Tiing-Leong Ang

Endosonography‐ vs. endoscopic retrograde cholangiopancreatography‐based strategies in the evaluation of suspected common bile duct stones in patients with normal transabdominal imaging

Backgroundu2002 Endosonography (EUS) and endoscopic retrograde cholangiopancreatography (ERCP) are highly accurate techniques for evaluating common bile duct stones.

Helicobacter pylori management in ASEAN: The Bangkok consensus report

Helicobacter pylori (H. pylori) infection remains to be the major cause of important upper gastrointestinal diseases such as chronic gastritis, peptic ulcer, gastric adenocarcinoma, and mucosa‐associated lymphoid tissue lymphoma. H. pylori management in ASEAN: the Bangkok consensus report gathered key opinion leaders for the region to review and evaluate clinical aspects of H. pylori infection and to develop consensus statements, rationales, and grades of recommendation for the management of H. pylori infection in clinical practice in ASEAN countries. This ASEAN Consensus consisted of 34 international experts from 10 ASEAN countries, Japan, Taiwan, and the United States. The meeting mainly focused on four issues: (i) epidemiology and disease association; (ii) diagnostic tests; (iii) management; and (iv) follow‐up after eradication. The final results of each workshop were presented for consensus voting by all participants. Statements, rationale, and recommendations were developed from the available current evidence to help clinicians in the diagnosis and treatment of H. pylori and its clinical diseases.

Comparative effects of liraglutide 3 mg vs structured lifestyle modification on body weight, liver fat and liver function in obese patients with non-alcoholic fatty liver disease: A pilot randomized trial

We compared the effects of weight loss induced by the glucagon‐like peptide 1‐agonist liraglutide with a structured lifestyle intervention in obese adults with non‐alcoholic fatty liver disease (NAFLD). Obese (body mass index ≥30 kg/m2, mean weight 96.0 ± 16.3 kg) non‐diabetic Asian adults, with NAFLD diagnosed by liver fat fraction (LFF) ≥ 5.5% on magnetic resonance imaging without other causes of hepatic steatosis, were randomized to a supervised program of dieting (restriction by 400 kilocalories/d) plus moderate‐intensity aerobic exercise (~200 min/wk; DE group, n = 12), or liraglutide at the 3 mg daily dose approved for weight loss (LI group, n = 12), for 26 weeks. Both DE and LI groups had significant (P < .01) and similar reductions in weight (−3.5 ± 3.3 vs −3.5 ± 2.1 kg, respectively, P = .72), LFF (−8.9 ± 13.4 vs −7.2% ± 7.1%, P = .70), serum alanine aminotransferase (−42 ± 46 vs −34 ± 27 U/L, P = .52) and aspartate aminotransferase (−23 ± 24 vs −18 ± 15 U/L, P = .53). In this first randomized study comparing the 2 weight‐loss modalities for improving NAFLD, liraglutide was as effective as structured lifestyle modification.

Multicenter randomised controlled trial comparing the high definition white light endoscopy and the bright narrow band imaging for colon polyps

AIM To compare high definition white light endoscopy and bright narrow band imaging for colon polyps’ detection rates. METHODS Patients were randomised to high definition white light endoscopy (HD-WLE) or the bright narrow band imaging (bNBI) during withdrawal of the colonoscope. Polyps identified in either mode were characterised using bNBI with dual focus (bNBI-DF) according to the Sano’s classification. The primary outcome was to compare adenoma detection rates (ADRs) between the two arms. The secondary outcome was to assess the negative predictive value (NPV) in differentiating adenomas from hyperplastic polyps for diminutive rectosigmoid lesions. RESULTS A total of 1006 patients were randomised to HD-WLE (n = 511) or bNBI (n = 495). The mean of adenoma per patient was 1.62 and 1.84, respectively. The ADRs in bNBI and HD-WLE group were 37.4% and 39.3%, respectively. When adjusted for withdrawal time (OR = 1.19, 95%CI: 1.15-1.24, P < 0.001), the use of bNBI was associated with a reduced ADR (OR = 0.69, 95%CI: 0.52-0.92). Nine hundred and thirty three polyps (86%) in both arms were predicted with high confidence. The sensitivity (Sn), specificity (Sp), positive predictive value and NPV in differentiating adenomatous from non-adenomatous polyps of all sizes were 95.9%, 87.2%, 94.0% and 91.1% respectively. The NPV in differentiating an adenoma from hyperplastic polyp using bNBI-DF for diminutive rectal polyps was 91.0%. CONCLUSION ADRs did not differ between bNBI and HD-WLE, however HD-WLE had higher ADR after adjustment of withdrawal time. bNBI surpassed the PIVI threshold for diminutive polyps.

Unexplained Small-Bowel Obstruction in a Patient with Presumptive Achalasia: Need for Early Recognition of Chronic Intestinal Pseudo-obstruction (CIPO)

Chronic intestinal pseudo-obstruction (CIPO) is a rare condition characterized by impaired gastrointestinal propulsion associated with features of intestinal obstruction (IO) in the absence of any mechanical cause [1–5]. Although gut involvement may be isolated or diffuse [1], the clinical picture is dominated by small-bowel involvement [2]. In contrast, esophageal involvement is usually clinically silent despite achalasia-like features evident on barium studies [3] or on esophageal manometry [5–8]. We report a patient who was treated for achalasia 10 years prior to his first presentation for small-bowel IO, and emphasize the need to consider CIPO early in the differential diagnosis of a patient with underlying achalasia presenting with unexplained small-bowel IO. In July 1998, a 38-year-old Chinese male was referred for worsening dysphagia and regurgitation. Barium swallow and gastroscopy revealed a dilated esophagus with smooth tapering at the gastroesophageal junction. A presumptive diagnosis of achalasia was made. He responded well to serial esophageal dilatations between July 1998 and January 2003 and defaulted follow-up. He represented in January 2009 with severe abdominal distension, vomiting, and constipation. In the preceding 6 months, he had experienced intermittent episodes of abdominal bloating, weight loss, and reduced frequency of bowel movements. He did not complain of dysphagia. Clinical and radiological investigations established a diagnosis of small-bowel IO without a mechanical cause. He was treated conservatively. A colonoscopy was normal. His chest X-ray was clear. A laparotomy was performed 2 weeks later for recurrent IO. Intraoperative findings revealed multiple dilated smallbowel loops without any structural lesion. Enterotomy, evacuation of small intestinal bezoar, and appendicectomy were performed. The diagnosis of CIPO was entertained following another three admissions for subacute IO. Failure of conservative management on the third occasion led to a second laparotomy, revealing dilated small-bowel loops. Full-thickness intestinal biopsies were performed. Histology revealed a complete absence of ganglion cells and neural hypoplasia but intact smooth muscles (Fig. 1a, b), supporting a diagnosis of a neuropathic degenerative variant [9] of CIPO. Eight weeks later, a third laparotomy was required, whereby resection of a contained small-bowel perforation, adhesiolysis, and a venting ileostomy were performed. The case patient had no prior history of metabolic, neurological, cardiovascular, or pulmonary disease or history of travel to any Chaga-prone endemic areas. No The authors do not have any conflict of interests.

Editorial: risk stratification for endoscopic surveillance of metachronous gastric cancer after endoscopic resection

Patients with early gastric cancer (GC) treated by endoscopic resection (ER) are at risk of developing metachronous GC. Helicobacter pylori eradication reduces this risk. Once chronic atrophic gastritis (CAG) has occurred, patients will remain at risk despite H. pylori eradication. The current practice is to perform annual endoscopic surveillance. It would be ideal to risk stratify these patients such that the need for endoscopy can be reduced. The combination of serum pepsinogen (PG) and H. pylori serology has been proposed for use in risk stratifying patients for endoscopy during GC screening. PG I and II are produced by gastric chief cells and mucous neck cells. PG II is also produced by pyloric gland cells. As CAG develops, chief cells are replaced by pyloric glands, leading to a decrease in PG I without PG II change. Low PG I with low PG I: II ratio is a marker of CAG. In severe H. pylori-induced inflammation without atrophy, PG II can be elevated, resulting in normal PG I but low PG I:II ratio. This has been associated with higher GC risk. In the ABC method of categorising gastritis severity, group A is H. pylori negative with normal PG and minimal risk for GC. The risk progressively increases from group B (H. pylori positive; PG normal) to C (H. pylori positive; PG low) and D (H. pylori negative; PG low). Kwon examined whether PG can predict the risk for metachronous GC after ER and investigated the effects of H. pylori eradication on metachronous GC incidence. Persistent H. pylori infection and low PG I:II ratio were risk factors for metachronous GC. PG I:II ratio increased after successful H. pylori eradication but there was no relationship with metachronous GC occurrence. Iguchi previously also reported that low PG I:II ratio was significantly associated with metachronous GC. PG levels can normalise after successful H. pylori eradication in the absence of CAG, but this may take 1215 months. The sensitivity and specificity of low PG for CAG from a meta-analysis were 0.69 (95% CI: 0.55-0.80) and 0.88 (95% CI: 0.77-0.94) respectively, while that for GC screening were 0.70 (95% CI: 0.66-0.75) and 0.79 (95% CI: 0.79-0.80) respectively. Another meta-analysis reported that PG (hazard ratio [HR], 3.5; 95% CI: 2.74.7) and H. pylori serology (summary HR, 3.2; 95% CI: 2.0-5.2) could discriminate between asymptomatic adults at high and low risk of GC. PG is not a tumour marker. It indicates CAG occurrence and reflects cancer risk. It cannot be used for GC screening but can help risk stratification. There is uncertainty about how PG levels change and whether they accurately reflect gastric mucosa status after H. pylori eradication. Extensive intestinal metaplasia without CAG is a risk factor for GC but will not be reflected by PG levels. Patients hesitant about endoscopic surveillance after ER may be counselled of their risk based on PG levels but would need to be aware of the limitations in order to make an informed decision on repeat endoscopy.