Reactivation of Hepatitis B After Ruxolitinib for MPN Hinges on Antivirals

The issue of reactivating hepatitis B and other chronic viruses such as herpes zoster after treatment for myeloproliferative neoplasms (MPN) is an emerging issue in hematologic malignancies, due to the power of newer therapies.

A recent retrospective analysis assessed the incidence of hepatitis B virus (HBV) reactivation among patients with myeloproliferative neoplasms (MPN) during and after treatment with ruxolitinib.

The issue of reactivation of HBV and other chronic viruses such as herpes zoster is an emerging issue in hematologic malignancies, due to the potency of the improved therapies. In general, the risk of HBV reactivation is different in patients with chronic HBV and resolved HBV.

Anti-CD20 monoclonal antibodies and ibrutinib have been linked with an increased risk of HBV reactivation in patients with previous infections, the authors noted. Ruxolitinib, a Janus kinase (JAK) inhibitor, weakens dendritic cell and T-cell functions, lowering cytokine production, which results in impaired control of silent infections and an increased risk of virus reactivation.

In prior trials, a few patients were reported to experience HBV reactivation after ruxolitinib, but the actual incidence of HBV reactivation in patients with MPN and chronic or resolved HBV infection during and after ruxolitinib treatment remains unclear.

This study was conducted in China; 224 patients with MPN were treated using ruxolitinib between February 2013 and February 2020.

Of the 224, 162 were excluded for being negative to all tests for HBV or for being positive for HBsAb only.

Of the 62 patients with resolved or chronic HBV treated with ruxolitinib, 58.1% were male, with a median age of 53.5. A little more than half had primary myelofibrosis; the remaining had various types of essential thrombocythemia or polycythemia vera.

Of 62 patients, 6 had chronic HBV, and 56 had resolved HBV infection. Of the 56 who had resolved infection, 43 patients had received combination treatment with thalidomide, prednisone, and stanozolol (TSP) during ruxolitinib treatment.

Of the 6 with chronic HBV, 2 did not take any antiviral prophylaxis and subsequently developed HBV reactivation and a flare of hepatitis.

The other 4 patients with chronic HBV infection did receive antiviral prophylaxis therapy before treatment with ruxolitinib did not develop HBV reactivation.

Of patients with resolved HBV infection who received antiviral prophylaxis, none of them experienced a reactivation of their infection.

The authors said the study had 3 limitations: retrospective observations were limited by patient variability in monitoring HBV; the study had a small sample size; and the study had relatively short media follow-up (23.21 months).

The authors said the study showed that HBV reactivation and hepatitis flare might occur a few months after ruxolitinib treatment in patients with chronic HBV infection who did not take antivirals prophylactically, especially in combination with TSP.

However, it was rare in patients with resolved HBV infection.

Reference

Duan MH, Cao XX, Chang L, Zhou DB. Risk of hepatitis B virus reactivation following ruxolitinib treatment in patients with myeloproliferative neoplasms. Hematology. 2021 Dec;26(1):460-464. doi: 10.1080/16078454.2021.1945234.