Risk of gastric carcinoma will be low in generations born at turn of the 20th and 21st centuries in Finland. Modelling NORDCAN data of the age group specific incidence rates of gastric cancer with PLS-regression and with attention to age ('age effect') and year of the birth ('cohort effect').

BACKGROUND AND METHODS: We examined in NORDCAN database how the annual age group-specific incidence rates (IR) of gastric cancer (GCA), and correspondingly the GCA risk, have declined in Finland during the twentieth century, and whether this decline corresponds to a decrease in the cohort-specific prevalence rate of Helicobacter pylori (Hp) gastritis that is considered an important precancerous risk condition for GCA. RESULTS: In modelling with partial least squares regression (PLSR), the logarithmically transformed IRs (ln(IR) of GCA were well explained with age and birth cohort as explanatory model variables. By considering the observed (actual) and the PLSR-modelled IRs, the IR of GCA (and the risk of GCA) has decreased gradually in Finland from 1900 onward, cohort by cohort. By prediction of the future with PLSR, the IRs of GCA will be markedly lower in all cohorts during the twenty-first century than in the twentieth century. By PLSR modelling, less than 10 GCA cases per 100,000 people are predicted to appear annually in cohorts (generations) born at the turn of the 20th and 21st centuries, even when these people will be 60-80 years old in the years 2060-2070. CONCLUSIONS: The IR of GCA and GCA risk progressively declined by cohort in Finland during the whole twentieth century. This decline corresponds in extent and time window to earlier observations in the decline of the prevalence rate of Hp gastritis in the same birth cohorts and supports the hypothesis of the role of Hp gastritis as an important risk condition of GCA.

When will Helicobacter pylori gastritis disappear in history in Finland?

OBJECTIVES: To predict how the10-year birth cohort specific prevalence rates of chronic non-atrophic (CG) and atrophic gastritis (AG), related to Helicobacter pylori (Hp) infection, will decline during the 21st century among the native adult Finns. MATERIALS AND METHODS: The predictions are based as continuums of our earlier observations of gradual and significant declines in birth cohort specific prevalence rates of CG and AG in endoscopic biopsies from gastric antrum and corpus of 2298 adult dyspeptic outpatients or asymptomatic volunteers born 1890-1977 that were endoscopied in 1972-1997 in Finland. RESULTS AND DISCUSSION: We could predict that the Hp related CG and AG will gradually disappear in history among the native Finns during the 21st century. From the 2020s onward, the CG and AG would decrease with time in prevalence rate, cohort-by-cohort, and would be more and more highlighted in the middle aged or elderly age groups only. Finally, since all birth cohorts (generations) infected with Hp have passed away by 2080, the Hp related gastrites would not appear anymore in notable counts among the native Finns. Correspondingly, gastric cancers and peptic ulcers (both duodenal and gastric), which are etiopathogenetically linked with Hp gastrites, would similarly become gradually more and more infrequent and rare disorders among native Finns during the 21st century.

Prevalence rates of heathy stomach mucosa, chronic non-atrophic and atrophic gastritis in endoscopic biopsies in adults born in Finland in 1890-1977.

BACKGROUND: Helicobacter pylori infection, chronic gastritis (CG) and atrophic gastritis (AG) are a continuum of consecutive events in the stomach mucosa. We studied the birth cohort and age group-specific prevalence rates of 'healthy' (N) and 'diseased' stomachs with CG or AG in endoscopic biopsies in adult people born in Finland in 1890-1977. MATERIALS AND METHODS: Study series consisted of 690 and 1608 adults with a diagnostic gastroscopy in 1972-1997. All subjects were divided to 10-year age groups and birth cohorts. Based on biopsy histology, relative frequencies (prevalences) of N, CG and AG were estimated by the observed number of cases with N, CG and AG in each study category. RESULTS: Prevalence rate of a histologically 'diseased' stomach (CG or AG) decreased and that of 'healthy' stomach (N) increased, cohort-by-cohort, from 1900 onward by rate 9-12% per every 10-year period in the two study subpopulations, respectively. Prevalences of CG remained unchanged over study groups when N, CG and AG were noted concurrently. By noting 'diseased' stomachs only, the prevalence rate of AG increased, and that of CG decreased with age, at rate 9-13% per every 10 years of calendar age. CONCLUSIONS: Over 70-year period from 1900 onward, the prevalence rate of 'diseased' stomach (CG or AG) decreased and that of 'healthy' (N) stomach increased in birth cohorts over 50%, by rate about 10% over every 10-year period of time. In birth cohorts, CG progressed to AG with aging of the subjects at a rate of about 10% over every 10 years of calendar age.

Challenges in evaluation of screening for gastric cancer among men based on nonrandomized design.

BACKGROUND: Objective was to quantify biases in screening for gastric cancer when comparing attenders to nonattenders using serum pepsinogen I (SPGI) level as primary test. METHODS: In mid 1990s, all men aged 51-65 years from two Finnish cities were invited to SPGI screening. Mortality and premature mortality in attenders were compared to nonattenders. Efficacy of screening was studied by 15 years' follow-up of standardized mortality ratio (SMR) and potential years of life lost (PYLL) due to gastric cancer. Bias due to selective attendance was quantified using corrective coefficients based on total cancer incidence and mortality, and gastric cancer-specific incidence and mortality for total population and nonattenders. RESULTS: In 1994-1996, men aged 51-65 years (16,872) were invited to SPGI assay and 12,175 men (72%) attended. SPGI was 25 microg/l or less in 610 (5%) men, indicating severe atrophic gastritis (AG). Post-screening gastroscopy was performed to 435 men with low SPGI. Of these, 168 men were referred for treatment due to abnormal focal lesions. Attributable proportions in reductions of SMR and PYLL from gastric cancer due to screening were 59% and 67%. After correcting for selective participation, attributable proportions were reduced to 23% and 39%. CONCLUSIONS: Biomarker screening by low SPGI among middle-aged men followed by upper gastrointestinal endoscopy decreased long-term and premature mortality due to gastric cancer. However, in spite of methodological corrections done, the results do not justify any firm conclusions or recommend general screening programs. Randomized trials are warranted for this purpose.

Risk of gastric cancer in Helicobacter pylori infection in a 15-year follow-up.

OBJECTIVE: We investigated the risk of gastric cancer among men with Helicobacter pylori (H. pylori) infection or atrophic gastritis (AG) in a 15-year follow-up. MATERIALS AND METHODS: Study population consists of 12,016 men aged 50-65 years at the beginning of the follow-up in 1994-1996. Serum levels of pepsinogen I (SPGI) and antibodies (IgG) to H. pylori (HpAb) were assayed from serums collected in 1994-1996. Incidence of gastric cancer in the study population was assessed in follow-up from 1994 to 2011 by data from the nationwide cancer registry. Based on SPGI and HpAb values, standardized incidence ratios (SIRs) of gastric cancer were calculated in three subgroups, that is, in those with a healthy stomach, those with H. pylori infection but without AG and those with AG. Risk ratios (RR) of gastric cancer were calculated using SIR of subgroups. RESULTS: During 15 years, seven gastric cancers appeared per 79,928 person years among men with healthy stomachs, 50 cancers per 92,533 person years in men with H. pylori infection but without AG, and 8 per 8658 person years in men with AG. Risk ratio (RR) of stomach cancer in men with H. pylori infection was 5.8 (95%CI: 2.7-15.3) compared to men with healthy stomachs, and 9.1 (95%CI: 2.9-30.0) in men with AG. There were no differences in cancer risk between cardia and distal stomach. CONCLUSIONS: Risk of gastric cancer is low in men with healthy stomachs. It is significantly increased in those with H. pylori infection and more in those with AG.

Chronic gastritis.

Prevalence of chronic gastritis has markedly declined in developed populations during the past decades. However, chronic gastritis is still one of the most common serious pandemic infections with such severe killing sequelae as peptic ulcer or gastric cancer. Globally, on average, even more than half of people may have a chronic gastritis at present. Helicobacter pylori infection in childhood is the main cause of chronic gastritis, which microbial origin is the key for the understanding of the bizarre epidemiology and course of the disease. A life-long and aggressive inflammation in gastritis results in destruction (atrophic gastritis) of stomach mucosa with time (years and decades). The progressive worsening of atrophic gastritis results subsequently in dysfunctions of stomach mucosa. Atrophic gastritis will finally end up in a permanently acid-free stomach in the most extreme cases. Severe atrophic gastritis and acid-free stomach are the highest independent risk conditions for gastric cancer known so far. In addition to the risks of malignancy and peptic ulcer, acid-free stomach and severe forms of atrophic gastritis may associate with failures in absorption of essential vitamins, like vitamin B12, micronutrients (like iron, calcium, magnesium and zinc), diet and medicines.

Natural coniferous resin lacquer in treatment of toenail onychomycosis: an observational study.

In in vitro tests, natural coniferous resin from the Norway spruce (Picea abies) is strongly antifungal. In this observational study, we tested the clinical effectiveness of a lacquer composed of spruce resin for topical treatment of onychomycosis. Thirty-seven patients with clinical diagnosis of onychomycosis were enrolled into the study. All patients used topical resin lacquer treatment daily for 9 months. A mycological culture and potassium hydroxide (KOH) stain were done from nail samples in the beginning and in the end of the study. Treatment was considered effective, if a mycological culture was negative and there was an apparent clinical cure. At study entry, 20 patients (20/37; 54%; 95% CI: 38-70) had a positive mycological culture and/or positive KOH stain for dermatophytes. At study end, the result of 13 patients was negative (13/19; 68%; 95% CI: 48-89). In one case (1/14; 7%; 95% CI: 0-21) the mycological culture was initially negative, but it turned positive during the study period. By 14 compliant patients (14/32; 44%; 95% CI: 27-61), resin lacquer treatment was considered clinically effective: complete healing took place in three cases (9%) and partial healing in 11 cases (85%). The results indicate some evidence of clinical efficacy of the natural coniferous resin used for topical treatment of onychomycosis.

Rationale in diagnosis and screening of atrophic gastritis with stomach-specific plasma biomarkers.

BACKGROUND AND AIMS: Atrophic gastritis (AG) results most often from Helicobacter pylori (H. pylori) infection. AG is the most important single risk condition for gastric cancer that often leads to an acid-free or hypochlorhydric stomach. In the present paper, we suggest a rationale for noninvasive screening of AG with stomach-specific biomarkers. METHODS: The paper summarizes a set of data on application of the biomarkers and describes how the test results could be interpreted in practice. RESULTS: In AG of the gastric corpus and fundus, the plasma levels of pepsinogen I and/or the pepsinogen I/pepsinogen II ratio are always low. The fasting level of gastrin-17 is high in AG limited to the corpus and fundus, but low or non-elevated if the AG occurs in both antrum and corpus. A low fasting level of G-17 is a sign of antral AG or indicates high intragastric acidity. Differentiation between antral AG and high intragastric acidity can be done by assaying the plasma G-17 before and after protein stimulation, or before and after administration of the proton pump inhibitors (PPI). Amidated G-17 will rise if the antral mucosa is normal in structure. H. pylori antibodies are a reliable indicator of helicobacter infection, even in patients with AG and hypochlorhydria. CONCLUSIONS: Stomach-specific biomarkers provide information about the stomach health and about the function of stomach mucosa and are a noninvasive tool for diagnosis and screening of AG and acid-free stomach.

The Sydney System for classification of gastritis 20 years ago.

The roots of research into gastritis go back into the early decades of the 20th century. Modern aspects of its classification and knowledge of its biological course and consequences were relatively well known even at the time that Helicobcter pylori was discovered by Robin Warren and Barry Marshall in 1982. This discovery, however, significantly changed the field, establishing that the commonest form of gastritis is simply an infectious disease, a finding that raised enormous interest in the subject amongst gastroenterologists, microbiologists, pathologists and basic researchers. However, many of these "new" players in the field often had a limited knowledge of the morphological aspects of gastric inflammations and chronic gastritis. As a consequence in the late 1980's a Working Party was set up to review the biology and natural course of chronic gastritis, to propose a new classification for gastritis, and to provide simple guidelines for reporting the pathology of gastritis in endoscopic biopsies in an attempt to bring uniformity to the subject and facilitate comparative studies in what was to be an era of high research activity. These guidelines, The Sydney System: A New Classification of Gastritis was presented to the World Congress of Gastroenterology in Sydney in 1990, and was later published as six papers in the Journal of Gastroenterology and Hepatology. Now, twenty years on, this review looks back on the birth of Sydney System and why it is still important and successful.

Hypochlorhydric stomach: a risk condition for calcium malabsorption and osteoporosis?

Malabsorption of dietary calcium is a cause of osteoporosis. Dissolution of calcium salts (e.g. calcium carbonate) in the stomach is one step in the proper active and passive absorption of calcium as a calcium ion (Ca(2+)) in the proximal small intestine. Stomach acid markedly increases dissolution and ionization of poorly soluble calcium salts. If acid is not properly secreted, calcium salts are minimally dissolved (ionized) and, subsequently, may not be properly and effectively absorbed. Atrophic gastritis, gastric surgery, and high-dose, long-term use of antisecretory drugs markedly reduce acid secretion and may, therefore, be risk conditions for malabsorption of dietary and supplementary calcium, and may thereby increase the risk of osteoporosis in the long term.

Prevalence of undiagnosed advanced atrophic corpus gastritis in Finland: an observational study among 4,256 volunteers without specific complaints.

OBJECTIVE: The objective of this observational study was to estimate the prevalence of advanced atrophic corpus gastritis (ACG) among Finnish adult volunteers without specific complaints using a biomarker blood test. The objective also was to assess the feasibility and acceptance of the biomarker test among the volunteers. MATERIALS AND METHODS: GastroView biomarker test (Biohit Oyj, Helsinki, Finland) was performed on mostly fingerprick blood samples from 4,256 volunteers (average age 56 years, range 18-92 years), independent of symptoms. GastroView biomarker test was offered to citizens at public events during 2007-2009. The test consisted of the measurement of pepsinogen I and II levels (and ratio) and H. pylori IgG antibody level in plasma by ELISA. RESULTS: Altogether 3.5% (150 individuals) of all 4,256 volunteers had ACG. In the age group of 70 or over, the prevalence of ACG increased to 8% (62 individuals). Altogether 19% (819 individuals) of all volunteers and 37% (56 individuals) of those with ACG had an ongoing H. pylori infection. In volunteers with ACG, the diagnosis was new in 95% (142 individuals), 5% (7 individuals) had received vitamin B12 supplementation and 13% (20 individuals) had received PPI medication according to a self-administered questionnaire; and 26% (39 individuals) reported gastrointestinal reflux like symptoms. CONCLUSIONS: This study shows that advanced ACG is a common disease among Finnish adults, and remains to be undiagnosed in most under the current healthcare practice. The biomarker test shows high feasibility and acceptance among the general public, and is simple to perform even in "field" conditions.

Clinical use of proton-pump inhibitors but not H2-blockers or antacid/alginates raises the serum levels of amidated gastrin-17, pepsinogen I and pepsinogen II in a random adult population.

OBJECTIVE: Proton-pump inhibitors (PPIs), H(2) receptor antagonists (H(2)RAs) and antacids/alginates reduce intragastric acidity and may thus influence normal gastric physiology. The purpose of this study was to examine the effect of these compounds on serum levels of amidated gastrin-17 (G-17) and pepsinogens (PGI & PGII) in a large, random, adult Swedish population sample with uninfected stomach mucosa. MATERIAL AND METHODS: The initial sample subjects (n=1000, mean age 50 years, range 20-80 years) completed a questionnaire on the use of acid inhibitory drugs 1 week and/or 3 months before study entry. All subjects (n=590) with normal gastric mucosa as delineated by serum biomarkers were included. Among them, serum levels of PGI, PGII and G-17 were compared between those who used acid inhibitory drugs and those who did not. RESULTS: The serum levels of G-17 or pepsinogens in the subjects who reported use of H(2)RAs (n=18) or antacid/alginates (n=66) during the previous 3 months did not differ from those in non-users (n=471). However, the median levels of G-17 and pepsinogens were significantly (p<0.001) higher among the PPI users (n=35) than among non-users: the levels were approximately doubled. The ratio of PGI/PGII was, however, similar between PPI users and non-users, or those using antacids/alginates or H(2)RAs. Among subjects using PPIs, the serum levels of pepsinogens correlated positively (p<0.01) with the serum levels of G-17. CONCLUSIONS: PPIs but not antacids/alginates or H(2)RAs markedly increase the fasting levels of serum amidated G-17 and pepsinogens among ordinary patients in everyday clinical practice.

Effects of Norway spruce (Picea abies) resin on cell wall and cell membrane of Staphylococcus aureus.

Resin salve prepared from Norway spruce (Picea abies) has been used for centuries in traditional medicine to treat skin diseases. The authors studied with transmission and scanning electron microscopy, and with electron physiology, changes in cell wall and cell membrane of Staphylococcus aureus after exposure of the bacterial cultures to resin. After exposure, cell wall thickening, cell aggregation, changed branching of fatty acids, and dissipation of membrane potential of the bacterial cells were observed. The authors conclude that spruce resin affects the cell viability via changes in the cell wall and membrane, and impairs, thereby, the synthesis of energy in the bacteria.

GastroPanel® Biomarker Assay: The Most Comprehensive Test for Helicobacter pylori Infection and Its Clinical Sequelae. A Critical Review.

BACKGROUND/AIM: Several clinical conditions seriously hamper the diagnostic accuracy of the commonly used tests for Helicobacter pylori (Hp), 13C-urea breath test (UBT) and stool antigen test (SAT). The present communication is a critical review of the potential limitations of UBT and SAT, and describes the approach on how these can be avoided. Drawbacks of the Hp tests: False-negative results are most often due to low bacterial load in the stomach due to: i) use of proton pump inhibitor medication; ii) use of antibiotics; iii) presence of atrophic gastritis and hypoacid stomach; iv); bleeding peptic ulcer; v) gastric cancer (GC) and vi) mucosal-associated lymphatic tissue lymphoma. The UBT also gives false-positive results when urease-producing bacterial species, other than Hp colonize an acid-free stomach. Importantly, neither UBT nor SAT are capable of diagnosing atrophic gastritis, thus missing the patients at highest risk for GC. GastroPanel® (Biohit Oyj, Finland) circumvents these shortcomings with a serological test consisting of a panel of stomach-specific biomarkers: pepsinogen I, pepsinogen II, gastrin-17 and Hp antibodies. GastroPanel® is a tool for non-invasive examination of i) dyspeptic patients for exclusion or diagnosis of Hp or atrophic gastritis, also disclosing the status of gastric acid output; ii) for screening of asymptomatic individuals at risk of GC; and iii) for comprehensive diagnosis of Hp infection. GastroSoft® application integrates the biomarker profile with the patient's medical information, accurately classifying the biomarker profiles into eight diagnostic categories. CONCLUSION: Given that Hp is the single most important risk factor of GC, the non-invasive diagnosis and screening of Hp should be based on more accurate and more comprehensive testing than UBT or SAT alone. The GastroPanel® is such test, being completely devoid of the known serious shortcomings of UBT and SAT.

Does the eradication of Helicobacter pylori delay the diagnosis of gastric cancer?

OBJECTIVE: To assess the frequency of gastric cancer patients having received eradication treatment of Helicobacter pylori, and whether this treatment has any influence on the delay in the diagnosis or the stage of the tumours at the time of the operation. MATERIAL AND METHODS: A total of 119 consecutive patients with gastric cancer were interviewed preoperatively between 2001 and 2003 at the Department of Surgery, Helsinki University Central Hospital. Abdominal symptoms, previous endoscopies, previous H. pylori testing and eradication therapies were recorded. RESULTS. Of these patients, 112 (94%) had abdominal symptoms before the cancer diagnosis, and in 110 patients (92%) these symptoms were alarming or had changed before the cancer diagnosis. Thirty-five patients (29%) had received H. pylori eradication therapy prior to the diagnosis of gastric cancer (15 after onset or change in symptoms, 10 more than 5 years prior to the cancer diagnosis). The median duration of alarm, new or changed symptoms was longer among patients with H. pylori eradication therapy after the onset or change in their symptoms as compared to other patients (12.0 versus 4.5 months, p=0.001). However, there was no difference in the tumour stages at time of the operation between the eradication and no eradication groups. A previous gastroscopy within 2 years prior to the cancer diagnosis was performed in 17 (14%) patients. Diffuse-type cancers were missed significantly more often in endoscopies than cancers of intestinal type. CONCLUSION: Previous H. pylori eradication may delay the detection of gastric cancer if it is given during symptoms caused by tumour.

Role of earlier gastroscopy in predicting findings on repeat gastroscopy in a population with a low H. pylori prevalence.

OBJECTIVE: Repeat gastroscopy is not recommended for patients without alarm symptoms and with a normal earlier gastroscopy. However, there is little information available on the consequences of this recommendation. The objective of this study was to examine the role of earlier gastroscopy results in predicting the findings at repeat gastroscopy. MATERIAL AND METHODS: Patients with previous gastroscopies presenting for a new gastroscopy during 2004-05 were included consecutively. A total of 293 patients who had undergone a gastroscopy a mean of 7.7 years (range 0.6-25.4 years) before the present gastroscopy were included in the study. The patients completed a questionnaire. The associations between the findings of the present gastroscopy and the findings of the previous gastroscopy and other patient characteristics were analysed by stepwise logistic regression. RESULTS: Nine percent of the patients were positive for Helicobacter pylori infection. An abnormal macroscopic finding, defined as any erosion, ulcer or other macroscopic finding with the exception of hiatus hernia, at the repeat gastroscopy was significantly positively associated with: 1) an abnormal finding at a previous gastroscopy (OR 2.94, 95% CI 1.48-5.85), 2) obesity (body mass index, BMI >30) (OR 2.89, 95% CI 1.28-6.55), 3) the presence of alarm symptoms (OR 2.68, 95% CI 1.29-5.56), and negatively associated with 4) the use of proton pump inhibitors (OR 0.48, 95% CI 0.24-0.98). The findings were not associated with age. CONCLUSIONS: Abnormal earlier gastroscopy findings, obesity and the presence of alarm symptoms were the strongest indicators of abnormal findings at repeat gastroscopy. Our results support a restrained gastroscopy policy in patients with no alarm symptoms and a normal earlier gastroscopy.

Serum biomarkers provide an accurate method for diagnosis of atrophic gastritis in a general population: The Kalixanda study.

OBJECTIVE: Serological biomarkers can be used for non-invasive diagnosis of gastritis and atrophic gastritis. The aim of this study was to compare the validity of serum levels of pepsinogen I (PGI) and II (PGII), gastrin-17 (G-17) and Helicobacter pylori antibodies (Hpab) with that of the gold standard histology for diagnosis of atrophic gastritis in a population sample from Northern Sweden. MATERIAL AND METHODS: In all, 1000 subjects underwent endoscopies with biopsies. Serum biomarkers were available in 976 subjects for independent diagnosis of gastric mucosal status using a predetermined diagnostic algorithm. RESULTS: Overall agreement between histology and serological biomarkers in diagnosing corpus atrophy was 96% (CI 95%: 95-97%). Sensitivity and specificity of markers for atrophic gastritis were 71% (CI 68-74%) and 98% (CI 97-99%) respectively, corresponding to 69% (CI 95%: 66-72%) and 98% (95% CI 97-99%) positive and negative predictive values. The positive likelihood ratio was 35.5 (95% CI: 35.0-36.0%). In subgroups with normal stomachs, H. pylori non-atrophic gastritis and H. pylori-negative gastritis by histology, the prevalence of corpus atrophy diagnosed with the biomarkers was 0.8% and 4.9%, respectively. In total, 6.6% of subjects in the study population had corpus atrophy according to the serological biomarkers. CONCLUSIONS. Serological biomarkers show a high degree of accuracy as a non-invasive method to diagnose corpus atrophy, which is common in the general population.

Serological biomarker testing helps avoiding unnecessary endoscopies in obese patients before bariatric surgery.

BACKGROUND: To assess the value of serological biomarker testing as a substitute for esophagogastroduodenoscopy (EGDS) in pre-operative assessment of patients referred for bariatric surgery. METHODS: Sixty-five obese patients with a mean age of 43 years (range: 21-65) and a mean body mass index (BMI) of 44 (range: 36-59) were studied. The patients were tested with a four-biomarker panel: pepsinogen I and II, gastrin-17 (basal and stimulated), and Helicobacter pylori (HP) antibodies (GastroPanel®, Biohit Oyj, Finland). On the basis of the biomarker test, the patients were classified into the HS (healthy stomach) group (n = 22) with the normal biomarker profile and the NHS (non-healthy stomach) group (n = 43). The classification of patients into HS and NHS was evaluated against the gold standard, i.e. EGDS with biopsies. RESULTS: The concordance (Cohen's kappa) between the biomarker test and gastric histology was 0.68; 95% CI 0.504-0.854, with an overall agreement of 84.6% (95% CI 73.9-91.4%). In the NHS group, all 43 patients had biopsy-confirmed chronic gastritis: 39 non-atrophic HP-gastritis, 4 atrophic antrum gastritis (AGA) of moderate severity.In the HS group only 6 patients had mild superficial H.pylori negative gastritis. Of the 22 HS subjects with the normal biomarker profile, 20 (31% of all 65) had no complaints either, while the remaining two had reflux symptoms with esophagitis. In the NHS group 10 patients had esophagitis and 8 had also reflux symptoms. CONCLUSIONS: The normal biomarker profile is an excellent surrogate for healthy stomach, implicating that pre-operative EGDS could have been avoided in 31% of our asymptomatic bariatric surgery patients who had the normal biomarker profile.

Pathology and molecular biology of gastric cancer.

Several attempts to classify gastric cancer (GCA) have been made over the past decades. Most successful, and widely used, is the classification by Laurén, which distinguishes, by microscopical morphology alone, two main cancer pathogeneses, diffuse (DGCA) and intestinal (IGCA) subtypes, which appear clearly as dissimilar clinical and epidemiological entities. Here we review the main differences in epidemiology, histopathology, and molecular pathology of the two main subtypes of gastric carcinomas based on Laurén classification. In clinical practice, however, clinical staging, particularly in predicting the survival, still remains superior to all classifications of gastric cancer independent of cancer type. The existence of local precursor lesions or conditions of IGCA tumours, i.e. Helicobacter pylori gastritis, atrophic gastritis (AG), intestinal metaplasia (IM), adenoma, dysplasia, and intramucosal neoplasia, is firmly established. The links of DGCA with intestinal-type epithelium, AG or IM are poor, or do not exist. So far, H. pylori gastritis is the only universal precursor condition for DGCA. It implies that AG and achlorhydria are of minor significance and infrequent in the development of DGCA but are important steps in that of IGCA. Despite an increasing body of data, the overall view on molecular pathology of GCA remains fragmentary. No consistent differences in the molecular pathology of GCA subtypes to meet the Laurén classification have been established. With the exception of TP53, no gene mutation occurring regularly in both histological types of GCA has been reported. Chromosomal aberrations and loss of heterozygosity seem to be non-specific and do not follow any consistent route in the progression of GCA. Microsatellite instability is more commonly found in IGCA than in DGCA. The present epigenetic data suggest that most of the decrease (or loss) of gene expression may be explained by promoter hypermethylation which is more often found in IGCA. In DGCA specific genes such as CDH1 are more often hypermethylated. Compared with GCA, in premalignant condition lesions gene mutations and chromosomal aberrations are infrequent. Epigenetic dysregulation might also represent a major mechanism for altered gene expression in premalignant stages in gastric carcinogenesis.