Transient elastography can stratify patients with Child-Pugh A cirrhosis according to risk of early decompensation.

BACKGROUND: Compensated cirrhosis has a variable prognosis depending on stage. There are currently no straightforward and robust tools in clinical practice to predict decompensation in Child-Pugh A cirrhosis. We set out to determine whether transient elastography (TE) could be used across liver disease aetiologies to determine risk of decompensation. PATIENTS AND METHODS: Participants were enrolled at two sites (Dublin and Nottingham) and followed up for a minimum of 2 years. The primary outcome of the study was liver decompensation, defined as the development of overt hepatic encephalopathy or ascites or presentation with bleeding varices. All patients received a TE examination to measure liver stiffness measurement (LSM) and had routine blood measurements taken at the baseline visit and on each subsequent visit. RESULTS: In 259 participants, the overall rate of liver-related outcome was 31 per 1000 person-years (95% confidence interval: 19-47 per 1000 person-years). Of the total population, 6 and 11% developed a liver-related outcome within 2 and 4 years of follow-up, respectively. There were no events in the population with a LSM less than 21 kPa. A LSM of more than 35 kPa was associated with a decompensation risk of 39% at 4 years. For each unit increase in the LSM above 20 kPa, the risk of liver-related outcome increased by 6% (hazard ratio=1.06; 95% confidence interval: 1.04-1.82) after adjusting for age, sex Mayo End Liver Disease Score, cohort source and aetiology. CONCLUSION: The risk of liver decompensation increased with increasing LSM in mixed aetiology compensated cirrhosis. LSM may be used to risk stratify patients, potentially reassure patients with low scores, and select patients with higher scores for experimental therapeutic studies with acceptable timelines.

Narrow band imaging and serology in the assessment of premalignant gastric pathology.

BACKGROUND: Patient outcomes in gastric adenocarcinoma are poor due to late diagnosis. Detecting and treating at the premalignant stage has the potential to improve this. Helicobacter pylori is also a strong risk factor for this disease. AIMS: Primary aims were to assess the diagnostic accuracy of magnified narrow band imaging (NBI-Z) endoscopy and serology in detecting normal mucosa, H. pylori gastritis and gastric atrophy. Secondary aims were to compare the diagnostic accuracies of two classification systems using both NBI-Z and white light endoscopy with magnification (WLE-Z) and evaluate the inter-observer agreement. METHODS: Patients were prospectively recruited. Images of gastric mucosa were stored with histology and serum for IgG H. pylori and Pepsinogen (PG) I/II ELISAs. Blinded expert endoscopists agreed on mucosal pattern. Mucosal images and serological markers were compared with histology. Kappa statistics determined inter-observer variability for randomly allocated images among four experts and four non-experts. RESULTS: 116 patients were prospectively recruited. Diagnostic accuracy of NBI-Z for determining normal gastric mucosa was 0.87(95%CI 0.82-0.92), H. pylori gastritis 0.65(95%CI 0.55-0.75) and gastric atrophy 0.88(95%CI 0.81-0.94). NBI-Z was superior to serology at detecting gastric atrophy: NBI-Z gastric atrophy 0.88(95%CI 0.81-0.94) vs PGI/II ratio < 3 0.74(95%CI 0.62-0.85) p<.0001. Overall NBI-Z was superior to WLE-Z in detecting disease using two validated classifications. Inter-observer agreement was 0.63(95%CI 0.51-0.73). CONCLUSIONS: NBI-Z accurately detects changes in the GI mucosa which currently depend on histology. NBI-Z is useful in the detection of precancerous conditions, potentially improving patient outcomes with early intervention to prevent gastric cancer.