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.     

Endoscopy-based Kyoto classification score of gastritis related to pathological topography of neutrophil activity

BACKGROUND Endoscopy-based Kyoto classification for gastritis and pathological topographic distribution of neutrophil infiltration are correlated with gastric cancer risk.AIM To investigate the association between Kyoto classification and the topographic distribution of neutrophil activity.METHODS Kyoto classification score, ranging from 0 to 8, consisted of atrophy, intestinal metaplasia, enlarged folds, nodularity, and diffuse redness. Neutrophil activity was scored according to the updated Sydney System using biopsy samples obtained from the greater curvature of the corpus and the antrum. The participants were divided into four categories, inactive stomach, antrumpredominant gastritis, pangastritis, and corpus-predominant gastritis, based on the topographic distribution of neutrophil activity. Effects of sex, age, body mass index, drinking habit, smoking habit, family history of gastric cancer, serum Helicobacter pylori(H. pylori) antibody, and Kyoto score on topography of neutrophil infiltration were analyzed.RESULTS A total of 327 patients(comprising 50.7% women, with an average age of 50.2 years) were enrolled in this study. H. pylori infection rate was 82.9% with a mean Kyoto score of 4.63. The Kyoto score was associated with the topographic distribution of neutrophil activity. Kyoto scores were significantly higher in the order of inactive stomach, antrum-predominant gastritis, pangastritis, and corpuspredominant gastritis(3.05, 4.57, 5.21, and 5.96, respectively). Each individual score of endoscopic findings(i.e., atrophy, intestinal metaplasia, enlarged folds, nodularity, and diffuse redness) was correlated with the topographic distribution of neutrophil activity. On multivariate analysis, the Kyoto score, age, and serum H. pylori antibody were independently associated with the topographic distribution of neutrophil activity.CONCLUSION The Kyoto classification score was associated with the topographic distribution of neutrophil activity.     

Kyoto classification in patients who developed multiple gastric carcinomas after Helicobacter pylori eradication

BACKGROUND Endoscopic Kyoto classification predicts gastric cancer risk; however, the score in the patients with primary gastric cancer after Helicobacter pylori(H. pylori) eradication therapy is unknown.AIM To elucidate the Kyoto classification score in patients with both single gastric cancer and multiple gastric cancers developed after H. pylori eradication.METHODS The endoscopist recorded the Kyoto classification at the endoscope and the Kyoto classification score at the time of the first diagnosis of gastric cancer after H. pylori eradication. The score was compared between single gastric cancer group and multiple gastric cancers group.RESULTS The Kyoto score at the time of diagnosis of 45 cases of gastric cancer after H. pylori eradication was 4.0 points in average. The score was 3.8 points in the single gastric cancer group, and 5.1 points in the multiple gastric cancers group. The multiple group had a significantly higher score than the single group(P = 0.016). In the multiple gastric cancers group, all the patients(7/7) had 5 or higher Kyoto score, while in single gastric cancer group, the proportion of patients with a score of 5 or higher was less than half, or 44.7%(17/38).CONCLUSION Patients diagnosed with gastric cancer after H. pylori eradication tended to have advanced gastritis. In particular, in cases of multiple gastric cancers developed after H. pylori eradication, the endoscopic Kyoto classification score tended to be 5 or higher in patients with an open type atrophic gastritis and the intestinal metaplasia extended to the corpus.     

Kyoto classification of gastritis: Advances and future perspectives in endoscopic diagnosis of gastritis

This editorial provides an update of the recent evidence on the endoscopy-based Kyoto classification of gastritis, clarifying the shortcomings of the Kyoto classification, and providing prospects for future research, with particular focus on the histological subtypes of gastric cancer (GC) and Helicobacter pylori (H. pylori) infection status. The total Kyoto score is designed to express GC risk on a score ranging from 0 to 8, based on the following five endoscopic findings: Atrophy, intestinal metaplasia (IM), enlarged folds (EF), nodularity, and diffuse redness (DR). The total Kyoto score reflects H. pylori status as follows: 0, ≥ 2, and ≥ 4 indicate a normal stomach, H. pylori-infected gastritis, and gastritis at risk for GC, respectively. Regular arrangement of collecting venules (RAC) predicts non-infection; EF, nodularity, and DR predict current infection; map-like redness (MLR) predicts past infection; and atrophy and IM predict current or past infection. Atrophy, IM, and EF all increase the incidence of H. pylori-infected GC. MLR is a specific risk factor for H. pylori-eradicated GC, while RAC results in less GC. Diffuse-type GC can be induced by active inflammation, which presents as EF, nodularity, and atrophy on endoscopy, as well as neutrophil and mononuclear cell infiltration on histology. In contrast, intestinal-type GC develops via atrophy and IM, and is consistent between endoscopy and histology. However, this GC risk-scoring design needs to be improved.     

胃黏膜肠上皮化生内镜诊断和分级的研究进展

胃黏膜肠上皮化生（gastric intestinal metaplasia,GIM）是一种癌前组织病理学改变,其临床意义在于对胃癌发生风险的提示,有着大面积肠上皮化生背景的胃黏膜具有较高的癌变风险;另外,不完全型GIM与肠型胃癌相关。因此,GIM的内镜下监测对及时发现和管理早期胃癌具有重要意义。可操作的GIM胃癌风险评估分级提供了较好地针对肠上皮化生的胃黏膜癌变风险评估,但每次评估需要标准的活检,增加了损伤风险,GIM内镜分级在此背景下被提出,但其应用受内镜诊断GIM的准确性和临床使用的便捷性所制约。笔者分析了各类内镜下诊断技术对GIM的诊断效果,结合人工智能辅助识别GIM面积,综述EGGIM评分的可行性。     

Comparison between the Linked Color and White Light Imaging Combined Score in the Evaluation of High-Risk Population of Gastric Cancer

Background: For patients undergoing gastroscopy, it is necessary to judge whether there is Helicobacter pylori infection, atrophy/intestinal metaplasia. This study aimed to evaluate and compare the light color imaging (LCI) and white light imaging (WLI) combined score during gastroscopy.Methods: Each included patient underwent normalized gastroscopy with WLI and LCI, and all notable findings were photographed. Four endoscopists reviewed the endoscopic images of each patient. The clinical information, results of the H. pylori tests were unavailable at review. The total LCI and WLI scores of each patient were calculated and their detection in high-risk populations of gastric cancer were evaluated. The diagnostic values of LCI and WLI for intestinal metaplasia were also calculated.Results: In total, 392 patients were included in the study. The degree of inflammation and proportion of active inflammation cases were significantly higher in the H. pylori gastritis group than in the non-H. pylori gastritis group; their endoscopic manifestations were also different. The LCI combined score improved the diagnostic value of each individual observation index in the diagnosis of H. pylori infection compared with the WLI combined score. The sensitivity, specificity, and accuracy were 91.9% (91.9% vs 81.5%), 91.1% (91.1% vs 80.2%), and 95.8% (95.8% vs 93.2%), respectively. The accuracy of LCI in the diagnosis of intestinal metaplasia was higher than that of WLI (83.4% vs 69.6%).Conclusion: The LCI and LCI combined score improved the diagnosis of H. pylori gastritis and intestinal metaplasia, and it is considered valuable in identifying the high-risk population of gastric cancer.     

High microsatellite instability predicts good prognosis in intestinal-type gastric cancers

Background and Aim: A subset of gastric cancers showed high microsatellite instability (MSI‐H). The reported clinicopathological features of MSI‐H gastric cancers are heterogeneous, and specific factors associated with prognosis have not been identified. Methods: We analyzed the clinicopathological characteristics and prognostic factors in a large series (161 cases) of MSI‐H gastric cancers, and compared the results to 315 cases of microsatellite‐stable or low microsatellite‐instable gastric cancers. Results: The frequency of MSI‐H gastric cancers was 9% (161/1786). MSI‐H gastric cancers have distinct clinicopathological features, including female sex, older age, antral location, well‐to‐moderate differentiation, intestinal‐type Lauren classification, expanding‐type Ming classification, a non‐signet‐ring cell component, the presence of a mucinous component, a moderate‐to‐severe lymphoid stromal reaction, and a lower tumor stage. The MSI‐H phenotype was associated with better prognosis (P = 0.044), and male sex (P = 0.035, hazard ratios [HR]: 0.23), intestinal‐/mixed‐type Lauren classification (P < 0.001, HR: 0.09) and lower tumor stages (1 and 2, P = 0.001, HR: 0.08) were independently‐favorable prognostic factors. Conclusions: With unique clinicopathological features, intestinal‐type MSI‐H gastric cancers are associated with good prognosis and can be classified as a different subset of gastric cancers.     

hsa-mi R-29c and hsa-miR-135b differential expression as potential biomarker of gastric carcinogenesis

AIM: To investigate the expression profiles of hsa-mi R-29 c and hsa-mi R-135 b in gastric mucosal samples and their values as gastric carcinogenesis biomarkers. METHODS: The expression levels of hsa-mi R-29 c and hsa-mi R-135 b in normal gastric mucosa, non-atrophic chronic gastritis, intestinal metaplasia and intestinaltype gastric adenocarcinoma were analysed using quantitative real-time PCR. The difference between hsa-mi R-29 c and hsa-mi R-135 b expression profiles in the grouped samples was evaluated by ANOVA and Student's t-test tests. The results were adjusted for multiple testing by using Bonferroni's correction. P values ≤ 0.05 were considered statistically significant. To evaluate hsa-mi R-29 c and hsa-mi R-135 b expressions as potential biomarkers of gastric carcinogenesis, we performed a receiver operating characteristic curve analysis and the derived area under the curve, and a Categorical Principal Components Analysis. In silico identification of the genetic targets of hsa-mi R-29 c and hsa-mi R-135 b was performed using different prediction tools, in order to identify possible genes involved in gastric carcinogenesis.RESULTS: The expression levels of hsa-mi R-29 c were higher in normal gastric mucosal samples, and decreased progressively in non-atrophic chronic gastritis samples, intestinal metaplasia samples and intestinal-type gastric adenocarcinoma samples. The expression of hsa-mi R-29 c in the gastric lesions showed that non-atrophic gastritis have an intermediate profile to gastric normal mucosa and intestinal-type gastric adenocarcinoma, and that intestinal metaplasia samples presented an expression pattern similar to that in intestinal-type gastric adenocarcinoma. This micro RNA(mi RNA) has a good discriminatory accuracy between normal gastric samples and(1) intestinal-type gastric adenocarcinoma; and(2) intestinal metaplasia, and regulates the DMNT3 A oncogene. hsa-mi R-135 b is up-regulated in non-atrophic chronic gastritis and intestinal metaplasia samples and down-regulated in normal gastric mucosa and intestinal-type gastric adenocarcinoma samples. Non-atrophic chronic gastritis and intestinal metaplasia are significantly different from normal gastric mucosa samples. hsa-mi R-135 b expression presented a greater discriminatory accuracy between normal samples and gastric lesions. This mi RNA was associated with Helicobacter pylori presence in non-atrophic chronic gastritis samples and regulates the APC and KLF4 tumour suppressor genes.CONCLUSION: Our results provide evidence of epigenetic alterations in non-atrophic chronic gastritis and intestinal metaplasia and suggest that hsa-mi R-29 c and hsa-mi R-135 b are promising biomarkers of gastric carcinogenesis.     

Role of N-Methyl-N-nitrosourea in the Induction of Intestinal Metaplasia and Gastric Adenocarcinoma in Mongolian Gerbils Infected with Helicobacter pylori

Background: Progression from intestinal metaplasia to neoplasia has not been demonstrated experimentally. The hypothesis that gastric adenocarcinoma arises from intestinal metaplasia was tested in a Mongolian gerbil model of Helicobacter pylori (H. pylori) infection. Methods: One hundred and fourteen specific pathogen-free gerbils were divided in five groups. A and D: infected with H. pylori and administered the carcinogen N-methyl-N-nitrosourea (MNU); C and E: received MNU; B: H. pylori, but no MNU. Animals were killed at 41 weeks, stomachs were mapped, and the relationship between metaplasia and cancer was assessed. Results: Intestinal metaplasia occurred more frequently in the H. pylori-infected, MNU-treated gerbils than in those receiving H. pylori inoculation only (P &lt; 0.01). Carcinomas arose only in H. pylori-infected animals receiving MNU (8 well differentiated, 2 poorly differentiated, and 10 signet ring). Intestinal metaplasia occurred more frequently in association with intestinal-type carcinoma. Conclusions: Intestinal metaplasia and adenocarcinoma arise in stomachs subjected to the same injuries (in this study, H. pylori and MNU). Only two intestinal-type carcinomas were contiguous to intestinal metaplasia; all other tumors developed most commonly at non-metaplastic sites. This suggests that in this animal model H. pylori and MNU induce several phenotypes of gastric cancer, but intestinal metaplasia may be a direct precursor only in a subset of the intestinal-type tumors.     

Most Gastric Cancer Occurs on the Distal Side of the Endoscopic Atrophic Border

Background: The endoscopic atrophic border indicates the extent of atrophic gastritis. The aims of this study were to examine the relation of intestinal and diffuse types of gastric cancer to the atrophic border and to study the pathologic condition of the atrophic border. Methods: In 83 patients with gastric cancer the extent of atrophic gastritis was assessed macroscopically. In 46 patients gastric biopsy specimens were also taken, to compare the histologic features of gastritis proximal and distal to the atrophic border. Results: Eighty-five per cent of gastric cancers (including 93% of intestinal type) occurred on the distal side of the atrophic border. Early diffuse gastric cancer arose closer to the atrophic border than intestinal-type cancer and was more likely to be sited proximal to it. Histologically, the grade of polymorphonuclear cell infiltration (inflammatory activity) and Helicobacter pylori density were significantly greater on the proximal side (P &lt; 0.05), whereas the grades of glandular atrophy and intestinal metaplasia were significantly greater distally (P &lt; 0.001). Conclusions: The atrophic border delineates the area of atrophic gastritis and intestinal metaplasia, and it is within the distal part of the stomach that gastric cancer occurs most frequently. Endoscopists should observe the distal side particularly carefully to identify early gastric cancer. The relationship of the two histologic types of cancer to areas of intestinal metaplasia and 'active' inflammation may have implications for the pathogenesis of cancer and, if so, for the potential protective effect of H. pylori eradication.     

Efficacy of Helicobacter pylori eradication for the prevention of metachronous gastric cancer after endoscopic resection for early gastric cancer

Helicobacter pylori(H.pylori)plays an important role in gastric carcinogenesis,as the majority of gastric cancers develop from H.pylori-infected gastric mucosa.The rate of early gastric cancer diagnosis has increased in Japan and Korea,where H.pylori infection and gastric cancer are highly prevalent.Early intestinal-type gastric cancer without concomitant lymph node metastasis is usually treated by endoscopic resection.Secondary metachronous gastric cancers often develop because atrophic mucosa left untreated after endoscopic treatment confers a high risk of gastric cancer.The efficacy of H.pylori eradication for the prevention of metachronous gastric cancer remains controversial.However,in patients who undergo endoscopic resection of early gastric cancer,H.pylori eradication is recommended to suppress or delay metachronous gastric cancer.Careful and regularly scheduled endoscopy should be performed to detect minute metachronous gastric cancer after endoscopic resection.     

The gastric mucosa in gastric cancer patients in a low-incidence area

BACKGROUND AND AIMS: Atrophic gastritis, intestinal metaplasia, and pyloric metaplasia are frequent precursors of noncardial intestinal-type gastric adenocarcinoma in populations in which both gastric cancer and Helicobacter pylori infection are common. We hypothesized that such lesions would be less prevalent in European gastric cancer patients. METHODS: Slides from patients who underwent gastrectomy for adenocarcinoma between 1997 and 2004 were reviewed. Tumors were categorized as intestinal or diffuse; non-neoplastic mucosa was evaluated for gastritis, atrophy, intestinal metaplasia and pyloric metaplasia. RESULTS: We studied 81 patients: 48 Swiss (mean age 68.5 years); 17 Italians (mean age 67.8 years); and 16 Iberians (mean age 54.8 years; P<0.001). Twelve tumors were proximal (all intestinal type), 12 in the corpus (six intestinal-type), and 57 antral (30 intestinal type). Patients with diffuse cancers were younger than those with intestinal type (P<0.05). Nineteen patients (23.4%) had a normal stomach; 30% of T1 tumors and 90% of T4s arose in a normal stomach (P<0.02). H. pylori gastritis was found in 47 patients (58%); they did not differ in age, sex, national origin, cancer location or type from those without gastritis. Intestinal metaplasia correlated with H. pylori gastritis (P=0.002). Pyloric metaplasia was infrequent and limited to rare microfoci. CONCLUSIONS: A quarter of the patients had a normal stomach, and pyloric metaplasia was distinctly uncommon. Approaches to prevention and early detection of gastric cancer based on bioptic or serological demonstration of atrophy and metaplasia could overlook at least 25% of the people at risk in certain populations and may need to be adapted to local conditions.     

Use of endoscopic assessment of gastric atrophy for gastric cancer risk stratification to reduce the need for gastric mapping

Abstract

Background/Aims: Stratification for gastric cancer risk typically involves histologic grading of gastric biopsies. This study aimed to compare endoscopic assessment of gastric atrophy and histologic gastric mapping for gastric cancer risk stratification in a region with relatively high risk of gastric cancer.

Methods: Endoscopic and histologic gastric cancer risk stratification were compared in Vietnamese patients with functional dyspepsia. Endoscopic gastric atrophy was graded according to the Kimura-Takemoto classification. High-risk histologic lesions were defined as gastric dysplasia, Operative Link on Gastritis Assessment (OLGA) gastritis stage III/IV, intestinal metaplasia in both the antrum and the corpus or incomplete intestinal subtype at any site. Two experienced pathologists, blinded to endoscopic information, jointly examined all specimens and reached a consensus. The presence of high-risk histologic lesions was compared among patients with different endoscopic grades of gastric atrophy.

Results: There were 280 subjects (mean age, 46.1?±?10?years, and male, 50%). The numbers of patients with moderate/severe grade of endoscopic gastric atrophy and high-risk histologic lesions were 126 (45.0%) and 46 (16.4%), respectively. The sensitivity, specificity, positive and negative likelihood ratios of moderate/severe endoscopic atrophic grade for detecting high-risk histologic lesions were 93% (95% CI 86%?100%), 65% (95% CI 58%?71%), 2.64 (95% CI 2.18???3.18) and 0.10 (95% CI 0.03???0.30), respectively.

Conclusions: Gastric cancer risk assessment using endoscopic or histologic methods provided similar results such that the absence or a mild grade of endoscopic gastric atrophy would preclude the need for histologic mapping.     

Most gastric cancer occurs on the distal side of the endoscopic atrophic border

BACKGROUND: The endoscopic atrophic border indicates the extent of atrophic gastritis. The aims of this study were to examine the relation of intestinal and diffuse types of gastric cancer to the atrophic border and to study the pathologic condition of the atrophic border. METHODS: In 83 patients with gastric cancer the extent of atrophic gastritis was assessed macroscopically. In 46 patients gastric biopsy specimens were also taken, to compare the histologic features of gastritis proximal and distal to the atrophic border. RESULTS: Eighty-five per cent of gastric cancers (including 93% of intestinal type) occurred on the distal side of the atrophic border. Early diffuse gastric cancer arose closer to the atrophic border than intestinal-type cancer and was more likely to be sited proximal to it. Histologically, the grade of polymorphonuclear cell infiltration (inflammatory activity) and Helicobacter pylori density were significantly greater on the proximal side (P < 0.05), whereas the grades of glandular atrophy and intestinal metaplasia were significantly greater distally (P < 0.001). CONCLUSIONS: The atrophic border delineates the area of atrophic gastritis and intestinal metaplasia, and it is within the distal part of the stomach that gastric cancer occurs most frequently. Endoscopists should observe the distal side particularly carefully to identify early gastric cancer. The relationship of the two histologic types of cancer to areas of intestinal metaplasia and 'active' inflammation may have implications for the pathogenesis of cancer and, if so, for the potential protective effect of H. pylori eradication.     

Helicobacter pylori infection and early gastric cancer

BACKGROUND: Helicobacter pylori has recently been associated with an increased risk of gastric cancer. This study aimed to examine the association between H. pylori, histologic chronic gastritis, and intestinal metaplasia in early gastric cancers of different histologic types. STUDY: Seventy-four patients who were surgically diagnosed as having early gastric cancer were included in this study. All tissue specimens were obtained from patients by endoscopic biopsy and were classified histopathologically as intestinal-type early gastric cancer in 55 patients and diffuse-type early gastric cancer in 19 patients. RESULTS: H. pylori infection was found in 67 patients (90.5%) but not found in seven (9.5%). And the prevalence of H. pylori infection with nongastric cancer patients was also high (68.5%). There was no significant difference between the intestinal-type and the diffuse-type early gastric cancer in chronic active gastritis and atrophic chronic gastritis. Intestinal metaplasia was observed more frequently in patients with the intestinal-type than with the diffuse-type early gastric cancer (P = 0.0102). CONCLUSIONS: Infection with H. pylori has an important relationship to both histopathologic types of early gastric cancer.     

Gastric mucosa in Mongolian and Japanese patients with gastric cancer and Helicobacter pylori infection

AIM: To investigate the characteristics of gastric cancer and gastric mucosa in a Mongolian populationby comparison with a Japanese population.METHODS: A total of 484 Mongolian patients with gastric cancer were enrolled to study gastric cancer characteristics in Mongolians. In addition, a total of 208 Mongolian and 3205 Japanese consecutive outpatients who underwent endoscopy, had abdominal complaints, no history of gastric operation or Helicobacter pylori eradication treatment, and no use of gastric secretion inhibitors such as histamine H2-receptor antagonists or proton pump inhibitors were enrolled. This study was conducted with the approval of the ethics committees of all hospitals. The triple-site biopsy method was used for the histologic diagnosis of gastritis and H. pylori infection in all Mongolian and Japanese cases. The infection rate of H. pylori and the status of gastric mucosa in H. pylori-infected patients were compared between Mongolian and Japanese subjects. Age(± 5 years), sex, and endoscopic diagnosis were matched between the two countries.RESULTS: Approximately 70% of Mongolian patients with gastric cancer were 50-79 years of age, and approximately half of the cancers were located in the upper part of the stomach. Histologically, 65.7% of early cancers exhibited differentiated adenocarcinoma, where as 73.9 % of advanced can cersdisplayed undifferentiated adenocarcinoma. The infection rate of H. pylori was higher in Mongolian than Japanese patients(75.9% vs 4 8. 3 %, P0.0001). When stratified by age, the prevalence was highest among young patients, and tended to decrease in patients aged 50 years or older. The anti-East-Asian Cag Aspecific antibody was negative in 99.4% of H. pyloripositive Mongolian patients. Chronic inflammation, neutrophil activity, glandular atrophy, and intestinal metaplasia scores were significantly lower in Mongolian compared to Japanese H. pylori-positive patients(P 0.0001), with the exception of the intestinal metaplasia score of specimen from the greater curvature of the upper body. The type of gastritis changed from antrumpredominant gastritis to corpus-predominant gastritis with age in both populations.CONCLUSION: Gastric cancer was located in the upper part of the stomach in half of the Mongolian patients; Mongolian patients were infected with non-East-Asiantype H. pylori.     

Postoperative mortality and morbidity after D2 lymphadenectomy for gastric cancer: A retrospective cohort study

BACKGROUND Surgery for gastric cancer is a complex procedure and lymphadenectomy is often mandatory.Postoperative mortality and morbidity after curative gastric cancer surgery is not insignificant.AIM To evaluate the factors determining mortality and morbidity in a population of patients undergoing R0 resection and D2 lymphadenectomy for gastric cancer.METHODS A retrospective analysis of clinical data and pathological characteristics(age,sex,primary site of the tumor,Lauren histotype,number of positive lymph nodes resected,number of negative lymph nodes resected,and depth of invasion as defined by the standard nomenclature)was conducted in patients with gastric cancer.For each patient we calculated the Kattan’s score.We arbitrarily divided the study population of patients into two groups based on the nomogram score(<100 points or≥100 points).Prespecified subgroups in these analyses were defined according to age(≤65 years or>65 years),and number of lymph nodes retrieved(≤35 lymph nodes or>35 lymph nodes).Uni-and multivariate analysis of clinical and pathological findings were performed to identify the factors affecting postoperative mortality and morbidity.RESULTS One-hundred and eighty-six patients underwent a curative R0 resection with D2 lymphadenectomy.Perioperative mortality rate was 3.8%(7 patients);a higher mortality rate was observed in patients aged>65 years(P=0.002)and in N+patients(P=0.04).Following univariate analysis,mortality was related to a Kattan’s score≥100 points(P=0.04)and the presence of advanced gastric cancer(P=0.03).Morbidity rate was 21.0%(40 patients).Surgical complications were observed in 17 patients(9.1%).A higher incidence of morbidity was observed in patients where more than 35 lymph nodes were harvested(P=0.0005).CONCLUSION Mortality and morbidity rate are higher in N+and advanced gastric cancer patients.The removal of more than 35 lymph nodes does not lead to an increase in mortality.     

GASTRIC CANCER DETECTED AFTER HELICOBACTER PYLORI ERADICATION

Background: Helicobacter pylori is associated with progression to gastric cancer. However, it is still unclear whether eradication therapy can prevent the development of gastric cancer. Methods: Subjects were 242 patients in whom success in eradication of Helicobacter pylori had been continuous for more than 3 years. Clinical, endoscopic and histological findings were compared retrospectively between those who developed gastric cancer (cancer group) and those who did not (non‐cancer group). Clinical features of each cancer case were also evaluated. Results: Gastric cancer was found in six of the 242 subjects (2.5%) during a mean follow‐up period of 4.6 years (range: 3.0–7.0). The mean age of the cancer group tended to be higher than that of the non‐cancer group. Endoscopy revealed a more severe grade of gastric corpus atrophy in the cancer group, and histological findings showed that the degree of intestinal metaplasia in the upper corpus was higher in the cancer group. Four of the six cancers were located in the gastric antrum. All were early cancers and five were of 0‐IIc type endoscopically. All were intestinal type histologically. Conclusions: Gastric cancer was discovered at a rate of 2.5% during the mean follow‐up period of 4.6 years after H. pylori eradication. Careful endoscopic follow up is necessary even after successful eradication, especially in cases characterized by an endoscopically high grade of gastric atrophy and pathologically severe intestinal metaplasia at the upper corpus.     

Precancerous lesions in the stomach: From biology to clinical patient management

Gastric cancer is the final step in a multi-stage cascade triggered by long-standing inflammatory conditions (particularly Helicobacter pylori infection) resulting in atrophic gastritis and intestinal metaplasia: these lesions represent the cancerization field in which (intestinal-type) gastric cancer develops. Intraepithelial neoplasia is consistently recognized as the phenotypic bridge between atrophic/metaplastic lesions and invasive cancer. This paper addresses the epidemiology, pathology, molecular profiling, and clinical management of advanced precancerous gastric lesions.