Steinfeld SD et al. (2006) Epratuzumab (humanised anti-CD22 antibody) in primary Sjögren's syndrome: an open-label phase I/II study. Arthritis Res Ther 8: R129

CD22 is thought to have a role in the disruption of B-cell homeostasis seen in primary Sjögren's syndrome, so Steinfeld and colleagues assessed the safety and efficacy of epratuzumab—a humanized antibody against CD22—in an open-label phase I/II study.

Overall, 16 white patients (14 female) with active, primary Sjögren's syndrome were scheduled to receive a 360 mg/m2 epratuzumab infusion at weeks 0, 2, 4, and 6; two patients did not receive all four infusions because of adverse reactions to treatment. Follow-up was performed at weeks 6, 10, 18, and 32. The authors used a composite end point (the Schirmer-I test, erythrocyte sedimentation rate, and unstimulated whole salivary flow) to assess response to treatment. Patient and physician global assessments, fatigue, and pain were measured with visual analog 0–100 mm scales.

Compared with baseline, patient and physician global assessments and fatigue were markedly improved after treatment with epratuzumab. Over half of the 15 patients who received ≥1 infusion achieved a ≥20% improvement in two disease activity parameters at week 6; nearly 70% of patients achieved this response at week 32. Within 18 weeks of treatment, mean B-cell levels had decreased; CD22 overexpression in peripheral B cells (observed at baseline) remained downregulated for at least 12 weeks post-treatment. Three patients had slightly elevated human anti-epratuzumab antibody titers, but without apparent clinical effects.

Interestingly, the number of responders was highest at week 32, which the authors suggest might indicate recovery of glandular tissue. They advise, therefore, that glandular biopsies be taken before and after treatment.