Videos

Drs Diana Isaacs and Natalie Bellini discuss selecting the right insulin delivery method for patients with diabetes, and the challenges that arise with insulin injectables.

Selecting Insulin Delivery Systems to Manage Diabetes

Drs Diana Isaacs and Natalie Bellini provide an overview of the types of insulin delivery systems used in type 1 diabetes (T1D) and type 2 diabetes (T2D), including injections, patches, and inhalable insulin.

Types of Insulin Delivery Systems for Diabetes Management

 We’ve talked a lot about the challenges associated with geographic atrophy, and the trouble is there are no FDA-approved treatments for this disease. Given that there are no treatments, Jay, how are you managing patients with geographic atrophy in your clinical practice?

 There are always 2 components to management. One is counseling and treatment recommendations, and the second is follow-up and what we do with that. I’ll hit on the first, which is risk-factor modification and doing whatever we can to lower risk factors: UV light protection, smoking cessation, exercise, diet. AREDS [Age-Related Eye Disease Study] and vitamins for geography atrophy aren’t clear cut. I’m curious what the rest of the panel does. I usually tell the patient it’s not going to hurt anything and that if it was me, I’d take them. It’s controversial. The data aren’t there if they’re bilateral of geographic atrophy, but I’d probably take them.

The final thing is when do you see these patients? Historically, we haven’t seen these patients as often, compared with our patients with wet macular degeneration, because there isn’t any rapid progression or intervention we’re offering. I see these patients every 4 to 6 months depending on what else is going on in their lives. In recent times—we’ll talk about some of the emerging treatment options—I’ve shortened that interval to get patients used to the idea that we may be seeing each other more often if treatment becomes available. But I’m curious what the rest of you do, especially regarding AREDS.

 I’ll go back to the AREDS trial, which did a post hoc analysis on geography atrophy. It showed no benefit on geographic atrophy lesion size or growth rate. If we’re going to recommend it, there may be some immediate in eye if the eyes are asymmetrical or if it was shown to decrease the rate toward CNV [copy number variations]. But AREDS vitamin hasn’t been shown to affect the growth rate of geographic atrophy. David, do you agree with that?

 Yeah, I agree 100%. I think about that same study when I have a patient with bilateral GA. I typically ask patients about their diet. I say that if you eat the all-American diet of hot dogs and ice cream each day, you may not be getting the nutrients that your retinal cells need. It’s OK to take the AREDS vitamins because you may be getting nutrients that could have some benefit. On the other hand, if you eat a very well-balanced diet, like a Mediterranean diet, and you’re careful about getting nutritious food, you’re probably getting enough of the nutrition based on that subgroup analysis from the AREDS study.

 AREDS vitamins aren’t FDA approved for treatment in these patients, but the use of these vitamins is in a post hoc analysis. Some of our patients have trouble with large pills. Fortunately, there’s a chewable option. I thought I’d mention it because it’s a practicality that’s important.

 The other practicality is cost. Insurance doesn’t approve this. For some of our patients, it’s not a problem. They’re willing to spend any dollar they have. But that’s also something we assess when we meet them the first time. Besides their lifestyle, what are their resources? Is it going to be a significant cost burden? As you said, Nancy, we don’t have data to support it. That’s when I’ll say that maybe we should lean toward the dietary modification things. It may be better to put your dollar there instead of toward the vitamin.

Jaynath R. Sridhar, MD, shares insights into managing geographic atrophy in his clinic given that there is no FDA-approved treatment.

Geographic Atrophy Management in Clinical Practice

 What about caregivers? What do you communicate to the caregivers? Do you use imaging as a tool? I’m hopeful that in the future we’ll have AI algorithms that’ll help us predict progression of disease a little better so we can advise the patients and caregivers, but what do you do now to advise the family?

 I think Jay hit on this point earlier, and he hit the nail right on the head, which is I typically use OCT [optical coherence tomography] imaging. I agree with Nancy, you said you use autofluorescence and if I had enough time in my private practice clinic, I would love to get autofluorescence on every macular degeneration patient. But that test sometimes takes time in our clinic, and we don’t have the resources to obtain that image, so often I’m using OCT. One thing I forgot to mention earlier is, I actually like the infrared on the OCT, and I should have mentioned that previously because the infrared shows the geographic atrophy lesion very well. It’s an easy thing on my OCT machine to show the patient and put the 2 images up side-by-side, maybe their baseline image and their present image, or show them each year how those GA [geographic atrophy] lesions have expanded. To Jay’s point, if the patient is dilated, it’s hard for them to see. A caregiver has a good understanding of what’s going on because these patients may be coming in and they’re still hitting the same visual acuity and they’re complaining, and the caregiver is thinking, “Well, the vision looks OK, they said the vision was all right, is my mom or dad, or loved one really having a worsening problem?” The infrared will show them, yes, this is a serious issue. This is a progressive disease. And every time you’re coming in, we’re seeing progression. It’s not something that’s slow. We see signs of progression each time you’re here.

 I agree with you, Dave. I love the infrared on OCT imaging. You can show progression of atrophy over time. This ties into Nancy’s point, when you were talking about preparation in terms of how the caregiver and the patient, what does true blindness mean with this condition? It’s important for the caregiver to understand, what is this person going to be able to do if they reach “the floor” of this disease? Well, they’ll still be able to do a lot of their activities of daily living, and I think that’s important for planning purposes, that they still can ambulate to a restroom, they often can take care of and groom themselves. The things that are going to be struggles are going to be reading, facial recognition, and watching television, if that’s something important to them. These entertainment things that are important to people’s lives. Those are the things that are drastic, and of course, driving is something that all patients and caregivers are thinking about. It’s a constant argument between caregivers and the patients, whether or not they can drive, and we end up being the arbiter, and that’s sometimes a tough conversation to navigate.

David R. Lally, MD, and Jayanth Sridhar, MD, comment on the use of imaging tools to for diagnosis and measuring progression of geographic atrophy.

Imaging Modalities in Geographic Atrophy

Ezetimibe, unfortunately, is not the most potent LDL [low-density lipoprotein]-lowering medication. It’s only around 18% or so LDL-lowering but in combination with bempedoic acid, you can get up to 40%. Then, with the other PCSK9 inhibitors, you can get 50% to 60% LDL-lowering. While we usually try ezetimibe in these very high-risk patients, we often need more, which is why I want to get back to what you brought up earlier: blood pressure. Somebody comes in and their blood pressure is above 160, you’re thinking combination therapy from the get-go. In clinical practice, we waste a lot of time starting with these low doses. Patients come back in 6 months, in a year. If they’re lucky, they get their dose increased; there’s a lot of inertia. In the GOULD registry that Alison had referred to, over these patients with ASCVD [atherosclerotic cardiovascular disease], these high-risk patients, over a 2-year period, only 17% actually have their lipid-lowering therapy intensified. Tell us about the approach for combination therapy. When should we be thinking about combination therapy? What do the guidelines say about combination therapy for lipids?

The broad message is to push on and to achieve the numbers that we need to achieve in patients, using the tools available and at our disposal. For many patients, that will be combination therapy. The ezetimibe trial is to show someone over 2-4 weeks that, “Yes, you’re not reacting.” We almost never do that in secondary prevention when the risk is higher. Even primary prevention in high-risk, we’ll say, “Well, we don’t want to spend that time waiting.” We’re really pushing on to additional therapies, using combination therapy, and doing it earlier especially in patients at very high risk; we’re going right to combination therapy, especially when patients start off with much higher LDL levels. We have a very low threshold for starting those agents, especially attending on inpatients services. If someone’s having a recurrent event on a statin alone, they need to aggressively move on, and to tailor that to the given patient using the tools you have available with these adjunctive medicines. We do that very early and aggressively, and after having established the rationale for the patient. I think anyone who practices prevention ends up doing motivational interviewing. When someone said to me, “Oh, that’s interesting. You’re really into motivational interviewing,” for the first time, I said, “Well, what is that?” I went back and then realized, well, gosh, this what we’ve been practicing for a very long time, creating a construct where you’re recognizing what the patient is bringing to the discussion. One of those fundamental tenets is that no patient is trying to hurt themselves. No one’s saying, “I was really hoping for a heart attack. I was really hoping you would place a stent.” They’re coming to this point where there may be a wrestling with a question about LDL lowering. Not because they want to harm themselves, but because they don’t fully understand the data, the evidence, and the options for pushing on and tailoring that to the patient. Explaining why they need combination therapy in the context of, “Well, then consider the alternative. If you’re having an event, to not being around. Or being compromised, or being on even more medicines, or having an interventional surgery.” I think that context really says, “Of course, I’ll take 2 medicines, because I need to do this, because the alternative is really dangerous.”

Thinking about combination therapy very early, in these very high-risk patients; to be intensifying therapy rapidly every 4-12 weeks, if they’re not at goal, to be intensifying to help overcome some of this inertia.

Erin D. Michos, MHS, FACC, FASPC; Pam Taub, MD, FACC, FASPC; Robert Busch, MD; Alison Bailey, MD, FACC; and Jorge Plutzky, MD; share benefits of combination therapy for lipid lowering in ASCVD and hypercholesterolemia.

The Role of Combination Therapy in Hypercholesterolemia

We talked about how so many patients are not at goal with statin therapy. One of the reasons is lack of adherence with their statin therapy. If we don’t see the anticipated 50% or more reduction [in low-density lipoprotein] with a high-intensity statin, they may not be adherent. One of the main drivers of adherence is patients stopping because of perceived statin intolerance. I was pleased that the NLA [National Lipids Association] recently this year 2022, updated and had a new statement specifically about statin intolerance. They also refined the definition of statin intolerance a little. It’s been defined differently across various statements. Alison, why don’t you walk us through the new definition of statin intolerance from this recent statement from the NLA?

Pam brought this up earlier in our talk today. There’s this concept of complete or partial statin intolerance, which is important because we’re not sure that any dose of statin is not beneficial. But complete intolerance means a patient doesn’t tolerate any dose of a statin, even a low dose a couple of times a week, because of adverse effects they attribute to the statin, which are frequently mental status changes, cognition is a big one that patients complain of. The most common are muscle complaints, statin-associated muscle adverse effects. Partial intolerance means patients will tolerate a low dose of the statin, but you can’t get to the dose you need to reduce events that we want, that more than 50% reduction, or a goal of less than 55 mg/dL in our high-risk patients. It’s really important, because we can send the message that taking some statin is still beneficial, and that’s OK. But we have lots of other options to work on to try to get your LDL [low-density lipoprotein] at a good level.

What is your approach to statin intolerance? The ACC [American College of Cardiology] expert decision statement we’ve mentioned also mentions statin intolerance in that document. As we’re thinking about these nonstatin therapies we’ve been discussing, maybe you can talk a little about what does the ACC say about this? What is your approach to statin intolerance?

Often, patients who may have had those experiences and are informed by resources we would question—what they’re seeing online, or a friend of a friend, and things that aren’t very well established—haven’t heard that laying out of the evidence and the rationale. I think that’s important. Folded into that is the idea that there are certain LDL levels we need to achieve, and we may be moving on to other therapies. I think that incorporation is what we see emerging in this discussion, an attempt to deal with statin intolerance, but then moving on, which is what we see in the ACC statement.

Because ultimately, you’re going to have some patients who are just not going to tolerate a statin, whether it’s partial or complete. To leave patients untreated without moving into some of these other therapies, I think is what we see incorporated in the ACC consensus update. If a patient’s not getting to the right number, then we do need to move on. If we’ve paid attention to the possibility that maybe they’re just mistaken, and they attributed an issue to the statin that wasn’t related to the statin, and that they haven’t gone through an explanation of the rationale, that we should move on. We have options for moving on, as we’ve talked about, bempedoic acid, ezetimibe, their combination, PCSK9 inhibitors, inclisiran; these are all tools that we can use in patients and help convey to them that this is separate from the statin, and we’re not expecting those same adverse effects.

That’s another thing we see, not infrequently, in the clinic, we’re going through this with statin intolerance. Probably 30% of the patients we see in our lipid clinic are referred for statin intolerance. We’ve gone through that, and they say, “I’ve had a problem with every statin that’s ever been made.” And you say, “Have you been on ezetimibe?” They will sometimes look at you like you’re crazy and say, “I told you, I can’t tolerate any statins.” You say, “Well, ezetimibe’s not a statin.” And they go, “Oh, I didn’t know that.” That becomes important as we move on to other therapies, such as bempedoic acid and PCSK9 inhibitors, that these are completely different, and there’s no reason to expect a similar kind of issue. One of the impressive things with the CLEAR Outcomes study is taking on patients with a statin intolerance, which can often be a challenging patient group, and working through that with another agent. It’s important for us to set the stage for patients to not be anticipating harm, which is this nocebo effect and can be very powerful. Not the placebo effect, where you expect it not to be doing anything, but the nocebo effect, where you’re anticipating harm, and then you experience it.

 Bob, why don’t you tell us a little more about the nocebo effect. There have been some studies that have examined the nocebo effect. What is your approach to that?

The one that I found very interesting was the GAUSS-3 trail that was done with evolocumab. To get the evolocumab, they took statin-intolerant patients who already had intolerance to several statins. They gave them 20 mg of atorvastatin for, I believe, 8 weeks, then switched them to placebo. You can be on statin, placebo, or placebo, statin. There were 4 possibilities: you could get symptoms on both; you could get symptoms on neither; you could symptoms on the statin, not on placebo; or symptoms on placebo, and not on the statin. The difference was 42% had symptoms while they were on the atorvastatin, and 26% had symptoms not on the atorvastatin but had it on the placebo. That difference of 16 percentage points there, that’s the nocebo effect, that you’re anticipating harm from the drug. Some people get statin intolerance when they open the bottle of the statin and put first one in their mouth. As Jorge very nicely said, you could hear from your neighbor or Doctor Oz on TV that statins are going to cause some problem, and the patient’s going to get that. Remember, keep the eye on the prize. You’re lowering heart disease, that’s why I’m giving you this. Whatever you could take, whether it’s an alternate dosing, or a lower dose, or some other dosing, and the other drugs that we were talking about, that would be imperative.

 There have been a couple of others, too. In addition to that, there was the SAMSON trial and the StatinWISE trial. I like that the design of the SAMSON trial took patients who reported statin intolerance and gave them 12 bottles, 1 for each month. One-third of these bottles had the statin, one-third had an identical match placebo, and one-third of the bottles were empty. They would use a different bottle each month. On the empty bottles, they didn’t take anything that month, and they knew they weren’t taking anything that month. Patients did have muscle symptoms when they were taking a statin compared to the months, they were taking nothing. But 90% had the same symptoms when they were taking the placebo, too. So it was thought that it was the act of taking the pill rather than the medication itself.

We know that there’s incredible safety data despite the fact that, in blinded trials, there isn’t much difference in statin-associated muscle symptoms. People have argued that, well, these trials screen. They have this run-in phase, look for tolerance. In real-world practice, up to 30% of patients report statin symptoms. Even though it may be a nocebo effect, it’s very real to them, and that can be really challenging. That’s why I do like to emphasize what Jorge said, with the guidelines, the NLA statement says that although we do want to try at least 2 statins, 1 at the lowest dose, in these very high-risk patients, we don’t need to keep wasting time to try all 6 statins and all kinds of combinations. We just need to move on, so that we can limit the time of exposure to these atherogenic particles and get patients on therapy quickly. But it is challenging, because although we know the nocebo effect is real, the symptoms are real to the patients and shouldn’t be discounted. Because they’re clinically meaningful, and we know that patients who stop their statins are at increased risk for events.

Erin, I think you’ve already mentioned this. But those patients who are labeled statin intolerant have an even higher risk of having events than our age-matched patients with atherosclerotic disease who are taking other medications. It’s for that really high-risk cohort that we have to find something else that’s beneficial to get the LDL down more.

I find it interesting, as you probably all encounter, the segment of my clinic that is physicians, some of them seeking me out because of statin intolerance. That’s an interesting subgroup, because as I approach this and say, “Well, is there a bias in this patient who’s anticipating harm and doesn’t want to take a statin?” In that group, the vast majority of them are upset that they can’t take one. That gives you this feeling that there are some people who just have a hard time with it, and that we need to move on, because we do have other alternatives. Sometimes ezetimibe is helpful even as just a test to say, “Well, this patient’s not reacting to ezetimibe.” Now I don’t have to worry so much that this is, as we say, supratentorial. As I say to patients, it would be like…I tell you that I have a peanut allergy, and you offer me an orange. I say, “Well, I have a peanut allergy.” You would say, “Well, what’s wrong with him? This is an orange, not a peanut.” That can help establish the fact that we’re now moving on to other therapies that shouldn’t cause those same kinds of issues. I do think there’s a subset of those patients, as supported by the physicians, including cardiologists I have, who say, “I really feel like I can’t do this.”

A panel of experts discusses recommendations for managing statin intolerance in patients with hypercholesterolemia.

Managing ASCVD in Patients With Statin Intolerance

Let's look now and dig deeper into a couple of those studies that have been done for EDS-FLU delivery. We'll talk about the 2 phase 3 studies, Navigate 1 and Navigate 2. Dareen, if you wouldn't mind introducing the study design and study endpoints, and then Drew can tell us the outcomes of the studies.

: Wonderful. Thank you so much. With the EDS-FLU studies, the 2 pivotal phase 3 trials were called Navigate 1 and 2, and as you can see with the accompanying slide, they each had about 300 some patients and each of those duplicative arms. They were all both randomized placebo controls involving patients who had number 1, nasal polyps, and number 2, moderate to severe congestion obstruction. And it is important to know that these patients would be if I saw them in my clinic did nasal endoscopy etcetera, they would have been candidates for potentially surgery, these weren't patients who had mild nasal polyps or something like that. And there were a variety of patients enrolled, including patients who did not have a history of surgery but also patients who had had previous surgery. Patients were randomized into 1 of 3 arms, including EDS-FLU 93 micrograms, EDS-FLU 186 micrograms and then 372 micrograms or placebo and they had to do it twice daily for 24 weeks. There were 2 co-primary endpoints. One was the mean change in congestion obstruction which we know is the most significant symptom as Dr Peters had discussed earlier that is the most frustrating for patients. The thing that they complain about the most. And certainly, the next would be the mean change in the endoscopic total polyp grade and this in fact was graded at 0 to 3, so a total score of 6, 3 on each side. It is slightly different than some of the other clinical studies that you might read, so that's important to know. And then some important secondary outcome endpoints, such as the sinonasal outcome test 22 which we know is an objective measure of disease severity, quality of life and some of those even non-nasal symptoms that we talk. I'm going to turn it over to Drew who is going to tell you about the results.

These are very similar study designs, and we have one outcome that is symptom based and then one outcome that is more objective looking at polyps score, and then the sinonasal outcome test or called the snot 22 score which is something that we pay careful attention to as something that correlates with our patient's quality of life. Looking at these results, I want to see how all these outcomes fair. And for Navigate 1, we see that there's a lot of improvement in both primary endpoints, statistical improvement. They met both of those primary endpoints, improvement in nasal congestion. And the endoscopic appearance also showed improvement in the size of the polyp. The polyp score improved and that also correlated not just this sense of nasal congestion but improvement in the total snot 22 score, which is a broader marker of quality of life. And the patients also reported that they felt- 80% of patients felt that they had significant improvement. I'll touch on the adverse effects or adverse events in a second. For Navigate 2, there's similar findings, again, these co-primary endpoints were both met. Improvement in congestion and polyp improvement, but there was also one other feature I want to call out. In some patients, there was a complete resolution of polyp, and in that study 25% of patients compared with only 8% in placebo. 25% with the EDS fluticasone had polyp elimination on at least one side. This speaks to a pretty significant effect all of these end points being met. Again, in this study improvement in this snot 22 score. And then another important part is as Dareen mentioned that these patients would have been eligible for surgery and depending on how much there's symptoms bothered them and their response to medical therapy may have in fact gone onto surgery. And in the patients that were treated with the EDS fluticasone, the patients that were eligible for surgery by the end of this study would have decreased by 62 to 67%. Big changes in what brought these patients into the study and how they ended up at the conclusion. And from a safety standpoint, there's no major differences between this device, the EDS fluticasone, and the typical nasal corticosteroid sprays that we've been using. So just some local irritation but nothing that goes beyond that.

Expert allergists provide an overview of the phase 3 studies with EDS-FLU for treatment of nasal polyposis.

EDS-PLU Studies for Treatment of Nasal Polyposis

 Dareen, this is for you. You do a lot of clinical trials. How do use clinical trials for patients, who for example, have stopped responding to their current treatment? Do you offer them other clinical trials?

My answer transitions to some of both of your points, in that, as I discussed, in some of these complicated patients with the excellent ENTs school of medicine in my area. We typically will try one of these biologics for about 6 months. I would like to see what you guys are thinking about that as well, and certainly if there's another option, we might try a different one. And, funny enough with these medications, unlike asthma, which clearly states this is an add on therapy with biologics, that's not very clear with all the biologics in terms of the use with nasal polyposis, which I find interesting because that the similar inflammation is underlying it. The best success is add-on treatment, meaning that we're addressing the underlying inflammation with something like EDS-FLU, as well as the use of biologics. But beyond that, one of the big barriers for us is that all these medications, IL-4, IL-13, anti-IgE, anti-eosinophils, IL-5, is that they are focused on that type 2 inflammation. And the deficit or the lack is that what about those patients who do not have a type 2 inflammation, or a sinophilic inflammation status. And in those patients, perhaps, that where is where the clinical trials may be utilized for them, with some of the newer developing therapies. Or perhaps, they do have that inflammation, but they are still having some lack of symptoms that are being addressed, and are still feeling some issues. And of course, we've assumed that we've worked these patients up for all the underlying diseases that we're worried about. But we have encountered these patients, you know, like some of the other disease states where we've treated them, the polyps have improved. We have much less inflammation, but the patients continue, for example, to have significant facial pain pressure. There are certainly opportunities for them going forward for some newer medications.

: That makes sense. We will move on from biologics. Naveen, you discussed this previously, but how do you see the role of steroid-eluting stents in the treatment of nasal polyps?

: Steroid-eluting stents have played a key role in my practice in treatment of polyps over the years now, and generally speaking, intraoperatively, I tend to use them in many patients with nasal polyps. Almost all, probably easily over 80% because of their ability to treat inflammation with eluting steroid epicyte to minimize the burden possibly of oral systemic steroids that - honestly, I used to give a lot more commonly in the setting of surgery before steroid implants. When we look at the studies on steroid implants, a meta-analysis that was performed in 2019 showed that compared to controls, the use of steroid-eluting implants decreased the need for post operative intervention, which can include scar tissue treatment, or adhesion lysis, repeat surgery, oral steroid use, improved patency of the frontal sinus ostium in particular, and reduced polyps score. Based on the data, they definitely play a key role. Like biologics, they do have an associated - significant associated cost per implant. We do need to pay attention to that when we make decisions on using those intraoperatively or even postoperatively. But the data is favorable. And yes, they have played a key role in the post-surgical setting. Again, we mentioned that all the implants can only be used in the setting of surgery or postoperatively after prior surgery.

Naveen Bhandarkar, MD, shares his thoughts on the role of steroid eluting stents in the treatment of Chronic Rhinosinusitis with Nasal Polyps (CRSwNP).

Use of Steroid Eluting Stents in Treatment of Chronic Rhinosinusitis with Nasal Polyps (CRSwNP)

 conference, Brett King, MD, PhD, gives a presentation generally along the topic of “the future of the field.” He notices often that his peers are less than enthusiastic for the conversation—“nobody wants to talk about the future when the future never comes,” he explained.

Well, the future came, and it’s all any of his peers want to talk about.

In the second segment of an interview with 

King, associate professor of dermatology at the Yale School of Medicine, discussed the outburst of JAK inhibitor agents in dermatology this year—easily making the emerged drug class the headline story of 2022.

“2022 has brought 2 new therapies for moderate to severe atopic dermatitis: abrocitinib and upadacitinib,” King said. “It brought the first ever treatment for alopecia treat: baricitinib. It brought the first ever treatment for vitiligo: ruxolitinib 1.5% cream. It brought an effective oral therapy for psoriasis: deucravacitinib. All JAK inhibitors. Holy cow, 2022 was the year of the JAK inhibitor. It’s just incredible—we’re able to do things with this class of medicine that we’ve never been able to do before.”

King also discussed his hopes for 2023 successes on the basis of this year’s developments. With a boom of agents reaching the market, he stressed the value of patience going forward.

“Honestly, I want to spend time in this moment,” King said. “But my answer is not that I want to see a pipeline with 4 new things. What I want to see a year from now is that all of us and patients have learned this important thing: it takes time.”

Speaking specifically to the ruxolitinib cream approval for vitiligo, he said clinicians need to advance “our knowledge and our sophistication in the care of these patients.”

“I want for this approval to advance the way we take care of, talk to and counsel our patients,” he said.

Brett King, MD, PhD, reviews how the drug class has altered the state of chronic skin disease management in this year alone.

2022: The Year of JAK Inhibitors

Earlier this year, the US Food and Drug Administration (FDA) 

 as the first agent designated to treat patients with 

Supported by a phase 3 clinical program portfolio that included data showing capability to repigment skin with the twice-daily JAK inhibitor, ruxolitinib cream was quickly regarded as a landmark breakthrough in dermatologic care—and representative of a promising drug class in investigation still, to boot.

Now, experts would like to take a minute more to learn about this breakthrough.

In the first segment of an interview with 

, Brett King, MD, PhD, associate professor of dermatology at Yale School of Medicine, discussed a recent 

 State of Science Summit he chaired on the subject of vitiligo management. Ruxolitinib cream was a headline discussion for King and his supporting panel—which included primary phase 3 investigator David Rosmarin, MD—though conversation deviated from standard excitement.

 that it’s critical to take time to interpret ruxolitinib cream, its benefit to patients, and its contribution toward better understanding vitiligo as a chronic disease.

“I think we all need to take a step back at timers like this, when we have a huge breakthrough, to measure what we know and what we don’t know,” King said. “One of the really great things about these sorts of advancements is that we learn a lot about the disease.”

King described the ruxolitinib approval as an opportunity for day-to-day clinicians and prescribers to reconsider their level of knowledge into vitiligo management, and to consider what the latest data on the JAK inhibitor should tell them about the disease course itself—warts and all.

“One of the really key things that have come from the ruxolitinib clinical trials is that it takes time to treat this disease,” King said. “You have to tell people, “This is going to take months.” We can erase red skin. We can erase plaques of psoriasis, literally in weeks. We cannot repigment the skin in weeks. It takes months.”

Nonetheless, King echoed the overwhelmingly positive sentiments shared by his peers on ruxolitinib cream’s status as a breakthrough in vitiligo care.

“There’s tremendous reward at the end,” he said. “We need to bring all this together to optimize benefits and treatment success for our patients.”

Why patience is key following the major FDA decision earlier this year.

Videos

Latest News