EULAR has published new guidelines for the use of medications in treating psoriatic arthritis (PsA).
This update was considered necessary given new developments in the field, including new trials of existing therapies and the approval of novel treatments. So it's worth reviewing.
I have listed the 10 key recommendations with some commentary:
- Treatment should be aimed at remission or minimal disease activity, with constant monitoring and appropriate therapy adjustments.
This mirrors the general move in rheumatoid arthritis (RA) to tighter monitoring and aiming for a therapeutic target in the belief that this will lead to less pain, suffering and long term damage.
- NSAIDs can be used to relieve musculoskeletal signs and symptoms.
And they are certainly used. I still find this class of agents very helpful.
- Conventional DMARDS should be used initially in patients with peripheral arthritis, swollen joints, structural damage coupled with inflammation, high ESR/CRP and/ or extra-articular manifestations, with methotrexate preferred for patients with skin involvement.
The options I use are Methotrexate as my go-to agent (with the understanding that I do not find it nearly as useful in PsA as I do in RA), Sulphasalazine (which does nothing for the skin component, psoriasis) and then Arava.
- Local injections of glucocorticoids should be considered as an adjunct; systemic glucocorticoids can be used with caution at low doses.
Sometimes, we don’t have a choice. Steroids are still often used to help manage symptoms. In PsA, our traditional DMARDs are on the whole not as effective and control can be frustratingly difficult to attain.
- A biologic treatment, usually a TNF inhibitor, should be started in patients with peripheral arthritis and poor response to at least one conventional DMARD.
This would be nice to do… if the drugs were more affordable and I could access them easier. Rightfully, but sometimes frustratingly, the bar to qualification for government-subsidised therapy in Australia is often hard to meet.
- If a TNF inhibitor is not appropriate, patients with poor response to at least one conventional DMARD can be started on a biologic targeting IL12/23 or IL17 pathways.
We really do need access to these agents in Australia. At the moment, we only have access to biologics with the same mode of action. For patients who do not respond adequately to these, or who do cannot tolerate this class of agents, there aren’t any options.
- If biologics are not appropriate, patients with poor response to at least one conventional DMARD can be started on a targeted synthetic DMARD such as a PDE4 inhibitor.
Again, we need access to this. It refers to Apremilast, marketed as Otezla. In Australia, it is not subsidised by the government at the moment. I have a few patients on this on a patient familiarisation program at the moment but the numbers and timeframe of this offer is limited.
- A biologic treatment, usually a TNF inhibitor, should be considered for patients with active enthesitis and/or dactylitis and poor response to NSAIDs
or glucocorticoid injections.
Dactylitis and enthesitis can be extremely challenging and very often, traditional DMARDs just aren’t that effective in helping these manifestations. Unfortunately, in Australia, the qualification process for TNF inhibitor therapy is based on joint counts. This makes it challenging when the major manifestations for the particular patient is not joint, but instead, tendon and enthesis.
- Biologics should also be considered for patients with predominantly axial disease that is active and not responding to NSAIDs.
As per my comment on point 8. It’s not easy to access the TNF inhibitor medication in Australia for this indication in PsA due to the assessment process being reliant on peripheral joint disease. I would often look to see if there is damage on X-rays of the sacroiliac spine so that the patient can have a concomitant diagnosis of Ankylosing Spondylitis and qualify for the TNF inhibitor medication via that pathway. Unfortunately, these X-ray changes only occur later in the disease, so again, a delay in effective treatment ensues.
- Switching to another biologic, including switching between TNF inhibitors, should be considered for patients who do not respond to an initial biologic.
I already employ this strategy. As mentioned, we don’t actually have any other biologics currently subsidised on the PBS (government scheme) so there’s little other option that to cycle through what we do have for those not doing so well.
With any luck, we will soon have access to Ustekinumab, which targets the IL12/23 pathway.
I hope you found the commentary useful. Please do share your thoughts.
You can access the full article here: http://ard.bmj.com/content/early/2015/12/07/annrheumdis-2015-208337.full.pdf+html