An excellent correlation between the Architect assay and the Elecsys HBsAg II assay (Roche Diagnostics) has been demonstrated.48 Using an automated onboard dilution step, the latter has a broad linear range that covers the HBsAg levels most frequently encountered and thus reduces the

need for manual dilutions, which are potential sources of error.49 Currently, the cost of these assays is not reimbursed in many countries, and they are not commercially available in the United States, so research-only tests are the only option at present. However, this can be expected to change in the future.50 Undoubtedly, there is still more to learn about the kinetics of the HBsAg decline and the ways to best use this in practice to optimize therapy. It remains to be confirmed whether HBsAg levels can reliably ABT-263 order Obeticholic Acid in vivo predict HBeAg seroconversion or HBsAg seroclearance. Studies in regions other than Europe and Asia are needed because the HBsAg kinetics for different HBV genotypes may differ during the natural course of the disease or in response to anti-HBV therapy. The on-treatment predictive value of HBsAg quantitation also needs to be studied in a sufficiently large number of patient

with consistent time points (e.g., weeks 12 and 24 of therapy) and with the same definition of response. The optimal HBsAg cutoff with the ideal PPV and NPV also awaits clarification. Prediction models combining the quantitation of HBsAg with HBV DNA and ALT levels should also be explored. Until these issues are resolved, HBsAg quantitation will not be ready for clinical practice. Nevertheless, with the assistance of HBsAg quantitation, we may

be on our way to establishing an individualized approach that might enable us to tailor anti-HBV treatments. The author thanks Karen Searle (Elements Communications, Ltd.) for her editorial assistance and Su-Chiung Chu for her secretarial assistance. “
“In their letter,1 Nakanuma and Sato provide evidence that peribiliary glands (PBGs) contain cells selleckchem implicated in the origin of intraductal papillary neoplasms of the bile duct. This fits well with the hypothesis that mucin-producing cholangiocarcinomas might arise from biliary tree stem/progenitor cells (BTSCs) located in the PBGs of large intra- and extrahepatic bile ducts.2 BTSCs are associated with mucin-producing cells within the liver and biliary tree.3 Figure 1 shows an example of a mucin-producing intrahepatic cholangiocarcinoma morphologically being the malignant counterpart of PBGs. Thus, intraductal papillary neoplasms could represent the preneoplastic lesions preceding the emergence of mucin-producing cholangiocarcinomas, supporting similarities between pancreatic and bile duct neoplasias. In response to injuries, pancreatic duct glands undergo a mucinous metaplasia that might lead to pancreatic cancer4; this could occur also in the biliary tree during pathologic processes with risk factors for cholangiocarcinoma, such as primary sclerosing cholangitis.