Epratuzumab, a CD22-targeted humanized monoclonal immunoglobulin G (IgG) 1 antibody, improved systemic lupus erythematosus (SLE) disease activity in patients with SLE and associated Sjogren syndrome, according to a study published in Arthritis & Rheumatology.1

B-cell activity has been implicated in the pathogenesis of Sjogren syndrome, and epratuzumab has previously demonstrated B-cell-specific immunological activity in a small number of patients with primary Sjogren syndrome.2-6 Although primary Sjogren syndrome develops independently, associated Sjogren syndrome is linked to coexisting autoimmune diseases, such as SLE. The prevalence of associated Sjogren syndrome varies from 6.5% to 19%.7-9

Researchers performed a post hoc analysis using data from the EMBODY 1 and EMBODY 2 trials (Clinicaltrials.gov identifiers: NCT01262365, NCT01261793) to determine the efficacy and safety of epratuzumab in 1584 patients with SLE, 113 of whom had a diagnosis of associated Sjogren syndrome.1 At 48 weeks, they found that treatment with epratuzumab in addition to standard therapies resulted in improved SLE-specific clinical outcomes compared with placebo in patients with associated Sjogren syndrome. However, no improvements in SLE-specific clinical outcomes were observed in patients who did not have associated Sjogren syndrome.

The researchers found that B-cell numbers, IgM, and anti-Sjogren-syndrome-related antigen-A levels were consistently reduced in all patients receiving epratuzumab. They add that B-cell reduction was faster in patients with associated Sjogren syndrome. There was no difference in the frequency of adverse events with epratuzumab compared with placebo.

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The authors concluded, “These data suggest that epratuzumab may have clinical benefits in certain subsets of SLE patients and so stratification of SLE patients may be appropriate. Further trials examining the effectiveness of epratuzumab in primary Sjogren’s would be required to confirm the effectiveness of epratuzumab in this population.”1

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References

  1. Gottenberg JE, Dörner T, Bootsma H, et al. Efficacy of epratuzumab, an anti-CD22 monoclonal IgG antibody, in systemic lupus erythematosus patients with associated Sjögren’s syndrome: post-hoc analyses from the EMBODY trials [published online January 30, 3018]. Arthritis Rheumatol. doi: 10.1002/art.40425
  2. Youinou P, Devauchelle-Pensec V, Pers JO. Significance of B cells and B cell clonality in Sjogren’s syndrome. Arthritis Rheum. 2010;62:2605-2610.
  3. Salomonsson S, Jonsson MV, Skarstein K, et al. Cellular basis of ectopic germinal center formation and autoantibody production in the target organ of patients with Sjogren’s syndrome. Arthritis Rheum. 2003;48:3187-3201.
  4. Risselada AP, Looije MF, Kruize AA, Bijlsma JW, van Roon JA. The role of ectopic germinal centers in the immunopathology of primary Sjogren’s syndrome: a systematic review. Semin Arthritis Rheum. 2013;42:368-376.
  5. Ambrus JL, Suresh L, Peck A. Multiple roles for B-lymphocytes in Sjogren’s syndrome. J Clin Med. 2016;5:87.
  6. Steinfeld SD, Tant L, Burmester GR, et al. Epratuzumab (humanised anti-CD22 antibody) in primary Sjogren’s syndrome: an open-label phase I/II study. Arthritis Res Ther. 2006;8:R129.
  7. Manoussakis MN, Georgopoulou C, Zintzaras E, et al. Sjogren’s syndrome associated with systemic lupus erythematosus: clinical and laboratory profiles and comparison with primary Sjogren’s syndrome. Arthritis Rheum. 2004;50:882-891.
  8. Fox PC. Autoimmune diseases and Sjögren’s syndrome. Ann N Y Acad Sci. 2007;1098:15-21.
  9. Patel R, Shahane A. The epidemiology of Sjögren’s syndrome. Clin Epidemiol. 2014;6:247.