Nearly half -- 48 percent -- of those without antibodies experienced a significant reduction of their arthritis symptoms while taking the drug, while only 13 percent of those who developed antidrug antibodies got similar relief.
And while 34 percent of patients without antibodies experienced remission, only 4 percent of those who developed antibodies did.
Patients who developed antibodies were also more likely to drop out of the study because of "treatment failure."
Humira is a tumor necrosis factor (TNF) inhibitor, which works by blocking the action of TNF, a substance known as a cytokine that contributes to the inflammation of rheumatoid arthritis and other conditions.
"If you make antibodies, then Humira doesn't block the action of TNF, and it doesn't work," Jan Wolbink said.
Dr. Olga Belostotsky, a rheumatologist and chief of allergy and immunology at Lennox Hill Hospital in New York City, said the research helps explain why some patients don't respond to Humira, and yet they do respond when switched to another drug in the same class of TNF inhibitors.
"It's because they don't have antibodies to the other drugs, even when it's another drug in the same group of medications," she said.
Belostotsky said the research suggests it's very important that patients start methotrexate to suppress the immune system before starting Humira.
What isn't known is why those 28 percent of patients developed antidrug antibodies while the rest didn't.
"Why antibodies develop in some people more than the others is unclear, and why people react more to some drugs than others is unclear," Belostotsky said.
The Arthritis Foundation has more on rheumatoid arthritis.
SOURCES: Gerrit Jan Wo
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