Christopher G. Bunick, MD, PhD, is an associate professor of dermatology at Yale University School of Medicine.

Christopher G. Bunick, MD, PhD

 (EPP) remains among dermatology's most under-recognized diagnoses, often mistaken for solar urticaria or polymorphic light eruption for years before clinicians identify its hallmark feature: severe burning pain after sun exposure with little or no visible skin change.

, hosts Lindsay Ackerman, MD, and Christopher Bunick, MD, PhD, spoke with Angelika Erwin, MD, PhD, founder and director of the Porphyria Center at Cleveland Clinic, about diagnosing and managing EPP and its X-linked counterpart, XLP.

On this episode of ABCs in Dermatology, Angelika Erwin, MD, PhD, founder and director of the Porphyria Center at Cleveland Clinic, joins hosts Lindsay Ackerman, MD, and Christopher Bunick, MD, PhD, to discuss a rare, often-missed photosensitivity disorder and how care for it is evolving.

ABCs in Dermatology: Updates in Erythropoietic Protoporphyria Management for 2026

EPP results from ferrochelatase deficiency, causing free protoporphyrin IX to accumulate in red blood cells, plasma, and skin. Pain typically strikes within minutes of sun exposure, most often on the backs of the hands, and can precede any visible finding. Onset usually occurs between ages 1 and 4, and diagnosis is frequently delayed for years because symptoms resolve before a clinician examines the skin. About 5% of patients develop protoporphyric hepatopathy, which in rare cases progresses to fulminant liver failure requiring transplantation paired with bone marrow transplant, since liver transplant alone is not curative.

Erwin outlined a diagnostic pathway starting with plasma total porphyrins, available through standard commercial labs, followed by erythrocyte protoporphyrin testing at specialized centers such as Mayo Clinic or ARUP to distinguish EPP from XLP based on the ratio of free to zinc-bound protoporphyrin. Urine porphyrins remain normal in both conditions and should not be used for screening. Genetic testing targets the FECH gene in EPP, an autosomal recessive condition typically involving a common low-expression allele paired with a disease-causing mutation, and the ALAS2 gene on the X chromosome in XLP.

Before afamelanotide's 2019 approval, management relied on physical sun avoidance, zinc oxide and titanium dioxide sunscreens, and UV-filtering window films, with limited benefit from oral beta-carotene. Afamelanotide, a subcutaneous implant given every 60 days, increased pain-free sun exposure by a mean of 69 hours over 6 months versus placebo in the US phase 3 trial

, though it is not approved in pediatric patients. Bitopertin, an oral glycine transporter 1 inhibitor now in phase 3 testing, reduces porphyrin production upstream in the heme biosynthetic pathway and has shown promise in patients as young as 12 years in earlier trials

Erwin also pointed to earlier-stage candidates, including an ABCG2 inhibitor, ex vivo FECH gene replacement, mRNA-based delivery, and dersimelagon, an oral melanocortin receptor agonist in phase 3 testing. She emphasized that suspected EPP warrants erythrocyte protoporphyrin or plasma porphyrin testing rather than urine studies, and that confirmed cases require coordinated monitoring of liver function and vitamin D levels alongside referral to a specialized porphyria center.

Langendonk JG, Balwani M, Anderson KE, et al. Afamelanotide for erythropoietic protoporphyria. N Engl J Med. 2015;373(1):48-59. doi:

Yeung AK, Bonkovsky HL, Balwani M, et al. Bitopertin shows efficacy in patients with erythropoietic protoporphyria: results from the randomized, double-blind, placebo-controlled AURORA trial. J Am Acad Dermatol. 2025. doi:

Articles

Erythropoietic protoporphyria and X-linked protoporphyria present in early childhood with rapid-onset, severe phototoxic burning pain and minimal visible erythema, leading to frequent misdiagnosis and prolonged diagnostic delay. Pathobiology centers on excess protoporphyrin IX from ferrochelatase deficiency (EPP) or ALAS2 gain-of-function (XLP), with rare but serious protoporphyric hepatopathy. Diagnosis hinges on plasma porphyrins and specialized erythrocyte protoporphyrin fractionation, not urine testing. Management has shifted from strict photoprotection to melanocortin-based and heme-pathway–targeted therapies.

Angelika Erwin, MD, PhD, joins the podcast to discuss diagnosing and managing EPP and XLP on ABCs in Dermatology.

 to clear or almost clear skin, rather than partial improvement, is emerging as the standard clinicians should hold themselves to across every affected body site, including the scalp, nails, and genitals. Special sites carry a disproportionate quality-of-life burden relative to their body surface area (BSA) and are increasingly recognized by clinical guidelines as sufficient grounds for systemic therapy on their own.

, Lindsay Ackerman, MD, and Christopher Bunick, MD, PhD, discussed data supporting transformational care in psoriasis, with a focus on risankizumab and the underappreciated burden of special-site disease.

Hosts discuss the latest updates in psoriasis management for 2026, including new data on risankizumab and changes in management for difficult-to-treat areas.

ABCs in Dermatology: Updates in Psoriasis Management for 2026

International Psoriasis Council guidelines now define systemic eligibility using 3 criteria: 

Disease in hard-to-treat areas such as the scalp, nails, palms, soles, or genitals

Failure of 2 topical therapies used for at least 4 weeks each 

Special-site involvement matters beyond symptom burden: scalp disease confers a fourfold higher risk of psoriatic arthritis, and nail disease a 3-fold higher risk, against a baseline lifetime psoriatic arthritis risk of roughly 30% to 35% across the psoriasis population.

In the phase 3 UltIMMa-1 and UltIMMa-2 trials, risankizumab, an IL-23 p19 inhibitor dosed every 12 weeks, achieved PASI 90 in about 75% of patients by week 16. In the head-to-head IMMerge trial, risankizumab sustained superiority over secukinumab through week 52. Long-term LIMMitless extension data showed durability, with response curves for modified non-responder imputation and as-observed analyses nearly superimposed, and roughly 54% of patients reaching PASI 100 by week 304. In the phase 3b IMMprint trial, risankizumab also demonstrated efficacy in palmoplantar psoriasis, an area with thicker epidermis that is traditionally difficult to clear.

The speakers noted structural differences among IL-23 p19 inhibitors, including epitope binding surface area and dissociation rate, may help explain efficacy differences observed across the class. Risankizumab has also shown a 10% to 20% efficacy advantage over the oral IL-23 receptor blocker icotrolimod in indirect comparisons, alongside evidence that IL-23 inhibition may delay psoriatic arthritis onset more effectively than other mechanisms.

Collectively, the data support a shift in benchmark thinking, from PASI 75 toward PASI 90 and 100, and reinforce special-site and nail involvement as legitimate, guideline-recognized triggers for systemic therapy rather than exceptions to standard BSA-based criteria.

Gordon KB, Strober B, Lebwohl M, et al. Efficacy and safety of risankizumab in moderate-to-severe plaque psoriasis (UltIMMa-1 and UltIMMa-2): results from two double-blind, randomised, placebo-controlled and ustekinumab-controlled phase 3 trials. Lancet. 2018;392(10148):650-661. doi:10.1016/S0140-6736(18)31713-6

Warren RB, Blauvelt A, Poulin Y, et al. Efficacy and safety of risankizumab vs. secukinumab in patients with moderate-to-severe plaque psoriasis (IMMerge): results from a phase III, randomized, open-label, efficacy-assessor-blinded clinical trial. Br J Dermatol. 2021;184(1):50-59. doi:10.1111/bjd.19341

Papp KA, et al. Long-Term Safety and Efficacy of Risankizumab to Treat Moderate-to-Severe Plaque Psoriasis: Final LIMMitless Phase 3, Open-Label Extension Trial Results. Am J Clin Dermatol. 2025. doi:10.1007/s40257-025-00964-6

Lebwohl M, Bukhalo M, Bissonnette R, et al. A randomized phase 3b study evaluating the safety and efficacy of risankizumab in adult patients with moderate-to-severe plaque psoriasis with non-pustular palmoplantar involvement. J Am Acad Dermatol. 2024. doi:10.1016/j.jaad.2024.07.1521

Podcasts

Hosts discuss the latest data in psoriasis and the case for treating scalp, nail, and genital psoriasis as systemic-eligible disease.

Live podcast episode of ABCs in Dermatology recorded at Revolutionizing Atopic Dermatitis 2026

 ABCs in Dermatology: Updates in Atopic Dermatitis at RAD 2026

New analyses are adding momentum to early systemic intervention in moderate-to-severe 

, with growth outcomes emerging as a previously underappreciated marker of disease control in children. The findings reinforce a broader shift across the AD biologic class toward measuring success beyond skin clearance alone.

, co-hosts Christopher Bunick, MD, PhD, and Lindsay Ackerman, MD, FAAD, discussed the maturing interleukin-4 (IL-4)/interleukin-13 (IL-13) biologic landscape in AD. The conversation, recorded live at the 

Revolutionizing Atopic Dermatitis (RAD) 2026 meeting

 in Nashville, Tennessee, spanned dupilumab (Dupixent), tralokinumab (Adbry), and lebrikizumab (Ebglyss).Because no head-to-head trials exist among the 3 agents, comparative efficacy data rely on indirect network meta-analyses. 

Roughly 30% of patients reach Eczema Area and Severity Index (EASI) 90 or Investigator Global Assessment (IGA) 0/1 by week 16, with response rates continuing to climb well beyond this early window. In dupilumab's long-term extension trial, more than 90% of patients who had not reached EASI 75 by week 16 achieved it by week 100. 

None of the 6 FDA-approved advanced AD therapies require routine laboratory monitoring, and tralokinumab and dupilumab have each published 5-year safety data showing predominantly mild to moderate adverse events without new safety signals. 

By contrast, around 1 in 5 patients with moderate to severe AD still receive oral corticosteroids. Even a 6-day prednisone dose pack raises the risk of sepsis, bone fracture, and venous thromboembolism for 30 days afterward.Pediatric growth emerged as a focal point. Extension data from the Liberty AD PS trial showed children treated early with dupilumab had a 3.7- to 4.2-fold greater likelihood of meaningful growth improvement versus peers on no systemic therapy, independent of corticosteroid exposure. Bunick described the underlying mechanism as likely multifactorial, reflecting reduced inflammation, lower corticosteroid use, and improved sleep.

Itch tracks closely with quality of life: registry data show quality of life drops sharply unless itch reaches a 0 or 1 on a 10-point scale. This prompted both hosts to counsel patients toward this stricter target rather than partial relief. Collectively, the data point to a biologic class no longer competing only on skin clearance, but increasingly on durability, safety, and capacity to address the systemic burden of AD across the lifespan.

Relevant disclosures for Bunick include AbbVie, South Beach Symposium, Almirall, Apogee Therapeutics, Arcutis Biotherapeutics, Daiichi Sankyo, Eli Lilly, LEO Pharma, US, Novan, Novartis, Ortho Dermatologics, Palvella Therapeutics, Pfizer Inc., Sanofi, Sun Pharmaceutical Industries Ltd., Timber Pharmaceuticals, and UCB. Relevant disclosures for Ackerman include AbbVie, Alumis, Amgen, Arcutis, Beiersdorf, Boehringer Ingelheim, Bristol Myers Squibb, Dermavant, Galderma, L'Oréal, Novartis, Sun Pharmaceutical, and UCB.

New AD biologic data highlight early systemic treatment, durable itch control, and improved pediatric growth—shifting goals beyond skin clearance.

ABCs in Dermatology: Updates in Atopic Dermatitis Live at RAD 2026

What Will Precision Dermatology Look Like in Atopic Dermatitis?

In another segment of his latest interview, Christopher Bunick, MD, PhD, associate professor of dermatology at Yale School of Medicine, described his views on the future of precision medicine in the atopic dermatitis space, speaking with 

2026 Revolutionizing Atopic Dermatitis (RAD) Conference

Bunick noted both the progress made so far toward this future and the scientific challenges that will continue to be seen before clinicians can reliably predict which medications will be best for individuals. He explained while atopic dermatitis therapy has entered an era of unprecedented therapeutic expansion, a true precision medicine future remains a work in progress.

“It's going to take a lot more understanding of what drives atopic dermatitis,” Bunick explained. “For example, understanding how OX40 ligand-targeted drugs, or any other drug, whether it's JAK inhibitors or the other biologics that are currently approved, may or may not cause disease modification requires us to actually study how are memory T-cells affected over short and long courses of therapy.”

He described current research efforts, including gene expression profiling, as having begun to provide key findings on how individuals may respond to different therapeutic classes, such as biologics and Janus kinase (JAK) inhibitors. However, Bunick also emphasized the field as not having yet attained a level whereby clinicians can confidently implement molecular signatures alone with the aim of matching patients with the optimal course of therapy.

According to Bunick, attaining that goal will involve gaining a much deeper understanding of the immunologic mechanisms known to drive atopic dermatitis. While cytokines such as IL-4, IL-13, and others have become important targets, he described researchers in this space as increasingly looking upstream in the disease process. Emerging investigations are assessing how immune cells contribute to disease activity and long-term disease control.

Bunick further explored the concept of disease modification, noting the increasing prominence of the topic as new therapeutic targets begin clinical development. The growing interest in drugs targeting pathways such as OX40/OX40 ligand, STAT6, and other immune regulators that may influence the underlying biology of the disease was highlighted by Bunick. An awareness of how these medications impact immune memory and long-term inflammatory responses may ultimately help determine whether durable disease modification is a potential aim for the future.

In his interview, Bunick additionally pointed to advances in transcriptomics, proteomics, and cellular immunology as areas that could potentially play a major role in the future of therapy prediction. Through the integration of molecular profiling with a deeper understanding of immune system behavior, those conducting such research may eventually be able to identify which patients will be most likely to see positive results from specific drugs prior to initiation of treatment.

Bunick has reported receiving consultant fees or serving as an investigator for AbbVie, Incyte, LEO Pharma and Pfizer.

Nguyen H, Bunick C, Cotter D, Shahriari M. Medical Crossfire and Clinical Case Challenge. Session presented at: 2026 Revolutionizing Atopic Dermatitis Conference; June 17-19, 2026; Nashville, TN.

Bunick C. Highlighting FDA-Approved Therapies in Atopic Dermatitis, With Chris Bunick, MD, PhD. HCPLive. June 25, 2026. 

https://www.hcplive.com/view/highlighting-fda-approved-therapies-atopic-dermatitis-chris-bunick-md-phd

Videos

The topic of precision medicine in dermatology is explored in this segment of Bunick's interview at RAD 2026.