[Hepatits B virus reactivation in patients receiving immunosuppressive therapy or chemotherapy and effective prophylactic management: a prospective observational study in a hospital over an 8-year period].

We investigated the development of hepatits B virus (HBV) reactivation in patients receiving immunosuppressive therapy or chemotherapy at our hospital for 8 years. Using the automatic checking system for HBV reactivation coded using medical information that has been in operation in our hospital since October 2012, we prospectively observed the occurrence status of HBV reactivation in immunosuppressive/chemotherapy cases for 8 years. HBV reactivation occurred in 31 of 1516 patients with HBV infection. It occurred annually between 1 and 7 cases in multiple clinical departments, and in 8 of 59 patients treated with rituximab, 10 of 653 patients treated with antineoplastic agents, 10 of 399 patients treated with steroids, and 3 of 212 patients treated with direct-acting antivirals. The cumulative incidence of HBV reactivation was 1.2%, 2.3%, and 3.4% at 1, 2, and 3 years, respectively. The results of Cox regression analysis showed that the incidence of HBV reactivation was significantly higher in patients who received rituximab (odds ratio:12.841) or steroid (hazard ratio:4.264) or those who tested positive for HBc antibody alone (hazard ratio:11.005). We observed the occurrence of HBV reactivation in HBV-infected patients treated with immunosuppressive therapy or chemotherapy. HBV reactivation by immunosuppressive therapy or chemotherapy still occurs, and further safety management and caution are required in the hospital.

Usefulness of KL-6 in the subtyping of intraductal papillary mucinous neoplasia of the pancreas, including carcinoma, dysplasia, and hyperplasia.

KL-6 is known as a useful serum biomarker of the disease activity in interstitial pneumonias. We investigated its usefulness as a biomarker for subtyping intraductal papillary mucinous neoplasms (IPMNs) of the pancreas. IPMNs are generally divided into 4 subtypes, namely pancreatobiliary (PB), intestinal (INT), gastric (GS), and oncocytic (ONC). Aside from the KL-6 antibody, the MUC1, MUC2, MUC5AC, MUC6, and MIB-1 antibodies were also examined. Eighteen IPMN cases were examined, including 12 cases of intraductal papillary mucinous carcinomas (IPMCs) simultaneously associated with dysplasia (IPMDs) and hyperplasia (IPMHs) and 6 IPMD cases with IPMH. KL-6 antibody was positive in the 8 IPMC cases, corresponding to a MUC2-negative PB subtype, but negative in 4 IPMC cases, corresponding to the INT subtype, which is positive for MUC2. IPMD of moderate-to-severe degree positively stained for the KL-6 antibody in the IPMC cases of the PB subtype but not in those of the INT subtype. The IPMH cases were mostly negative for KL-6, similar to the mild IPMD cases. In the 6 cases of mild IPMD and/or IPMH, KL-6 and MUC2 expressions were mostly negative. In conclusion, the KL-6 antibody is immunohistochemically a good biomarker of the PB subtype of IPMC, but not the INT subtype. Identifying IPMN subtypes based on KL-6 stainability would be useful. Clinicopathological studies with more IPMC cases might be needed for further progress in this field of study.