António Sousa Guerreiro

Curcumin Inhibits Gastric Inflammation Induced by Helicobacter Pylori Infection in a Mouse Model

Helicobacter pylori (H. pylori) infection triggers a sequence of gastric alterations starting with an inflammation of the gastric mucosa that, in some cases, evolves to gastric cancer. Efficient vaccination has not been achieved, thus it is essential to find alternative therapies, particularly in the nutritional field. The current study evaluated whether curcumin could attenuate inflammation of the gastric mucosa due to H. pylori infection. Twenty-eight C57BL/6 mice, were inoculated with the H. pylori SS1 strain; ten non-infected mice were used as controls. H. pylori infection in live mice was followed-up using a modified 13C-Urea Breath Test (13C-UBT) and quantitative real-time polymerase chain reaction (PCR). Histologically confirmed, gastritis was observed in 42% of infected non-treated mice at both 6 and 18 weeks post-infection. These mice showed an up-regulation of the expression of inflammatory cytokines and chemokines, as well as of toll-like receptors (TLRs) and MyD88, at both time points. Treatment with curcumin decreased the expression of all these mediators. No inflammation was observed by histology in this group. Curcumin treatment exerted a significant anti-inflammatory effect in H. pylori-infected mucosa, pointing to the promising role of a nutritional approach in the prevention of H. pylori induced deleterious inflammation while the eradication or prevention of colonization by effective vaccine is not available.

Infections on the rise: Raoultella spp., clinical and microbiological findings from a retrospective study, 2010-2014.

We performed a retrospective analysis of clinical and laboratory data over 5 years in a tertiary centre to assess clinical and microbiological characteristics of patients with Raoultella spp. infection. Raoultella spp. were deemed responsible for clinical infections in 57 patients (R. planticola, n = 32 and R. ornithinolytica, n = 25). The most prevalent diagnoses for R. planticola were cystitis (50%; n = 16) followed by bacteraemia and pneumonia (9.4%; n = 3); for R. ornithinolytica, cystitis (36%; n = 9) followed by pneumonia (24%; n = 6). Immunodeficiency was present in 18 patients (56.3%) with R. planticola and in 16 patients (64%) with R. ornithinolytica infection. Of these, 55.6% and 37.5% had diabetes and 27.8% and 18.% were solid organ transplant recipients, respectively. All isolates were sensitive to third-generation cephalosporins, fluoroquinolones and aminoglycosides. Mortality of infections with R. planticola (n = 5; 15.6%) was higher than for R. ornithinolytica (n = 2; 8.0%), but the difference was not statistically significant.

Serum Zn levels in dysphagic patients who underwent endoscopic gastrostomy for long term enteral nutrition

BACKGROUND AND AIMS Dysphagic patients who underwent endoscopic gastrostomy (PEG) usually present protein-energy malnutrition, but little is known about micronutrient malnutrition. The aim of the present study was the evaluation of serum zinc in patients who underwent endoscopic gastrostomy and its relationship with serum proteins, whole blood zinc, and the nature of underlying disorder. METHODS From patients that underwent gastrostomy a blood sample was obtained minutes before the procedure. Serum and whole blood zinc was evaluated using Wavelength Dispersive X-ray Fluorescence Spectroscopy. Serum albumin and transferrin were evaluated. Patients were studied as a whole and divided into two groups: head and neck cancer (HNC) and neurological dysphagia (ND). RESULTS The study involved 32 patients (22 males), aged 43-88 years: HNC = 15, ND = 17. Most (30/32) had low serum zinc, 17/32 presented normal values of whole blood zinc. Only two, with traumatic brain injury, presented normal serum zinc. Serum zinc levels showed no differences between HNC and ND patients. There was no association between serum zinc and serum albumin or transferrin. There was no association between serum and whole blood zinc. CONCLUSIONS Patients had low serum zinc when gastrostomy was performed, similar in HNC and ND, being related with prolonged fasting and unrelated with the underlying disease. Decrease serum zinc was unrelated with low serum proteins. Serum zinc was more sensitive than whole blood zinc for identifying reduced zinc intake. Teams taking care of PEG-patients should include zinc evaluation as part of the nutritional assessment, or include systematic dietary zinc supply.

Role of 13C-Urea Breath Test in Experimental Model of Helicobacter pylori Infection in Mice

Background:  Animal models have been widely used to study Helicobacter pylori infection. Evaluation of H. pylori infection status following experimental inoculation of mice usually requires euthanasia. The 13C‐urea breath test (13C‐UBT) is both sensitive and specific for detection of H. pylori in humans. Thus, it would be very useful to have such a test with the same accuracy for the follow‐up of this infection in animal models of gastric infection. Accordingly, the purpose of this study was to develop and evaluate a 13C‐UBT method for following the course of H. pylori infection in a mouse model.

Serum Zinc Evolution in Dysphagic Patients that Underwent Endoscopic Gastrostomy for Long Term Enteral Feeding

BACKGROUND AND OBJECTIVES Patients undergoing endoscopic gastrostomy (PEG) present with protein-energy malnutrition (PEM) but little is known about zinc status. Our aim was to evaluate serum zinc, its relationship with serum proteins and with the nature of the underlying disorder, during the first 3 months of PEG feeding. METHODS AND STUDY DESIGN Prospective observational study during a 3-month period after gastrostomy. Data was collected at initial PEG procedure (T0), after 4 (T1) and 12 weeks (T3). Initial evaluation included: age, gender, disorder causing dysphagia, Neurological Dysphagia (ND) or Head and Neck Cancer (HNC), NRS-2002, BMI, albumin, transferrin, zinc. At T1 and T3, a blood sample was collected for zinc, albumin, transferrin. Serum zinc evaluation was performed with ICP-AES - Inductively Coupled Plasma-Atomic Emission Spectroscopy. Patients were fed with homemade meals. RESULTS A total of 146 patients (89 males), 21-95 years were studied: HNC-56, ND-90 and low BMI in 78. Initial low zinc in 122; low albumin in 77, low transferrin in 94; low values for both proteins in 66. Regarding the serum protein evolution, their levels increase T0-T3, most patients reaching normal values. zinc has a slower evolution, most patients still displaying low zinc at T3. Significant differences between the 3 moments for zinc (p=0.011), albumin (p<0.0001) and transferrin (p=0.014). CONCLUSION PEG patients are prone to PEM and zinc deficiency. Most patients present decreased zinc, suggesting that zinc deficiency is common in PEG candidates and is not corrected during 3 months of enteral feeding. Zinc deficiency should be expected and teams taking care of PEG patients should use zinc supplementation.

SELENIUM IN DYSPHAGIC PATIENTS WHO UNDERWENT ENDOSCOPIC GASTROSTOMY FOR LONG TERM ENTERAL FEEDING.

BACKGROUND AND AIMS endoscopic gastrostomy (PEG) patients usually present protein-energy malnutrition, but little is known about selenium deficiency. We aimed to assess serum selenium evolution when patients underwent PEG, after 4 and 12 weeks. We also evaluated the evolution of albumin, transferrin and Body Mass Index and the influence of the nature of the underlying disease. METHODS a blood sample was obtained before PEG (T0), after 4 (T1) and 12 (T3) weeks. Selenium was assayed using GFAAS (Furnace Atomic Absorption Spectroscopy). The PEG patients were fed through homemade meals. Patients were studied as a whole and divided into two groups: head and neck cancer (HNC) and neurological dysphagia (ND). RESULTS we assessed 146 patients (89 males), between 21-95 years old: HNC-56; ND-90. Normal values of selenium in 79% (n=115); low albumin in 77, low transferrin in 94, low values for both serum proteins in 66. Low BMI in 78. Selenium has slow evolution, with most patients still displaying normal Selenium at T3 (82%). Serum protein levels increase from T0 to T3, most patients reaching normal values. The nature of the underlying disease is associated with serum proteins but not with selenium. CONCLUSIONS low serum selenium is uncommon when PEG is performed, after 4 and 12 weeks of enteral feeding and cannot be related with serum proteins levels or dysphagia cause. Enteral nutrition using customized homemade kitchen meals is satisfactory to prevent or correct Selenium deficiency in the majority of PEG patients.

Low serum chromium is rare in patients that underwent endoscopic gastrostomy for long term enteral feeding

BACKGROUND Patients that underwent Percutaneous Endoscopic Gastrostomy (PEG) present with protein-energy malnutrition. Trace elements are required in small quantities and Chromium (Cr) displays a major role in the metabolism. OBJECTIVE This study aims to evaluate Cr levels and its relationship with serum proteins, BMI and underlying diseases during the first 3 months of PEG feeding. METHODS Prospective observational study during 3-months, when PEG was performed (T0), after 4 (T1), and 12 weeks (T3). Initial evaluation included: age, gender, underlying disease, NRS-2002, BMI, serum albumin, transferrin and Cr concentration. At T1 and T3 a blood sample was collected for Cr, albumin and transferrin. A Graphite Furnace Atomic Absorption Spectroscopy was used to assess Cr. According with the underlying disease, patients were divided into two groups: head and neck cancer (HNC) and neurological dysphagia (ND). All patients were fed with homemade meals. RESULTS A one hundred and twenty-nine patients (80 males), 26-95 years old were studied: HNC-52; ND-77. The observed data included low mean values of BMI from 71 patients; low Cr-8, low albumin-70, low transferrin-85 and 57 with both proteins low. Albumin was associated with survival time ( P =0.024) and there was a significant correlation between albumin and Cr (r=0.217, P =0.012). A good evolution of Cr and proteins values was observed, with no low Cr levels at T3. CONCLUSION Low serum Cr is rare in PEG-patients, with no relationship to other studied parameters. For the minority of patients displaying low Cr before gastrostomy, homemade PEG meals seem to be effective.

Helicobacter pylori infection: the role of intestinal

no.: WS1.1 HELICOBACTER PYLORI INFECTION AND MARKERS OF GASTRIC CANCER RISK IN ALASKA NATIVE PEOPLE J. Keck,* K. Miernyk,* L. Bulkow,* J. Kelly, B. McMahon, F. Sacco, T. Hennessy* and M. G. Bruce* *Centers for Disease Control and Prevention, Anchorage, AK, USA; Alaska Native Tribal Health Consortium, Anchorage, AK, USA Background: Alaska Native gastric cancer incidence and mortality rates are 3 to 4-times higher than general US population rates. We evaluated pepsinogen I, pepsinogen I/II ratio, anti-H. pylori and CagA antibodies, and blood group to determine their association with gastric cancer development in Alaska Native people. Methods: We conducted a retrospective case-control study that matched gastric cancers reported to the Alaska Native Tumor Registry from 1969–2008 to three controls on known demographic risk factors for H. pylori infection, using previously collected sera from the Alaska Area Specimen Bank. Conditional logistic regression evaluated the associations between serum markers and gastric cancer. Results: We included 122 gastric cancer cases with sera predating cancer diagnosis (mean = 13 years) and 346 matched controls. One hundred and twelve cases (91.8%) and 285 controls (82.4%) had evidence of previous or ongoing H. pylori infection as measured by anti-H. pylori antibodies. Gastric cancer cases had 2.63-fold increased odds of positive anti-H. pylori antibodies compared with their matched controls (p = .01). In a multivariate model, non-cardia gastric cancer (n = 94) was associated with anti-H. pylori antibodies (adjusted OR 3.92, p = .004) and low pepsinogen I (aOR 6.04, p = .04). We found no association between gastric cancer and blood group, anti-CagA antibodies, or pepsinogen I/II ratio. Conclusions: Alaska Native people with gastric cancer had increased odds of previous H. pylori infection. Low pepsinogen I might function as a pre-cancer marker for non-cardia cancer. Impact: Future research to identify Alaska Native individuals with increased gastric cancer risk includes H. pylori genotype and host characteristic studies. Abstract no.: WS1.2 CLUSTERING OF HELICOBACTER PYLORI STRAINS FROM GASTRIC CANCER C. Wang, S. Zhan and Q. Dong Qingdao Municipal Hospital, Qingdao City, Chinano.: WS1.2 CLUSTERING OF HELICOBACTER PYLORI STRAINS FROM GASTRIC CANCER C. Wang, S. Zhan and Q. Dong Qingdao Municipal Hospital, Qingdao City, China Genetic differences between strains play an important role in the determination of clinical outcomes of Helicobacter pylori infection. This study aimed to determine the sequencing types of H. pylori strains from gastric cancer. Materials and Methods: Twenty-two strains of H. pylori were enrolled, including 12 strains from patients with gastric cancer. MLST was used to determine the sequencing type. Results: The seven genetic loci of H. pylori were PCR amplified and sequenced. Those sequences of the seven genes were concatenated, and aligned with the sequences of strains from Europe (5), Africa (5), Asia (5) and other parts of China (16) extracted from the MLST database. A neighbour-joining tree with a kimura 2-parameter model was subsequently constructed. The results showed that all 22 strains, as well as Asia strains from database fell into the HpEastAsia haplogroup which could divided into two groups, groups I and II. Group I consisted of seven cancer strains but only one non-cancer strain of H. pylori, in addition to five strains form database. Fisher’s exact test revealed a statistically significant difference (p = .027). Discussion and Conclusion: The clustering of cancer strains of H. pylori is consistent with a recent report showing that the phylogeopraphic origin of H. pylori is a determinant of gastric cancer risk. This may reflect the consequence of long-term interaction of the bacterium with individual hosts of different genetic ground. The results suggested that the sequencing types could possibly be used to predict the clinical outcomes of H. pylori infection. Abstract no.: WS1.3 LACK OF ASSOCIATION BETWEEN GENE POLYMORPHISMS OF ANGIOTENSIN CONVERTING ENZYME, NOD-LIKE RECEPTOR 1, TOLL-LIKE RECEPTOR 4 AND FAS/FASL WITH THE PRESENCE OF HELICOBACTER PYLORI-INDUCED PREMALIGNANT GASTRIC LESIONS AND GASTRIC CANCER IN CAUCASIANS J. Kupcinskas,* T. Wex, J. Bornschein, M. Selgrad, M. Leja, L. Jonaitis* and P. Malfertheiner *Department of Gastroenterology, Lithuanian University of Health Sciences, Kaunas, Lithuania; Clinic of Gastroenterology, Hepatology and Infectious Diseases, Otto von Guericke University, Magdeburg, Germany; Faculty of Medicine, University of Latvia, Digestive Diseases Center, Hospital Lizeners, Riga, Latvia Background: Several polymorphisms of genes involved in the immunological recognition of Helicobacter pylori and regulating apoptosis and proliferation have been linked to gastric carcinogenesis, however reported data are partially conflicting. The aim of our study was to evaluate potential associations between the presence of gastric cancer (GC) and high risk atrophic gastritis (HRAG) and polymorphisms of genes encoding Angiotensin converting enzyme (ACE), Nod-like receptor 1 (NOD1), Toll-like receptor 4 (TLR4) and FAS/FASL. Methods: Gene polymorphisms were analyzed in 574 subjects (GC: n = 114; HRAG: n = 222, controls: n = 238) of Caucasian origin. ACE I/D (rs4646994), NOD1 796G>A (rs5743336), TLR4 3725G>C (rs11536889), FAS 1377G>A (rs2234767), FAS 670A>G (rs1800682) and FASL 844T>C (rs763110) were genotyped by different PCR approaches and RFLP analysis. Results: Frequencies of genotypes in our study are similar to the data reported on subjects of Caucasian ethnicity. There was a tendency for NOD1 796G/G genotype to be associated with increased risk of HRAG (62.4% vs 54.5% in controls, p = .082). FAS 670G/G genotype was more frequent in HRAG when compared to controls, 23.9% and 17.2% respectively, however it failed to reach significance level (p = .077). We did not find any significant associations for all examined polymorphism in relation to GC or HRAG. NOD1 796G>A and TLR4 3725G>C gene polymorphisms were also not linked with Helicobacter pylori seropositivity status. Conclusions: ACE, NOD1, TRL4 and FAS/FASL gene polymorphisms are not linked with gastric carcinogenesis in Caucasians, and therefore they should not be considered as potential biomarkers for identifying individuals with higher risk for GC. Abstract no.: WS1.4 ATROPHIC GASTRITIS BY THE OLGA STAGES AND HELICOBACTER CAGA SEROPOSITIVITY IN GASTRIC CANCER T. Vorobjova,* K. Kull,* H. Saar,* R. Labotkin,* A. Zimmermann and H. Maaroos* *University of Tartu, Tartu, Estonia; University of Bern, Bern, Switzerlandno.: WS1.4 ATROPHIC GASTRITIS BY THE OLGA STAGES AND HELICOBACTER CAGA SEROPOSITIVITY IN GASTRIC CANCER T. Vorobjova,* K. Kull,* H. Saar,* R. Labotkin,* A. Zimmermann and H. Maaroos* *University of Tartu, Tartu, Estonia; University of Bern, Bern, Switzerland Introduction: Operative Link on Gastritis Assessment (OLGA) express extent of gastric atrophy in terms of gastritis staging, which severity should be related to gastric cancer. Aim: To study how the OLGA stages of atrophic gastritis are associated with the morphological type, and Helicobacter pylori CagA positivity in gastric cancer. Patients: Twenty two gastric carcinoma patients (8 male, 14 female; mean age 64 ± 12) were operated on. The intestinal type of carcinoma was diagnosed in 12, diffuse in 8, mixed and indeterminate type in two cases (according to Lauren). Methods: Gastric mucosa samples (altogether up to 15) from the each operation specimen were stained with haematoxylin and eosin. Tissue material was received from the primary tumour and the tumour surrounding antral and corpus mucosa. The stage of atrophy by OLGA was established by combining the extent of histologically scored atrophy with the topography of atrophy. IgG antibodies to H. pylori cell surface proteins and CagA were evaluated using ELISA. Results: Of the 12 patients with intestinal type of gastric cancer eight had OLGA stage III or IV, four had OLGA stage II and nobody had OLGA stage I (p < .05). Five patients with diffuse cancer had OLGA stage I and II, two had III stage and one had IV stage. There was no association of OLGA stage or cancer type with CagA positivity. Conclusion: Gastric cancer patients represented all stages of gastric atrophy from OLGA stage I to OLGA stage IV which was not associated with cancer type and CagA seropositivity. a 2011 Blackwell Publishing Ltd, Helicobacter 16 (Suppl. 1): 77–143 79 WS1 Gastric Cancer

Nutraceuticals: a new therapeutic approach against

no.: WS1.1 HELICOBACTER PYLORI INFECTION AND MARKERS OF GASTRIC CANCER RISK IN ALASKA NATIVE PEOPLE J. Keck,* K. Miernyk,* L. Bulkow,* J. Kelly, B. McMahon, F. Sacco, T. Hennessy* and M. G. Bruce* *Centers for Disease Control and Prevention, Anchorage, AK, USA; Alaska Native Tribal Health Consortium, Anchorage, AK, USA Background: Alaska Native gastric cancer incidence and mortality rates are 3 to 4-times higher than general US population rates. We evaluated pepsinogen I, pepsinogen I/II ratio, anti-H. pylori and CagA antibodies, and blood group to determine their association with gastric cancer development in Alaska Native people. Methods: We conducted a retrospective case-control study that matched gastric cancers reported to the Alaska Native Tumor Registry from 1969–2008 to three controls on known demographic risk factors for H. pylori infection, using previously collected sera from the Alaska Area Specimen Bank. Conditional logistic regression evaluated the associations between serum markers and gastric cancer. Results: We included 122 gastric cancer cases with sera predating cancer diagnosis (mean = 13 years) and 346 matched controls. One hundred and twelve cases (91.8%) and 285 controls (82.4%) had evidence of previous or ongoing H. pylori infection as measured by anti-H. pylori antibodies. Gastric cancer cases had 2.63-fold increased odds of positive anti-H. pylori antibodies compared with their matched controls (p = .01). In a multivariate model, non-cardia gastric cancer (n = 94) was associated with anti-H. pylori antibodies (adjusted OR 3.92, p = .004) and low pepsinogen I (aOR 6.04, p = .04). We found no association between gastric cancer and blood group, anti-CagA antibodies, or pepsinogen I/II ratio. Conclusions: Alaska Native people with gastric cancer had increased odds of previous H. pylori infection. Low pepsinogen I might function as a pre-cancer marker for non-cardia cancer. Impact: Future research to identify Alaska Native individuals with increased gastric cancer risk includes H. pylori genotype and host characteristic studies. Abstract no.: WS1.2 CLUSTERING OF HELICOBACTER PYLORI STRAINS FROM GASTRIC CANCER C. Wang, S. Zhan and Q. Dong Qingdao Municipal Hospital, Qingdao City, Chinano.: WS1.2 CLUSTERING OF HELICOBACTER PYLORI STRAINS FROM GASTRIC CANCER C. Wang, S. Zhan and Q. Dong Qingdao Municipal Hospital, Qingdao City, China Genetic differences between strains play an important role in the determination of clinical outcomes of Helicobacter pylori infection. This study aimed to determine the sequencing types of H. pylori strains from gastric cancer. Materials and Methods: Twenty-two strains of H. pylori were enrolled, including 12 strains from patients with gastric cancer. MLST was used to determine the sequencing type. Results: The seven genetic loci of H. pylori were PCR amplified and sequenced. Those sequences of the seven genes were concatenated, and aligned with the sequences of strains from Europe (5), Africa (5), Asia (5) and other parts of China (16) extracted from the MLST database. A neighbour-joining tree with a kimura 2-parameter model was subsequently constructed. The results showed that all 22 strains, as well as Asia strains from database fell into the HpEastAsia haplogroup which could divided into two groups, groups I and II. Group I consisted of seven cancer strains but only one non-cancer strain of H. pylori, in addition to five strains form database. Fisher’s exact test revealed a statistically significant difference (p = .027). Discussion and Conclusion: The clustering of cancer strains of H. pylori is consistent with a recent report showing that the phylogeopraphic origin of H. pylori is a determinant of gastric cancer risk. This may reflect the consequence of long-term interaction of the bacterium with individual hosts of different genetic ground. The results suggested that the sequencing types could possibly be used to predict the clinical outcomes of H. pylori infection. Abstract no.: WS1.3 LACK OF ASSOCIATION BETWEEN GENE POLYMORPHISMS OF ANGIOTENSIN CONVERTING ENZYME, NOD-LIKE RECEPTOR 1, TOLL-LIKE RECEPTOR 4 AND FAS/FASL WITH THE PRESENCE OF HELICOBACTER PYLORI-INDUCED PREMALIGNANT GASTRIC LESIONS AND GASTRIC CANCER IN CAUCASIANS J. Kupcinskas,* T. Wex, J. Bornschein, M. Selgrad, M. Leja, L. Jonaitis* and P. Malfertheiner *Department of Gastroenterology, Lithuanian University of Health Sciences, Kaunas, Lithuania; Clinic of Gastroenterology, Hepatology and Infectious Diseases, Otto von Guericke University, Magdeburg, Germany; Faculty of Medicine, University of Latvia, Digestive Diseases Center, Hospital Lizeners, Riga, Latvia Background: Several polymorphisms of genes involved in the immunological recognition of Helicobacter pylori and regulating apoptosis and proliferation have been linked to gastric carcinogenesis, however reported data are partially conflicting. The aim of our study was to evaluate potential associations between the presence of gastric cancer (GC) and high risk atrophic gastritis (HRAG) and polymorphisms of genes encoding Angiotensin converting enzyme (ACE), Nod-like receptor 1 (NOD1), Toll-like receptor 4 (TLR4) and FAS/FASL. Methods: Gene polymorphisms were analyzed in 574 subjects (GC: n = 114; HRAG: n = 222, controls: n = 238) of Caucasian origin. ACE I/D (rs4646994), NOD1 796G>A (rs5743336), TLR4 3725G>C (rs11536889), FAS 1377G>A (rs2234767), FAS 670A>G (rs1800682) and FASL 844T>C (rs763110) were genotyped by different PCR approaches and RFLP analysis. Results: Frequencies of genotypes in our study are similar to the data reported on subjects of Caucasian ethnicity. There was a tendency for NOD1 796G/G genotype to be associated with increased risk of HRAG (62.4% vs 54.5% in controls, p = .082). FAS 670G/G genotype was more frequent in HRAG when compared to controls, 23.9% and 17.2% respectively, however it failed to reach significance level (p = .077). We did not find any significant associations for all examined polymorphism in relation to GC or HRAG. NOD1 796G>A and TLR4 3725G>C gene polymorphisms were also not linked with Helicobacter pylori seropositivity status. Conclusions: ACE, NOD1, TRL4 and FAS/FASL gene polymorphisms are not linked with gastric carcinogenesis in Caucasians, and therefore they should not be considered as potential biomarkers for identifying individuals with higher risk for GC. Abstract no.: WS1.4 ATROPHIC GASTRITIS BY THE OLGA STAGES AND HELICOBACTER CAGA SEROPOSITIVITY IN GASTRIC CANCER T. Vorobjova,* K. Kull,* H. Saar,* R. Labotkin,* A. Zimmermann and H. Maaroos* *University of Tartu, Tartu, Estonia; University of Bern, Bern, Switzerlandno.: WS1.4 ATROPHIC GASTRITIS BY THE OLGA STAGES AND HELICOBACTER CAGA SEROPOSITIVITY IN GASTRIC CANCER T. Vorobjova,* K. Kull,* H. Saar,* R. Labotkin,* A. Zimmermann and H. Maaroos* *University of Tartu, Tartu, Estonia; University of Bern, Bern, Switzerland Introduction: Operative Link on Gastritis Assessment (OLGA) express extent of gastric atrophy in terms of gastritis staging, which severity should be related to gastric cancer. Aim: To study how the OLGA stages of atrophic gastritis are associated with the morphological type, and Helicobacter pylori CagA positivity in gastric cancer. Patients: Twenty two gastric carcinoma patients (8 male, 14 female; mean age 64 ± 12) were operated on. The intestinal type of carcinoma was diagnosed in 12, diffuse in 8, mixed and indeterminate type in two cases (according to Lauren). Methods: Gastric mucosa samples (altogether up to 15) from the each operation specimen were stained with haematoxylin and eosin. Tissue material was received from the primary tumour and the tumour surrounding antral and corpus mucosa. The stage of atrophy by OLGA was established by combining the extent of histologically scored atrophy with the topography of atrophy. IgG antibodies to H. pylori cell surface proteins and CagA were evaluated using ELISA. Results: Of the 12 patients with intestinal type of gastric cancer eight had OLGA stage III or IV, four had OLGA stage II and nobody had OLGA stage I (p < .05). Five patients with diffuse cancer had OLGA stage I and II, two had III stage and one had IV stage. There was no association of OLGA stage or cancer type with CagA positivity. Conclusion: Gastric cancer patients represented all stages of gastric atrophy from OLGA stage I to OLGA stage IV which was not associated with cancer type and CagA seropositivity. a 2011 Blackwell Publishing Ltd, Helicobacter 16 (Suppl. 1): 77–143 79 WS1 Gastric Cancer