Gastric Cancer: How Can We Reduce the Incidence of this Disease?

Gastric cancer remains a prevalent disease worldwide with a poor prognosis. Helicobacter pylori plays a major role in gastric carcinogenesis. H. pylori colonization leads to chronic gastritis, which predisposes to atrophic gastritis, intestinal metaplasia, dysplasia, and eventually gastric cancer. Screening, treatment, and prevention of H. pylori colonization can reduce the incidence of gastric cancer. Other interventions that may yield a similar effect, although of smaller magnitude, include promotion of a healthy lifestyle including dietary measures, non-smoking, low alcohol intake, and sufficient physical activity. This chapter reviews interventions that can lead to a decline in gastric cancer incidence in high and low incidence countries

Natural History of Barrett’s Esophagus

Barrett’s esophagus (BE) is a very common condition. We have obtained fairly profound knowledge of the natural history of this condition. This results from many cross-sectional and cohort studies, many describing patients undergoing long-term surveillance. Their consent to use their clinical data has improved our knowledge to the benefit of these same and other patients. The prevalence of BE increases with age both in men and in women. This increase starts at a younger age in men than in women. The incidence of high-grade dysplasia and cancer in BE depends on segment length, gender, and age. The latter two likely indicate the duration of the presence of BE in an individual patient. Other factors that influence the incidence of dysplasia and cancer are smoking behavior and use of certain medications such as PPIs, statins, and NSAIDs. Surveillance of BE and treatment of dysplasia can impact the incidence of and mortality due to esophageal adenocarcinoma. This is of major benefit to a subgroup of BE patients. The epidemiology and burden of disease ask for further efforts to develop targeted screening, surveillance, and intervention techniques in coming years

Patients' preferences regarding shared decision-making in the treatment of inflammatory bowel disease: Results from a patient-empowerment study

Shared decision-making is gaining favor in clinical practice, although the extent to which patients want to be involved in choosing their treatment varies substantially. Because data are lacking on the preferences of patients with chronic diseases such as inflammatory bowel disease (IBD), we wanted to assess IBD patients' preferences about being involved in such decisions. Methods: Adult IBD patients were asked to anonymously complete an online survey on their preferences. Non-parametric tests (χ2) were used to determine the relationship between responses and respondents. Results: The questionnaire was completed by 1,067 patients, 617 with Crohn's disease and 450 with ulcerative colitis. Patients' mean age was 43 (SD 13.7) years; the majority were female (66%). In total, 866 patients (81%) reported it as 'very important' to be actively involved in the decision-making process, and another 177 (17%) rated it as 'quite important'. When asked how their treatment could be improved, 537 patients (50%) wanted close, equitable collaboration with their physician. This preference was significantly associated with a disease duration of ≤8 years (p = 0.03). Gender and type of IBD were not significantly associated with patients' preferences. Conclusions: This study demonstrates IBD patients' desire to be actively involved in the decision-making process. Further research is needed on physicians' perspectives on shared decision-making, and on finding predictive factors for developing a model for shared decision-making in IBD. Copyrigh

Barrett's oesophagus: Epidemiology, cancer risk and implications for management

Although endoscopic surveillance of patients with Barrett's oesophagus has been widely implemented, its effectiveness is debateable. The recently reported low annual oesophageal adenocarcinoma risk in population studies, the failure to identify most Barrett's patients at risk of disease progression, the poor adherence to surveillance and biopsy protocols, and the significant risk of misclassification of dysplasia all tend to undermine the effectiveness of current management, in particular, endoscopic surveillance programmes, to prevent or improve the outcomes of patients with oesophageal adenocarcinoma. The ongoing increase in incidence of Barrett's oesophagus and consequent growth of the surveillance population, together with the associated discomfort and costs of endoscopic surveillance, demand improved techniques for accurately determining individual risk of oesophageal adenocarcinoma. More accurate techniques are needed to run efficient surveillance programmes in the coming decades. In this review, we will discuss the current knowledge on the epidemiology of Barrett's oesophagus, and the challenging epidemiological dilemmas that need to be addressed when a

The minimal incubation period from the onset of Barrett's oesophagus to symptomatic adenocarcinoma

Background:The interval between the onset of Barrett's oesophagus (BO) and oesophageal adenocarcinoma (OAC) can be termed the incubation period. However, the unrecorded onset of BO precludes its direct observation.Methods:Determining the range of intervals between BO diagnosis and OAC within the longest observational BO follow-up study. Exclusion criteria were presence of high-grade dysplasia (HGD) or OAC at baseline, death within <2 years of BO diagnosis, oesophagectomy without HGD/OAC and loss to follow-up. A total of 133 patients (M/F 73/60) were taken into account.Results:In 1967 person years of follow-up there were 13 cases of HGD/OAC, (0.66% p.a.; 95% CI 0.58-0.74), 96 patients died without HGD/OAC and 24 survived without HGD/OAC. The mean intervals between BO diagnosis and either HGD/OAC, death or end of follow-up were 10.8, 12.6 and 25.5 years, respectively, and the mean ages at endpoint were 72.5, 80.0 and 68.3 years, respectively. The survivors without HGD/OAC had a lower age at BO diagnosis (mean 42.8 vs 61.2 and 67.4 years, P=0.001). Baseline presence of low-grade dysplasia was associated with progression to HGD/OAC (log rank P=0.001).Conclusion:The Rotterdam BO follow-up cohort revealed a long incubation period between onset of BO and development of HGD/OAC, in patients without HGD/OAC at baseline as illustrated by 24 patients diagnosed with BO at a young age and followed for a mean period of 25.5 years. Their tumour-free survival established a minimum incubation period, suggesting a true incubation period of three decades or more

NSAIDs, statins, low-dose aspirin and PPIs, and the risk of oesophageal adenocarcinoma among patients with Barrett's oesophagus: A populationbased case-control study

Objectives: Non-steroidal anti-inflammatory drugs (NSAIDs), proton pump inhibitors (PPIs), low-dose aspirin and statins may decrease the risk of oesophageal adenocarcinoma (OAC) among patients with Barrett's oesophagus (BO). However, previous studies did not adequately address bias and confounding. Our objective was to estimate the risk of OAC among patients with BO exposed to NSAIDs, statins and PPIs. Design: Case-control study nested within a BO cohort. Setting: Two primary care databases (the UK and the Netherlands (NL)). Participants: Cases were adults ≥18 years of age with OAC or high-grade dysplasia (HGD) diagnosis ≥1 year after BO diagnosis. Controls were matched on age, sex, year of BO diagnosis and database. Exposure: Drug use was assessed from BO diagnosis until matching date. Outcome measure: Adjusted ORs with 95% CI were calculated by conditional logistic regression. Results: Within the BO cohort (n=15 134), 45 OAC (UK: 40, NL: 5) and 12 HGD cases (NL: 12) were identified. ORa for OAC during NSAID use was 1.2 (95% CI 0.6 to 2.5) and during statin use for <3 years 0.5 (95% CI 0.1 to 1.7). When including HGD cases (n=57), ORa for NSAID use was 0.9 (95% CI 0.5 to 1.8) and for statin use <3 years 0.5 (95% CI 0.1 to 1.7). Higher doses of statins showed lower estimates for OAC and HGD, though not statistically significant. Low-dose aspirin and PPIs did not significantly decrease the risk of OAC and HGD. Conclusions: In this population-based nested case- control study, use of NSAIDs, PPIs, low-dose aspirin or statins did not reduce the risk of HGD and OAC among patients with BO. These findings indicate that for an unselected group of patients with BO chemoprevention by use of drugs to reduce progression to HGD and OAC should not be directly considered as routine care

Management of biliary complications following damage control surgery for liver trauma

Background: The liver is the most frequently injured solid intra-abdominal organ. The major cause of early death following severe liver trauma is exsanguination. Although perihepatic packing improves survival in severe liver trauma, this leaves parenchymal damage untreated, often resulting in post-traumatic biliary leakage and a subsequent rise in morbidity. The aim of this study was to analyze the incidence and treatment of biliary leakage following the operative management of liver trauma. Methods: Patients presenting between 2000 and 2009 to Erasmus University Medical Centre with traumatic liver injury were identified. Data from 125 patients were collected and analyzed. Sixty-eight (54 %) patients required operation. All consecutive patients with post-operative biliary complications were analyzed. Post-operative biliary complications were defined as biloma, biliary fistula, and bilhemia. Results: Ten (15 %) patients were diagnosed with post-operative biliary leakage following liver injury. Three patients with a biloma were treated with percutaneous drainage, without further intervention. Seven patients with significant biliary leakage were managed by endoscopic stenting of the common bile duct to decompress the internal biliary pressure. One patient had a relaparotomy and right hemihepatectomy to control biliary leakage and injury of the right hepatic duct. Conclusion: Biliary complications continue to occur frequently following damage control surgery for liver trauma. The majority of biliary complications can be managed without an operation. Endoscopic retrograde cholangiopancreatography (ERCP) and internal stenting represent a safe strategy to manage post-operative biliary leakage and bilhemia in patients following liver trauma. Minor biliary leakage should be managed by percutaneous drainage alone

Mutation prediction models in Lynch syndrome: evaluation in a clinical genetic setting

Background/aims: The identification of Lynch syndrome is hampered by the absence of specific diagnostic features and underutilization of genetic testing. Prediction models have therefore been developed, but they have not been validated for a clinical genetic setting. The aim of the present study was to evaluate the usefulness of currently available prediction models. METHODS: We collected data of 321 index probands who were referred to the department of Clinical Genetics of the Erasmus Medical Center because of a family history of colorectal cancer. These data were used as input for five previously published models. External validity was assessed by discriminative ability (AUC: area under the receiver operating characteristic curve) and calibration. For further insight, predicted probabilities were categorized with cut-offs of 5%, 10%, 20% and 40%. Furthermore, costs of different testing strategies were related to the number of extra detected mutation carriers. RESULTS: Of the 321 index probands, 66 harboured a germline mutation. All models discriminated well between high risk and low risk index probands (AUC: 0.82-0.84). Calibration was well for the Premm1,2 and Edinburgh model, but poor for the other models. Cut-offs could be found for the prediction models where costs could be saved while missing only few mutations. CONCLUSIONS: The Edinburgh and Premm1,2 model were the models with the best performance for an intermediate to high-risk setting. These models may well be of use in clinical practice to select patients for further testing of mismatch repair gene mutations