is dependent on the topographic type of gastritis; i.e. whether the inflammation and atrophy occur in the antrum (chronic antral gastritis), corpus (chronic corpus gastritis) or in both the antrum and corpus simultaneously (chronic pangastritis). Gastritis of different topographic types associates with different gastric diseases. In patients with H. pylori-related antral or pangastritis, peptic ulcer disease, and in particular duodenal ulcer, is common (with an incidence exceeding 20% after 10 years' follow-up), as compared with peptic ulcer disease, which is very rare in patients with a normal stomach. Gastric ulcer may sometimes occur in patients with a rather atrophic stomach, but both gastric and duodenal ulcers are extremely rare in patients in whom the gastritis accompanies severe atrophic changes in the corpus mucosa. Routine biopsies from the antrum and corpus, and interpretation of the results in the light of the data on gastritis and its atrophic sequelae, allow the gastroenterologist to predict the risk and likelihood of peptic ulcer disease in patients with gastritis.

Adult↗