Targeting High Disease Activity in PsA
This disease affects many parts of the body so a multi-faceted approach utilizing different therapies is required.
Targeting High Disease Activity in PsA
Doctors can use a variety of formulas to determine whether patients with rheumatoid arthritis (RA) have uncontrolled inflammation – often known as high disease activity. But it’s not as straightforward for psoriatic arthritis (PsA), a much more complicated disease that can strike many different parts of the body. Still, the goal is the same as for RA and other forms of inflammatory arthritis: near or complete clearing of symptoms.
Susan Goodman, MD, a rheumatologist at Hospital for Special Surgery in New York City, says achieving these aims in PsA is challenging because so many domains (skin, nails, spine, joints, tendons and ligaments) are involved. No single treatment will address all of them.
“When talking about PsA, we’re talking about multiple things, and some things respond to certain treatments and others don’t,” she says.
Joint Pain and Swelling
Joint pain is one example. The first treatment prescribed for PsA is usually methotrexate, a disease-modifying anti-rheumatic drug (DMARD) that suppresses an overactive immune system. But Dr. Goodman points out there’s little evidence that methotrexate can actually slow joint destruction in PsA. One of the few randomized controlled trials of the drug found it was no better than placebo for PsA patients. Still, many doctors find it benefits some people. There’s no question that methotrexate can improve skin symptoms – the FDA approved it for psoriasis decades ago. But it’s not useful for other aspects of PsA, like enthesitis and axial (spinal) disease. And it can cause serious liver, kidney, lung and bone marrow problems.
When methotrexate doesn’t control inflammation, the next step may be a type of DMARD called a biologic. The first choice is usually adalimumab (Humira) or infliximab (Remicade) – drugs that block the inflammatory protein, tumor-necrosis factor (TNF). If one TNF blocker doesn’t work, your doctor may try another or switch to a different class of biologics. These include drugs like secukinumab (Cosentyx) and Ixekizumab (Taltz), which target interleukin (IL)-17, another inflammatory protein. All biologics are powerful, costly medications with potentially serious side effects, including TB and some forms of cancer.
There’s almost no data on axial disease in PsA, so doctors tend to treat it like ankylosing spondylitis, a type of spinal arthritis. If you have active disease and changes to your spine, your doctor might start you on a non-steroidal anti-inflammatory drug (NSAID) such as ibuprofen (Advil, Motrin) or naproxen (Aleve), then switch to a biologic. Dr. Goodman says early data suggest IL-17 blockers may stop the disease from getting worse. “TNF inhibitors are good for symptom control,” she says, “but IL-17 inhibitors are more beneficial.”
Exercise and physical therapy are essential to strengthen muscles and maintain normal posture.
NSAIDs are usually the only treatment needed for low disease activity. Sometimes they’re combined with a steroid injection into a single swollen finger or toe. For severe symptoms, your doctor may prescribe a TNF blocker like infliximab.
You’re likely to start with an NSAID and physical therapy; these may be enough to reduce symptoms. If not, you may move on to a TNF blocker like infliximab, though at least one study has shown that enthesitis often clears on its own or without the need to change treatment.
“Psoriasis should always be co-managed with a dermatologist,” Dr. Goodman says. And treatment is highly individualized, depending on the severity of plaques, where you have them and how they affect your life. The first choice for even severe symptoms may be a topical steroid, Vitamin D analog or combination of the two, sometimes in conjunction with laser or UV light treatments. There are also new systemic treatments for psoriasis that target different inflammatory pathways. For example, tildrakizumab (Ilumya), guselkumab (Tremfya) and ustekinumab (Stelara) block the cytokine, IL-23, which plays a key role in autoimmunity.
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