Anyone who has ever had hepatitis B can have the virus wake up when rituximab strips out their B cells, sometimes months later and sometimes fatally. A blood test before the first dose, and a tablet for those who need it, prevents almost all of it.
Anti-CD20 antibodies remove the B cells that keep hepatitis B suppressed, so the virus can return in anyone with current infection (HBsAg positive) and in anyone with past, resolved infection (HBsAg negative but anti-HBc positive). Reactivation presents as a rise in HBV DNA followed by hepatitis, and it can appear up to a year after the last dose of rituximab, which is why prophylaxis continues after treatment ends.
What is done. Test HBsAg, anti-HBc and anti-HBs, and hepatitis C antibody and HIV, before the first anti-CD20 dose. HBsAg-positive patients receive antiviral prophylaxis throughout treatment and for at least twelve months after the last anti-CD20 dose. Anti-HBc-positive, HBsAg-negative patients receive either prophylaxis or close HBV DNA monitoring, depending on local policy and risk. A randomised trial in 121 HBsAg-positive patients with untreated diffuse large B-cell lymphoma receiving R-CHOP compared entecavir with lamivudine: HBV-related hepatitis occurred in 0 per cent against 13.3 per cent, reactivation in 6.6 against 30 per cent, and chemotherapy was disrupted in 1.6 against 18.3 per cent. Entecavir or tenofovir, not lamivudine, is the prophylaxis.
The same caution applies to obinutuzumab, to CD20 bispecific antibodies and to CAR-T, all of which deplete B cells for longer than rituximab does. Hepatitis B status is also checked before alemtuzumab and before any transplant.
Backbone ribbon from PDB 6VJA. RCSB PDB 6VJA. The ribbon widens where the chain is folded into a regular pattern and narrows where it is a loose loop.
Showing the molecule this term concerns: Rituximab.
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