RESEARCH - Denosumab inhibits structural damage in RA patients

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Denosumab Inhibits Structural Damage in Rheumatoid Arthritis Patients

By Will Boggs, MD

NEW YORK (Reuters Health) Jun 25 - Denosumab -- a monoclonal antibody

that binds RANKL, which is necessary for osteoclast development --

inhibits structural damage in rheumatoid arthritis patients, according

to a report in the May issue of Arthritis & Rheumatism.

" This patient research validates the basic research regarding the role

of RANKL/RANK/OPG in osteoclast activation/recruitment and subsequent

joint erosion, " Dr. Stanley B. Cohen told Reuters Health. " If further

studies confirm this observation, this will provide us another tool to

prevent joint damage. "

Dr. Cohen from Metroplex Clinical Research Center, Dallas, Texas and

colleagues in the Denosumab Rheumatoid Arthritis Study Group evaluated

the ability of denosumab versus placebo every 6 months to decrease the

progression of structural damage in a phase II study of 218 patients

with rheumatoid arthritis who were receiving methotrexate.

The MRI erosion score changed significantly less from baseline to 6

months in the denosumab groups than in the placebo group, the authors

report.

Just under 40% of the placebo patients had stable or improved MRI

erosion scores at 6 months, compared with 51% of patients who received

denosumab 60 mg and 64% of patients who received denosumab 180 mg.

Erosion scores increased more in the placebo group than in the 60-mg

and 180-mg denosumab groups at 6 and 12 months, the researchers note,

but there was no evidence of an effect of denosumab on the joint space

narrowing score.

Denosumab treatment was also associated with a sustained decrease in

markers of bone turnover and an increase in bone mineral density, the

investigators say.

Rates of adverse events were comparable among the treatment and placebo groups.

" The impact on erosions should be similar to TNF inhibitors, as TNF

stimulates RANK ligand, which denosumab blocks. " Dr. Cohen explained.

" From the discovery of this pathway in the late 1990s it was only a

decade until proof of concept in patients, " Dr. Cohen added. " This

points out how rapidly basic discoveries are translating into

potential for improved patient outcomes. "

Arthritis Rheum 2008;58:1299-1309.

http://www.medscape.com/viewarticle/576665

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