Given by injection just underneath the skin, rilonacept (IL-1 Trap) blocks interleukin-1, aprotein involved in inflammation. A new study of 10 people with severe goutshows that it substantially decreases both disease activity and pain.
The findings were presented at the American College of Rheumatology’s AnnualScientific Meeting in Boston.
“Lots of gout patients can’t take standard anti-inflammatory drugs suchas nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, or systemic steroids because theymay have kidney problems, heart problems, or diabetes,” explains researcher Robert Terkeltaub,MD.
Terkeltaub is section chief of rheumatology-allergy at the VA Medical Centerin San Diego and a professor of medicine at the University of California, SanDiego. “Now we can help break the inflammatory loop in these patients,”he says.
“IL-1 is a lynch pin of gout inflammation, and if we can block the lynchpin, we can stop the inflammatory cascade,” Terkeltaub tells WebMD.
Gout is a condition characterized by “flares” of intense pain,redness, inflammation, and warmth in the affected joint. It is caused byan accumulation of uric acid crystals in joints, which can also build up inother areas of the body. As the disease progresses, these flares may becomemore frequent and patients may develop joint deformity and large deposits ofcrystals, which can become visible under the skin (called tophi). Patients withgout can also develop kidney stones and kidney damage.
Uric acid is found naturally in the body. In gout, there is generally aproblem with either too much production of uric acid or problems in getting ridof the uric acid, or both. During an attack, gout is typically treated withdrugs that cool inflammation. In addition, uric-acid-lowering drugs aresometimes prescribed.
Some uric-acid-lowering drugs actually cause flares, and it is possible thenew drug may be used along with drugs to lower uric acid to help prevent suchflares.
In the new study of 10 people (average age 62) with severe, chronic gout,participants received two weekly injections of a dummy drug followed by sixweekly injections of rilonacept. In the second through eighth week of thestudy, 70% of participants had at least a 50% improvement in their pain; 60% ofparticipants had at least a 75% improvement in their pain. By contrast, none ofthe participants showed improvement while they were receiving the dummyinjections.
Levels of C-reactive protein in the blood, a marker of inflammation,decreased about 59% by the end of rilonacept therapy. Mild to moderatereactions at the drug injection sites were reported, but there were no deathsor serious adverse effects reported from this study.
“It’s really gratifying to see patients that are considered the worst ofthe worst respond,” Terkeltaub says. “If it works in the worst of theworst, we are hopeful it will work in the less than worst of theworst.”
Michael Hershfield, MD, a professor of medicine and biochemistry at DukeUniversity School of Medicine in Durham, N.C., tells WebMD that “a druglike this or any other that blocks IL-1 could prevent flares that occur when weare having a dramatic effect in lowering uric acid levels. The two could workvery well together.” Hershfield developed a new uric-acid-lowering drugcalled pEG-Uricase, which is now in clinical trials.
All in all, the new drug “looks very promising,” he says. “Thereis a lot more recognition of the problem of severe refractory gout and a lot ofpeople working on different approaches at the anti-inflammatory and theuric-acid-lowering level,” he says.