Endoscopic three-categorical diagnosis of Helicobacter pylori infection using linked color imaging and deep learning: a single-center prospective study (with video).

BACKGROUND: Helicobacter pylori (H. pylori) eradication is required to reduce incidence related to gastric cancer. Recently, it was found that even after the successful eradication of H. pylori, an increased, i.e., moderate, risk of gastric cancer persists in patients with advanced mucosal atrophy and/or intestinal metaplasia. This study aimed to develop a computer-aided diagnosis (CAD) system to classify the status of H. pylori infection of patients into three categories: uninfected (with no history of H. pylori infection), currently infected, and post-eradication. METHODS: The CAD system was based on linked color imaging (LCI) combined with deep learning (DL). First, a validation dataset was formed for the CAD systems by recording endoscopic movies of 120 subjects. Next, a training dataset of 395 subjects was prepared to enable DL. All endoscopic examinations were recorded using both LCI and white-light imaging (WLI). These endoscopic data were used to develop two different CAD systems, one for LCI (LCI-CAD) and one for WLI (WLI-CAD) images. RESULTS: The diagnostic accuracy of the LCI-CAD system was 84.2% for uninfected, 82.5% for currently infected, and 79.2% for post-eradication status. Comparisons revealed superior accuracy of diagnoses based on LCI-CAD data relative based on WLI-CAD for uninfected, currently infected, and post-eradication cases. Furthermore, the LCI-CAD system demonstrated comparable diagnostic accuracy to that of experienced endoscopists with the validation data set of LCI. CONCLUSIONS: The results of this study suggest the feasibility of an innovative gastric cancer screening program to determine cancer risk in individual subjects based on LCI-CAD.

Endoscopic Kyoto classification of Helicobacter pylori infection and gastric cancer risk diagnosis.

Recent advances in endoscopic technology allow detailed observation of the gastric mucosa. Today, endoscopy is used in the diagnosis of gastritis to determine the presence/absence of Helicobacter pylori (H. pylori) infection and evaluate gastric cancer risk. In 2013, the Japan Gastroenterological Endoscopy Society advocated the Kyoto classification, a new grading system for endoscopic gastritis. The Kyoto classification organized endoscopic findings related to H. pylori infection. The Kyoto classification score is the sum of scores for five endoscopic findings (atrophy, intestinal metaplasia, enlarged folds, nodularity, and diffuse redness with or without regular arrangement of collecting venules) and ranges from 0 to 8. Atrophy, intestinal metaplasia, enlarged folds, and nodularity contribute to gastric cancer risk. Diffuse redness and regular arrangement of collecting venules are related to H. pylori infection status. In subjects without a history of H. pylori eradication, the infection rates in those with Kyoto scores of 0, 1, and ≥ 2 were 1.5%, 45%, and 82%, respectively. A Kyoto classification score of 0 indicates no H. pylori infection. A Kyoto classification score of 2 or more indicates H. pylori infection. Kyoto classification scores of patients with and without gastric cancer were 4.8 and 3.8, respectively. A Kyoto classification score of 4 or more might indicate gastric cancer risk.

Helicobacter pylori Infection, Gastric Cancer and Gastropanel.

Gastric cancer (GC) is one of the most widespread types of cancer worldwide. Helicobacter pylori infection has been clearly correlated with gastric carcinogenesis. At present and in the near future, the most important challenge is and will be the significant reduction of mortality due to GC. That goal can be achieved through the identification of higher-risk patients, such as those with atrophic gastritis, intestinal metaplasia and dysplasia. In this review we intend to discuss the importance of diagnosing H. pylori infection and chronic atrophic gastritis in preventing gastric cancer, using a new non-invasive test called GastroPanel. This test is a classification algorithm including four biochemical parameters pepsinogen I and II (PGI and PGII), gastrin-17 (G17), and anti-Helicobacter pylori antibodies (Ig G anti-Hp) measured in fasting sera, which allows to classify patients as having atrophic or non-atrophic gastritis and to find whether gastritis is associated or not with H. pylori infection. GastroPanel is not a "cancer test", but it can and should be used in the screening and diagnosis of subjects with a high cancer risk; still, a careful diagnostic made by superior digestive endoscopy is compulsory to find possible precancerous or cancerous lesions at an early and curable stage.

Helicobacter pylori: Helicobacter pylori gastritis--a novel distinct disease entity.

A global consensus report on Helicobacter pylori gastritis has been developed. Topics discussed include whether dyspepsia caused by H. pylori infection is separate from functional dyspepsia or not, the evaluation method for H. pylori-induced gastritis, eradication therapy for H. pylori gastritis to prevent gastric carcinogenesis and management after H. pylori eradication.

Kyoto global consensus report on Helicobacter pylori gastritis.

OBJECTIVE: To present results of the Kyoto Global Consensus Meeting, which was convened to develop global consensus on (1) classification of chronic gastritis and duodenitis, (2) clinical distinction of dyspepsia caused by Helicobacter pylori from functional dyspepsia, (3) appropriate diagnostic assessment of gastritis and (4) when, whom and how to treat H. pylori gastritis. DESIGN: Twenty-three clinical questions addressing the above-mentioned four domains were drafted for which expert panels were asked to formulate relevant statements. A Delphi method using an anonymous electronic system was adopted to develop the consensus, the level of which was predefined as ≥80%. Final modifications of clinical questions and consensus were achieved at the face-to-face meeting in Kyoto. RESULTS: All 24 statements for 22 clinical questions after extensive modifications and omission of one clinical question were achieved with a consensus level of >80%. To better organise classification of gastritis and duodenitis based on aetiology, a new classification of gastritis and duodenitis is recommended for the 11th international classification. A new category of H. pylori-associated dyspepsia together with a diagnostic algorithm was proposed. The adoption of grading systems for gastric cancer risk stratification, and modern image-enhancing endoscopy for the diagnosis of gastritis, were recommended. Treatment to eradicate H. pylori infection before preneoplastic changes develop, if feasible, was recommended to minimise the risk of more serious complications of the infection. CONCLUSIONS: A global consensus for gastritis was developed for the first time, which will be the basis for an international classification system and for further research on the subject.

Analysis of vacA/cagA genotypes/status in Helicobacter pylori isolates from Iranian children and their association with clinical outcome.

BACKGROUND/AIM: More than 50% of Iranian children are infected with Helicobacterpylori; however, no data exist about the association of vacA/cagA genotype/status with disease outcomes in them. We analyzed association of vacA/cagA genotypes/status of children's isolates with gastric inflammation status as the first step in H. pylori pathogenesis. MATERIALS AND METHODS: Antral biopsies for culture and histopathology were taken from 328 children in 1997-2009. vacA (s, m) alleles and cagA statuses of the isolates were determined by PCR. Histopathology was performed according to the Sydney system; gastritis was scored as normal, mild, moderate, severe, and follicular. RESULTS: A total of 159 culture-positive cases, with no mixed infections, were enrolled in the study. Of them, 60% were cagA-positive; 21.4%, 37.1%, 16.3%, and 25.2% cases were slm1, slm2, s2m1, and s2m2, respectively. Histopathology showed normal (4.4%), mild- chronic (31.4%), moderate-chronic (38.4%), severe-chronic (10.7%), and follicular gastritis (15.1%) cases. Thirty-four (21.4%) of the children had ulcers. Correlation (P < 0.05) was observed between more severe (moderate, severe, follicular) status and both vacAs1 allele and cagA-positive status. No significant relation was observed between genotype/status of vacA/cagA and ulcers (P > 0.05). CONCLUSION: vacAs1 and cagA are associated with more severe gastric inflammation in Iranian children. Association ofvacAs1 and cagA with more severe pathology in Iran may be similar to that of other parts of the world.

Gastroesophageal cancer: focus on epidemiology, classification, and staging.

Gastroesophageal cancer (GEC), comprising proximal esophagogastric junction (EGJ) and distal gastric cancer (GC), is a significant public health concern. The epidemiology of these tumors has significantly changed over the past several decades especially in developed countries. There is a recognized decrease in incidence and mortality of distal GC and an increase in incidence and mortality of proximal EGJ cancer. The changing epidemiology is thought to be mainly due to changing trends of risk factors such as lower incidence of Helicobacter pylori infection and increasing incidence of obesity and gastroesophageal reflux. Histologically, EGJ cancers are adenocarcinoma (AC), while distal esophagus may be squamous cell carcinoma (SCC) or AC. Distal GC is predominantly AC. Following anatomical and histological distinction, tumors are staged with endoscopic ultrasound (EUS), computerized tomography (CT), and often positron emission tomography (PET) with or without diagnostic laparoscopic and peritoneal washing. Accurate staging of tumors, with emphasis on excluding occult metastasis, is imperative to avoid unnecessary surgical resection. Therefore, it is crucial to understand how these tumors are classified, the associated epidemiology, and the current standards of staging prior to selecting the appropriate course of therapy. In this review we will discuss the epidemiology, classification, and staging of locally advanced GEC.

Helicobacter enterohepáticos distintos de Helicobacter pylori / Enterohepatic Helicobacter other than Helicobacter pylori

El género Helicobacter engloba bacterias Gram negativas que en un principio se consideraban pertenecientes al género Campylobacter, y desde 1989 se clasificaron en un género separado debido a características bioquímicas diferentes, con más de 24 especies identificadas y otras aún en estudio. H. pylori es el más conocido y tiene un importante papel etiopatogénico en la patología péptica y cáncer gástrico. Otros Helicobacter enterohepáticos (HEH) distintos de H. pylori colonizan el intestino, el árbol biliar y el hígado de animales y seres humanos con potencial patógeno. Las dificultades para el correcto aislamiento de estos microorganismos limitan la descripción de su prevalencia real y de las patologías que provocan. Múltiples estudios intentan desvelar las diferentes implicaciones clínicas de los HEH. Patologías como la hepatopatía crónica, hepatitis autoinmune, hepatocarcinoma, enfermedad hepatobiliar autoinmune, litiasis biliar, colangiocarcinoma y cáncer de vesícula biliar, cáncer de páncreas, diverticulitis de Meckel, apendicitis aguda y enfermedad inflamatoria intestinal se han relacionado con diferentes especies de HEH con diferentes resultados, aunque con una mayor prevalencia que en sujetos sanos. No obstante, estos datos son insuficientes para sacar conclusiones definitivas por el momento. Por último, el papel más conocido de los HEH en la patología intestinal es la producción de cuadros diarreicos agudos y crónicos referidos inicialmente como Campylobacter. H. pullorum se ha identificado en pacientes con gastroenteritis aguda. La correcta identificación de HEH como productores de gastroenteritis infecciosa radica en su sensibilidad antibiótica, generalmente sensible a macrólidos y resistente a quinolonas (AU)

The Helicobacter genus includes Gram negative bacteria which were originally considered to belong to the Campylobacter genus. They have been classified in a separate genus since 1989 because they have different biochemical characteristics, with more than 24 species having been identified and more still being studied. H. pylori is the best known. It has an important etiopathogenic role in peptic ulcer disease and gastric cancer. Enterohepatic Helicobacters (EHH) other than H. pylori colonize the bowel, biliary tree and liver of animals and human beings with pathogenic potential. The difficulties existing to correctly isolate these microorganisms limit the description of their true prevalence and of the diseases they cause. Many studies have tried to discover the different clinical implications of EHH. Diseases like chronic liver disease, autoimmune hepatitis, hepatocarcinoma, autoimmune hepatobiliary disease, biliary lithiasis, cholangiocarcinoma and gallbladder cancer, Meckel´s diverticulum, acute appendicitis and inflammatory bowel disease have been related with different EHH species with different results, although their prevalence is greater than in healthy subjects. However, these data are currently not sufficient to draw definitive conclusions. Finally, the best known role of EHH in bowel disease is production of acute and chronic diarrhea pictures initially referred to as Campylobacter. H. pullorum has been identified in patients with acute gastroenteritis. The correct identification of EHH as producers of infectious gastroenteritis is found in its antibiotic susceptibility. It is generally macrolidesusceptible and quinolone-resistant (AU)

The EGFR expression in gastric mucosa of children infected with Helicobacter pylori.

PURPOSE: Epidermal growth factor receptor (EGFR) modulates balance between proliferation and apoptosis in gastric mucosa of the gastrointestinal tract. The aim of the study was to evaluate immunohistochemically the EGFR expression in epithelial and gland cells of antral mucosa in children infected with Helicobacter pylori (H. pylori). MATERIAL/METHODS: The study included 44 children, aged from 5 to 18 years (mean age 13+/-3.4 years) with dyspeptic symptoms, of whom 30 (68.2%) children were infected with H. pylori, 14 (31.8%) children constituted controls. Endoscopic and histopathological assessment of antral mucosa samples was performed according to the Sydney System. Samples taken from gastroscopy were prepared to evaluate EGFR expression in epithelial and gland cells of antrum mucosa according to the manual of a detection kit of EnVision+System-HRP (DAKO). RESULTS: In children H. pylori infected, the EGFR expression in epithelial cells of antral mucosa equaled on average 82.5+/-15 cells/mm2 and ranged from 45.0 to 98.0 cells/mm2 as well as differed statistically significantly when compared to controls (10.2+/-5.0 cells/mm2) (p<0.001). In children with H. pylori infection, the EGFR expression in gland cells of antral mucosa ranged from 2.0 to 85.0 cells/mm2 (mean 25.7+/-22.6 cells/mm2); was lower and differed statistically significantly from controls (54.2 +/- 29.6 cells/mm2) (p<0.001). In children H. pylori infected, there was a statistically significant difference (p<0.001) between the EGFR expression in epithelial and in gland cells of antral mucosa. CONCLUSION: The increased EGFR expression in epithelial cells in comparison with gland cells of antral mucosa in children with H. pylori infection may suggest its role in regeneration processes of gastric mucosa.

Helicobacter pylori gastritis updated Sydney classification applied in our material.

(Full text is available at http://www.manu.edu.mk/prilozi). BACKGROUND. Hp inhabits the stomach of more than 50% of humans and is the most frequent cause of chronic gastritis worldwide. The purpose of this research has been to present the importance of combining topographical, morphological and etiological information of diagnostic evaluation on grading gastritis in our material according to the Updated Sydney Classification, as well as to represent the frequency and the evaluation of Hp gastritis after eradication in order to prevent the development of gastric cancer. MATERIALS AND METHODS. 154 cases of gastric mucosa (endoscopic biopsies) which were fixed in buffered neutral formalin and embedded in paraffin were invwstigated. Tissue sections (5microm thick) were cut and stained with H&E, May Grunwald Giemsa and Silver stain. The biopsy cases were analysed in an attempt to assess the major histopathological features of gastritis. The histopathological major variables were graded on a scale of 3 (mild, moderate and severe). RESULTS. There were 36 (23.37%) cases positive for Hp (22.2%, 72.2%, 5.5%). Atrophy was positive in 23 (14.93%) cases with the scale (47.8%; 47.8%; 4.34%). Dysplasia was positive in 13 (8.44%) cases with the scale (84.6%; 7.6%; 7.6%). Intestinal metaplasia was positive in 25 (16.2%) with the scale (76%; 20%, 4%). There were 6 (3.8%) cases of MZL, which were treated appropriately. CONCLUSIONS. Our data indicate the importannce of early eradication of Helicobacter pylori in order to prevent the eventual development of gastric cancer. These findings should influence the treatment of gastric cancers. Key words: Updated Sydney System of Classification, Hp gastritis, morphology.

[An update on rickettsiosis]. / L'actualité des rickettsioses.

Rickettsiae are strictly intracellular bacteria belonging to the Rickettsiaceae family. They are transmitted by various arthropods species, which are either vectors or reservoirs for the bacteria. The specific association between Rickettsieae and the vector are extensively studied, moreover Rickettsieae associated diseases are part of a continuously evolving field. Nevertheless, some rickettsiosis, such as epidemic typhus, have been described since the 16th century. Emerging diseases related to these bacteria are being investigated as well as new species, the implication of which is not always clear in human pathology when they are discovered. Some of these diseases are benign, others may be potentially fatal. Clinicians must therefore be aware of them. These issues are reviewed.

OLGA staging for gastritis: a tutorial.

Atrophic gastritis (resulting mainly from long-standing Helicobacter pylori infection) is a major risk factor for (intestinal-type) gastric cancer development and the extent/topography of the atrophic changes significantly correlates with the degree of cancer risk. The current format for histology reporting in cases of gastritis fails to establish an immediate link between gastritis phenotype and risk of malignancy. The histology report consequently does not give clinical practitioners and gastroenterologists an explicit message of use in orienting an individual patient's clinical management. Building on current knowledge of the biology of gastritis and incorporating experience gained worldwide by applying the Sydney System for more than 15 years, an international group of pathologists (Operative Link for Gastritis Assessment) has proposed a system for reporting gastritis in terms of stage (the OLGA staging system). Gastritis staging arranges the histological phenotypes of gastritis along a scale of progressively increasing gastric cancer risk, from the lowest (stage 0) to the highest (stage IV). This tutorial aims to provide unequivocal information on how to consistently apply the OLGA staging system in routine diagnostic histology practice.

Diagnóstico no invasivo de Helicobacter pylori: ¿serología, prueba de aliento con C-urea o antígenos de Helicobacter pylori en material fecal? / Noninvasive diagnosis of Helicobacter pylori: serología, test of breath with C-urea or antigens of Helicobacter pylori in fecal material?

La infección por Helicobacter pylori se constituye como la infección crónica más frecuente en la especie humana. Esta infección se asocia con la patogénesis de enfermedades del estómago como la gastritis, la úlcera péptica duodenal, la úlcera péptica gástrica, el cáncer gástrico y los linfomas tipo MALT del estómago, y una gran variedad de enfermedades extradigestivas incluyendo enfermedades he matológicas, dermatológicas, cardiovasculares y autoinmunes. El diagnóstico de la infección por Helicobacter pylori se puede establecer por métodos invasivos, dependientes de la endoscopia digestiva alta, y por métodos no-invasivos, que no requieren endoscopia, como son la serología, la prueba de aliento con urea marcada con 13C y la detección de antígenos de Helicobacter pylori en materia fecal. En este módulo se analizará la utilización de las pruebas no-invasivas en el diagnóstico y manejo de la infección por Helicobacter pylori, de tal manera que el médico esté en condiciones de solicitar e interpretar adecuadamente las pruebas disponibles en el medio.Palabras claves: Helicobacter pylori, diagnóstico, serología, prueba de aliento con 13C urea, detección de antígenos en materia fecal.

Summary: Infection by Helicobacter pylori is the most common chronic infection in human kind. Helicobacter pylori infection has been associated with the pathogenesis of gastric diseases such as gastritis, duodenal ulcer, gastric ulcer, gastric cancer and MALT lymphomas, and with a wide variety of extradigestive diseases including hematologic, dermatologic, cardiovascular and autoimmune. Diagnosis of Helicobacter pylori infection can be established by invasive methods, by means of endoscopy, and by non-invasive methods including serology, 13C-urea breath test and Helicobacter pylori antigen stool test. The present module describes and compares these non-invasive methods for the diagnosis and treatment of Helicobacter pylori infection, to inform the physician about the differences between...

Relationship between the severity of hepatitis C virus-related liver disease and the presence of Helicobacter species in the liver: a prospective study.

AIM: To determine the presence of Helicobacter species DNA in the liver of chronic hepatitis C (CHC) patients with and without cirrhosis as compared to controls, and to identify the bacterial species involved. METHODS: Seventy-nine consecutive patients (HBV and HIV negative) with a liver sample obtained after liver biopsy or hepatic resection were studied: 41 with CHC without cirrhosis, 12 with CHC and cirrhosis, and 26 controls (HCV negative). Polymerase chain reactions (PCRs) targeting Helicobacter 16S rDNA and species-specific were performed on DNA extracted from the liver. A gastric infection with H pylori was determined by serology and confirmed by 13C-urea breath test. RESULTS: Overall, Helicobacter 16S rDNA was found in 16 patients (20.2%). Although positive cases tended to be higher in CHC patients with cirrhosis (41.6%) than in those without cirrhosis (17.0%) or in controls (15.4%), the difference was not statistically significant (P = 0.08). H pylori-like DNA was identified in 12 cases and H. pullorum DNA in 2, while 2 cases remained unidentified. Gastric infection with H pylori was found in only 2 of these patients. CONCLUSION: Our results do not confirm the association of Helicobacter species DNA in the liver of CHC patients with advanced liver disease. The lack of correlation between positive H pylori serology and the presence of H pylori-like DNA in the liver may indicate the presence of a variant of this species.

Gastroenteritis and transmission of Helicobacter pylori infection in households.

The mode of transmission of Helicobacter pylori infection is poorly characterized. In northern California, 2,752 household members were tested for H. pylori infection in serum or stool at a baseline visit and 3 months later. Among 1,752 person considered uninfected at baseline, 30 new infections (7 definite, 7 probable, and 16 possible) occurred, for an annual incidence of 7% overall and 21% in children <2 years of age. Exposure to an infected household member with gastroenteritis was associated with a 4.8-fold (95% confidence interval [CI] 1.4-17.1) increased risk for definite or probable new infection, with vomiting a greater risk factor (adjusted odds ratio [AOR] 6.3, CI 1.6-24.5) than diarrhea only (AOR 3.0, p = 0.65). Of probable or definite new infections, 75% were attributable to exposure to an infected person with gastroenteritis. Exposure to an H. pylori-infected person with gastroenteritis, particularly vomiting, markedly increased risk for new infection.

Comparative classification and grading of Helicobacter pylori gastritis in patients with gastric cancer and patients with functional dyspepsia.

BACKGROUND: It has previously been shown that corpus-dominant grade and activity of Helicobacter pylori gastritis in combination with intestinal metaplasia in the antrum or corpus are risk markers for the development of stomach cancer. If one point is scored for each of these three parameters, a gastric cancer risk index is obtained that permits prediction of the risk of gastric cancer developing on the soil of H. pylori gastritis. The aim of the present study was to evaluate the accuracy of the gastric cancer risk index based on a large number of patients compared with dyspeptic controls. METHODS: In 415 biopsied patients with gastric carcinoma, biopsy specimens taken from the antrum and corpus were investigated retrospectively. From this group of patients, 244 patients positive for H. pylori were compared with 244 sex- and age-matched H. pylori-infected patients with functional dyspepsia. RESULTS: H. pylori gastritis was detected in 395 carcinoma patients (95.2%). The 244 sex- and age-matched patients significantly more frequently had corpus-dominant H. pylori gastritis (compared with NUD controls). The incidence of intestinal metaplasia was also significantly increased. For a gastric cancer risk index score of 3 points (i.e. corpus pronounced grade and activity of gastritis, and intestinal metaplasia in antrum or corpus), a sensitivity of 93% and a specificity of 85% for the presence of gastric carcinoma can be calculated. CONCLUSION: Using the proposed risk index, the topographic grading of H. pylori gastritis in the antrum and corpus enables the diagnosis of a 'risk gastritis' to be made.

A proinflammatory genetic profile increases the risk for chronic atrophic gastritis and gastric carcinoma.

BACKGROUND & AIMS: Pro-inflammatory polymorphisms within the genes interleukin (IL)-1B and IL-1RN are associated with risk for gastric carcinoma (GC) in Helicobacter pylori-infected individuals. We aimed to determine the association between variation of the tumor necrosis factor (TNF)-alpha gene and the risk for chronic atrophic gastritis (CAG) and GC. We also investigated the extent to which the combined effect of proinflammatory genetic polymorphisms (IL-1B, IL-1RN, and TNF-alpha), and the combined effect of TNF-alpha and bacterial genotypes each influence such a risk. METHODS: In a case-control study including 306 controls, 221 individuals with chronic gastritis, and 287 GC patients, the TNF-alpha-308 and IL-1B-511 bi-allelic polymorphisms, the IL-1RN variable number of tandem repeats (VNTR), and the H. pylori genes vacA (s and m regions) and cagA were genotyped. RESULTS: We found that carriers of the TNF-alpha-308*A allele are at increased risk for GC development with an odds ratio (OR) of 1.9 (95% confidence interval [CI], 1.3-2.7). For both CAG and GC, the odds of developing disease increased with the number of high-risk genotypes. Individuals carrying high-risk genotypes at the 3 loci are at increased risk for CAG and GC with an OR of 5.8 (95% CI, 1.1-31.0) and 9.7 (95% CI, 2.6-36.0), respectively. The risk for GC was not affected significantly by the combination of bacterial and TNF-alpha-308 genotypes. CONCLUSIONS: These findings show that a proinflammatory polymorphism in the TNF-alpha gene is associated with increased risk for GC, and that it is possible to define a specific genetic profile associated with highest risk for CAG and GC.

Effect of cytochrome P4502C19 genotypic differences on cure rates for gastroesophageal reflux disease by lansoprazole.

BACKGROUND AND OBJECTIVES: The acid-inhibitory effect of lansoprazole depends on differences in cytochrome P450 (CYP) 2C19 genotypes. We assessed whether therapeutic effects of lansoprazole on gastroesophageal reflux disease (GERD) depended on the CYP2C19 genotype status in relation to the grade of GERD. METHODS: A total of 65 patients with GERD (grades A-D) completed treatment with lansoprazole, by taking 30 mg orally once a day for 8 weeks. The CYP2C19 genotype status of patients was determined by polymerase chain reaction-restriction fragment length polymorphism analysis. Before and after treatment, esophageal endoscopy was performed. GERD was considered to be cured on the basis of endoscopic findings at the end of treatment. Plasma lansoprazole levels could be determined at 3 hours after the last 30-mg dose of lansoprazole in the 27 genotyped patients. RESULTS: Cure rates for GERD depended significantly on the CYP2C19 genotype status, as well as the grade of GERD before treatment. Cure rates in the homozygous extensive, heterozygous extensive, and poor metabolizer groups were 45.8%, 67.9%, and 84.6%, respectively. Cure rates in the groups with GERD grade A, grade B, and grade C or D were 85.0%, 60.0%, and 45.0%, respectively. The cure rate in patients with the homozygous extensive metabolizer genotype of CYP2C19 with a GERD grade of C or D was very low (16.7%). Plasma lansoprazole levels in patients with the homozygous extensive metabolizer genotype were the lowest of the 3 groups. CONCLUSIONS: CYP2C19 genotype status, as well as the grade of GERD before treatment, is one of the determinants for the success or failure of treatment of GERD with lansoprazole. The low cure rate in patients with the homozygous extensive metabolizer genotype appeared to be a result of these patients having the lowest plasma lansoprazole levels among the 3 genotype groups.

Gastric Helicobacter species infection in murine and gerbil models: comparative analysis of effects of H. pylori and H. felis on gastric epithelial cell proliferation.

C57BL/6 mice and Mongolian gerbils were infected with Helicobacter felis and Helicobacter pylori SS1 strain to investigate the effects of different Helicobacter species on gastric inflammation and epithelial cell proliferation in different animal models. At 4 weeks, gerbils infected with H. pylori or H. felis developed antral gastritis. Onset of gastritis varied between the models, with mice infected with H. pylori having minimal inflammation at 8 weeks. In mice, H. felis, but not H. pylori, induced significantly increased epithelial cell proliferation in the cardia and corpus at 8 weeks, but no changes were observed at 4 weeks. In gerbils, both H. pylori and H. felis significantly increased antral epithelial cell proliferation at 4 weeks. Epithelial cell proliferation induced by H. felis in gerbils was twice that stimulated by H. pylori. These studies demonstrate host differences in the development of Helicobacter species-induced gastric inflammation and a marked difference in epithelial cell proliferation induced by H. pylori and H. felis in 2 animal models.

[Morphology of gastritis and Helicobacter pylori infection]. / Morfoloska slika gastritisa i infekcije Helicobacterom pylori.

Helicobacter pylori infection almost invariably results in chronic gastritis. The Sydney System (1990) emphasised the importance of combining topographical, morphological and etiological aspects in attempt to make clinical useful diagnosis of chronic gastritis. The aims of revised Sydney System in Houston (1994), Texas, were to improve terminology of chronic gastritis emphasising distinction between nonatrophic and atrophic gastritis, and in addition to determinate special forms of gastritis. The special forms of gastritis were described and diagnostic criteria were provided. Principles and grading of histological division of Sydney System were only slightly modified, grading being improved by the provision of a visual scale. Endoscopy and histological findings of 1062 patients from University Hospital Merkur were compared to evaluate the value of endoscopic division of Sydney System, and the modified grading proposed by Houston classification. There was no correlation between endoscopic and histological findings. Localisation of inflammatory cells was either 1) superficial or 2) diffuse in the mucosa, respectively. In Helicobacter pylori positive patients the most common finding was chronic active gastritis, and in Helicobacter pylori negative superficial and inactive chronic gastritis.