Background: We have previously demonstrated a negative relationship between the prevalence of Helicobacter pylori and gastro‐oesophageal reflux disease (GERD). Aim: To study the effects of H. pylori infection on the severity of GERD. Methods: Ethnic Chinese patients with frequent heartburn and/or endoscopic oesophagitis were studied. Endoscopic examination was performed to assess the severity of oesophagitis (modified Savary–Miller grading) and the presence of hiatus hernia. Biopsies were taken for rapid urease testing and confirmation of Barrett’s oesophagus. Risk factors which may affect the severity of oesophagitis (age, sex, smoking, drinking, diabetes mellitus, hiatus hernia, H. pylori status and body mass index) were evaluated by a multiple regression model. The cagA status of H. pylori infected GERD and age‐and‐sex matched controls were determined by Western blot. Age‐and‐sex matched non‐reflux patients were recruited as controls for comparison. Results: Two hundred and twenty‐five patients with GERD were studied, of whom 77 (34%) were infected with H. pylori. Oesophagitis and Barrett’s oesophagus were found in 140 patients (62%) and six patients (3%), respectively. H. pylori infected patients had significantly less severe oesophagitis compared to the uninfected group (P=0.022). All patients with Barrett’s oesophagus were uninfected. Factors that predicted severe oesophagitis included age over 60 years (P < 0.001) and hiatus hernia (P < 0.001). H. pylori infection was the only factor that showed a negative correlation with severe oesophagitis (P=0.011). The prevalence of the cagA positive strain in endoscopy‐negative GERD, erosive oesophagitis and control subjects was 70, 76 and 78%, respectively (P=0.75). Conclusions: H. pylori infection is associated with milder GERD.

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The discovery of the novel KIF5B-ALK variant further consolidated the role of aberrant ALK signaling in lung carcinogenesis.

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Prader-Willi syndrome (PWS) is a chromosomal disorder characterized by the presence of hyperghrelinemia, hyperphagia, and obesity. The optimal treatment for PWS patient remains controversial. Here, we present our experience of treating PWS with laparoscopic mini-gastric bypass (LMGBP) and laparoscopic sleeve gastrectomy (LSG). Three patients with genetic diagnosis of PWS and body mass index (BMI) greater than 40 kg/m(2) were referred for bariatric surgery. All of them had completed 2-year postoperative follow-up. Body weight, BMI, and ghrelin levels were recorded before and after surgery. They were two females and one male. Their age ranged from 15 to 23 years old, and the mean BMI was 46.7 kg/m(2) (range 44-50). Two patients underwent LSG and one patient underwent LMGBP. After a median follow-up of 33 months (range 24-36 months), mean weight loss and percentage of excessive weight loss at 2 years were 32.5 kg (24.9-38.3 kg) and 63.2 % (range 50.5-86.2 %), respectively. The mean fasting active ghrelin level decreased from 1,134.2 pg/ml preoperatively to 519.8 pg/ml 1 year after surgery. No major complication was observed. Iron deficiency anemia was observed in the patient who underwent LMGBP. Significant reduction of body weight and level of serum ghrelin can be achieved with minimal morbidity by LSG or LMGBP in patients with PWS.