Difficult-to-Treat RA

Why some RA patients don’t respond to conventional therapies

If your patient has tried and failed multiple RA treatments, their disease may be driven by autoinflammation.1,2

“Before Kineret, I tried many different treatments to get my symptoms under control, but many of them didn’t work for me.” —Peggy, RA patient

RA exists along a spectrum.

Though RA is primarily defined as an autoimmune disease, the distinction between autoimmune and autoinflammatory disease isn’t clear cut. Because there are various interactions and similarities between the innate and adaptive immune systems, they may be viewed as two ends of the same spectrum.3,4 Some patients have RA that is closer to the autoinflammatory end of that spectrum.1

RA autoimmune and autoinflammatory spectrum

Where does your patient’s RA fall?

Understanding which end of the spectrum your patient’s disease leans toward can be challenging, but there are key clues to watch for. Along with treatment history, you may want to consider any elevated acute-phase reactants and extra-articular signs of inflammation, including 1,5-7:

  • Fever
  • Rash
  • Headache
  • Fatigue
  • Musculoskeletal symptoms (arthralgia, arthritis, myalgia)
  • Conjunctivitis
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“I spent two years trying and failing multiple RA drugs, never knowing which drug might treat some symptoms but exacerbate others.... I began to feel that my rheumatologist and I were firing shots into the air and hoping we hit something.” —Megan, RA patient

Steroid resistance can be a telling clue.

Since RA is typically considered an autoimmune disease, therapies targeting the adaptive immune system (like steroids) are often prescribed. But autoinflammatory disease isn’t usually well controlled by these types of therapies.6 There may be several factors at play, including8,9:

Overexpression of cytokines

The overexpression
of cytokines that
suppress steroid

Dysregulation of steroid receptors

of steroid receptors9

Signaling of inflammatory pathways

The signaling
of inflammatory

Genetic mutations


Could your patient’s difficult-to-treat RA be driven by autoinflammation?