scholarly journals A meta-analysis and systematic review on subtypes of gastric intestinal metaplasia and neoplasia risk

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ning Wei ◽  
Mengyue Zhou ◽  
Siyu Lei ◽  
Zhiheng Zhong ◽  
Ruihua Shi

Abstract Background Gastric intestinal metaplasia (GIM) is a significant risk factor for gastric cancer. Risk of gastric cancer/dysplasia between complete intestinal metaplasia (CIM) and incomplete intestinal metaplasia (IIM) was controversial. Our study aimed to pool relative risk (RR) of cancer/dysplasia of IIM compared with CIM in GIM patients. Methods PubMed, EMBASE, Cochrane Library and Web of Science were searched for studies concerning cancer/dysplasia in GIM patients. Random-effects or fixed-effects model was utilized for pooling RR. Sensitivity and publication bias analyses were conducted. Stability of results would be evaluated in case of publication bias. Results 12 studies were included. Compared with CIM, pooled RR of cancer/dysplasia in IIM patients was 4.48 (95% CI 2.50–8.03), and the RR was 4.96 (95% CI 2.72–9.04) for cancer, and 4.82 (95% CI 1.45–16.0) for dysplasia. The pooled RR for cancer/dysplasia in type III IM was 6.27 (95% CI 1.89–20.77) compared with type II + I IM, while it was 5.55 (95% CI 2.07–14.92) compared with type II IM. Pooled RR between type II IM and type I IM was 1.62 (95% CI 1.16–2.27). Subgroup analyses showed that IIM was associated with a higher risk of gastric cancer/dysplasia in Western population (pooled RR = 4.65 95% CI 2.30–9.42), but not in East Asian population (pooled RR = 4.01 95% CI 0.82–19.61). Conclusions IIM was related to a higher risk of cancer/dysplasia compared with CIM. Risk of developing cancer/dysplasia from type I, II, and III intestinal metaplasia increased gradually.

2020 ◽  
Vol 2020 ◽  
pp. 1-13 ◽  
Author(s):  
Xiaoyan Dong ◽  
Wenyan Gao ◽  
Xiaoling LV ◽  
Yazhen Wang ◽  
Qing Wu ◽  
...  

Purpose. Long noncoding RNAs (lncRNAs) have been widely studied, and single nucleotide polymorphisms (SNPs) in lncRNAs are considered to be genetic factors that influence cancer susceptibility. The lncRNA GAS5, MEG3, and PCAT-1 polymorphisms are shown to be possibly associated with cancer risk. The aim of this meta-analysis was to systematically evaluate this association. Methods. Studies were selected from PubMed, Web of Science, Embase, Google Scholar, Cochrane Library, the Chinese National Knowledge Infrastructure (CNKI), and the Chinese Biomedical Literature Database (CBM) through inclusion and exclusion criteria. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using the random-effects model or fixed-effects model to assess the association between lncRNA polymorphisms and cancer susceptibility. Metaregression and publication bias analyses were also conducted. All analyses were performed using the Stata 12.0 software. Results. Sixteen articles (covering 13750 cases and 17194 controls) were included in this meta-analysis. A significant association between SNP rs145204276 and gastric cancer risk was observed (del vs. ins: OR=0.79, 95%CI=0.72‐0.86; del/del vs. ins/ins+del/ins: OR=0.74, 95%CI=0.59‐0.91; del/ins vs. ins/ins: OR=0.84, 95%CI=0.67‐1.05). For rs16901904, a decreased cancer risk was observed in three genetic models (C vs. T: OR=0.79, 95%CI=0.70‐0.90; CC vs. CT+TT: OR=0.49, 95%CI=0.37‐0.65; CC vs. TT: OR=0.49, 95%CI=0.37‐0.66). No statistical significance was found in the metaregression analysis. For all of the included SNPs, no publication bias was found in all genotype models. Conclusions. The rs145204276 SNP in lncRNA GAS5 is likely to be associated with gastric cancer risk, whereas the rs16901904 SNP in lncRNA PCAT-1 bears association with a decreased cancer risk.


2011 ◽  
Vol 58 (1) ◽  
pp. 39-52 ◽  
Author(s):  
Marjan Micev ◽  
Milena Cosic-Micev

Recent epidemiological studies in Serbia revealed that gastric carcinoma is the third and the fifth main cause of cancer morbidity in men and women, respectively. Despite the declining incidence of gastric cancer, it remains the second most common cause of cancer-related deaths as it is worldwide. A well-defined carcinogenic inflammation-metaplasia-dysplasia-cancer sequence typically precedes the development of most gastric adenocarcinomas. Alterations such as gastric mucosal atrophy and intestinal metaplasia are merely markers of increased risk, while gastric epithelial dysplasia (GED) represent a direct precursor of cancer. DNA damage and increased mucosal proliferation secondary to H pylori infection, combined with a suitable host susceptibility phenotype (eg, genetic polymorphisms in interleukin IL-1B, IL-1RN, and tumor necrosis factor a TNF-a genes), are important factors in this progression pathway. However, only a small minority of patients infected with H. pylori eventually develops gastric cancer, and eradication of H pylori in these patients does not seem to eliminate the risk of cancer completely. It has been shown that atrophy may be a better indicator of risk of cancer than intestinal metaplasia, and remains to be validated in routine clinical practice according to recent proposal for new quantitative methods. It is often associated with pseudopyloric gland metaplasia in the gastric corpus mucosa, which expresses a type of trefoil peptide, the spasmolytic polypeptide (termed spasmolytic polypeptide-expressing metaplasia or SPEM) and has been shown to be linked more closely to gastric cancer than intestinal metaplasia. Better histological characterization of adenomatous (or type I), hyperplastic (foveolar or type II) and tubule-neck (mucocellular or type III) GED, two-tiered grading system (low and high grade dysplasia) as well as the introduction of Padova and Vienna international classificatons of dysplasia seem to be more helpful in GED survillance and comparative studies. A combination of histopathological features, serum markers such as pepsinogen I, and molecular tests that analyze host susceptibility polymorphisms and bacterial virulence factors, may allow development of strategies for early detection of cancer in the future. At present, pathobiology of gastric cancerogenesis is far from known, despite the progressive knowlegde on predisposing environmental conditions and genetic and epigenetic abnormalities, including tumour supressor genes, oncogenes, microsatellite instability and hypermethylation or the significance of E-cadherin mutational status association with hereditary diffuse gastric cancer syndrome. Recent evidence regarding the importance of several histopathologically derived prognostic factors, such as resection margin status and lymph node metastases and their implications have also been discussed. We aim to review these aspects, with special relevance to gastric cancer specimen reporting.


Gut ◽  
2021 ◽  
pp. gutjnl-2021-324057
Author(s):  
Jonathan W J Lee ◽  
Feng Zhu ◽  
Supriya Srivastava ◽  
Stephen KK Tsao ◽  
Christopher Khor ◽  
...  

ObjectiveTo investigate the incidence of gastric cancer (GC) attributed to gastric intestinal metaplasia (IM), and validate the Operative Link on Gastric Intestinal Metaplasia (OLGIM) for targeted endoscopic surveillance in regions with low-intermediate incidence of GC.MethodsA prospective, longitudinal and multicentre study was carried out in Singapore. The study participants comprised 2980 patients undergoing screening gastroscopy with standardised gastric mucosal sampling, from January 2004 and December 2010, with scheduled surveillance endoscopies at year 3 and 5. Participants were also matched against the National Registry of Diseases Office for missed diagnoses of early gastric neoplasia (EGN).ResultsThere were 21 participants diagnosed with EGN. IM was a significant risk factor for EGN (adjusted-HR 5.36; 95% CI 1.51 to 19.0; p<0.01). The age-adjusted EGN incidence rates for patients with and without IM were 133.9 and 12.5 per 100 000 person-years. Participants with OLGIM stages III–IV were at greatest risk (adjusted-HR 20.7; 95% CI 5.04 to 85.6; p<0.01). More than half of the EGNs (n=4/7) attributed to baseline OLGIM III–IV developed within 2 years (range: 12.7–44.8 months). Serum trefoil factor 3 distinguishes (Area Under the Receiver Operating Characteristics 0.749) patients with OLGIM III–IV if they are negative for H. pylori. Participants with OLGIM II were also at significant risk of EGN (adjusted-HR 7.34; 95% CI 1.60 to 33.7; p=0.02). A significant smoking history further increases the risk of EGN among patients with OLGIM stages II–IV.ConclusionsWe suggest a risk-stratified approach and recommend that high-risk patients (OLGIM III–IV) have endoscopic surveillance in 2 years, intermediate-risk patients (OLGIM II) in 5 years.


2012 ◽  
Vol 75 (4) ◽  
pp. AB240
Author(s):  
Justin M. Gomez ◽  
James T. Patrie ◽  
Jeanetta Frye ◽  
Bryan G. Sauer ◽  
Vanessa M. Shami ◽  
...  

Rheumatology ◽  
2019 ◽  
Vol 59 (5) ◽  
pp. 930-939 ◽  
Author(s):  
Wenhui Xie ◽  
Shiyu Xiao ◽  
Yanrong Huang ◽  
Xiaoying Sun ◽  
Dai Gao ◽  
...  

Abstract Objectives To explore the risk of new and recurrent cancer in adult RA patients with prior malignancy and subsequently exposed to biologic therapies. Methods Separate searches were performed of PubMed, EMBASE and Cochrane Library and conference proceedings for observational studies reporting cancer incidence or recurrence in patients with RA and prior malignancy treated with biologics and conventional synthetic DMARDs (csDMARDs). Mantel-Haenszel fixed-effects method was conducted to calculate relative risk and 95% CI. Results A total of 12 studies involving 13 598 patients and 32 473 patient-years of follow-up were included (10, 3 and 1 studies for TNF inhibitors [TNFi], rituximab and anakinra, respectively). The crude incidence of new and recurrent cancer per 1000 patient-years were 34.4 for TNFi, 32.3 for rituximab, 32.3 for anakinra and 31.8 for csDMARDs. In the quantitative meta-analysis, biologics were not associated with an increased risk of new or recurrent cancer compared with csDMARDs in patients with RA and prior cancer (TNFi: relative risk = 0.95, 95% CI = 0.83, 1.09; rituximab: relative risk = 0.89, 95% CI = 0.52, 1.53). Secondary analyses of stratification of cancer types, the interval between initiation of TNFi and prior cancer diagnosis, and duration of TNFi exposure, found similar results. Conclusion Compared with csDMARDs, there is no increased risk of developing cancer overall or some specific subtypes in RA patients with a prior cancer receiving biologics. More investigations are warranted to explore the risk of cancer development in individual cancer as well as to determine optimal time to initiate biologic therapy after the diagnosis of cancer or completion of cancer treatment.


2013 ◽  
Vol 2013 ◽  
pp. 1-4 ◽  
Author(s):  
Tarek Almouradi ◽  
Tadd Hiatt ◽  
Bashar Attar

Gastric intestinal metaplasia is an important stage in the development of gastric cancer. Limited data is available regarding the prevalence of gastric intestinal metaplasia in the United States. We conducted a retrospective review of esophagogastroduodenoscopies performed in our endoscopy unit between the months of April and October 2010 to evaluate the prevalence and the epidemiologic and endoscopic features of gastric intestinal metaplasia in an underserved population in the United States.


2016 ◽  
Vol 62 (1) ◽  
pp. 56-59
Author(s):  
Silvia Cosmina Drasovean ◽  
Diana Elena Morărașu ◽  
Ofelia Daniela Pascarenco ◽  
Olga Brsunic ◽  
Danusia Maria Onișor ◽  
...  

AbstractBackground and Aim: Gastric intestinal metaplasia represents a risk factor for intestinal type of gastric cancer. Gastric intestinal metaplasia seems to be associated with Helicobacter pilory infection in relatives of patients with gastric cancer. The aim of this study was to determine the prevalence, clinical, endoscopic and histological features of gastric intestinal metaplasia. Material and Methods: We retrospectively analyzed the esophagogastroduodenoscopies with biopsies performed between January 1, 2014 and October 31, 2014. Collected and analyzed data included age, gender, symptoms, endoscopic and histological findings. Results: Four hundred eighty-two patients were included in the study. One hundred thirty-seven patients had gastric intestinal metaplasia, which presented a prevalence was 28,4%. A similar distribution between gender was observed with a significant increase of gastric intestinal metaplasia with age (p=0,0001). Regarding the indication for endoscopy, the prevalence of gastric intestinal metaplasia was: 17 % among patients with dyspeptic syndrome, 2 % in patients with anemia and 5 % in patients examined for other symptoms. Endoscopic findings showed gastric intestinal metaplasia was significantly associated with atrophic gastritis (p=0.0001), erythematous gastritis (p=0.0079), while there was no association with erosive gastritis (p=0.24) and peptic ulcer (p=0.19). Conclusions: Gastric intestinal metaplasia is frequently recorded in patients undergoing in esophagogastroduodenoscopies with associated biopsies. Endoscopic findings like erythema and atrophy is strongly associated with gastric intestinal metaplasia emphasizing the importance of sampling biopsies.


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