Psoriatic arthritis (PsA) is finally getting the attention it deserves after spending a long time in the shadows of its big brother rheumatoid arthritis. But are we making progress in treating the disease or are we just procrastinating? We speak to internationally renowned expert Professor Iain McInnes to get his view on where we are and how far we have to go.

PsA is not RA

The disease has often been regarded as a little brother to rheumatoid arthritis and it’s only in the last five years that it has gained the recognition it deserves, says Professor McInnes.

The disease is actually quite common, with psoriasis affecting three percent of the population with a third of these people developing psoriatic arthritis.

As Professor McInnes points out the figure is not that dissimilar to the number of people living with rheumatoid arthritis.

However, until recently most therapies used to treat PsA were borrowed from RA despite the diseases having entirely different clinical phenotypes and time course, tissue distribution, and tissue cell and molecular features.

“They [treatments] weren’t really conceived because of the PsA condition and the understanding of its pathology …they were used because they worked in other inflamed joints” he told the limbic.

But PsA is more than synovitis, it’s a disease of enthesitis, tendon bone insertion, synovium, skin and bone, explains Professor McInnes.

The immune system deals with different challenges in different tissues and the consequences of that immune response are very different.

In an evolutionary sense, the type of immune response that develops in the gut is different from the skin, it is different from the eye and different from the joint and all for a very good reason, says Professor McInnes.

For instance if you have an inflamed eye and become blind the eye is useless, whereas if you have an inflamed bit of skin it will eventually heal.

“The immune system has evolved to make really important decisions about how much damage you can tolerate in a tissue,” he says.

“We shouldn’t expect one medicine to deliver perfect results in each of these different tissues”.

“We already know this because we have medicines that work in the skin and not the joint, or the joint and not the skin, and we have medicines that work a bit in both.”

The progress – more targets on the way

The treatments currently approved or under investigation to treat PsA include conventional DMARDS, TNF blocking biologics, IL-17A inhibitors, kinase inhibitors, PDE4 inhibitors and IL-12/IL-23 inhibitors.

The progress is that we’re now looking at a lot of new targets directed at the real pathogenesis of the disease, says Professor McInnes.

We’re also starting to look at the right treatment strategy although there’s still a lot of work to do in this area.

At present there isn’t enough evidence on how to use treat to target (T2T) strategies in PsA but the TICOPA study suggests that a T2T strategy confers benefit.

Interestingly, says Professor McInnes, the study showed more side effects in the group who were treated intensively compared to those who received conventional care.

“The early signs are that some T2T strategy will be helpful but I think we have to be quite clever and imaginative in how we make that strategy and what we use as the targets – maybe a different target for skin, joints, tendon.

“We need more data, it’s as simple as that… we don’t have the tools we need at the moment,” he says.

A little bit of procrastination

According to Professor McInnes the procrastination in all of this is that there’s still room for improvement in getting the joint disease of people with PsA to a state of low disease activity.

“The triumph of the latest medical advance is still only a partial advance in the totality of the disease,” he said.