In people without a history of gastrectomy and those who have not recently had antibiotics or proton ,pump inhibitors, urea breath tests had high diagnostic accuracy while serology and stool antigen tests were less accurate for diagnosis of Helicobacter pylori infection.This is based on an indirect test comparison (with potential for bias due to confounding), as evidence from direct comparisons was limited or unavailable. The thresholds used for these tests were highly variable and we were unable to identify specific thresholds that might be useful in clinical practice.We need further comparative studies of high methodological quality to obtain more reliable evidence of relative accuracy between the tests. Such studies should be conducted prospectively in a representative spectrum of participants and clearly reported to ensure low risk of bias. Most importantly, studies should prespecify and clearly report thresholds used, and should avoid inappropriate exclusions.

Both environmental and genetic factors have a role in the aetiology of gastric cancer. The nature of the genetic factors has not been well-studied and, outside of a few rare cancer syndromes, the genes involved have not been identified. Having a first-degree relative with gastric cancer is a consistent risk factor for gastric cancer, although the magnitude of the odds ratio (OR) associated with a positive family history varies with the ethnic group and with the geographic region. In published case -control studies, the odds ratio varies from approximately 2 to 10, depending on the country. Unlike other common adult cancers, the risk of gastric cancer in migrants is similar to that of the population of origin and does not approach that of the host population in the first generation postmigration. It is hoped that molecular studies, including genomewide association studies (GWAS), will illuminate the genetic factors underlying this important association.

There is no association between Hp eradication and development of new cases of GERD in the population of dyspeptic patients. However, in cohort studies, there seems to be a twofold higher risk of development of erosive GERD in patients with PUD. The effect in RCTs of patients with PUD did not show a significant difference.

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AIMTo quantify the risk of gastric cancer in first-degree relatives of patients with the cancer.METHODSA comprehensive literature search was performed. Case-control trials comparing the frequency of a positive family history of gastric cancer in patients with gastric cancer, vs non-gastric cancer controls were retrieved. Studies with missed or non-extractable data, studies in children, abstracts, and duplicate publications were excluded. A meta-analysis of pooled odd ratios was performed using Review Manager 5.0.25. We performed subgroup analysis on Asian studies and a sensitivity analysis based on the quality of the studies, type of the outcome, sample size, and whether studies considered only first-degree relatives.RESULTSThirty-two relevant studies out of 612 potential abstracts (n = 80690 individuals) were included. 19.0% of the patients and 10.9% of the controls had at least one relative with gastric cancer (P < 0.00001). The pooled relative risk for the development of gastric cancer in association with a positive family history was 2.35 (95%CI: 1.96-2.81). The Cochran Q test for heterogeneity was positive (P < 0.00001, I² = 92%). After excluding the three outlier studies with the highest relative risks, heterogeneity remained significant (P < 0.00001, I² = 90%). The result was not different among Asian studies as compared to others and remained robust in several sensitivity analyses. In the 26 studies which exclusively analysed the history of gastric cancer in first-degree relatives, the relative risk was 2.71 (95%CI: 2.08-3.53; P < 0.00001).CONCLUSIONIndividuals with a first-degree relative affected with gastric cancer have a risk of about 2.5-fold for the development of gastric cancer. This could be due to genetic or environmental factors. Screening and preventive strategies should be developed for this high-risk population.

INTRODUCTIONAchalasia is a primary oesophageal motor disorder characterized by incomplete relaxation of the lower oesophageal sphincter on swallowing and aperistalsis of the oesophageal body.1 Histopathological examination of the achalasic oesophagus demonstrates a loss of inhibitory myenteric plexus ganglionic cells. The loss of inhibitory ganglion cells secreting nitrous oxide and vasoactive intestinal peptide and the persistence of cholinergic stimulatory cells appear to be the primary pathophysiological defects.2 The mainstay of therapy is directed towards the reduction of lower oesophageal sphincter pressure resulting in improved oesophageal emptying by gravity. Pharmacological therapy, endoscopic dilatation, botulinum toxin injection and surgical myotomy are the primary therapeutic modalities. Pneumatic balloon dilatation is a commonly used treatment modality. Studies have found that balloon dilatation provides good to excellent symptomatic relief in 86±100% of cases. 3±6 In a large prospective study, Barkin et al. reported that dilatation with a 3.5-cm balloon provided symptomatic response in 90% of patients. 6 The advantages of this technique include the opportunity for a 1-day out-patient procedure, SUMMARY Background: Therapeutic options for achalasia include pharmacological therapy, surgical myotomy, pneumatic dilatation and intrasphincteric botulinum toxin injection. Aim: To compare botulinum toxin injection with pneumatic dilatation in a randomized trial. Patients/methods: Forty adults with newly diagnosed achalasia were randomized to receive botulinum toxin (n 20) or pneumatic dilatation (n 20). Symptom scores were evaluated at 1, 6 and 12 months. Clinical relapse was de®ned as a symptom score greater than 50% of baseline. Relapsers received a second botulinum toxin injection or pneumatic dilatation. Results: The cumulative 12-month remission rate was signi®cantly higher after a single pneumatic dilatation

SUMMARY BackgroundDespite initial evidence in the literature, nonsteroidal anti-inflammatory drugs (NSAIDs) have not been widely used to prevent post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis (PEP).