Predictive biomarkers for Barrett's esophagus: so near and yet so far.

Barrett's esophagus (BE) is the strongest risk factor for the development of esophageal adenocarcinoma. However, the risk of cancer progression is difficult to ascertain in individuals, as a significant number of patients with BE do not necessarily progress to esophageal adenocarcinoma. There are several issues with the current strategy of using dysplasia as a marker of disease progression. It is subject to sampling error during biopsy acquisition and interobserver variability among gastrointestinal pathologists. Ideal biomarkers with high sensitivity and specificity are needed to accurately detect high-risk BE patients for early intervention and appropriate cost-effective surveillance. To date, there are no available molecular tests in routine clinical practice despite known genetic and epigenetic aberrations in the Barrett's epithelium. In this review, we present potential biomarkers for the prediction of malignant progression in BE. These include markers of genomic instability, tumor suppressor loci abnormalities, epigenetic changes, proliferation markers, cell cycle predictors, and immunohistochemical markers. Further work in translating biomarkers for routine clinical use may eventually lead to accurate risk stratification.

New diagnostic and therapeutic frontiers in eosinophilic esophagitis.

Eosinophilic esophagitis (EoE) is a relatively new disease that is increasingly recognized as a chronic inflammatory condition with currently evolving diagnostic and therapeutic aspects. There is data to support the rising prevalence of EOE especially in western countries. EoE is an emerging cause of dysphagia and food bolus impaction in adults as well as abdominal pain, feeding disorders, and gastroesophageal reflux-like symptoms in younger patients. EoE is ever more recognized as a separate disease process that is more complicated than eosinophilic infiltration from gastroesophageal reflux disease. Food and environmental antigens both play significant roles in stimulating T-helper (Th-2) inflammatory response. Current therapeutic options include use of proton-pump inhibitors, immunosuppressive drugs, elimination diets, and esophageal dilatation. Simple elimination of food and environmental antigen exposure can be challenging in adults due to the difficulty in accurately identifying triggering antigens and adherence to restrictive diets from a wide range of putative food allergens. Novel therapeutic options are being presented as potential treatments that target chemokines and specific immunologic mechanisms for EoE. This review will aim to summarize the latest and evolving approaches to EoE diagnosis and management. In the future, biomarkers of inflammatory response may help diagnose, treat, and stratify individual patients for better treatment outcomes with this chronic disease.

Early treatment improves outcomes in acute hepatitis C virus infection: a meta-analysis.

Acute hepatitis C virus infection is associated with high rates of spontaneous clearance and variable rates of treatment-induced clearance. The benefit of early treatment versus awaiting spontaneous clearance is unknown, as is the optimal timing of treatment.We performed a MEDLINE and EMBASE search for the time period 1950 to October 2008. All English language abstracts using the search terms acute hepatitis C, hepatitis C and acute and hepatitis C and acute disease or acute infection were reviewed. Bibliographies were reviewed.Twenty-two studies including 1075 patients met the inclusion criteria. The sustained virologic response (SVR) rate for treated patients was 78%, significantly higher than 55.1% in untreated patients (OR = 3.08, 95% CI: 1.8-4.8 P value <0.0001). Mean time from diagnosis to spontaneous clearance was 9.7 weeks (SD 6.5). SVR rates varied inversely with time from acute HCV diagnosis. SVR rates for treatment within 12 weeks was 82.5% (95% CI: 75.6-89.3), significantly better than the clearance rates in untreated patients (P < 0.001). Response rates fell to 66.9% for treatment between 12 and 24 weeks, and decreased further to 62.5% for treatment beyond 24 weeks. Rates of viral clearance in treated patients with acute hepatitis C virus infection were significantly higher than that in untreated patients. Treatment rates were highest when treatment was initiated within 12 weeks of diagnosis. Based on these findings, we would advocate a 12 week period of observation for spontaneous clearance before treatment initiation. If no clearance has occurred by 12 weeks, treatment should be initiated.