Another interesting concept here is understanding psoriatic arthritis. It’s an interesting comorbidity, and we have the opportunity as dermatology providers to be able to pick up on that potential complication, and to address it early. Many of these patients don’t understand that the disease can be linked, and that the destruction that comes from psoriatic arthritis can be permanent and can impact their activities of daily living and even their ability to work. It’s important to approach that and to evaluate that as a part of your new patient encounter, and on subsequent patient encounters as well, because those are symptoms that can develop over time.

I totally agree, and I love what you said, Matt, about starting the conversation by sitting down, because I’ve had patients who’ve said they’ve been to multiple providers. Sometimes when patients have severe psoriasis, they’ve said that the provider doesn’t even go into the room, they just stand at the door and look at them and say, “You have really bad psoriasis, I can’t help you. This is a chronic disease, and you just need to learn to live with it,” which is devastating for a patient to hear. The severity as you mentioned, can be graded in several ways. First of all, how much of their body surface is affected, and typically, you hear mild, moderate, and severe. We tend to gauge it by body surface area [BSA] being 1 palm, or 1% BSA, and 0% to 5% is considered mild disease, 5% to 10% BSA is considered moderate, and anything above 10% is considered severe. But I think you made an excellent point of getting to know the patient and understanding how their psoriasis impacts them. For example, a patient may have psoriasis just on their scalp, which is a relatively small body surface area, maybe 2%, 3%, 4% BSA, which is technically considered mild. However, if you have those big, thick, white plaques of psoriasis all over your scalp, it is so itchy and it feels like somebody stuck papier-mache on your scalp. Think about the psychological impact of wearing that for the world to see. That can be severe disease, even though it’s a smaller body surface area.

You made a very excellent point in that you don’t just look at their skin, but you assess for other symptoms, such as joint stiffness and pain, which can be an indicator of early psoriatic arthritis. We know about 30% of patients with psoriasis can develop psoriatic arthritis. From the initial interview, sitting down with the patient, hearing their story, understanding where they’ve come from, and also starting to assess for the comorbidities, and educating patients along the way with each visit—this makes it less overwhelming for patients, and helps them to realize that you truly are a provider who is in it for the long haul with them.

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Videos

Advanced practice providers share their perspectives on assessing and grading the disease severity of plaque psoriasis.

Plaque Psoriasis: Assessing Disease Severity

What about the clinical manifestations of plaque psoriasis?

George hit on it a little. We see the classic psoriasis: scaling, erythematous plaques that are often bilateral or symmetrical, involving elbows and knees. The scalp is a very common area that is involved and difficult to treat, I might add, but we also have other forms of psoriasis. You want to remember that you can have inverse psoriasis. It is not the classic, scaling plaque that you might see with regular psoriasis. It might present as beefy, red, macerated skin in the groin, not unlike HS [hidradenitis suppurativa] or other comorbidities that share the same cytokine. I think you want to look at all the parts of the body: nails, scalp, the skin, and certainly, do not forget the genitals. I find that is one that, as dermatologists, we often forget to look at because we do not want to go there. We did a study in our clinic that showed that patients do not bring it up, but would like people to look there, because they often cannot. They might have itchy skin and they do not put that together and realize it is psoriasis. You do not see pictures of that often. I think the thing to think about is what George said, because of the pathophysiology, these inflammatory cytokines share characteristics with a lot of other disease states. We must think of immune-mediated inflammatory disease as a whole group and psoriasis is just 1 of them. We must be aware, when we examine our patients, to look for HS, to ask them questions about IBD [inflammatory bowel disease] because they all share those same cytokines. The end result is scaling in the skin, the scalp, mucosa, and other places.

 Talking about the cytokines makes me think about background comorbidities. Tell us about some of the comorbidities associated with psoriatic disease and what the impact is on those comorbidities.

Obviously, the one that is the elephant in the room is psoriatic arthritis, correct? We all know that psoriasis and psoriatic arthritis go together, but there are a number of them, like obesity or metabolic syndrome. We know that the same inflammatory cytokines are involved in making atherosclerotic plaque. We have coronary artery disease, obesity, psoriatic arthritis, and even inflammatory bowel disease, because they share some of the common cytokines such as TNF [tumor necrosis factor]. Those sorts of things occur in much greater incidences in patients with psoriasis. We need to ask our patients about those comorbidities, because that too can help when you come down to what your treatment algorithm is going to be. We want to treat as many of the disease processes with 1 drug as we can. It is logical to ask those questions of patients and then look for other disease processes that have much higher incidences in patients with psoriasis.

 Neal, do you have any other comments relating to comorbidities, your perspective, how you approach patients, and the impact on comorbidities as it relates to psoriatic disease?

I think Erin hit a big one about being cognizant about what is under the hood with a lot of these patients. If we are not looking into their weight, their lifestyle, their cardiovascular risk, and history, then all of that discussion of systemic therapy could be for naught. I think, as a specialty, we need to ramp up our inquiries of these patients and how much is going on in their medical history. I want to go back to one of the things George said about the characterization of the immune mechanisms, hypersensitivity, and autoimmune diseases. These are words that get thrown around a lot by patients who sit there on Dr Google and go to the chat rooms.

I always must make sure that I am reminding patients about what is truly autoimmune. In some cases, they tend to cross more the Th2 [T helper cell type 1] side of the fence if anything, but we do not want patients to equate psoriasis with lupus in terms of approaches because they may be the exact opposite part of the immune shelf. I think the one thing that both George and Erin brought up nicely is process. If we are not stopping the process in its tracks and are just constantly mopping up the mess, we are not going to get patients out of their own way in terms of their futures. We want patients to think about what their outcome is going to be in 6 months, not just 6 days or 6 weeks. We want them to think about what we can do to change the quality of their lives with these interventions. I think a lot of that goes hand in hand with the way we define it ourselves.

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Erin Boh, MD, PhD, FAAD, shares insight into clinical manifestations of plaque psoriasis, and panelists emphasize how disease characteristics may be mistaken for signs and symptoms of commonly comorbid diseases.

Plaque Psoriasis Signs, Symptoms, and Comorbidities

 My recommendation, for clinicians and clinicians talking to the parents of kids with ADHD [attention-deficit/hyperactivity disorder], is to ground them in the science but connect and create the hope around what it means to have the condition when treated. When I say “ground them in the science,” we’re helping people understand it’s not their fault. This is not about bad parenting. I have an ADHD child, so I know what it feels like to think, “How did I screw this up?” Even though intellectually you can say, “I did what I was supposed to do to help my child.” So we ground folks in the neuroscience.

That’s why I spent time on the neurobiology genetics. This is not about bad parenting. Pull out some information verbally or in a picture to show what we mean in the frontal lobe. Quiet and underactive kids with ADHD, when you treat them appropriately—whether it’s exercise, nonstimulant medications, or stimulant medications—you’re engaging that frontal lobe of the brain. It’s like turning on a switch. All the circuitry is there; it’s all normal. It’s just flipping on that switch to help people focus, concentrate, filter out background noise, and understand even a little bit.

It takes only a couple of minutes to describe it in that way. Use an analogy. One of the analogies I like to use is the electrical circuits in your household. They’re all there. They’re just quiet until you flip the light switch on. There’s nothing abnormal. It just needs to be turned on. That’s what our medications do. They flip the switch and engage the circuitry. The brain is a bunch of electrical circuits. When you put things in terms people can understand, it’s less scary. It makes it less scary to proceed with the medication when people understand that that’s what the medication is doing; it’s flipping the switch.

When something is a boring, mundane task that we all face day to day, regardless of how smart we are, how emotionally stable we are, there are things that are boring and that makes it hard to focus. Normalize it in that regard, and emotionally connect. The creating hope part is the data I gave you about ADHD and outcomes that are scary. But if you look at treated ADHD, it normalizes outcomes down to the non-ADHD individual. You’re changing the functional outcomes. You’re changing the person’s relationships with themselves and others—their family, their ability to succeed in terms of their schoolwork, their work life, and their relationships. Creating that hope simply by treating ADHD has been 1 of the most rewarding things about specializing in this field.

As clinicians, there are many areas can diagnose but don’t have good treatment options. With ADHD, the wonderful aspect is that this is a treatable condition. You can change the course of outcomes for patients by making an accurate diagnosis, being thorough with your treatments, adjusting your treatments, and constantly monitoring and tweaking as you go in the pharmacological and the nonpharmacological aspects. That’s the message we need to provide our clients and health care providers.

Theresa R. Cerulli, MD, provides advice for clinicians on how to increase understanding of attention-deficit/hyperactivity disorders (ADHD) and encourage therapy adherence for both children and parents.

Promoting Therapy Adherence in Pediatric ADHD

 Ehsan, we’ve got a lot of data on regression, a reduction in the rates of vision-threatening complications using anti-VEGF agents infrequently as every 4 months. This is not particularly aggressive treatment. There doesn’t appear to be today widespread adoption of this type of management in patients that have the threat for vision loss in diabetes. How does this work for you in clinical practice? How do you apply this data as you see patients with diabetic eye disease?

There are so much great data to unpack from PANORAMA and from Protocol W. As you alluded to, there’s been slow uptake in our field. Although anytime you’re dealing with something that’s potentially paradigm shifting in terms of the way we handle or manage a condition that we used to observe, there’s going to be a gradual phase-in and phase-out to start adopting these therapies. At this point in my practice, I’m fairly comfortable offering anti-VEGF therapy to my patients with severe NPDR [nonproliferative diabetic retinopathy]. If there’s a mistake that colleagues who are a bit averse to it may be making, it’s not even having that discussion with patients. In my practice, I’m all about educating my patients, letting them know what’s available, trying to get them to engage, understanding their disease process, and letting them know that treatment options are available. Here are some studies, here’s what they showed. And I let them be an active decision maker in that process, rather than me practicing paternalistic medicine and saying, “I’m not even going to say anything to this patient other than, ‘Come back in 3 or 4 months.’”

That type of care with diabetic retinopathy potentially lends itself to increased noncompliance more than anything in the long run. I’ve been pleasantly surprised that when I share these data from Protocol W and from PANORAMA, and the findings essentially corroborate one another, that our risk of progressing to vision-threatening complications is substantially reduced. I’ve been pleasantly surprised at the number of patients who want to do therapy.

There are a couple of take-home points from that. No. 1, consistency is more important than frequency. What I mean by that is, we saw in year 2 from PANORAMA, the every-8-weeks arm that switched to as-needed treatment, their level of DRSS [Diabetic Retinopathy Severity Scale] improvement fell off a cliff. It doesn’t get talked about much because that was an as-needed treatment arm. Remember that in year 1 that you had an 80%, 2-step improvement. In year 2, that dropped all the way down to 50%. And the reason was patients were being undertreated and they got an average of 1.8 injections of the 6 eligible injections. Whereas that every-4-month arm group essentially maintained their 2-step improvement. It was 65% in year 1 and 62% in year 2 across much less injections.

The way I look at it is, consistency is more important than the frequency. If we can get a patient to a regular interval that’s comfortable for them, that they’re compliant with, whether it’s 4 months or 6 months, then that’s great. Part of this is also the psychology. I think about things as if I were that patient. I don’t have retinopathy, and I hope I never do, but I think about it in terms of going to the dentist. If I’m going to a clinical care provider, and that visit is being tied to something procedural, then I’m far more likely to be compliant with that visit, knowing that something is being proactively done for me. Rather than just showing up, somebody looking at something and saying, everything is fine.

When push comes to shove, if I have something else going on, as Joe alluded to, diabetes is not entirely a disease of noncompliance. We have patients who care very much about their visits but are forced to choose. They’re working class, so they can’t take that many days off. They may have to juggle seeing the eye care provider with the kidney doctor, with the cardiologist, maybe they’re hospitalized. Sometimes they just end up missing these appointments, not because they don’t want to be there but because they’re forced to. If I can tie in a procedure, my belief is—and we have some real-world data forthcoming that suggest that—adherence to visits ends up increasing when we’re tying that injection to it.

I’ll end with 1 anecdote of a patient I saw earlier this week. We talked about turning back the hands of time. This was probably 1 of my earlier patients who elected to want to start treating his severe NPDR. His right eye had severe NPDR, and his left eye was moderate. We said we’d just start therapy. He had no DME [diabetic macular edema], by the way; his vision was 20/20. He was an engineer, very educated, and wanted to know everything about diabetes. I remember him the first time he came to see me. He presented the PANORAMA paper printed up. He brought it to me, and he wanted to start therapy, and we did so with his right eye. I tried to do my own algorithm, where I extended his treatment. I eventually lost him for over a year.

He came back just this week. His right eye was still at about a severe NPDR state, and the FA [fluorescein angiography] looked somewhat comparable to before. But his fellow eye that was moderate had progressive proliferative diabetic retinopathy with vitreous hemorrhage during that interval period. And it’s just an N-of-1, it’s just 1 anecdote, but that’s the type of patient I’m thinking about. Because you could have the most compliant patient in the world, but diabetes is a terrible multisystem disease that will inevitably cause someone to become noncompliant and miss a visit. But by treating that patient, did we potentially lengthen the leash and help prevent a terrible outcome from coming by the time they do inevitably get back to us?

Joe, these are very powerful data. What do you think it’s going to take for us to change the way we think as a retina community to begin to prevent vision loss vs treating the end-stage complications? Are there data that we need? Is there just time? Are there factors you can identify that may change this line of thinking in the future?

 For 1, training younger physicians to understand the disease is important. When I was training, if it didn’t change an outcome—and at that time it was vision—then we didn’t institute that therapy. I was always trained to look at vision as an outcome. Now we’re talking about trying to change the disease process, so to speak, where vision is not effective, which is a little harder to gauge. By training younger physicians in understanding the historical standpoint of eyes, because the data are prevalent. The progression of retinopathy hasn’t changed since we had been doing the studies in the 1970s. That has been consistent. And if you have an eye that has moderate disease, we know what the rate of progression is over the next 5 years. We know what the rate of progression is—you have severe disease if it’s untreated. And when you have sight-related problems, you know what the progression is. From a historical standpoint, that needs to be told to younger physicians. That’s No. 1.

No. 2, for me, it took a patient to have that outcome where it happened on my watch, and because they missed an appointment, for whatever reason, they got worse. I don’t want that to happen again. When I talk to patients with these issues, she always comes up in my mind. The other eye we were able to save. She also has proliferative disease. She’s still 20/20 in that eye, but in the eye that developed the tractional detachment, we never gained vision better than hand motion. And she never misses an appointment now. She’s 3 years out. She’s constantly undergoing therapy, and the impact that we’ve made on her is important.

When you have personal testimonies, when you have personal patients, that’s a sounding bar that helps us to make a change. It makes the paradigm shift, which may go against what you were originally taught. For me, I’ve learned every day with my patients, and that discussion with my patients is critical; knowing more about their lifestyles, and how this disease is a little different from what we see with our patients with AMD [age-related macular degeneration] who are normally brought in by a caregiver. These are individuals, these are our colleagues, and these are people who work next to you. That’s the reason I find this disease so fascinating. There’s not 1 thing you can point to, but personal stories, and having your patients not do well, is a strong testament to changing your behavior so it won’t happen again. If you can decrease that, it’s just imperative.

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Drs Ehsan Rahimy and Joseph M. Coney analyze the implications of clinical trial data on the management of nonproliferative diabetic retinopathy.

Updates in the Management of Non-Proliferative Diabetic Retinopathy

Joe, I’m going to start with you talking about the role of the available anti-VEGF agents in the treatment of DR [diabetic retinopathy]. We’ve got 2 approved agents, ranibizumab and aflibercept. How do you use these agents overall in managing patients with diabetic eye disease?

 Both are great drugs. Both have turned back the hands of time in terms of their disease. When I was in a residency or fellowship not long ago, everyone had progression of the disease; they were all getting lasers. They would still bleed; you’ll have these tractional components. I just don’t see that with the current landscape. It’s also true for when you have nonproliferative disease. When we did our clinical trials for DME [diabetic macular edema], I don’t think any of us thought about what we were doing to the level of retinopathy. We noticed this as a by-product of how we were treating patients in clinical trials and, obviously, what we saw in our clinics day-to-day.

We have great studies that have shown—PANORAMA being the most recent—that if eyes have come in at the severe nonproliferative state, you can reduce their level of disease 2-fold 65% to 80% of the time. This was by customizing doses that they received injection after loading doses, even if it was at 16, 18, or 8 weeks. You have the flexibility to use these agents how you see them fit into that particular patient. In the long term, I don’t know how long I need to maintain these patients. Those are questions that someone on the panel can ask.

Once I get that improvement, how often should I follow patients? I typically use a widefield angiogram. Sometimes I’ll skip an injection, and I’m surprised when I see the neovascularization come back. That if it was severe or maybe had early PDR with low-risk characteristics, I’m very surprised on the changes I see. I’m starting to treat patients a little longer but space them out further. This is a landscape I’m still getting more comfortable with. The more I see these patients do well, the more I’m a very big proponent that if they have disease states that I know that over the next 4 years can have sight-threatening problems, then I tend to start therapy earlier.

Diana, we’re going to lean on you for some clinical trial results. Joe alluded to the PANORAMA study, talking about a 65% to 80% rate of 2-step reduction in diabetic retinopathy severity. Can you give us your thoughts on the PANORAMA study as well as the recently released data from Protocol W? Both trials evaluated aflibercept for the treatment of nonproliferative diabetic retinopathy [NPDR]. Give us the lowdown on these trials and your thoughts about how they were performed and what the results look like for you in clinical practice.

 Over the past few years, we’ve received an abundance of clinical trial data providing level 1 evidence that demonstrates that intravitreal VEGF inhibition with aflibercept is effective and safe at treating moderately severe to severe nonproliferative diabetic retinopathy. Both the PANORAMA study and Protocol W were randomized clinical trials that looked at different dosing regimens of aflibercept compared with sham treatment. They followed these patients over time to see what the benefits and risks would be for the treatment of moderately severe to severe NPDR. Recall that any patient in these clinical trials did not have diabetic macular edema at the time of enrollment. The results of these trials showed that intravitreal VEGF inhibition with aflibercept was safe and effective, and it decreased the risk for vision-threatening complications.

What does this mean? In the sham treatment arm, if you were observed over the 2-year period, you had a 50% risk of developing a vision-threatening complication such as diabetic macular edema or progression to proliferative diabetic eye disease. On the other hand, if you were randomized to aflibercept, this risk was dramatically decreased to less than 15%. It shows that prophylactic proactive treatment with VEGF inhibition could decrease the risk of vision loss over time. This is exciting for the field, and we can see that practice patterns are beginning to change and retina specialists are thinking and treating patients earlier in their disease state.

What’s the most important data point from these studies? PANORAMA was a study where the primary outcome was a 2-step progression in diabetic retinopathy. That was the primary outcome. We’ve been programmed to pay attention to primary outcome data in level 1 trials. Is that the most important data point, or are some of the secondary data points—such as vision-threatening complications—more relevant to us in clinical practice?

 The reduction in vision-threatening complications is the most clinically meaningful for us and for the patients. As you said, the primary end point was looking at severity scale of their diabetic eye disease and the reduction, and these studies met those primary end points. But when we’re talking to patients and we’re understanding how we can preserve their vision, vision-threatening complications is where the money is. That’s where we can help patients preserve their central and peripheral vision.

Diana, we observed these reductions in diabetic retinopathy severity when we were all involved in the clinical trials evaluating anti-VEGF agents for DME. We saw similar reduction rates, slightly less, reduction rates in patients treated for DME. Can you talk about the data we saw in RISE and RIDE, as well as VISTA DME and VIVID-DME that informed these primary treatment of retinopathy clinical trials?

: If you recall, when we first used VEGF inhibitors in diabetic eye disease, it was for vision-threatening diabetic macular edema. When we were treating these patients every month or every 2 months, investigators also noticed that there was an additional benefit because these agents also improved the diabetic retinopathy severity score in these eyes. Because of this evidence, additional clinical trials were launched, specifically looking at eyes who had moderately severe to severe nonproliferative disease at baseline in the absence of diabetic macular edema. The key point with these new clinical trials is that the treatment burden for treating eyes with nonproliferative diabetic retinopathy is less. We don’t have to treat them intensively every month or 2. We saw that aflibercept in these clinical trials could be given every 4 months and still have a beneficial effect.

A panel of experts reviews data on nonproliferative diabetic retinopathy treatments from the PANORAMA, Protocol W, RISE, and RIDE studies.

A Review of Clinical Trial Data in Non-Proliferative Diabetic Retinopathy

 presentation titled, “Paradigm Shifts in the Management of Plaque Psoriasis—Advanced Practice Provider Perspectives.” I’m Matthew Bruner, physician assistant at the Dermatology & Skin Surgery Center in Stockbridge, Georgia. I am joined today by my friend and colleague Lakshi Aldredge, nurse practitioner of the dermatology service of the VA Portland Health Care System in Portland, Oregon. Our discussion focuses on the role of nurse practitioners [NPs] and physician assistants [PAs] in patient care and improving outcomes of plaque psoriasis. We will also discuss the safety and efficacy of available treatments. Welcome, Lakshi, let’s begin.

: Hi, Matt. I’m delighted to be here with you, and I’m excited to have this conversation.

Lakshi, when you think about your patients, and how plaque psoriasis impacts their lives, can you tell me how you think it impacts them in their physical lives, as well as mentally and in their social lives?

: Absolutely, Matt. You and I have taken care of psoriasis patients for many years, and the real joy in taking care of patients with psoriasis is because this is a long-term relationship you develop with them. Because as you know, we don’t have a cure for psoriasis. Psoriasis is an autoimmune-mediated disease, much like diabetes and some thyroid diseases. These patients suffer when they know that they have a condition that is very visible on their skin that everyone sees. And they’ve been told there’s no cure for it. It is a disease that warrants NPs and PAs and any providers to look at patients holistically, and that means not only looking at their clinical and physical manifestations of their disease, but also the psychosocial aspect of the disease. These patients have myriad comorbidities also that can go along with their psoriasis. Patients with more moderate to severe psoriasis can be at risk for developing type 2 diabetes, cardiovascular disease, liver disease, even Crohn disease. Given all the impacts that psoriatic disease can play on a patient’s physical well-being, but also on their mental health, knowing that they have a chronic disease, that they could have developed these more significant comorbidities, it becomes part and parcel of caring for the whole patient, when NPs and PAs take care of these patients. I like to start by telling patients that I’m going to be with them throughout their journey of psoriasis and psoriatic disease, and that I plan to work with them with the goal of getting them as clear as possible, and also helping them to control those other comorbidities. And you know, Matt, I’m sure that you have seen many psoriasis patients. One of the biggest challenges is trying to understand how we, first of all, describe psoriasis and how to determine how severe the disease is. When you look at your patients, how do you start that conversation about assessing the severity of their psoriasis?

For me, that conversation starts from a sitting position. That’s one of the most important things as a practitioner, to come into the room, sit down with the patient and meet with them eye to eye to talk to them about where they’ve been, what they’re going through, what kind of previous treatments they’ve had, how they view it impacting their lives, because patients are individualistic. Especially when you think about the psychosocial impact, the higher rates of depression and suicidality in these patients, you need to approach your patient with an understanding of where they’re coming from, and what their treatment goals are. Then I like to do an examination. Sometimes patients have a preconceived notion of their diagnosis before they arrive. Many of them I find have less education about their condition. They don’t understand the comorbidities, and that’s an important discussion to have with the patients, both on day 1 of the visit when you meet them, but also on those subsequent visits as reminders to make sure they’re having their regular screenings with their primary care provider, as well as making sure that you’re reaching their treatment goals. Sometimes as providers, we have our own preconceived notions of treatment goals.

The clinical and psychological impact of plaque psoriasis on a patient’s overall well-being.

Impact of Psoriasis on a Patients’ Overall Well-Being

 I’ve been subspecialized within ADHD [attention-deficit/hyperactivity disorder] for about 20 years, so it’s been exciting to see all the changes and improvements and the wonderful advancements in the field. But we’re not done. There’s more to come. I just explained how viloxazine, as a new chemical entity, has a very specific labeling by the FDA. It’s not easy to achieve. It must be something novel and different. With viloxazine, it’s new and exciting to me.

What’s still to come is that the adult data have been completed and submitted to the FDA. What we’ll see, hopefully by April 2022, is a response from the FDA, whether viloxazine gets approved for use in adults. I see a wonderful opportunity there. We have only 1 drug FDA approved for adults as a nonstimulant to treat ADHD, and that’s atomoxetine. That was a long time ago. That’s when I started in the field, and we’re going back over 18 years since we had another option. Hopefully, we’ll have another option for adults.

Here we’re talking about the risk with substance abuse. This comes up for me. The exciting news is that viloxazine may also be approved for adult use. We have only 1 other medication right now, and that’s a nonstimulant. This comes up in professional sports, for example. I work with MLB [Major League Baseball]. When I’m evaluating players for ADHD, because so many of the medications prescribed are stimulants and are banned substances because of the performance enhancement possibilities, that leads to abuse. For some people it’s highly regulated. Most of the time, players have to try a nonstimulant first and fail that before they qualify for trying a stimulant medication, regardless of whether they have the diagnosis accurately documented. The reason is to prevent abuse. We don’t want to go down that road if we don’t have to.

For adults who need an alternative, I just gave you a clear example that comes up in my clinical practice. The option of having a second choice besides atomoxetine for treating adults with ADHD in a nonstimulant fashion on the horizon. Besides that medication in the pipeline, there was 1 recently approved in 2021 that’s also interesting. It’s a prodrug methylphenidate formulation that just became available this year. Most people haven’t even heard of that. You’ve already had a prodrug amphetamine for many years, and that’s lisdexamfetamine. In the amphetamine family, there’s been a prodrug stimulant, but we hadn’t had 1 in methylphenidate until this year.

I’m seeing some progress in using technology to collect objective information in brain functioning and behaviors. Collecting objective information may help with our diagnostic options and approaches. For example, a company in California approached me that’s looking at using eye-tracking technology and measurements to assess and diagnose ADHD. There’s some information to show the way an ADHD person eye tracks and follows targets regarding their cognitive function compared with a non-ADHD individual. Right now, that technology is used in other ways. It is used in professional sports. It’s been used in the military. It would be interesting to find out where the cutoffs are between ADHD and non-ADHD in such objective measures so that maybe we can improve our diagnostic protocol.

Dr. Theresa Cerulli reflects on exciting updates and unmet needs in the management and treatment of pediatric attention deficit hyperactivity disorders (ADHD).

Emerging Treatments and Unmet Needs in Pediatric ADHD

Hello and welcome to this HCPLive® Peer Exchange titled, “Changing Treatment Approaches in the Management of Plaque Psoriasis.” I am Dr Brad Glick and I am a board-certified dermatologist and a clinical assistant professor of dermatology at the FIU [Florida International University] Herbert Wertheim College of Medicine in Miami, Florida. Joining me today in this discussion are my colleagues, Dr Neal Bhatia, who is director of clinical dermatology at Therapeutics Clinical Research in San Diego, California. I am also pleased to be joined by Dr Erin Boh, professor and chair of dermatology at the Tulane University School of Medicine, New Orleans. Finally, joining us is Dr George Han, associate professor of dermatology at the Zucker School of Medicine at Hofstra/Northwell, in New York. Welcome everyone. Our discussion today is about the standard of care in the management of plaque psoriasis, along with the newer interleukin-23 inhibitor class of biologic drugs. We shall also focus on the long-term safety and efficacy data of these interleukin-23 inhibitors. Welcome everyone, and let’s go ahead and get started. I am going to start off with Dr Han. Briefly review for us the pathogenesis of plaque psoriasis.

Thank you, Dr Glick, and thanks for having me. It is a pleasure to be here today. I think that is a loaded question, but we will try to summarize. Our understanding of psoriasis has evolved considerably in the last 20 years or so. It used to be thought of as classically Th1 [T helper cell type 1] versus Th2 [T helper cell type 2], and now we have started to really understand and appreciate the importance of the Th17 [T helper 17 cells] pathway, partly because of our research in psoriasis. We like to think of psoriasis, nowadays, as the activation and perhaps the hyperactivity of what should be normal inflammatory mechanisms. In that sense, there are some corollaries to autoimmune disease processes. The real question has become, what is the trigger? There are some candidates out there for that: LL37…TSO. 

There are various things that have been found in patients with psoriasis that seem to act as an autoantigen, triggering some of the inflammation we have seen, but nothing is so consistent yet. What we do know, though, is that whatever the trigger is, there are probably multiple hits of genetic susceptibility, plus an environmental trigger that makes the patient have these activated dendritic cells that then are a source of increased cytokines and T-cell activation, proliferation, and expansion that eventually results in this proinflammatory cascade. We have found that, in this proinflammatory cascade, the key mechanistic pathway seems to be IL [interleukin]-23–induced activation of Th17 cells leading to increased IL-17, and finally to keratinocyte hyperproliferation. There are various aspects of this feedback loop, including immune-like cells and other processes that occur to create this long-term, chronic disease that we know as psoriasis and worsening inflammation.

Environmentally speaking, what would you say are specific triggers for psoriasis?

We have classical triggers, like medications; certain medicines we have thought of traditionally as triggers for psoriasis. For a large number of patients, stress certainly seems to be one that kicks off their psoriasis. Of course, we know for certain forms of psoriasis, like guttate psoriasis, certain infections like streptococcal infections can be at fault. But I think for the vast majority of patients, it is just that at some point, the disease activity becomes great enough that it starts manifesting on their skin and tends to be rather progressive in a lot of patients.

Dr Boh, would you like to add any comments there?

No; I think that covers it very well. I do think some of the other stressors are some of the same comorbidities we see with psoriasis—for instance, obesity. Then, once you start this inflammatory cytokine cascade, it spills over into other disease processes, which then puts added stress on your body. I think it is so integrated that we must look at psoriasis as a whole, and not just skin or just 1 aspect.

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An expert dermatologist, George Han, MD, PhD, provides a brief overview of the pathogenesis of plaque psoriasis and reviews some common environmental triggers.

Pathogenesis of Plaque Psoriasis

Whether it is new treatments in development or new guidelines in managing 

 infections (CDI), there is plenty to discuss in this field.

That is why it is so important for experts to come together to discuss new research and different perspectives.

State of Science program, a group of 4 C difficile investigators and clinicians discussed several different portions of CDI care and research.

The program, called Institutional Perspectives in Infectious Diseases: Management of C. Difficile and led by Bincy Abraham, MD, MS, Houston Methodist, was held on Nov. 9.

Also joining the panel were Eamon Quigley, MD, Daniel Bushyhead, and Kerri L. Glassner, DO, all of Houston Methodist.

Bincy Abraham, MD, led the State of Science program on C difficile infections.

The State of C Difficile Care

If ABX464 eventually gains US Food and Drug Administration (FDA) approval for patients with 

, it could spark future research testing the treatment for other indications, including Crohn’s disease, rheumatoid arthritis, and potentially others.

In fact, the treatment was once thought to be a potential medication for cancer.

Recently, there was data released showing the novel, orally administrated small molecule treatment resulted in 82.1% (n = 23) of patients who went into an ongoing, phase 3, maintenance trial in clinical remission remained in remission with the once-daily oral 50 mg treatment.

In addition, 49.3% (n = 36) of patients who were not in clinical remission at the end of the induction phase achieved a de novo clinical remission during the first year of maintenance.

, Hartmut J. Ehrlich, MD, CEO of Abivax and Philippe Pouletty, MD, chairman of the board of directors at Abivax, said an ulcerative colitis approval from either the US or European regulatory bodies could yield future research in the other diseases mentioned.

“Clearly, when you show safety and efficacy in 1 disease like ulcerative colitis,” Ehrlich said. “From the mechanism of disease propagation, Crohn’s disease is very similar. In the end, for the regulators what is important is for every disease, you are showing the required efficacy and safety data.”

The treatment also has potential in Crohn's disease and rheumatoid arthritis.