This is a really important topic because so many times when people develop a new problem with their HS, some practitioners or offices are quick to refer them out. A good example is an abscess. One of these cysts turns into an abscess, it’s actively draining. I believe most people are comfortable with doing an incision and drainage. But many times people and clinicians are underutilizing intralesional injections. This is a quick procedure that can provide a lot of relief and less scarring for the patient. Obviously, there are limitations to that. But for some of the bigger areas that are more involved and resistant to I&Ding [incision and drainage] or intralesional injections, doing a deroofing procedure can provide a lot of benefit for patients. This is a way to keep the patient in your practice, have good continuity of care, and treat them effectively without referring them to a general surgeon. There are lots of resources available for that procedure, but that is something that I encourage everyone to get better at doing because it really provides a lot of relief for those patients with HS.

Ask your patients about HS. There is definitely a knowledge gap for practitioners across all specialties. And many times patients are not forthcoming with having this disease. And so when you’re seeing someone who comes in for acne, or you’re seeing someone who comes in and you’re draining an abscess, have the conversation and ask them, “Do you have these anywhere else? How many cysts have you had in your life?” Oftentimes, that opens up a good conversation, and patients will be more forthcoming with having this disease. Also, for the patients who have HS, talk to them about the benefit of early treatment. We’ve discussed this here, but a lot of people feel that biologic treatment is only necessary when they have severe disease or stage III Hurley disease, and that is not the case. Early intervention in this window of opportunity can provide people with an improved quality of life, less surgery, less sequelae from this disease, so that is really important. And also, develop a good multidisciplinary team. People in the medical community—some have very strong personalities. And it may take a little bit of time to find a group of individuals you trust to refer. Whether it’s a psychiatrist or a surgeon or whoever you’re working with for these patients, making sure that you’re on the same page about what it takes to truly treat this disease effectively is so important. And the last is to make sure you’re going to tell your patients that you’re going to follow them closely, you’re going to be seeing them frequently, you’re going to make sure that their medications are working for them. If they develop a hot spot or a draining abscess, make sure that you tell them that you’ll get them in quickly to manage this to prevent them from going to ERs [emergency rooms] and urgent care facilities. And just having polypharmacy, because so many times these patients are being bounced around. So just let them know that you care and that you’ll be there with them throughout this journey.

An expert in dermatological conditions discusses office-based procedures that can benefit patients with HS and shares clinical pearls for the management of the disorder.

Clinical Pearls for the Management of HS

Andrew Baker PA-C, MBA

Devrey Martin is a Master’s Student in Forensic Psychology at the University of Denver with interests in the overlap of forensic psychology with health psychology and neuropsychology. During her first year, Devrey has been involved in traumatic brain injury research and writing for an advocacy newsletter. She aims to provide forensic evaluations and assessments while advocating for prison reform.

Devrey Martin, BS

Advancing Retinal Disease Treatment – The Next Generation of Anti-VEGF Therapies

1:25- Rationale for high dose aflibercept

22:29- Faricimab and role of ang-2 inhibition

Ehsan Rahimy, MD; David G. Miller, MD, and Jordana Fein, MD, discusses how 8 milligram aflibercept and faricimab, newer anti-VEGF therapies for retinal diseases, offer improved durability with comparable safety profiles to existing treatments, allowing less frequent injections while maintaining equivalent vision outcomes.

Advancing Retinal Disease Treatment – The Next Generation of Anti-VEGF Therapies 

Ehsan Rahimy, MD

Future Directions for Psoriasis Treatment

Video content above is prompted by the following:

Panelists discuss how the future of psoriasis treatment is evolving toward more personalized approaches with earlier biologic intervention for patients with high-impact disease regardless of body surface area, improved assessment tools that better capture disease burden, greater consideration of comorbidities and quality-of-life impacts, increased diversity in clinical trials, expanded patient education, innovative delivery systems, combination therapies, and targeted treatments for specific psoriasis phenotypes—all aimed at addressing current treatment gaps and moving closer to disease modification rather than merely symptom management.

James Song, MD

Jennifer Flemming, MD, is an associate professor of medicine and public health sciences at Queen's University.

Flemming describes increasing rates of AH among adolescents and young adults, with females facing the greatest increases and worse outcomes than males.

Understanding the Shifting Burden of Alcohol-Associated Hepatitis

 (AH) is on the rise among adolescents and young adults, but long-term liver-related outcomes for affected individuals vary by sex, according to findings from a recent study.

The population-based study of more than 3000 patients 13-39 years of age in Canada highlights rapid increases in the rates of AH in this patient population over the past 2 decades, especially among women. Additional analyses reveal female sex is independently associated with a 47% greater risk of cirrhosis and/or decompensation, and the cumulative incidence of liver-related mortality at 10 years is higher among women than men.

According to alcohol-associated liver disease practice guidance from the American Association for the Study of Liver Diseases, women have a greater risk of liver injury compared with men for any level of drinking. Additionally, while rates of alcohol use disorder and high-risk drinking have grown in recent years, some of the greatest increases have been observed among women.

“Myself, in addition to many others, noticed this switch in the demographic of individuals who were coming in with acute alcohol-associated hepatitis,” Jennifer Flemming, MD, an associate professor of medicine and public health sciences at Queen's University, told 

, explaining how AH has historically been known to affect middle-aged men but has recently been observed more frequently in younger individuals, especially females.

To determine the extent of this phenomenon, she and a group of colleagues conducted a population-based retrospective cohort study of 3340 adolescents and young adults 13-39 years of age with an incident diagnosis of alcohol-associated hepatitis without a history of cirrhosis and/or decompensation in Ontario, Canada.

“What we found, concerningly, is that rates of [AH] were going up in all ages in this young group,” Flemming said. “When we stratified it based on sex, kind of similar to what we were seeing clinically, we saw that the rates were going up much higher among females.”

Flemming went on to emphasize the importance of multidisciplinary management of alcohol-associated liver disease and underlying alcohol use disorder, citing the importance of addressing both the liver-related and 

 aspects of these conditions. Additionally, she called attention to the need to develop sex-based interventions addressing the heightened risk of alcohol-associated liver disease observed in female patients.

Editors’ note: Flemming has no relevant disclosures.

Brooks A. Young Women Face Worse Long-Term Alcohol-Associated Hepatitis Outcomes Than Men. 

. January 8, 2025. Accessed January 13, 2025. 

https://www.hcplive.com/view/young-women-face-worse-long-term-alcohol-associated-hepatitis-outcomes-than-men

Crabb DW, Im GY, Szabo G, et al. Diagnosis and Treatment of Alcohol‐Associated Liver Diseases: 2019 Practice Guidance From the American Association for the Study of Liver Diseases. Hepatology. doi:10.1002/hep.30866

Jennifer Flemming, MD: Understanding the Shifting Burden of Alcohol-Associated Hepatitis

Jennifer Flemming, MD

The last piece is about education. This is important because to make a good shared decision-making process with the patient, they have to be on the same page. There’s a huge amount of education that has to happen. Of course, we all have luxurious amounts of time. You guys usually have, what, 1 to 2 hours for a new visit? Maybe longer—it’s only a few patients a day. No. We’re crunched. You have crunched time, and you have so much to cover. Sometimes the visit has many factors: where have you been? What are you using currently? What are your hopes, your fears, concerns? Then you get derailed. All they want to talk about is food. What food should we avoid? If we mention that, it can derail the whole visit. You’re trying to get to the next step to figure out how to get their skin better, and they’re doing this.

That doesn’t take into account the paperwork that has to happen after: the insurance forms, the prior authorization, the patient support stuff—all these things. How do we do that? One thing that’s so important is to bring external resources. I’m obsessed with handouts. I’m the king of handouts. Every time I see anybody for anything, they’re going home with a handout, and it’s usually going to list my action plan: what to do when you’re flaring up and what to do when you’re better. That’s such a big deal for me because it’s cut a lot of calls. Not 100%, but many calls [are answering the questions], “Which do I do first? Do I put this 1 on and then this 1?” I put them in numeric order. “In the morning, you’re going to do 1, 2, and 3.” We can really bring them through that.

The other piece that’s important is utilizing some of the national organizations that have patient support resources. I’m very conflicted because I’m a board member of the National Eczema Association. I don’t get paid any money. In fact, I donate a lot every year. I love the National Eczema Association. They’re a nonprofit organization that does a lot of patient advocacy support and education. I try to have my patients go to their website , to get signed up, to learn a little more about it. It’s nice when it doesn’t have to come directly from us. Sometimes they have a rapport with us, they understand us, but it’s nice to hear someone else’s voice, to get another opinion. That can help and give them some of the tools that can help them ask the good questions at the next visit, because I don’t like to be pushy. 

On the first visit, sometimes I say, “Here are some options. I want you to think about this. Here’s some homework for you to read. Let’s talk, either by phone”—if they’re from out of state or from far away—“or when I see you in a few weeks, we’ll make our decisions at that point.” How do you guys feel about the education burden that we have?

I agree. All of our patients are—if they haven’t already before they come to the visit—going to Google and Facebook to crowdsource and ask for advice from trusted friends and family members beyond their trusted allergist or dermatologist. Beyond the sheet that has all those important, point-by-point instructions, there needs to be a trusted links list. Something like the [National] Eczema Association and our national societies, which have great patient handouts. Let them kind of go down the rabbit hole online in a safe place, in a place they’re going to get good information.

Giving links and trusted sources are really helpful. But I also find that having that patient back with a short turnaround time is important. We’re all busy, but in patients with atopic dermatitis, we give them homework, we give them food for thought, but they need to come back shortly thereafter with questions fresh in mind. [Once they’re] able to move the ball along the field, get closer to that touchdown, get closer to that goal line, we can make management decisions incrementally. It’s OK to make management decisions incrementally for these patients. If you do that, they’ll follow you along that pathway.

I was going to make 1 quick [point]. We’ve alluded to the food thing. There may be some listeners [wondering], “Why are they laughing about the food? Why aren’t they talking about that?” I can speak a little for Dr Jain because I just attended 1 of his amazing lectures about food allergy and atopic dermatitis. The point—and the way I say it to my patients—is that I wish the food were the cause. When food is the cause, it’s easy. Arguably, you don’t actually have atopic dermatitis. You have an eczematous food reaction—you’re done, you don’t need us, you don’t need any of this. But for many patients, food may be playing some role. It might be inflammatory. They may have some food triggers. Of course, there’s a huge concurrence of real food allergies that are IgE mediated.

It’s a complex, messy thing, but it’s often not where the money is to get the skin better. There’s this tension because the patients want to focus on the diet, “How can I fix my diet to get better?” [We say], “I don’t know.” Even if you did a super-severe, extreme diet—we’ve all had patients with literal malnutrition because they’ve been so stringent on their diet, and their eczema is still terrible. It’s trying to redirect, not because we’re trying to push drugs on somebody, but because we’re trying to help them. Some of the patients and families have done this for years. I’ll just sit there and say, “You would’ve found it without me. You’ve cut everything out. You’re feeding the child rocks and water, but his eczema is still bad. I don’t think it’s food. I want it to be too, but can we work on other things?”

One of the little tools in my toolbox that I’ll share—this is a pretty universal thing; we all feel the pain of this is that I often say to families who are fixated on it, “When the skin is super inflamed, like now, when it’s a mess, it’s similar to when you get up on the wrong side of the bed.” You’re in a bad mood. No matter what anybody says to you, you’re going, “Grr.” Somebody says, “Good morning,” and you’re, “Grr.” But when you get up and you’re in a good mood, even if someone says, “You’re a jerk,” you say, “Have a great day.” It rolls off you.

It’s very difficult to evaluate what’s triggering your skin when it’s a mess, so I say, “Let’s get it better.” Let’s spend a little time cleaning things up. If there are still triggers, we can then see with much clearer eyes If they had an aha moment when they ate—fill in the blanks—dairy, gluten, strawberries, whatever it may be. That definitely made it worse. But right now, we can’t even see that. I put that there not because we don’t take it seriously. We do, but it could take up all the time. Sometimes that’s all people want to talk about. We have to redirect, because I want to get people better. Do you guys agree with that? Not to derail it too much, but it’s so important.

Absolutely. When we talk about what works and what helps patients get buy-in, we take for granted that we understand this pathology of atopic dermatitis, but they don’t. You just spoke about this with regard to their focus on foods or other things, what mindset they come in with. We need to take a step back and teach them that this is a disease where there’s barrier dysfunction, helping them understand that we’re learning that this is true not only of atopic dermatitis but also other type 2 inflammatory diseases, whether it’s asthma, allergic rhinitis, chronic rhinosinusitis with nasal polyps, eosinophilic esophagitis.

We know that there are these similarities with this barrier dysfunction, and that barrier dysfunction leads to this inflammation. That’s how you develop food allergies. It happens first there. We need to help them understand this so that they get the focus away from some things that they have preconceptions about, and then we can educate them about the options to manage that and help restore that function to help their skin better. That’s hugely helpful. When this comes from reputable sources like the National Eczema Association, the AAD [American Academy of Dermatology], our societies in allergy, getting that same message repeatedly helps.

We did some survey on patients’ perceptions about bathing. You hear these patients coming in, saying that they’ve been told 15 things about what they should do with bathing, and they’re just confused. So to have some science to back this up gives us credibility, and that allows for the buy-in that ultimately leads to success in skin improvement.

Educating patients about their disease course is very important at the outset. It’s important to set expectations, and there’s no more important way for me to do that than to tell them this is not something you’re doing. It’s not your fault. It’s a genetic skin condition, and it’s a condition that waxes and wanes over time. There are going to be periods when you forget that you have eczema. There are going to be periods when it’s very flared. Our job is to control those flares so that you’re not having flares very often and when you do have flares, to not be concerned about treating them at the first sign of trouble.

One way to do that is to talk about the use of steroids and how to properly use them so that they’re not afraid to use them. Another way is to use nonsteroidal medications that might promote less fear within the patient or the parents so that they use them at the first sign of trouble. I always say that it’s like a little fire that’s burning. The sooner you put it out, the better off you’ll be—but you have to completely put it out. If you use your medication for a few days and then there are still some embers there, it will come right back. It’s important to set those expectations.

A third thing that’s very important to talk about is avoiding systemic steroids. Very commonly, patients come to the office with chronic waxing-and-waning flares. It’s a vicious cycle, and it’s usually triggered by the use of systemic steroids, either injectable or oral prednisone or Medrol dose packs. What happens is the patient’s skin rebounds once they come off their systemic steroids. It’s important to educate parents, patients, and providers that using systemic steroids should be a bridge to some other therapy and should not in and of itself be the plan to treat someone’s atopic dermatitis. In the long term, they have adverse effects. In the short term, they’re going to create a rebound that’s only going to continue their waxing-and-waning flare cycle.

Shared insight on the best ways to educate patients on their atopic dermatitis and explain the nuances of available therapies.

Educating Patients on Atopic Dermatitis and Inflammation 

Marc Serota, MD

Mercedes E. Gonzalez, MD, is a clinical assistant professor at the FIU Herbert Wertheim School of Medicine and the Phillip Frost Department of Dermatology at the Miller School of Medicine.

 that the US Food and Drug Administration (FDA) had accepted their supplemental New Drug Application (sNDA) for roflumilast cream 0.05% (Zoryve) as a topical for children with mild to moderate 

 team spoke with a clinical trial investigator for the INTEGUMENT-PED study.

Mercedes E. Gonzalez, MD, is a clinical assistant professor at the FIU Herbert Wertheim School of Medicine and the Phillip Frost Department of Dermatology at the Miller School of Medicine. Gonzalez spoke with the 

 team about roflumilast’s recent data and its use as a once-daily topical phosphodiesterase-4 (PDE4) inhibitor in children aged 2 - 5 years.

Findings on Roflumilast Cream 0.5% for Children with Atopic Dermatitis, with Mercedes Gonzalez, MD

“This was a pediatric atopic dermatitis that included patients 2 years to 5 years of age who had mild to moderate atopic dermatitis and had to have at least 3% body surface area to be enrolled in the trial,” Gonzalez said. “This was a 4-week trial. It was a randomized, placebo-controlled trial. Patients were randomized 2 to 1 to receive roflumilast 0.05% cream versus a vehicle, and they were followed for 4 weeks. The primary efficacy endpoint was IGA improvement. So this was an improvement in IGA score of 0 or 1, as well as an EASI 75 at 4 weeks.”

The findings highlighted by Gonzalez represented the conclusion of the INTEGUMENT-PED study, during which the research team followed up the INTEGUMENT-1 and INTEGUMENT-2 phase 3 analyses.

 437 subjects were included in the trial who were given roflumilast cream and 215 were in the vehicle arm.

Gonzalez’s team highlighte that at the 4-week mark, there was a significantly higher proportion of individuals included in the roflumilast cream cohort who had visibly attained an EASI-75 (39.4% versus 20.6%; 

 < .0001), as well as Validated Investigator Global Assessment for atopic dermatitis (vIGA-AD) Success (25.4% versus 10.7%; 

 < .0001) and Worst Itch-Numeric Rating Score (WI-NRS) Success (35.3% versus 18.0%; nominal 

“Because of the data, I'm able to say that there's a significant chance that itch is going to improve quickly and that the skin lesions are going to go away pretty quickly within that 4-week time frame,” Gonzalez explained. “In addition, it does not have the side effects associated with the traditional topical corticosteroids. The rates of adverse events in the trial were extremely low, with less than 1% reporting stinging and burning from this medication. So that's important.”

It has been noted previously that the FDA has a PDUFA target action date set for October 13, 2025 for the roflumilast cream 0.05% application.

 For more information on this subject, view the full interview video posted above.

The quotes contained in this interview summary were edited for clarity.

Arcutis Biotherapeutics. U.S. FDA accepts Supplemental New Drug Application For Arcutis’ ZORYVE® (roflumilast) cream 0.05% for the treatment of children aged 2 to 5 with mild to moderate atopic dermatitis. Arcutis Biotherapeutics. February 26, 2025. Accessed February 26, 2025. 

https://www.arcutis.com/u-s-fda-accepts-supplemental-new-drug-application-for-arcutis-zoryve-roflumilast-cream-0-05-for-the-treatment-of-children-aged-2-to-5-with-mild-to-moderate-atopic-dermatitis/

Eichenfield, L.F., Serrao, R., Berk, D.R., et al (2025). Efficacy and Safety of Once-Daily Roflumilast Cream 0.05% in Pediatric Patients Aged 2–5 Years With Mild-to-Moderate Atopic Dermatitis (INTEGUMENT-PED): A Phase 3 Randomized Controlled Trial. Pediatric Dermatology. 

This interview highlights recent findings on roflumilast cream 0.05% for patients aged 2 to 5 years with mild to moderate atopic dermatitis.

Findings on Roflumilast Cream 0.05% for Children with Atopic Dermatitis, with Mercedes Gonzalez, MD

Mercedes Gonzalez, MD

Reynold Panettieri, Jr, MD, Robert Wood Johnson Medical School 

Robert S. Rosenson, MD is a professor of cardiology at the Icahn School of Medicine at Mount Sinai.

Solbinsiran, a GalNAc-conjugated small interfering RNA targeting hepatic angiopoietin-like protein 3 (ANGPTL3), at a dose of 400 mg, achieved sustained reductions in apolipoprotein B concentration among patients with 

American College of Cardiology (ACC) 2025 Annual Scientific Sessions

, results from the Phase 2 PROLONG-ANG3 study showed solbinsiran was well tolerated, with a low incidence of adverse events, but its impact on cardiovascular outcomes has yet to be determined.

“These data related to the efficacy and the safety of the medication set the foundation for a phase three cardiovascular outcome trial,” trial investigator Robert S. Rosenson, MD, a professor of cardiology at the Icahn School of Medicine at Mount Sinai, told 

. “I'm quite excited about ANGPTL3 inhibitors as adjunctive therapy to what we have available today

Mixed dyslipidemia is characterized by raised levels of circulating triglycerides and low-density lipoprotein cholesterol (LDL) linked to an elevated likelihood of atherosclerotic cardiovascular disease (ASCVD). Solbinsiran achieved targeted reductions in both levels of triglycerides and LDL-C in a Phase 1 trial.

Investigators sought to further evaluate the therapy, specifically its durability and efficacy, in reducing concentrations of atherogenic lipoprotein in adults with mixed dyslipidemia. A double-blind, parallel-arm, randomized, placebo-controlled trial, the team enrolled adults with mixed dyslipidemia at 41 clinical units across 7 countries.

Enrollment criteria included patients receiving moderate-intensity or high-intensity statins, with concentrations of fasting triglycerides between 1.69 mmol/L and 5.64 mmol/L, LDL-C of >1.81 mmol/L, and non-HDL-cholesterol of ≥3.36 mmol/L.

Patients were randomly assigned 1:2:2:2 to either solbinsiran 100 mg or solbinsiran 400 mg, solbinsiran 800 mg, or placebo, by subcutaneous injection on Days 0 and 90. Follow-up occurred for at least 270 days in all patients. The primary outcome was the percent change in apoB concentration from baseline to Day 180 with solbinsiran, compared with placebo, as analyzed by an efficacy estimand: patients who received ≥1 dose of solbinsiran.

Among 585 screened patients, 205 were enrolled between July 2022 and March 2024. The population was more than half (54%) female, and the median age was 57 years. Randomization assigned patients to solbinsiran 100 mg (n = 30), solbinsiran 400 mg (n = 58), solbinsiran 800 mg (n = 59), or placebo (n = 58).

Baseline mean concentrations were 111 mg/dL for apoB, 2.64 mmol/L for triglycerides, and 3.16 mmol/L for LDL-C. Upon analysis, the placebo-adjusted percent change in apoB concentration at Day 180 was –2.8% (95% CI, –15.5 to 11.9; 

 =.69) for solbinsiran 100 mg, –14.3% (95% CI, –23.6 to –3.9; 

 =.0085) for solbinsiran 400 mg, and –8.3% (95% CI, –18.3 to 2.9; 

Safety analysis revealed treatment-emergent adverse events in 18 (60%) of 30 patients in the solbinsiran 100 mg cohort, 30 (52%) of 58 patients in the solbinsiran 400 mg cohort, 26 (44%) of 59 patients in the solbinsiran 800 mg cohort, and 37 (65%) of 57 patients in the placebo cohort. Notably, the 400 mg dose was associated with reductions in hepatic fat fraction of 27.6%.

“By these therapies, often we're thinking about adverse changes in the liver with statins, fibrates, and other agents. These data contrast and actually show improvement in the hepatic fat fraction,” Rosenson told 

. “I'm quite encouraged about the opportunities for some of our very difficult to treat patients.”

Learn more about the trial in an interview with Rosenson at ACC.25.

Solbinsiran Significantly Reduces apoB in Mixed Dyslipidemia in Phase 2 Trial

Ray, Kausik K et al. Durability and efficacy of solbinsiran, a GalNAc-conjugated siRNA targeting ANGPTL3, in adults with mixed dyslipidaemia (PROLONG-ANG3): a double-blind, randomised, placebo-controlled, phase 2 trial. The Lancet, Volume 0, Issue 0. March 31, 2025. Accessed March 31, 2025.

Ray KK, Linnebjerg H, Michael LF, et al. Effect of ANGPTL3 inhibition with solbinsiran in preclinical and early human studies. JACC (in press) 10.1016/j.jacc.2025.03.005

At ACC.25, Robert S. Rosenson, MD, discusses the efficacy and safety of solbinsiran, an ANGPTL3 inhibitor, in a population with mixed dyslipidemia.

Robert S. Rosenson, MD

 You touched on the brand-new drug anifrolumab. It’s another breakthrough in lupus, developed for SLE [systemic lupus erythematosus]. In the mid-1990s, they found that interferons were highly expressed in SLE, and particularly in the pathogenesis…

 Maybe so. But the trials had showed efficacy in both high and low responders, but maybe we’ll get there later.

 Yeah, it’s interesting. But it means you need to inhibit it a little—that’s all, right? There’s only so much you can get with interferon-alpha blocker probably.

 But it’s so new, we don’t know yet, right?

 Right. But that drug was developed out of genome-wide studies and that showed multiple SNPs, or single-nucleotide polymorphisms, in genes that encoded for the expression of interferon alpha. It’s this idea of rational drug design that’s being applied to SLE, that had been applied to other rheumatic diseases. We’re finally here, where we’re going to be at the breakthrough with new therapies.

 I’m very curious because it’s been approved in the United States for a number of months. Are you now—I mean 

 in the plural, so rheumatologists practicing in the United States—gaining experience with anifrolumab? Is it available?

 We are. It’s becoming available in the community setting. Most academic centers are getting it on their formulary. I have patients on the medication, and I’m doing a clinical trial incorporating that medication with Joan Merrill. We’re starting pick up, and it’s still too early to know how important this may be in the treatment of lupus and when it should be employed in SLE. As you know, the study showed an effect that was fairly rapid, so that there was a divergence of the treatment curves at 2 or 3 months, from what I recall. There was a particular improvement in skin disease with lupus. This might be an agent that 1 may try for rapid amelioration of skin manifestation of lupus.

 Interesting. There are also data that in the skin, interferon is upregulated. If you do a molecular analysis, you can see that.

 That stands to reason. But I’m also still intrigued by how lupus may be several pathophysiologies. In some people you have the high interferon signature or the low interferon signature, going back to belimumab you have patients for whom B-cell activity is very high, and they have all these other antibodies. Other patients might have lupus, but they may have only antinuclear antibodies and not the other ones. There could be a difference also. It might be that in the future, which is what I hope, we’ll do these analyses, immunological analyses, and it will tell us this patient should be treated with anifrolumab, this patient should be treated with belimumab, this patient will do best with a conventional therapy. That’s also possible. We might be able to start doing it that way. We’re not there yet by a long shot, but I want it for the future.

 Right, and there may be cycles of therapy. They may want to treat patients with anti-interferon therapy followed by B-cell therapy or combinations, particularly if there’s severe disease, and we’ll learn how to use them in combination to get our patients better. But it’s an exciting breakthrough.

 Interesting. I was involved in a combination trial with—I don’t know if you knew about this—the combination of belimumab with rituximab. That’s quite strange because rituximab is not approved for lupus. It’s used off-label, but it’s not approved. Then there’s a trial. There were several trials where these were combined with the idea that you could get some sort of a synergy. It’s a very interesting scientific concept, and it could work. The patients in the trials did well, but it was not so clear that the combination gave an added benefit. That’s still a little unclear. Some parameters said they did, but others said that it was the same. It will be very interesting to see it.

 You showed this data in an abstract at the American College of Rheumatology, am I right?

 I was a coauthor, so there were others who showed it.

 Right. After 52 weeks, though, you had stopped therapy, so of course lupus will flare. One wondered why these were not continued.

The rationale for using a newer monoclonal antibody therapy, anifrolumab, to manage patients with systemic lupus erythematosus.

Authors