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We compared the degree of mucosal colonisation by aerobic and anaerobic bacteria with special attention to Helicobacter pylori in the antrum of the stomach of 19 non-ulceral dyspepsia (NUD), 18 duodenal ulcer (DU) and seven gastric ulcer (GU) patients. In the three cases of normal mucosa bacteria were present in quantities below 103 c.f.u./g and no H.pylori were detected. H.pylori was isolated from the antral mucosa of all patients with DU and GU and of 12 (63 per cent) NUD patients. A high colonisation rate (> 105 c.f.u./g) was found in 25 cases (56 per cent). In NUD patients with superficial gastritis the high degree of colonisation was due to H.pylori, but in the cases of GU and DU with the same state of the mucosa high numbers of H, pylori occurred in association with other microbes (P < 0.02). In the eight cases of slight atrophic gastritis (NUD, GU and DU) the population level of H, pylori was low accompanied by high numbers of other microorganisms. The aetiological role of H.pylori in the development of gastritis is discussed.

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. Resufrs: 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.

Maaroos H-I, Kekki M, Vorobjova T, Salupere V, Sipponen P. Risk of recurrence of gastric ulcer, chronic gastritis, and grade of Helicobacter pylori colonization. A long-term follow-up study of 25 patients. Scand J Gastroenterol 1994;29:532-536.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 gastritic 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.

The course of chronic gastritis in the antrum and body was followed up for 7 years in 112 patients with gastric ulcer (GU). As controls served 155 subjects collected at random from the same geographical area. At the start of the study (first examination) there was a slight predominance of antrum gastritis in the series, but during the follow-up period (second examination at 4 years (61 out of 112 patients) and third examination at 7 years (39 out of 112 patients)) a distinct body gastritis gradually predominated in GU patients. The healing tendency of active ulcer was accompanied by a more pronounced progression of body gastritis. The rate of body gastritis progression was very rapid and was calculated to be 11-fold as compared with that in the population at large. No immunological phenomena were associated with the body atrophy process.

Selective adult-type hypolactasia, the main cause of primary malabsorption of lactose, shows considerable variation in terms of its symptoms, which mainly depend on the amount of milk consumption. The article discusses congenital lactase deficiency and familial lactose intolerance. Links between hypolactasia and non-specific abdominal complaints, coronary heart disease and cataract are presented. The decrease in lactase activity in the brush border of jejunal mucosa, associated with diseases of the mucosa or any other condition which damages the enterocytes, is discussed as a cause of secondary hypolactasia. It is shown that adult-type primary hypolactasia and selective lactose malabsorption represent a major problem in the everyday work of general practitioners, particularly in populations where hypolactasia is common. Therefore, the examination and treatment of non-selected patients with vague abdominal complaints is important in primary health care. As the need for calcium in humans is largely met by the intake of milk, the consumption of milk has to be in amounts that are tolerable for the individual.

The prevalence and density of Helicobacter pylori (HP) colonisation was assessed twice, with an interval of six years from antral and corpus biopsies from a randomly collected Estonian urban population sample. Positive HP colonisation was found in either at 1st or 2nd or in both examinations in 85 out of 86 subjects in whom gastritis without atrophy (chronic inflammation without atrophic changes, SG) either developed or remained during the follow-up at the SG level. There was a clear intraindividual tendency to keep the grade of HP colonisation at an unchanged level during the follow-up: the hypothesis of random variation of HP colonisation during follow-up could be statistically rejected. Close to half of the subjects had at both examinations an identical grade of HP colonisation in the antral or corpus mucosa. Distinct changes in HP colonisation were observed in three instances: (1) the appearance of HP colonisation occurred concomitantly with appearance of gastritis; (2) the development of antrum atrophic gastritis (AG) occurred with concomitant diminution and eventual disappearance of HP in the antral side, and (3) normalization of antral mucosa occurred with persistence of corpus AG with concomitant disappearance of HP colonisation at both sites of the stomach mucosa. The grade of HP colonisation increased with increase in severity of SG and decreased with the progression of AG changes. In the antrum at the SG level a distinct increase was seen both in the grade of HP colonisation and in the severity of SG up to middle age, but in the corpus mucosa only HP colonisation but no SG progression was seen in the younger age-groups. In the antrum, a life-long correlation was found between HP colonisation and inflammatory reaction. The efficiency of immune response against HP colonisation was calculated by using the ratio of SG score to grade of HP colonisation (IRR). The youngest age group (15-19 years at 1st examination) had a significantly higher immune response ratio (IRR) than other age groups. With regard to antral gastritis, those subjects whose SG regressed during the follow-up had a higher IRR than the other subjects. Parietal cell antibodies (PCA) developed in 2 subjects. Both the two subjects had positive HP colonisation at the 1st examination. In addition, one of them preserved HP positivity at the 2nd examination. These findings suggest that autoimmune mechanisms may start in subjects previously exposed to HP-related gastritis.

To study the prevalence and course of chronic gastritis (CG), 142 adult subjects collected at random from an Estonian urban area were endoscopically and bioptically examined at a six-year interval. The histology of the antral and corpus mucosae was evaluated by grading gastritis without ("superficial gastritis"; SG) and with atrophy ("atrophic gastritis"; AG) into mild, moderate and severe categories. A total of 135 (95%) and 139 (98%) subjects showed CG in the 1st and 2nd examinations, respectively. The CG healed in one subjects (0.7%), and in 5 out of 7 subjects with normal stomach in the 1st examination the CG started during the follow-up. No change in the severity of CG was seen in 24% of subjects with gastritis in the 1st examination. The main trend of CG was a slow, "one-step progression" in severity of inflammation and appearance of atrophy and intestinal metaplasia. Inflammation progressed significantly, especially in the young age groups and in the antrum in particular. The prevalence of AG increased linearly with age in corpus (mean annual risk 1.25%). Parietal cell antibodies (PCA) were found in 2 subjects in the 1st examination, and a further 2 subjects developed these antibodies later. Three of four PCA-positive subjects belonged to a subgroup of 8 elderly subjects who had corpus AG at both examinations and who also showed normal or normalizing mucosa in the antrum. It is concluded that CG is a slowly progressive disease advancing with time and, once started, rarely healing spontaneously.

Serum alpha1-antitrypsin (A1AT) allo-and phenotypes (including M1, M2 and M3 alleles) were studied in 99 patients with gastric ulcer (GU) and 56 patients with duodenal ulcer (DU) using agarose isoelectric focusing. The results were compared with the A1AT data of a random population sample of similar genetic background (1422 persons). An increase in M2 allotype and M1M2 phenotype as well as a decrease in Z allotype of A1AT was seen in GU in comparison to DU and the random population. There were no particular clinical features which would distinguish patients with M2 allotype from the remainder of the GU group. However, a trend toward elevated serum pepsinogen I and II levels in patients with M2 allotype was seen. When the pepsinogen levels were compared in the GU patient groups with and without M2 allotype, matched between themselves by the state of the gastric mucosa, a statistically significant difference was revealed between pepsinogen II levels in these two groups. No associations were found between DU and any of the A1AT phenotypes.

Gastroscopy with biopsies was performed in 178 children with upper abdominal pain. Of them 109 (61%) had gastritis and 104 (58%) Helicobacter pylori (HP) in antrum and/or corpus. Gastritis consisted in most cases (87% of antral and 86% of corpus gastritis) of mild superficial round cell infiltration. Mucosal atrophy was not found. Accumulation of granulocytes was present in 43 patients and lymphonoduli were found in 33 patients, usually in connection with gastritis. Gastritis affected only the antrum in 18%, only the corpus in 5% and both antrum and corpus in 62% of the cases of gastritis. There was a good correlation between morphology and bacteriology in the antrum and a satisfactory one in the corpus. However, in some cases gastritis was present without bacteria and in some cases a normal mucosa was associated with bacteria. Gastritis and HP prevalences showed a general increasing trend with age, but significances were with one exception lacking. It is tentatively concluded that gastritis begins in childhood as a slight and chronic superficial infiltration affecting usually antrum and corpus simultaneously. In the majority of cases gastritis is associated with HP infection, which seems to start the process. It is possible that the HP-related gastritis is a common cause of abdominal complaints in children; however, convincing evidence is lacking.

Argyrophil cell (AC) hyperplasia in corpus mucosa was investigated in 53 patients with chronic gastric ulcer disease not previously treated with antisecretory drugs. Mucosal biopsies were taken stepwise from the posterior wall in the corpus area of the stomach. Of 117 biopsy sites, 28 showed gastritis without atrophy, 85 showed chronic atrophic gastritis of varying degrees while 4 biopsies showed a normal mucosa. About one third (38%) showed a normal AC pattern. Of the remaining two thirds (62%), 45% had simple AC hyperplasia, 18% had linear and 37% had micronodular AC hyperplasia. A strong association was found between focal (linear/micronodular) AC hyperplasia and chronic atrophic gastritis. It is concluded that focal AC hyperplasia is a common phenomenon in gastric ulcer patients and is inherently related to the spontaneous development of atrophy in the corpus mucosa of these patients.

We have examined the occurrence of Helicobacter pylori (HP) infection in 86 Estonian gastric ulcer (GU) and 25 duodenal ulcer (DU) patients. Diagnosis of the HP infection was made histologically (modified Giemsa) from gastric biopsy specimens, and serologically by parallel use of two enzyme-linked immunosorbent assays for IgG antibodies to HP in patient sera. The infection was diagnosed simultaneously by all three methods in 84% of the GU and 84% of the DU patients. The infection was revealed histologically in 88% of the GU and 92% of the DU patients, and serologically by either of the two methods in 94% and 92% of the GU and DU patients, respectively. HP infection was absent by all three methods in one GU patient only, this patient being the only subject who showed normal gastric mucosa in conventional histology. These observations show that HP infection is very common in patients with peptic ulcer in Estonia. In addition, the findings suggest that the serological assays will find a small proportion (15%) of ulcer patients with antibodies against HP but no histologically detectable bacteria.

The purpose of the study was to evaluate the long-term effects of vagotomy on the morphological status and Helicobacter pylori infestation of the gastric mucosa. Endoscopy with biopsies (2 from antrum and 2 from corpus) was performed in 317 patients on whom vagotomy had been performed on an average 8 years earlier. The success of the vagotomy was estimated by the endoscopic Congo Red technique in 270 cases. Non-operated 187 duodenal ulcer patients were examined endoscopically and bioptically in a similar way and used as a reference series. Helicobacter pylori (HP) was determined by Giemsa staining of biopsy specimens in both series. In non-operated duodenal ulcer patients, gastritis and HP behaved as expected from the data in literature: antral gastritis was present in nearly all cases (96%), while the corpus mucosa was normal or the process was retarded at the stage of superficial gastritis (76%) and atrophic changes were virtually lacking (1%), On the basis of the Congo Red test the vagotomized patients were separated into two groups: successfully operated, i.e., complete vagotomy, and incomplete vagotomy groups. The results of the examinations were independent of the kind of vagotomy performed, but related significantly to its completeness. The incomplete and complete groups differed significantly. The prevalence of atrophic changes (29%) in the corpus was significantly higher and that of superficial gastritis (69%) lower in the complete than in the incomplete vagotomy group, in which the prevalences were 12% and 85%, respectively. Likewise the prevalence and density of HP was lower in the complete vagotomy group but the difference was not statistically significant. The antral mucosa did not significantly differ morphologically in the two groups, but the overall prevalences of HP and of high density colonization of the bacterium was significantly lower in the complete group. Summarizing, the effects of vagotomy were dependent upon the success rather than the type of vagotomy, and the most significant long-term effects of successful vagotomy were the appearance and progression of atrophic changes in the corpus and the overall decrease of HP positivity as compared with patients with incomplete vagotomy.

A series of 38 patients with high gastric ulcer (GU) was examined twice a seven-year interval. One-third of the patients had an active ulcer at the second examination. Chronic gastritis was evaluated, and the level of Helicobacter pylori (HP) colonisation assessed semiquantitatively. The results were compared with age and sex matched non-ulcer controls. The GU series differed from the controls in having a higher degree of HP colonisation in gastric mucosa. The relative risks (RR) in predicting high GU connected with high HP colonisation were significantly elevated, both in the antrum (RR = 6.0-4.8) and in the corpus (RR 5.0-4.4), and still higher when combined HP colonisation values were used (RR 9.5-7.1). The persistence of active ulcer (GU+) was associated with a very high level of HP colonisation, with absence of corpus atrophic gastritis at the first examination and with young patients. Half of the GU+ patients had the maximum grade of combined HP colonisation in both examinations. The study indicates that the presence of HP infection as well as the level of HP colonisation are of importance in both the development and chronicity of peptic GU disease.

A series of 143 subjects representing an Estonian urban population was examined for the occurrence and extent (absent, mild, moderate, severe) of Helicobacter pylori colonization in antral and body biopsy specimens (Giemsa staining). These data were correlated with the presence and grade of chronic gastritis (normal, mild, moderate, or severe superficial chronic gastritis; mild, moderate, or severe atrophic gastritis) in the antrum and the body. Gastritis of any grade was found in the antrum and/or the body in 140 (98%) subjects. The overall extent of H. pylori colonization in the whole series did not differ between the antrum and the body. Of 93 subjects with superficial gastritis, H. pylori was found in the antrum and/or the body in 87 (94%) cases. Of 47 subjects with atrophic gastritis in the antrum and/or the body, H. pylori was not found in 12 (25%). In subjects with gastritis the absence of H. pylori either in the antrum or in the body was relatively common (in 30 of 143 subjects). The grade of superficial gastritis showed a highly significantly positive correlation with the extent of H. pylori colonization in the antrum but not in the body, Correspondingly, the grade of atrophic gastritis in the antrum correlated negatively to the grade of colonization. The total absence of H. pylori was particularly associated with the absence of gastritis in the antrum. Conversely, severe body H. pylori colonization was found in subjects who had atrophic antral gastritis, and severe antral colonization in subjects who had at least moderate superficial antral gastritis and who showed a coexistent normal or slight superficial gastritis in the body. We concluded that the presence and extent of H. pylori colonization are strongly linked to specific profiles of antrofundal gastritis.