Among 63 papers accepted (27 on pathology, gastritis, atrophic gastritis and 36 on neo-plastic diseases), seven papers were selected as oral presentations.

P. Sipponen from Helsinki, Finland, (07.01) examined the frequency of atrophic gastritis associated deficiency of vitamin B12 and high serum homocysteine in the general population in old age. The study population consisted of 12,252 men (aged 51-65 years). Serum pepsinogen I (S-PGI) was assayed in all, and the 635 men (5%) with S-PGI <25 µg/l formed Series A ("males with atrophic corpus gastritis"). Control series C ("males without atrophic corpus gastritis)" was formed as a sample of men (N=402) with S-PGI ≥50 µg/l. Serum levels of vitamin B12, folate, total homocysteine and Helicobacter pylori antibodies were assayed. The conclusion of the study was that low serum B12 and high serum homocysteine, associated with atrophic corpus gastritis, are common (prevalence 2.5%) in an elderly general population. An on-going H. pylori infection occurs in three-quarters of these cases.

S. Sebastian from Dublin, Ireland, (07.07) examined the usefulness of screening for premalignant lesions in first degree relatives of gastric cancer patients.  Thirty-eight first-degree relatives of gastric cancer patients were invited to undergo screening. Endoscopic biopsies taken from the corpus, antrum, incisura and cardia were graded according to the Sydney system. Fasting and meal stimulated serum samples were taken for analysis of pepsinogen I, II and gastrin-17. Dyspeptic patients with no family history of gastric cancer undergoing endoscopy were taken as controls. Intestinal metaplasia (IM) was identified in a significantly higher proportion of screened subjects than the controls (9/38 vs 2/30) . One patient had high-grade dysplasia. Serum PGI and PGI to PGII ratio predicted the presence of intestinal metaplasia in 6 of the 9 patients. Fasting and meal stimulated gastrin level was lower in first-degree relatives of gastric cancer compared to controls.The conclusion was that screening of first-degree relatives of gastric cancer detects significant premalignant lesions. The majority of these appear to be related to H. pylori infection.

G.I. Perez-Perez from New York, USA, (07.15) evaluated the correlation between clinical and serological markers under different gastrointestinal conditions. They studied 328 patients. Serum samples were obtained to determine H. pylori and CagA status, and PGI and PGII levels. Biopsies from the gastric antrum, body, and esophagus were obtained. Patients were classified based on histology results. They concluded that PGI/PGII ratio is a non-invasive indicator of gastric mucosal changes, and can identify risk of IM. Negative associations between PGI levels and Barrett’s esophagus indicate a potential utility in defining the risk for this disease (BE risk).

In the presentation by M. Held from Stockholm, Sweden, (07.16) the authors estimated the age- and calendar year-specific prevalence of atrophic corpus gastritis to see if it had diminished in parallel with gastric cancer incidence. They also investigated risk factors for atrophic gastritis. In 1990, 1994 and 1999, representative samples of 1326, 1464, and 1499 subjects, respectively, were drawn from the 35-64 year old population in two counties in northern Sweden. They determined serum concentrations of PGI and used 28 µg/L as the upper cutpoint for atrophic corpus gastritis. For each subject, they selected three controls with pepsinogen I >28 µg/L, matched by age and year of sampling. H. pylori and CagA serostatus was determined by immunoblot. H. pylori and questionnaire data (gender, body mass index, snuff intake and education) were related to the risk of atrophic gastritis. The conclusion was that none of the questionnaire data was significantly associated with atrophic corpus gastritis risk. A downward trend in atrophic corpus gastritis prevalence was evident only among the oldest. Atrophy was linked to CagA but not to H. pylori seropositivity.

H.M. Mitchell from Sydney, Australia, and Johannesburg, South Africa, (10.16) examined the IL-1 gene polymorphisms in Sowetan subjects and their relationship with H. pylori associated disease. IL-1B -511 and IL-1RN polymorphisms were assessed in 95 patients attending for endoscopy, 31 with non-ulcer dyspepsia (NUD), 41 duodenal ulcer (DU), 17 gastric ulcer (GU) and 6 gastric cancer (GC). IL-1B -511 and +3954 single nucleotide polymorphisms were determined by real time PCR and IL-1RN polymorphisms by PCR. The conclusion of the study was that, as previously reported, carriage of IL-1-511T/T was associated with GC. The virtual absence of the IL-1RN*2/2 allele in Sowetans may explain the low incidence of GC in this population.

Telomerase is an enzyme associated with cellular immortalization and plays an important role in carcinogenesis. Telomerase consists of 2 subunits, telomerase RNA template (hTR) and telomerase reverse transcriptase protein (hTERT). In the paper by A. Karameris and T. Rokkas from Athens, Greece, (10.17) the aim was to define hTR activity in the serum of H. pylori related gastric carcinoma patients and to compare these findings with the immunohistochemical expression of telomerase in bioptic material taken from the same patients. Telomerase activitity in serum was measured by using OneStep RT-PCR in 45 H. pylori-related gastric carcinoma cases whereas the expression of telomerase in the tissues was assessed immunohistochemically using a anti-telomerase moab. Positive and negative controls were also included. Increased hTR activity as well as immunohistochemical expression of tissue telomerase was detected in 43/45 cases examined. In normal gastric mucosa, weak hTR expression was noted, limited to basal cells of gastric glands. hTR activity and telomerase expression was found to be higher in IM of type III than in types I and II (4:2:1, accordingly). H. pylori-negative controls constantly expressed very low levels of hTR activity. The conclusion was that H. pylori infection may be a strong trigger for hTR overexpression possibly through activation of epithelial “stem cells” during the procedure of intestinal metaplasia.

Gastric body mucosa atrophy represents a lesion which predisposes to gastric cancer. Disturbances in the gastric differentiation process might play a role for the evolution of gastric atrophy. Sonic Hedgehog has recently been implicated as a crucial factor in gastric organogenesis and gland differentiation. In their study G. Faller et al. from Erlangen, Germany, (07.05)  investigated the expression of key factors in the Sonic Hedgehog-pathway, namely Sonic Hedgehog (Shh) and its receptor Patched (Ptc) in normal and pathologic stomach mucosa. Gastric biopsy specimens from normal gastric mucosa (n=10), chronic non-atrophic gastritis (n=16), atrophic gastritis (n=11) and gastric cancer (n=26) were included. Expression of Shh and Ptc was analyzed by immunohistochemistry. In normal body mucosa and in non-atrophic body gastritis Shh was strongly expressed in parietal cells. Ptc was also expressed in gastric chief cells. In atrophic gastritis and in gastric cancer Shh expression was almost completely lost and was absent in intestinal metaplasia (IM). Ptc was markedly reduced in atrophy and only weakly positive in IM and gastric cancer.They concluded that the decreased expression of the Shh pathway in atrophic gastritis and gastric cancer might reflect altered differentiation processes within the gastric unit and contributes to the development of gastric atrophy.