My name is Oliver FitzGerald. I'm based at University College Dublin. And one of the abstracts that I enjoyed listening to at the EULAR meeting recently was presented by Laura Coats on the CONTROL study.
So the CONTROL study was addressing the question as to if you have a patient who's got persistent disease despite treatment with methotrexate, is it best to gradually increase the dose of methotrexate in order to gain control of the disease, or is it a better option to add in adalimumab at that point, an anti-TNF inhibitor.
So they had-- it was a 16-week study. The primary outcome measure was MDA, and they started patients on either gradually increasing methotrexate up to the maximum tolerated dose or adding in adalimumab.
So what they found was that adding in adalimumab was a better option in terms of the numbers of patients that achieved MDA. In addition, the side-effect profile was slightly worse with increasing methotrexate, largely relate to normal methotrexate-related adverse events. And the patients who were on adalimumab overall did better in all of the measures that were used in the study.
So what this tells us is that if you're adopting a treatment strategy for patients with psoriatic arthritis who have persistent disease already on treatment with methotrexate that it's a better option to consider adding in a TNF rather than increasing the dose of methotrexate, which I think is a useful lesson and something that can be applied easily in a clinical setting.
Another abstract I enjoyed was in the same session from David Simon and the Georg Schett group in Erlangen in Germany. The Schett group have been focusing on bone changes that occur in patients with psoriatic arthritis, and they have some very elegant studies of CTs of the joints in patients with psoriatic arthritis that clearly appear to differentiate them from patients with rheumatoid arthritis.
But in this study what they were looking at were structural bony changes that occurred in patients with psoriasis, and they wondered whether the presence of such changes might be associated with the subsequent development of psoriatic arthritis. So they had, I believe, about 114, 115 patients with psoriasis who had some symptoms but no signs of psoriatic arthritis, and they did CT scans of their second and third MCP joints, and they identified a number of patients who had these structural bony changes with what looked like enthesophytes at the edges of the joints. And they looked to see whether these changes and also bone-mineral-density changes might be associated with the subsequent development of psoriasis.
And the bottom line was-- with psoriatic arthritis. The bottom line was these structural changes and the reduction in bone-mineral density at the enthesophytes appeared to be predictive of patients that would go on to develop psoriatic arthritis. They're certainly more frequently found in those who develop psoriatic arthritis during the roughly 18 months of follow up.
It's a small study, small numbers of patients, and small numbers of patients develop psoriatic arthritis, but it's an interesting study and perhaps gives us some clues as to what we should be looking for in our psoriasis patients who might develop some psoriatic arthritis. So I think some lessons are potentially learned from these kinds of studies.
A further study that I found of interest at the EULAR meeting was a study presented by Dr. Gladman which was focusing on biomarkers that were measured during the course of the phase II filgotinib studies in patients with psoriatic arthritis. So filgotinib is a JAK1 inhibitor. And what they did was they took serum samples at various stages of follow up in the filgotinib study and measured a number of different biomarkers, including inflammatory cytokines and other measures to look to see what they might tell us about the changes that were occurring in both musculoskeletal and also in skin.
So filgotinib had, in the phase II study, shown a good effect in terms of both ACR responses but also PASI responses. And what they showed was that there appeared to be a difference in which biomarkers correlated with musculoskeletal response and which biomarkers correlated with PASI which I certainly thought was of interest. So the markers like COP, serum amyloid A appeared to correlate with measures of musculoskeletal disease whereas I-17 and other inflammatory cytokines appear to be more related to skin responses, which I certainly thought was of interest and perhaps not terribly surprising in that the I-17 inhibitors are so effective in terms of skin disease.
But nonetheless, I think that it gave us some insight into what the mechanisms, I guess, for treatments like JAK inhibitors may be affecting multiple biomarkers within the disease spectrum. So interesting.
So the final abstract I wanted to mention was one presented by Iain McInnes, president of EULAR, who presented data from a study, the EXCEED study, which was a comparison of secukinumab and adalimumab in patients with psoriatic arthritis. The dose of secukinumab that was used was 300 milligrams. That was compared with the usual standard 40-milligram dose of adalimumab. There were about 425 patients in each arm, and the primary outcome measure was superiority of secukinumab as compared to adalimumab.
So interestingly, the secukinumab failed to meet the primary outcome measure. It was not superior to adalimumab. It looked about the same both at the time of the primary outcome measure but also in terms of more longer-term follow up, it didn't appear to be any different to adalimumab.
Unsurprisingly, secukinumab outperformed adalimumab in relation to skin responses. And while Iain McInnes suggested that there was some difference in terms of some of the musculoskeletal measures in favor of secukinumab it looked really that there wasn't a whole lot of difference between the two.
I guess what that's telling us is that secukinumab and adalimumab are about the same for patients with psoriatic arthritis in terms of musculoskeletal involvement, but if you have bad skin disease, secukinumab does appear to perform better.
I guess my interest in this would be how do we know-- is it the same patients that are responding to-- the same type of patients that are responding to secukinumab and adalimumab? How do we choose which patient should go on which drug? And we still really don't know other than if they've got bad skin disease. We really don't know which treatment to choose, and there's more work to be done in that area certainly. Thank you.