Transition from Psoriasis to Psoriatic Arthritis
Dr. Peter Nash reports on studies addressing the transition from PSO to PsA at EULAR 2026.
Transcription
Hi everyone, Peter Nash reporting for RheumNow from EULAR London 2026. I've got a little theme, a couple of abstracts and a couple of presentations talking about the transition of psoriasis to psoriatic arthritis, how we can prevent it perhaps and how we can use some imaging to help.
So the first is an Austrian group that have put together a nice prospective longitudinal program where they've taken a couple of hundred people who are at risk of developing psoriatic arthritis but don't have any enthesitis, don't have any swelling, negative inflammatory markers, they only have PSO and they have some morning stiffness and they have an improvement with NSAIDs but that's about all, and they have done a nice lot of work with this group and even at the baseline they find 4% have rheumatologist-diagnosed PsA and they're going to follow this group over a length of time. Now we did a similar thing in eight dermatology clinics and we turned up about 8% PsA patients hiding amongst the PSO population.
Now the next transition is, is anything can stop that transition from PSO to PsA. So the Greeks have done an OP72. They have done a retrospective observational cohort study where they took PSO derm-diagnosed but no PsA and they're all on a biologic for over 6 months and they followed these patients up over 17 years and they looked to see how many developed rheumatology-diagnosed PsA. 394 patients, sorry, and in the 17 years 22% developed frank PsA and of that 22%, given that they were all given a biologic by their dermatologist for their rash, 45% of them happened to be on a TNF when they developed PsA, 14% on an IL-17 inhibitor, 10% IL-23, and 11% on an IL-12/23. So these are 394 people, 22% actually have PsA that evolves and they diagnose it and they had been on a variety of different biologics, and there was a hazard ratio difference adjusting for the disease time on a biologic and methotrexate background, and the IL-17s and the IL-23s and the IL-12/23s — there was no difference between them, but you were more likely to prevent and not get progression on those agents compared to a TNF in a group all of them on a biologic. So that was of some interest.
People including Lehi have presented ultrasound to help pick the PsA in the PSO population. But previous meetings have shown, and this is abstract 2613, that if you use a technique called FAP-PET you can show fibroblast activation, and the fibroblast is going to become very interestingly more important as a measure of chronicity in rheumatoid, in PsA, in people who are not responding and not going into remission, and it's a watch-this-space as a number of companies are developing anti-fibrotic drugs. But this FAP-PET CT — if you have a high index compared to if you don't, you're six times more likely to develop psoriatic arthritis whilst you started off with psoriasis compared to those who do not have an elevated FAP-PET CT. It's an expensive research tool, but people are looking for ways to pick PsA in a PSO population and do something about it early.
So the first is an Austrian group that have put together a nice prospective longitudinal program where they've taken a couple of hundred people who are at risk of developing psoriatic arthritis but don't have any enthesitis, don't have any swelling, negative inflammatory markers, they only have PSO and they have some morning stiffness and they have an improvement with NSAIDs but that's about all, and they have done a nice lot of work with this group and even at the baseline they find 4% have rheumatologist-diagnosed PsA and they're going to follow this group over a length of time. Now we did a similar thing in eight dermatology clinics and we turned up about 8% PsA patients hiding amongst the PSO population.
Now the next transition is, is anything can stop that transition from PSO to PsA. So the Greeks have done an OP72. They have done a retrospective observational cohort study where they took PSO derm-diagnosed but no PsA and they're all on a biologic for over 6 months and they followed these patients up over 17 years and they looked to see how many developed rheumatology-diagnosed PsA. 394 patients, sorry, and in the 17 years 22% developed frank PsA and of that 22%, given that they were all given a biologic by their dermatologist for their rash, 45% of them happened to be on a TNF when they developed PsA, 14% on an IL-17 inhibitor, 10% IL-23, and 11% on an IL-12/23. So these are 394 people, 22% actually have PsA that evolves and they diagnose it and they had been on a variety of different biologics, and there was a hazard ratio difference adjusting for the disease time on a biologic and methotrexate background, and the IL-17s and the IL-23s and the IL-12/23s — there was no difference between them, but you were more likely to prevent and not get progression on those agents compared to a TNF in a group all of them on a biologic. So that was of some interest.
People including Lehi have presented ultrasound to help pick the PsA in the PSO population. But previous meetings have shown, and this is abstract 2613, that if you use a technique called FAP-PET you can show fibroblast activation, and the fibroblast is going to become very interestingly more important as a measure of chronicity in rheumatoid, in PsA, in people who are not responding and not going into remission, and it's a watch-this-space as a number of companies are developing anti-fibrotic drugs. But this FAP-PET CT — if you have a high index compared to if you don't, you're six times more likely to develop psoriatic arthritis whilst you started off with psoriasis compared to those who do not have an elevated FAP-PET CT. It's an expensive research tool, but people are looking for ways to pick PsA in a PSO population and do something about it early.
If you are a health practitioner, you may Login/Register to comment.
Due to the nature of these comment forums, only health practitioners are allowed to comment at this time.