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

An older couple wearing sunglasses holds hands and walks through tall grass in a field on a clear day while looking at each other

“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

A horizontal cylindrical shape represents the spectrum of rheumatoid arthritis. On the left of the shape it says "AUTOIMMUNE" with 13 human-shaped icons above it. On the right side of the shape it says "AUTOINFLAMMATORY" and has only 3 human-shaped icons above it

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
  • Muscle weakness
  • Keratoconjunctivitis sicca or dry eye
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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:

A group of randomly scattered dots

The overexpression
of cytokines that
suppress steroid
sensitivity9-11

An inverted triangular shape consisting of rows of hexagons. The first 4 rows of hexagons fit perfectly together while the next three rows appear jumbled and do not fit together

Dysregulation
of steroid receptors9

Three arrows intertwine and point upward

The signaling
of inflammatory
pathways9

A double helix

Genetic
mutations9

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