Psoriatic Arthritis From the Dermatologist's Perspective
I'm joined by my colleagues Dr Mona Shahriari and Dr Jason Hawkes. Would you guys like to introduce yourselves? Mona, do you want to start?
Mona Shahriari, MD, FAAD: Thank you so much, Tina, for having me. I'm a dermatologist out of Connecticut. I run a clinical trial center, so I live and breathe inflammatory skin disease, including psoriasis. I'm very excited for the conversation.
Bhutani: Love it. Jason?
Jason E. Hawkes, MD, MS: Hi, everyone. Like Mona, I'm also a dermatologist and run a clinical trial center. I'm co-owner, chief scientific officer, and investigator at Oregon Medical Research Center in Portland, Oregon. We treat all inflammatory diseases, including psoriasis and psoriatic arthritis.
Screening Tools for the Dermatologist
Bhutani: We couldn't have a better group to discuss this topic. I think this is really important, because I know I've heard from many people that when we talk about psoriatic arthritis, people say, oh, that's a rheumatologist's problem. Whenever they think a patient might have psoriatic arthritis or they're worried about it, they send them straight to the rheumatologist.
The issue in my area, and probably similar to yours, is it's really hard to get into a rheumatologist. The access is quite tough. From my perspective, I think it's important for us to at least screen our patients, try to get as close to a diagnosis as possible, and potentially even start treatment if we think that this patient is progressing pretty quickly.
To start, I would love to know your approach when you are suspecting psoriatic arthritis. Let's even step back. Maybe you have a patient with psoriasis, and we know they have psoriasis on their skin. How are you screening them at your visits, or are you screening them at your visits, for psoriatic arthritis?
Shahriari: Honestly, I think as dermatologists, we're in a unique position because 85% of our psoriatic arthritis patients are going to present with skin as the first sign of their arthritic disease. I tell my residents all the time that you have to fully undress your patient. Do that head-to-toe exam and look for inverse psoriasis, scalp psoriasis, and nail psoriasis, because all of those can clue you into this patient being maybe at slightly higher risk for psoriatic arthritis.
I include a joint screening as part of any workup of any of my psoriasis patients, even if they have mild disease. Data show that whether they have mild, moderate, or severe psoriasis, they can still be at risk for psoriatic arthritis. I can always go into how I screen, but I'd love to hear, Jason, if you do anything differently.
Hawkes: I love that tip. I think that's really important, to have patients fully undress. I think we do that primarily because these high-impact sites are more difficult-to-treat because they don't always want to talk about these areas — like the genitals, for example, or even scalp. I think in the same way, many patients aren't talking about their joints because they haven't made the connection between their skin disease and their joint disease.
When getting them into a gown and doing the full-body exam, I like to focus on the skin first. We talk about their psoriasis, but then I like to walk them back and say, you know, you've got a disease that primarily manifests in the skin, but you may start to have other health issues. You introduce the concept of comorbidities and then you ask, do you know your psoriasis can involve your joints?
Then you start walking through some of those symptoms because it kind of feels like a natural progression. Obviously, swollen joints and painful joints. We talk about the osteoarthritis vs psoriatic arthritis, which is helpful.
Dactylitis is one of those tried and true symptoms; when it's there and present, then there's a good likelihood of psoriatic arthritis. We spend a large amount of time teasing out the joint pain pattern because many people have joint pains in general. The problem is that many of those patients don't have psoriatic arthritis. Instead, they might have osteoarthritis or fibromyalgia.
The good thing with the skin is that it's the easy part. When you see psoriasis, most of the time you know it, but joint pain in the absence of skin disease, that's much more difficult. We also get patients from rheumatology to try to help tease out whether their joint pain's associated with a nonspecific rash such as eczema or is this really psoriatic arthritis in the setting of mild plaque psoriasis?
The Importance of Asking the Right Questions
Bhutani: To Mona's point, I think we are lucky that when patients are coming into our clinic, they most likely already have psoriasis. It's our job to tease apart the other parts of it. Sometimes, like you said, when they have joint pain without skin disease and they end up in rheumatology, it's much harder oftentimes to nail down or be very confident with the diagnosis. We often get inflammatory arthropathy or something along those lines. They don't really put their money down and say it's psoriatic arthritis, unless they have psoriasison the skin.
Jason, you mentioned a few questions that you ask about swollen joints and tender joints. I also talk about morning stiffness. Fatigue is a big one. I think fatigue is one of these that is a huge sign of psoriatic arthritis, but who doesn't feel tired? Even teasing that apart, is this normal fatigue from somebody who's very busy living life, or is it actual, pathologic fatigue that shouldn't be happening at age 35 or something like that?
Are there other specific questions that you guys are asking, or alternatively, do you guys use any formal questionnaires like the Psoriasis Epidemiology Screening Tool (PEST) questionnaire or any psoriatic arthritis screening tools in your clinic?
Hawkes: I don't necessarily use the PEST formally — like we don't hand somebody a sheet at check-in. I think the questions are easy to remember. I've mentioned a couple of them already. Heel pain, plantar fasciitis is a common problem, so I certainly ask about that, and the morning stiffness. Also, describing what it feels like to have plantar fasciitis, sacroiliac (SI) joint pain, etc.
We start looking, as Mona mentioned, at the nails and the scalp, and looking for tender joints. I've had a few patients that basically said, my joints feel fine. But I looked and I saw one of their knees that was swollen and red, and they just figured it was due to something else. I think those are parts of the history that then couple with our exam, and we start to put the two things together — the skin and the joint findings.
Shahriari: Jason, to echo that point, psoriatic arthritis is a clinical diagnosis. We don't have biomarkers that can help us nail down that specific diagnosis, so it is really crucial to get that history. Sometimes I say just because the joint swelling and tenderness isn't present on that day in the exam room, it doesn't mean they don't have psoriatic arthritis.
Somebody who has psoriasis of the skin, has pitting of the nails, maybe some scalp involvement, too, and then they have this remote history of a swollen joint, but today, I can't elicit anything. Do they not have psoriatic arthritis? I think keeping all the domains of psoriatic arthritis in mind is very important.
I use Dr Merola's mnemonic, it's as easy as 'PSA,' to remember the questions that I ask. P stands for pain, so you ask about the peripheral joints, pain in the heel, and pain in the elbow. S is for stiffness, so any stiffness after periods of immobility. A is for questions about axial disease.
As dermatologists, sometimes we might not be sure. A PEST questionnaire is a good idea. It's an easy five- to six-question questionnaire that is easy for patients to do when they're waiting for us, given how busy some of our clinics are. I know I'm always running behind.
Decision-Making Surrounding Medication Selection
Shahriari: I do think, if I'm in doubt, why not give them a drug that covers the joints until they can see the rheumatologist? There's really no harm that I could do. Either I didn't adequately treat the joints and they'll add something, or they get diagnosed with something else and they're still on a medicine that covers their skin well. I don't know if you guys have a different approach.
Bhutani: No, I agree. Sometimes I even use some of the highly effective treatments that we have as a diagnostic tool. I say, if your joint pains and your fatigue — let's say they're nonspecific — get better if I treat them with a biologic agent, for example, it kind of nails it into my head that, okay, this probably was psoriatic arthritis and I was right vs this might be something else, like fibromyalgia or osteoarthritis that Jason mentioned earlier. Sometimes I even use our treatments to help me confirm or feel more confident about the diagnosis in those patients where I'm questioning it a little bit.
Hawkes: I think it highlights the gaps. As mentioned, there are no biomarkers. When we think about the testing for psoriatic arthritis, outside of x-rays and maybe ultrasound, which dermatology really doesn't do, we really don't have a good lab test. We're talking about patients that are rheumatoid factor negative, but we know that some patients with rheumatoid arthritis aren't going to have positive serology.
We don't really have a good biomarker for PsA. Even with the treatments, the treatments for the joints are so far behind immunologically where the skin is. We've pushed the needle of skin improvement so high to where we're getting eight or nine out of 10 patients almost completely clear. We're not really talking about American College of Rheumatology (ACR) scores of 90 or 100. Rather, we're talking about ACR 50 and 70 as being big, dramatic changes in the joints.
I think this is important for patients to understand, too, because even when we use therapies when patients do have psoriatic arthritis, their joints don't always respond. Even with an agent that has an indication for both skin and joint. These are the patients that keep me up at night.
For the uncomplicated, straightforward plaque psoriasis patient, we have many great agents. Even for those same agents that are approved, we don't always see a joint response. It uncovers the gap that we have, the real need in psoriatic disease to really advance therapies for the joints. To have a biomarker would be worthwhile, especially for those patients who have subclinical joint disease, because that's the timepoint where we can make the biggest difference by preventing permanent joint destruction.
Bhutani: It's funny. I just gave a talk with a rheumatologist recently and he said, I always hate going after the dermatologist because like you said, we're talking about Psoriasis Area and Severity Index (PASI) score of 90 or 100, and then he comes in and says, the ACR score is 20. You're right, it's not as impressive, although even an ACR of 20 can be very impactful for a patient who's living with psoriatic arthritis. I still think it's important to put that into perspective.
Mona, I think you were about to say something?
Shahriari: I was just going to say, along the lines of the gaps, I think skin of color is another place where there is work to be done. Diagnosing psoriasis can be challenging in skin of color, which is partly why psoriatic arthritis is actually less likely to be diagnosed in a timely fashion. In many patients with skin of color, the pain associated with the arthritis may also be misdiagnosed, which can further lead to delays in therapy. There was a mentor of mine who used to use the phrase 'time is bone,' and the more time that goes by, the more bone that we lose.
I think it's really important, especially in patients who may have melanin-rich skin, to have that index of suspicion that maybe it is a psoriatic arthritis that they're dealing with and not some other nonspecific arthritis.
Bhutani: I always tell my patients when they come in with just skin disease that we can try other things. We can try topicals, we can do phototherapy, and we can try other things to see if it helps. We might still end up on a systemic agent, but I still say that we can give it a try if it makes you more comfortable.
With psoriatic arthritis, I don't give them that option. I describe it to them as almost like scarring. Once that scar is there, once the bone has started to be destroyed, we can't get it back. Those changes are irreversible, and that's why early treatment is so critical.
We briefly mentioned it earlier, but I wanted to go over the different types of psoriatic arthritis, or let's say the features or what are called the domains of psoriatic arthritis. GRAPPA, which is the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis, has put out these domains for psoriatic arthritis. Two of the domains are axial disease vs peripheral disease. Does one of you want to go into the details of that a little bit, and then we'll go into the other domains?
Hawkes: It makes sense in just the anatomical sense of peripheral disease vs axial disease. There was a great talk by one of the rheumatologists in Europe that basically said, don't make it more complicated than that. We're talking about the axis (spine and SI joints) or we're talking about peripheral disease (joints of the arms and legs). There are nuances between the two, and there is a gradient or spectrum for how they present.
For peripheral disease, we're really talking about those joints away from the spine and hips or pelvis. By classifying the two types, I think that's really in the hope that maybe we find a group where, for example, peripheral disease responds better than axial disease, or the other way around. Drilling down is on these two types helps us approach personalized medicine or tailored treatments based on their pattern of joint involvement. I think this is the dream for rheumatology, just like the dream for dermatology is to know which rash responds to a very specific medication or a subtype, for example.
Bhutani: Agreed. I think it's important to also highlight that the reason it's important to recognize the axial vs peripheral disease is that sometimes the axial disease tends to be, first of all, a little bit tougher to diagnose,and then second of all, it's a little slower to respond or a little harder to treat. It's important to separate those pieces. I think that's why they've been separated into these other domains.
The other things we talk about are dactylitis and enthesitis. These are endpoints that are oftentimes looked at in clinical trials. Dactylitis is swelling and inflammation of that entire finger — what we call 'sausage digits.' Enthesitis is inflammation of those points where the tendons enter the bone — so, the tender tendons. Most classically, we talk about the Achilles tendon, but many other tendons can be involved.
A Focus on the Joints
Bhutani: Mona, are these areas that you are evaluating during your physical exam? I know we talked about screening questions, but are you looking for these types of things in your exam?
Shahriari: That's an excellent question. I think if you tell a dermatologist to do a joint exam, they're going to freak out and say, wait, what are you asking me to do? I'm not doing a joint-by-joint exam the way that a rheumatologist would do. No one would even expect me to do that. I do try to put pressure on some of those key areas, kind of like Jason mentioned, such as the SI joint. I touch the elbows, the heels, and areas that tend to be hotspots. I even palpate the fingers. It's just part of my exam.
I'm touching the patient's joints, squeezing down, and I ask if anything feels tender. I think it's a really easy way for us to be able to pick up on some of these symptoms, but I do find both enthesitis and dactylitis wax and wane. Even if they don't have it during that visit, I still ask about it because if they had a remote history of it, it still means they are positive for this particular domain of psoriatic arthritis.
Bhutani: To Jason's point earlier, I think while doing that exam is a great time to get that education in, because oftentimes their appointments are short. While you're doing the exam, you can talk to them about why you're doing it, what psoriatic arthritis is, and how many patients are affected. It's a really great time to also plug your education, even if they don't have any tender or swollen joints at that point.
In the final couple of minutes, I wanted to ask you guys about treatments and if there are certain treatments that you lean toward in patients who have psoriatic arthritis. Maybe we can even get into the nuances of the peripheral vs axial disease or if they have more dactylitis or enthesitis. Are there any drugs that you are leaning toward or any classes of drugs?
Hawkes: I think big picture, when we're talking about those patients who have psoriatic arthritis, with or without skin disease, in general, my experience has been what many others have shared where the anti-interleukin (IL)-23s don't have as good of success in the joints as other agents, such as anti-IL-17 medications.
This was obvious to me when we did some of the clinical trials where we had patients whose skin did great on the anti-IL-23s, but their joints worsened, and for some of these patients, going back to a TNF inhibitor or an IL-17, even if their skin maybe lost some response, their joints improved. I think we haven't fully teased that out yet.
However, there are some patients who do really well with the skin and the joints with IL-23s in general. I think the anti-IL-17s may work a little bit better in skin and joints, although they're also given more frequently.
Additionally, it's always interesting to me to think about how w e sometimes dose the skin higher than the joints. I wonder if we shouldn't be doing exactly the opposite, where we should be dosing the joints higher and more frequently than the skin. It may be that anti-IL-23 medications don't work as well because of the way they're administered compared to the IL-17s, for example.
It's really interesting to think about the JAK inhibitors, where some medications that we know are approved for psoriatic arthritis only but really weren't studied or pursued in plaque psoriasis. I think that underscores some of the differences in the immunology there as well.
We certainly have a group of immune cells, which are not necessarily under the regulatory control of IL-23. I think that's part of the potential explanation, but I think we also start to see more of a mixed bag, probably some type 1 disease inflammation that probably contributes to psoriatic arthritis.
We talk about psoriatic skin disease leading to joint disease, but PsA may have some of its own unique immunology that I don't think we fully appreciate because many of our assumptions are based on data from the skin that we just hope translate to the joints. I think those assumptions haven't always played out to be true. In general, the IL-17s for dermatology and rheumatology have been a leader for these reasons, maybe because it balances IL-17 blockade with the ideal frequency of dosing.
Shahriari: I think just to build upon, Jason, your comments on the TNF inhibitors, I seldom if ever prescribe them anymore nowadays. As a dermatologist, I do think the safety profile of IL-17s and IL-23s are superior. If a patient has uveitis, I might consider a TNF just from that standpoint. I do love the safety of the IL-23s, though, so I try to tease out that axial component to see if an IL-17 is warranted.
If I don't see anything that stands out for axial disease, many times I do start with the IL-23. If I'm not getting full improvement of the joints, and if their symptoms are persisting beyond the 6-month mark, then I consider that this might be someone I should either refer to rheumatology for another opinion or I consider switching to an IL-17. Sometimes it's important to have rheumatology weigh in because [patients] may have an osteoarthritis superimposed on the psoriatic arthritis that is leading to symptoms that cannot be treated with targeted psoriatic therapies. Do you guys do it differently?
Bhutani: I think that's my approach as well. It's changed over time. I used to lean towards the IL-17s as my go-to if they had psoriatic arthritis. Mona, like you mentioned, I think I'm using more of the IL-23s, given the safety profile and the benefits of dosing that the patients really love. If it's not helping or if it's only partially helping their joints, then we might consider going to an IL-17 at that point, or even back to a TNF inhibitor, like you said, Jason. For example, etanercept, which we don't use in dermatology anymore, rheumatologists are still prescribing it.
I think it gets back to your point about how that efficacy in the skin does not always equate to the efficacy in the joints. There is this mismatch there.
Hawkes: I just had a patient actually today who has very clear classic plaque psoriasis, bad joint disease, and has basically failed all of the IL-23s and the IL-17s. She had a rheumatologist and went on adalimumab and had excellent response. The skin hasn't been great, but the joints were dramatically improved and mostly pain-free.
Again, it underscores the gaps in PsA, but I always tell patients that for skin, we can pretty much clear it as we have many good options. Treating joints is sometimes a moving target. It's a dynamic process. I think it's important and it makes perfect sense to start a drug that's really convenient and works great in skin like the anti-IL-23 or 17s. Nothing's amazing in the joints, but we're getting better and better. We start there and work our way backward based on the clinical response. I think that makes sense.
Bhutani: Thank you both for taking time out of your day to have this great discussion. I think we have come so far in the treatment of psoriasis and psoriatic arthritis, but I think our conversation also tells us how much we still have to learn.
I hope that all of us will continue that hard work and continue to help find our patients a cure, hopefully, in the future. Thank you so much.
Shahriari: Thank you.
Hawkes: Thank you.
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- Fast Company
Want to develop greater willpower and determination? A new study shows how to use the Navy SEAL 40% rule
Imagine you've worked hard. You've worked long. Mentally, physically you're done. But then I offer you $1,000 if you can keep going for another 10 minutes. And suddenly you're good to go. Hold that thought. Mental toughness. Determination. Willpower. Perseverance. However you describe it, the ability to push through mental and physical fatigue to achieve long-term goals is often what sets successful people apart. When others stop trying, the last person to give up—especially on themselves— is often the person who succeeds. But why do some people keep going when others won't? In part because they understand, if only intuitively, the 40% rule, a concept popularized by Dave Goggins in Jesse Itzler's book Living With a SEAL. The premise is simple. When our minds say we're exhausted, fried, and totally tapped out, we're really only 40% done: We still have 60% left in our tanks. So why do we stop? According to a new study published in Journal of Neuroscience, two brain regions activate when you feel mentally fatigued. (Physical fatigue is, in effect, mental fatigue. Your muscles don't give up when you're tired. Your mind gives up long before; otherwise you wouldn't stop until you physically collapse.) One culprit is the right insula, an area deep in the brain associated with feelings of fatigue. The other is the dorsal lateral prefrontal cortex, areas on both sides of the brain that control working memory. All of these areas work together to decide when it's time to avoid more cognitive effort—to decide when you're done. Except the decisions they make aren't particularly accurate. According to the researchers: Our study was designed to induce cognitive fatigue and see how people's choices to exert effort change when they feel fatigue, as well as identify locations in the brain where these decisions are made. However, there may be a discrepancy between perceptions in cognitive fatigue and what the human brain is actually capable of doing. Take incentives. When participants were fatigued, they were more likely to choose to pass up on higher levels of reward for more effort. The more fatigued they became, the greater the reward had to be. But with the right reward, they would—and obviously could—keep going. That makes intuitive sense. Deciding to give up is always a benefits/rewards decision. If you're creating a sales demo, you won't put in more effort unless you think it's worth it: If more work will create an appreciably better result, or if the demo's potential outcome is sufficiently great. Your brain weighs the effort against the outcome. That's why my offering you $1,000 for 10 more minutes makes you suddenly find mental or physical energy reserves you didn't think you had. Another factor is time. A study published in PLoS One found that people asked to pedal an exercise bike set at a certain resistance level as long as they could lasted about 12 minutes, until they said they could do no more. But when they were then asked to repeat a five second, maximum-effort power test, they could produce three times more power than they did during the endurance test. Their muscles weren't depleted. Their mind was depleted. Even if you think you're exhausted, cranking out another five seconds is (relatively) nothing. The endurance test is a different beast. Stuck on a bike, hamster-wheeling away, heart pounding and legs screaming, and not knowing how long the pain will last? Indefinite effort is physically and mentally draining, a combination that makes it much harder to keep pushing past what you perceive as your limit. Even though you could, if offered the right incentive. That's the primary takeaway. The ability to push through mental or physical fatigue is a trait you can definitely develop. But over the shorter term, if you want to keep going, the key is to find reasons—meaningful reasons—to stay the course. Getting in better shape so your clothes fit better is a worthwhile goal; getting in better shape so you can live a longer, healthier life and be there for your family is a meaningful goal. Finishing a sales demo because you'll make the call tomorrow is a worthwhile goal, but crafting a demo that will truly resonate with a potential long-term client—which will help you build a thriving business—is a meaningful goal. The key is to find a greater, more long-term 'why,' one that will outweigh the feeling that you're done. And to set time limits on your effort. Not knowing when you'll be done? You'll probably decide in, say, 30 minutes, even if you could go longer. But if you say, 'I'll give this one more hour,' now there's a limit, one you'll find the energy reserves to reach. When you think you're done, you really aren't. Your right insula and dorsal lateral prefrontal cortex have just decided you are. And you can just as easily—with the right incentives, and the right perspective—decide you're not done. — By Jeff Haden
