| objective: HBV reactivation is a well-know and potentiallylife-threatening complication in chronic HBV carriers receiving systemicchemotherapy for cancer treatment. The current guidelines recommendthe use of preemptive antiviral drugs for chronic carriers undergoingchemotherapy or immunosuppressive therapy for hematologicmalignancies and solid tumors. This prospective study was conducted todetermine whether TACE could induce reactivation of HBV andexacerbation of underlying chronic hepatitis B in HBsAg-positive HCCpatients, and to examine possible risk factors to HBV reactivation.Methods: From March2008to September2011in the Affiliated Hospitalof LuZhou Medical College,67HBsAg positive patients newlydiagnosed as HCC were enrolled in the study, and the clinical data werestudied retrospectively. A total of55patients who received126sessionsof TACE were assigned as treatment group; TACE was performed withcis-platinum (60mg/m2), mitomycin (6mg/m2) or combined withadriamycin (20mg/m2) and lipiodol (5–25ml) or gelfoam; the controlgroup (n=12) included patients who did receive surgical resection (3),percutaneous ethanol injection therapy (PEIT)(4), and conservativemanagement (5) during the study period. Before study entry, all patients underwent baseline examinations including complete blood counts,prothrombin time (PT), a-fetoprotein (AFP) levels, liver function tests,serum HBV DNA quantification, detection of hepatitis B surface antigen(HBsAg), anti-HBs, anti-HBc, HBeAg, anti-Hbe and anti-hepatitis Cvirus (anti-HCV), Follow-up laboratory examinations, including liverfunction test, common blood counts, were performed Biweekly, HBeAgand HBV DNA quantification were performed at4-8wk after TACE inthe case group. The control group was given the same follow-uplaboratory examinations at least4wk after baseline examinations, TACEefficacies was evaluated in all patients after1month by dynamic spiralCT or MRI of for evaluation of response and determine whether TACEshould be performed repeatly. All patients were followed-up no less than3months. Results:1. IN total, HBV reactivation occurred in24patients(23with chemo-lipiodolization and1with PEIT, P<0.05), and of the24patients,9(25%)(All were occurred in TACE group, P<0.05) developedhepatitis.2. HBeAg seropositivity (47.8%vs22%, P=0.04) andchemotherapeutic agents (P=0.03) were found to be significantlycorrelated with HBV reactivation. On multivariate analysis using alogistic regression analysis, HBeAg seropositivity (OR:26.21, CI:2.46-278.74, P<0.05) and chemotherapeutic agents (OR:0.09, CI:0.01-0.92, P<0.05) was the independent predictor of HBV reactivation inpatients receiving chemo-lipiodolization.3. Thirty patients (26.5%) in the chemo-lipiodolization group developed hepatic decompensation, Amongthem,7patients (4with hepatitis) had HBV reactivation, HBeAgseropositivity, prothrombin time, and Portal vein thrombosis correlatedwith the hepatic decompensation (P<0.05). Conclusion:1. Transarterialchemo-lipiodolization can reactivate HBV, and HBeAg-positive HCCpatients receiving chemo-lipiodolization should be closely monitored forHBV reactivation.2. Univariate and Multivariate analysis revealed thatHBeAg seropositivity and chemotherapeutic agents correlated withchanges in HBV DNA status after TACE.3. HBeAg seropositivity,prothrombin time, and Portal vein thrombosis correlated with the hepaticdecompensation.4. Although HBV reactivation may result inexacerbation of liver damage, careful post-procedure monitoring andmanaging is needed. |
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