Long-term hepatic consequences of chemotherapy-related HBV reactivation in lymphoma patients

Abstract

Aim: To investigate the long-term consequences of chemotherapy-related HBV reactivation in patients with lymphoma.

Methods: This study was based on the database of published prospective study evaluating HBV reactivation in HBV lymphoma patients during chemotherapy. Deteriorated liver reserve (DLR) was defined as development of either one of the following conditions during follow-up: (1) newly onset parenchyma liver disease, splenomegaly or ascites without evidence of lymphoma involvement; (2) decrease of the ratio (albumin/globulin ratio) to less than 0.8 or increase of the ratio of INR of prothrombin time to larger than 1.2 without evidence of malnutrition or infection. Liver cirrhosis was diagnosed by imaging studies.

Results: A total of 49 patients were included. The median follow-up was 6.2 years (range, 3.9-8.1 years). There were 31 patients with and 18 patients without HBV reactivation. Although there was no difference of overall survival (OS) and chemotherapy response rate between the two groups, DLR developed more frequently in patients with HBV reactivation (48.4% vs 16.7%; P = 0.0342). Among the HBV reactivators, HBV genotype C was associated with a higher risk of developing DLR (P = 0.0768) and liver cirrhosis (P = 0.003). Four of five patients with sustained high titer of HBV DNA and two of three patients with multiple HBV reactivation developed DLR. Further, patients with a sustained high titer of HBV DNA had the shortest OS among the HBV reactivators (P = 0.0000). No patients in the non-HBV reactivation group developed hepatic failure or liver cirrhosis.

Conclusion: Chemotherapy-related HBV reactivation is associated with the long-term effect of deterioration of hepatic function.

Figure 1

OS of total 49 HBV carriers’ undergoing chemotherapy for non-Hodgkin’s lymphoma, according to HBV reactivation status (P = 0.601) (A); comparison of liver reserve between HBV reactivators and HBV non-reactivators (P = 0.0342) (B).

Figure 2

Relationship between genotype and liver cirrhosis in HBV reactivators (P = 0.003).

Figure 3

OS in HBV reactivation patients with different reactivation patterns (P = 0.000). (MA: multiple reactivations; PR: protracted/resolved; PU: protracted/ unresolved.).