From the Journals

Mepolizumab proves effective for eosinophilic granulomatosis with polyangiitis

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Directions for future research

The study by Michael E. Wechsler, MD, and his associates can be considered proof of concept. Now, researchers must turn to identifying biomarkers that predict the success or failure of mepolizumab in patients.

Researchers must also elucidate the fate of eosinophils in the tissues, especially in vasculitic lesions, after treatment with mepolizumab. And they should address possible synergistic activity when the drug is given together with immunosuppressants such as azathioprine and cyclophosphamide.

In addition, future studies should include patients who have organ-threatening or life-threatening eosinophilic granulomatosis with polyangiitis, who were excluded from this trial but who are most in need of novel treatments.

Ratko Djukanovic, MD, is with the University of Southampton (England) and the National Institute for Health Research Southampton Biomedical Research Centre. Paul M. O’Byrne, MD, is with the Firestone Institute for Respiratory Health within St. Joseph’s Healthcare and McMaster University in Hamilton, Ont. Dr. Djukanovic and Dr. O’Byrne both reported financial relationships with pharmaceutical companies outside their editorial. They made these remarks in an editorial accompanying Dr. Wechsler and colleagues’ report (N Engl J Med. 2017 May 18. doi: 10.1056/NEJMe1704402).


 

FROM NEW ENGLAND JOURNAL OF MEDICINE

Adding mepolizumab to standard-of-care glucocorticoids with or without immunosuppressive agents can induce remission in many patients who have eosinophilic granulomatosis with polyangiitis (EGPA), according to a report published online May 18 in the New England Journal of Medicine.

Proof-of-concept studies have demonstrated the efficacy of subcutaneous mepolizumab, an anti–interleukin-5 monoclonal antibody, in EGPA, so Dr. Wechsler and his colleagues assessed the safety and efficacy of a 1-year course of mepolizumab (300 mg) as add-on therapy in a double-blind, randomized, phase III trial, which involved 136 adults treated at 31 academic medical centers in nine countries. The study was sponsored by GlaxoSmithKline and the National Institute of Allergy and Infectious Diseases.

The first of two primary efficacy endpoints was the total accrued weeks of remission. A total of 28% of the mepolizumab group achieved remission for at least 24 weeks, compared with only 3% of the placebo group, for an odds ratio of 5.91.

The second primary efficacy endpoint was the proportion of patients in remission at both week 36 and week 48. Again, significantly more patients in the mepolizumab group (32%) than in the placebo group (3%) met this end point (OR, 16.74).

Mepolizumab also proved superior to placebo regarding numerous secondary endpoints, the investigators said (N Engl J Med. 2017 May 18. doi: 10.1056/NEJMoa1702079). More patients who received active treatment achieved remission within the first 6 months of treatment and remained in remission for a full year (19% vs. 1%; OR, 19.65). The time to first relapse was significantly longer for mepolizumab, with only 56% of that group experiencing a relapse within 1 year, compared with 82% of the placebo group. The annualized relapse rate was half as high with mepolizumab (1.14) as with placebo (2.27).

In addition, patients in the mepolizumab group were more likely to reduce their doses of glucocorticoids (OR, 0.20) or discontinue the drugs altogether (18% vs. 3% taking placebo).

Mepolizumab was most effective among the 79 patients who had a high absolute eosinophil count (150 or more cells per cubic millimeter) at baseline. In this subgroup, 33% of patients taking mepolizumab achieved remission for 6 months or more, compared with none of the patients taking placebo (OR, 26.1).

Although the effectiveness of mepolizumab in this difficult-to-treat population was noteworthy, only about half of the patients given the active treatment achieved remission as defined by the study protocol. It is unclear why the drug was not effective in the other half of patients. One possible reason is that some manifestations of the disorder are not driven by eosinophils. Another is that nonresponsive patients may have sustained longstanding, irreversible vasculitic damage that is no longer amenable to anti–interleukin-5 therapy.

Alternatively, it’s possible that mepolizumab reduced eosinophils in the blood but not those in the body tissues of nonresponsive patients or that the patients who didn’t respond well simply required a higher dose of the drug, Dr. Wechsler and his associates said.

The NIAID is now supporting a study of blood, urine, sputum, and tissue samples from some of these participants “to address questions related to disease risk and pathological features, as well as response to treatment,” they added.

Many authors reported receiving payments from pharmaceutical companies, including several from GlaxoSmithKline. Four authors are employees of the company.

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