Psychological characteristics predict likelihood of GERD symptoms but not structural state of esophagus. Male gender and obesity are risk factors for erosive esophagitis; whereas female gender and neuroticism are more likely to be associated with GERD symptoms.

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Sera from 14 patients with duodenal ulcer and their families were tested for IgG antibodies to Helicobacter pylori. Fourteen serologically negative patients and their families served as controls. Index patients and their family members who were serologically positive were advised to undergo endoscopic biopsy. Gastric biopsy tissues were subjected to HaeIII restriction analysis of nested polymerase chain reaction products of the urease gene. By serology, 28 (49.0%) of 57 in index families and 11 (27.5%) of 40 in control families tested positive. A higher prevalence rate was found in children of index patients (11/31, 35.5%) than in those of control patients (1/18, 5.6%; P < .05). On DNA analysis, 11 patterns were found in 13 patients, and 6 families underwent endoscopy. Children in 5 families exhibited identical patterns to those of their siblings and, in 3 of the 5 families, identical to the pattern of 1 of the parents. These results suggest that parent-to-child transmission and common infection source are probable causes of intrafamilial clustering of H. pylori.

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This pilot study suggests a trend for an inverse association between anti-HBc levels and clinical relapse in CHB patients off entecavir.

Summary Background Mac‐2 binding protein glycosylation isomer (M2BPGi) is an emerging biomarker for risk prediction of liver disease, but data remain sparse for patients with chronic hepatitis B (CHB) who are treated with nucleos(t)ide analogues (NA). Aim To clarify serial changes in M2BPGi and its association with subsequent hepatocellular carcinoma (HCC) development in NA‐treated CHB patients. Methods We enrolled 384 previously untreated CHB patients who received NAs. Among them, 195 had baseline cirrhosis (n = 142:48:5 for Child A:B:C). Sera were collected at NA initiation, and after 1 and 2 years. Serum M2BPGi levels were measured and expressed as cut‐off index (COI) at different time points. The association between M2BPGi and HCC was evaluated by the Cox proportional hazard model. Results The median M2BPGi levels significantly decreased from 1.68 COI at baseline, to 1.0 at year 1, and 0.88 at year 2. During median follow‐up of 72.7 months, HCC occurred in 37 patients, 36 of whom had cirrhosis. In patients with cirrhosis, baseline M2BPGi level was associated with HCC risk (adjusted hazard ratio, 1.07 per COI; 95% CI, 1.01‐1.14) on the multivariable Cox analysis, whereas levels at year 1 or 2 were not independently predictive. A risk score for HCC was developed using baseline M2BPGi, age and body mass index with c statistics of 0.77, 0.79 and 0.87 at 3, 5 and 10 years, respectively. Conclusions Serum M2BPGi level significantly decreases after NA treatment in CHB patients. Baseline level can be factored into the risk prediction of HCC in NA‐treated patients with cirrhosis.

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