- Research has shown that the use of JAK inhibitors can weaken rheumatoid arthritis patients’ responses to shingles vaccination.
- In a study from Japan, patients with rheumatoid arthritis who started tofacitinib after they received the first dose of a two-dose shingles vaccine had similar antibody levels by 12 weeks to those who waited until after the second dose.
- While patients in the first group had an earlier improvement in their arthritis compared with the second group, Clinical Disease Activity Index scores were similar by week 12.
Patients with rheumatoid arthritis who started a JAK inhibitor after they received one dose of a two-dose shingles vaccine series had similar varicella zoster virus (VZV) antibody levels by 12 weeks to those who waited until after the second dose, an exploratory randomized trial from Japan showed.
At week 12, VZV-specific antibody titers increased in patients who initiated tofacitinib (Xeljanz) after the first dose of the recombinant zoster vaccine on day 1 (geometric mean fold rise [GMFR] 2.66) and in those who initiated the JAK inhibitor after the second vaccine dose at week 8 (GMFR 2.91), with a between- group ratio of 1.10 (95% CI 0.73-1.64), indicating similar responses, reported Yuko Kaneko, MD, PhD, of Keio University School of Medicine in Tokyo, and colleagues.
While patients in the first group had an earlier improvement in their arthritis at weeks 4 and 8 compared with the second group, Clinical Disease Activity Index (CDAI) scores were similar by week 12 (5.2 vs 7.4), they noted in the Annals of Internal Medicine.
“By 12 weeks, antibody responses were similar between strategies, suggesting that JAK inhibitor use may delay but does not prevent vaccine-induced immunity,” Kaneko and colleagues wrote.
While effective for rheumatoid arthritis, JAK inhibitors are associated with an increased risk for shingles, or herpes zoster. Although a recombinant zoster vaccine can be given during immunosuppressive therapy, “the optimal strategy to balance immunogenicity and disease control remains unclear,” the authors explained.
Previous research has shown that the use of JAK inhibitors, abatacept (Orencia), and rituximab can weaken patients’ responses to shingles vaccination, while immunogenicity is mostly preserved in patients taking conventional synthetic and biologic anti-rheumatic drugs, including tumor necrosis factor and interleukin-6 inhibitors.
The decision to wait on JAK inhibitor therapy depends on disease severity and shingles risk. “When feasible, completing vaccination before JAK inhibitor initiation may enhance early immunogenicity, but this must be balanced against the need for prompt disease control,” Kaneko and team pointed out.
The multicenter, open-label STOP-HZ study enrolled patients ages 50 and older who were starting tofacitinib. Participants received the recombinant zoster vaccine at day 1 and week 8, and 29 were randomized to initiate tofacitinib at day 1 (mean age 66.8, 75.9% women), while 30 were randomized to start therapy at week 8 (mean age 66.2, 73.3% women). Across the two groups, 27.6% and 20%, respectively, had a history of herpes zoster.
The proportion of patients achieving at least a 1.5-fold increase in antibody titers at week 4 was lower in the group who initiated tofacitinib at day 1, but proportions were similar at week 12. The VZV-specific T-cell response did not change in either group.
Waiting to start tofacitinib was linked to more arthritis exacerbations, but fewer adverse events. Exacerbation occurred in 6.9% of the day-1 group and 13.3% of the week-8 group. Adverse events occurred in 58.6% and 23.3%, respectively, including infection (24.1% and 6.7%).
Study limitations included its small sample size and short follow-up period, in addition to no incidences of clinical herpes zoster. The study also wasn’t powered to make between-group comparisons.
