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

In a recent review on emerging therapies for atopic dermatitis, Christopher G. Bunick, MD, PhD, and colleagues highlighted a notable limitation in the treatment landscape: many of those treated with existing monospecific biologics do not achieve optimal or sustained disease control.

, Bunick emphasized that although currently available medications targeting individual pathways have led to improved outcomes, they often fail to fully impact the breadth of inflammation and symptom burden.

 In response, Bunick and colleagues outlined a rapidly expanding pipeline of bispecific and trispecific antibodies designed to simultaneously target multiple inflammatory and neuroimmune pathways.

In this new Q&A segment of his interview with 

, he touched on these emerging therapies being developed to address both immune-driven inflammation and itch signaling concurrently, noting several key points about his team’s findings and their significance:

Based on the early clinical data your team reviewed, what signals would you say are most encouraging in terms of efficacy, itch control, and durability of response?

For me, last year at EADV, we saw our first glimpse of what the multi-targeted biologics could achieve. What I refer to there is an early phase 1 study from galvokimig. Now this is a molecule that's targeting IL-13 with a tralokinumab-like epitope, but also has the ability to target like by bimekizumab, IL-17 A and F. And what this answered for us was a couple of things. Number one, it asked the question, ‘Can tackling some of the cytokines historically associated with psoriasis improve atopic dermatitis?’

We know from a number of molecular studies that there is overlap between psoriasis and atopic dermatitis in terms of some of the molecular drivers; some of the transcriptomic analyses show the overlap between these diseases. Therefore, it actually makes a lot of sense that inhibiting some of the cytokines that go both ways and that can be involved in psoriasis and can be involved in atopic dermatitis, hitting the breadth of those cytokines, it sort of makes sense.

We really didn't have that masterful proof, in my opinion, until we saw galvokimig, the ability of a biologic to achieve that. We saw in this phase 1 study…this was IV galvokimig, not the final product that's ultimately going to end up in atopic dermatitis patients, but this phase 1 study was IV galvokimig. What it did show was that at Week 12, about 47% of patients achieved EASI 90, which is an incredibly high and fast response for that level of response. That really signaled to me that there's now a connection between the underlying scientific data saying that the atopic dermatitis and psoriasis patients can overlap in some of their molecular drivers.

We know this also from the fact that there are a number of atopic dermatitis patients who kind of have this immune phenotype, switching between atopic dermatitis and psoriasis. We know this happens, and certainly, there are also other examples, such as the flare of the head and neck atopic dermatitis, which may be largely IL-22 driven. We see these things in the clinic every day: the psoriasiform type shift in our atopic dermatitis patients, the head and neck atopic dermatitis. The reality is that galvokimig showed that this can, in fact, really push the levels of what a biologic can achieve.

In addition to galvokimig, we also have tilrekimig. This is a tri-specific antibody that targets the cytokines IL-4, IL-13, and TSLP. Some data was just released around the AAD 2026, which showed that this drug, in its phase 2 studies, actually met its endpoint in achieving EASI 75 response. It is now moving onto phase 3. One of the drugs where we saw an effect that we didn't want to see was one of the tri-specifics being developed by Johnson & Johnson, which showed that it didn't hit the efficacy bar that they were looking for in order to advance the program. One of the tri-specific agents in development has already been discontinued. This was targeting IL-4 receptor alpha and IL-31.

While we've had a couple of very positive responses from galvokimig and tilrekimig in some of the early phase 1 and phase 2 data, galvokimig and tilrekimig represent two really good phase 1 and phase 2 responses that give us clues that this multi-target approach is going to work from a biologic perspective and for atopic dermatitis. We also have another bi-specific antibody developed by J&J targeting the IL-4 receptor alpha and IL-31 cytokines that did not hit the efficacy bar that the company was looking for, and they have discontinued further development of that program.

This goes to show that in developing the bi- and tri-specific antibodies for atopic dermatitis, it is not as simple as just mixing and matching. There's a lot of science that goes into trying to develop a bi- or tri-specific that is much more complicated than developing a mono-targeted biologic. Then again, how you target these agents, the sizes of the molecules, the tissue penetration of these molecules, all matter, and they can all differ. I do think that these complexities in both pharmacodynamics and pharmacokinetics of these drugs are very important to pay attention to, and it's not a given just because we see a good itch response from nemolizumab versus dupilumab or any of the other biologics. The reality is, just mixing and matching isn't necessarily guaranteed to work.

We've seen some successes. We've already seen a failure, and it's going to be really interesting to see over the coming months to years, how this entire landscape plays out. I do believe very strongly, regardless of whether a drug succeeds to the very end and gets clinical approval, or whether that drug ultimately doesn't meet that new efficacy threshold and doesn't make it into FDA approval and into the patients and into the clinics. The reality is that we are going to learn a lot about the disease itself. We're going to learn so much about the pathophysiology of atopic dermatitis, how to manipulate different cytokine and receptor pathways underlying atopic dermatitis, as well as other th two driven diseases. I think that that is also one of the major benefits of the program that we're seeing in the multi-targeted biologics, [which is] how we're going to learn about other diseases. This is because the reality is, these multi-targeted biologics aren't going to stay combined to atopic dermatitis. They're going to be expanded into other diseases, particularly they're already being explored in hidradenitis suppurativa.

Looking ahead, how do you envision these multi-specific biologics fitting into the current treatment landscape, especially compared with Janus-kinase (JAK) inhibitors and existing biologic options?

Well, right now, when we think about the drugs for atopic dermatitis that have the best chance of hitting an optimal target or a minimal disease activity state for our patients, the reality is the JAK inhibitors, upadacitinib and abrocitinib, and all the network meta-analyses and head-to-head clinical trials that have occurred, that the JAK inhibitors have set the response bar in terms of EASI 90 and EASI 100 in terms of composite EASI 90, and Itch 01. In reality, the JAK inhibitors have raised that ceiling because of their ability to target multiple cytokines driving the atopic dermatitis. That is what they do. They can hit IL-4, IL-13, and IL-31. They can also hit IL-22, TSLP, and interferon gamma. All of that is what underlies the success that we've seen with JAK inhibitors in not only raising how well they treat the skin disease of atopic dermatitis, but how they reduce very quickly the itch burden that our patients feel. That is really what the multi-targeted biologics are trying to accomplish.

They're trying to match or exceed what the JAK inhibitors have been able to do, and that is having greater skin control, greater itch relief, and all the patient-reported outcomes. Can we ultimately improve these patients to the point where the quality of life, from a biologic standpoint, really continues to improve and grow? That is why half-life extension is so important. Because part of that narrative in terms of patient convenience and patient comfort, comes from the fact that if you're going to have to take an injection, it is difficult]. A lot of patients, when they have to take an injection, the injection fatigue can be real. The reality is, if you're taking it every 3 months or every 6 months, it's a lot different than needing to take an injection every 2 weeks.

For any additional information, view Bunick’s interview segment posted above.

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

Amid-Toby G, Alani O, Bunick CG. Bispecific and trispecific antibodies in atopic dermatitis: a review of the emerging clinical pipeline. Front. Drug Discov. 6:1766021. 

Bunick C. Bispecific and Trispecific Antibodies in Atopic Dermatitis, With Christopher Bunick, MD, PhD. HCPLive. April 24, 2026. Accessed April 28, 2026. 

https://www.hcplive.com/view/bispecific-trispecific-antibodies-atopic-dermatitis-christopher-bunick-md-phd

Articles

Multi-specific antibodies are being advanced to overcome suboptimal depth and durability seen with many monospecific biologics in atopic dermatitis, aiming to co-modulate inflammatory and pruritic circuitry. Early clinical signals suggest that broadened cytokine coverage can drive rapid, high-level responses, while setbacks underscore that target pairing and molecular engineering are nontrivial. JAK inhibitors currently define the efficacy ceiling through pleiotropic pathway inhibition and rapid itch reduction, setting a benchmark these biologics must meet or exceed. Longer half-lives and less frequent dosing may improve adherence and patient experience.

Atopic Dermatitis

Atopic Dermatitis condition center page, audiences can find a variety of coverage mediums for medical news and updates, including articles, video interviews, podcasts, and breaking news on dermatitis research, treatment, and drug development.

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The HCPLive dermatology page is a resource for medical news and expert insights on skin disease. This page features expert-led coverage, articles, videos and research on the therapies and development of treatments for dermatologic conditions, and more.

Positive Signals for Bispecific and Trispecific Antibodies in Atopic Dermatitis, With Christopher Bunick, MD, PhD

Tatyana Kushner, MD, is an associate professor of medicine in the division of gastroenterology and hepatology at Weill Cornell Medicine.

Brelovitug AZURE-1 Trial Results in Hepatits D Explained, With Tatyana Kushner, MD

Chronic hepatitis D virus (HDV) infection remains one of the most severe and underrecognized forms of viral hepatitis, often accelerating progression to cirrhosis, liver failure, and hepatocellular carcinoma. Despite its clinical impact, HDV continues to be overlooked in routine practice. For patients already living with hepatitis B virus (HBV), coinfection with HDV can dramatically worsen outcomes, yet gaps in awareness, diagnosis, and treatment persist across the care continuum.

, Tatyana Kushner, MD, discussed these challenges alongside new data from the phase 2b portion of the AZURE-1 study evaluating brelovitug, an investigational therapy for chronic HDV infection. While HDV is estimated to affect approximately 2–5% of individuals with HBV globally, she noted prevalence can be significantly higher in certain regions, highlighting important geographic variability.

Brelovitug is an investigational monoclonal antibody targeting HBsAg, designed to neutralize both HBV and HDV

Phase 2b AZURE-1 met its primary endpoint at Week 24, combining virologic response (HDV RNA reduction) and ALT normalization

Virologic response reached 100% with weekly dosing and 75% with monthly dosing, with 0% in the delayed-treatment arm

Treatment was generally well tolerated, with no reported discontinuations and low rates of serious adverse events

Still, even in high-resource settings, screening rates remain strikingly low, with Kushner pointing to data from New York City showing that < 10% of patients with HBV had ever been tested for HDV, underscoring substantial gaps in case identification.

Several factors contribute to these shortcomings. Differences in clinical guideline recommendations ranging from universal screening endorsements by organizations such as the European Association for the Study of the Liver and the World Health Organization to risk-based strategies from the American Association for the Study of Liver Diseases have created variability in clinical practice. Limited provider awareness further complicates diagnosis, sometimes resulting in missed or incorrect testing. As a result, many patients are only identified once they have progressed to advanced liver disease, making management more difficult.

Treatment limitations have historically compounded these challenges, with no therapies currently approved by the US Food and Drug Administration specifically for HDV.

“In the US, there's currently no FDA approved treatment for delta hepatitis, so providers may think ‘Why would we test for this condition if we don't have any currently FDA approved treatments?’,” Kushner said.

The only recommended option, pegylated interferon, has modest efficacy and is frequently associated with significant tolerability issues, leading many patients to decline or discontinue therapy.

Against this backdrop, emerging data for brelovitug signal a potential shift in the HDV treatment landscape. According to results from the phase 2b AZURE-1 study, the therapy met its primary endpoint, demonstrating meaningful antiviral activity in patients with chronic HDV infection. 

Specifically, results showed 100% of patients in the 300 mg once weekly arm and 75% of patients in the 900 mg once every 4 weeks arm achieved virologic response (≥2 log10 reduction in HDV RNA from baseline or undetectable HDV RNA [<LLOQ, TND]), as compared to 0% in the delayed treatment arm. Additionally, the primary composite endpoint of virologic response and alanine aminotransferase (ALT) normalization was achieved in 45% and 35% of patients in the 300 mg QW and 900 mg Q4W arms, respectively, as compared to 0% of patients in the delayed treatment arm.

Kushner emphasized that these findings are particularly encouraging given the unmet need for effective and tolerable options.

Beyond efficacy, early data suggest brelovitug may offer advantages in tolerability compared with interferon-based approaches, which have long been limited by systemic side effects. Additionally, its dosing profile, potentially allowing for weekly or even monthly administration, could represent a meaningful improvement in convenience and adherence compared with more burdensome regimens.

While additional data and regulatory review are still needed, the AZURE-1 findings highlight growing momentum in HDV research. As awareness and screening efforts evolve in parallel with therapeutic innovation, clinicians may be better equipped to identify and manage this historically underrecognized disease.

Editors’ Note: Kushner reports relevant disclosures with Gilead, Abbvie, GSK, Ipsen, Mirum, and Madrigal.

US Centers for Disease Control and Prevention. Hepatitis D Basics. April 24, 2024. Accessed April 28, 2026. 

https://www.cdc.gov/hepatitis-d/about/index.html

Ghany MG, Pan CQ, Lok AS, et al. AASLD ISDA Practice Guideline on treatment of chronic hepatitis B. 

. Published online November 4, 2025. doi:10.1097/HEP.0000000000001549

Mirum Pharmaceuticals. Mirum Pharmaceuticals Announces Primary Endpoint Met in Phase 2b Portion of the AZURE-1 Study of Brelovitug in Chronic Hepatitis Delta Virus. April 27, 2026. Accessed April 28, 2026. 

https://ir.mirumpharma.com/news/news-details/2026/Mirum-Pharmaceuticals-Announces-Primary-Endpoint-Met-in-Phase-2b-Portion-of-the-AZURE-1-Study-of-Brelovitug-in-Chronic-Hepatitis-Delta-Virus/default.aspx

Videos

Brelovitug met the primary endpoint for virologic response and ALT normalization in the phase 2b portion of the AZURE-1 trial.

Hepatology

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Hepatitis C page, resources on the topics of medical news and expert insight into HCV can be found. Content includes articles, interviews, videos, podcasts, and breaking news on hepatitis C virus research, treatment, and drug development.

New Phase 2b AZURE-1 Data Signal Progress in Chronic Hepatitis D Treatment, With Tatyana Kushner, MD

Martina J. Porter, MD, is a dermatologist at Beth Israel Deaconess Medical Center.

Contextualizing JAK Safety With Povorcitinib in HS, With Martina Porter, MD

The 54-week STOP-HS data for povorcitinib showed deepening inflammatory response, broad and sustained improvements across patient-reported outcomes in people with moderate-to-severe 

Povorcitinib is an investigational oral JAK1-selective inhibitor - the JAK inhibitor class carries FDA black box warnings for major adverse cardiovascular events (MACE) and thromboembolic events, and these labels that loom over any new agent in the class.

Martina L. Porter, MD, of Harvard Medical School and Beth Israel Deaconess Medical Center in Boston, presented the 54-week STOP-HS data at the 2026 American Academy of Dermatology (AAD) Annual Meeting, and sat down with 

to discuss povorcitnib’s safety and efficacy data in the context of JAK safety signals.

The STOP-HS1 (NCT05620823) and STOP-HS2 (NCT05620836) phase 3 trials enrolled a combined 1,227 adults with moderate-to-severe HS, randomized 1:1:1 to povorcitinib 75 mg once daily, 45 mg once daily, or placebo for 12 weeks, followed by a 42-week blinded extension through week 54. The HS population enrolled in these trials shares several features with patients historically associated with elevated cardiovascular and thromboembolic risk in other JAK inhibitor programs: high rates of obesity, significant smoking history, and elevated systemic inflammatory burden. These are the same comorbidity factors implicated in the cardiovascular safety signals that emerged from JAK inhibitor trials in older rheumatoid arthritis populations and contributed to the class-wide black box labeling. Porter acknowledged this concern directly, noting it was among the most frequent questions she fielded at the meeting.

The STOP-HS safety data through 54 weeks did not reveal a pattern consistent with amplified risk in this higher-comorbidity population. Across both studies, thromboembolic events were infrequent, and MACE occurred in 1 patient (0.3%) in STOP-HS2. Porter noted that this MACE event — an ischemic cerebrovascular event — was also counted within the thromboembolic event category per the study's classification scheme, meaning that the total cardiovascular and thromboembolic event count is partially overlapping rather than additive. Serious treatment-emergent adverse events (AEs) occurred in 3.7% to 6.4% of patients across arms, and laboratory abnormalities were relatively uncommon — a finding Porter suggested may reflect the relative JAK1 selectivity of povorcitinib compared with less selective agents in the class, since hematologic abnormalities in particular tend to be mediated through JAK2 rather than JAK1 signaling.

She also noted that the absence of a dose-dependent safety signal across the 45 mg and 75 mg arms was specifically reassuring. JAK inhibitor AEs typically track with degree of JAK pathway inhibition, and a flat safety profile across doses is consistent with a compound that achieves meaningful JAK1 engagement without proportional off-target JAK2 or JAK3 effects. The most common treatment-emergent AE was acne, occurring in 16.4% to 21.1% of patients — a rate Porter contextualized as likely reflecting 2 overlapping factors: the known acne association with JAK inhibitor use as a class, and the demographic profile of the STOP-HS population, which skews toward younger women who may be on oral contraceptives as a trial requirement, some formulations of which have known acne-promoting effects independent of JAK inhibition. The acne observed was predominantly mild in severity and did not drive meaningful discontinuation.

At the primary efficacy endpoint of HiSCR50 at week 12, both doses achieved statistical significance versus placebo in both studies — 40.2% (45 mg) and 40.6% (75 mg) versus 29.7% for placebo in STOP-HS1 (

 <.025), and 42.3% for both doses versus 28.6% for placebo in STOP-HS2 (

 <.01) — with responses deepening through week 54 to HiSCR50 rates of 60.2% to 67.5% across studies and doses on continuous povorcitinib. Up to 29.0% of patients achieved HiSCR100 at week 54. Porter's overall assessment of the safety profile was that it is consistent with the established JAK class picture but without the amplification in cardiovascular or thromboembolic events that the comorbidity burden of the HS population might have been expected to produce — a finding she characterized as meaningful precisely because it was not the obvious outcome given the patient profile.

“[I thought the safety data] looked quite good for a HS clinical population. And I say this because HS clinical trials and Hs patients tend to have a lot more adverse events that occur. And we see this even in the beginning of the trial, when it's placebo controlled, that the patients on placebo have very high rates of adverse events, and it's probably related to their comorbidity burden,” Porter said.

Relevant disclosures for Porter include Abbvie, Bristol Myers Squibb, Janssen, Eli Lilly, Novartis, Pfizer, UCB, Trifecta Clinical, Incyte, and Anaptys Bio.

Porter ML, et al. Povorcitinib in moderate-to-severe hidradenitis suppurativa: 54-week results from the phase 3 STOP-HS1 and STOP-HS2 trials. Presented at: AAD Annual Meeting; Denver, Colorado; March 27-31, 2026.

Porter ML, et al. Povorcitinib efficacy in biologic-experienced patients with moderate-to-severe hidradenitis suppurativa: subgroup analysis from STOP-HS1 and STOP-HS2. Presented at: AAD Annual Meeting; Denver, Colorado; March 27-31, 2026.

54-week STOP-HS safety data for the JAK1-selective inhibitor povorcitinib showed no dose-dependent safety signal and few laboratory abnormalities.

Hidradenitis Suppurativa

Hidradenitis Suppurativa condition center page, audiences can find a variety of coverage mediums for medical news and updates, including articles, video interviews, podcasts, and breaking news on dermatology research, treatment, and drug development.

This episode focuses on how GHD presents clinically in pediatric patients across different age groups and the quality-of-life implications of missed or delayed treatment. Dr. Alter explains that in newborns and infants, GHD often manifests as hypoglycemia — since both growth hormone and cortisol maintain blood glucose — and, in male infants, microphallus. Beyond the first few years, GHD typically presents later, most commonly between ages 10 and 13, and the severity of presentation tends to correlate with age of onset. Younger patients are more likely to have organic or structural causes. The panel discusses the challenge of distinguishing true GHD from physiologic pre-pubertal growth deceleration. Dr. Yang notes that in the U.S., there is a tendency to treat borderline cases, whereas European colleagues may take a watch-and-wait approach. Data suggests that roughly half of these pre-pubertal patients may self-correct once puberty begins and retest as normal. When GHD is genuine and left untreated, consequences extend beyond height. Dr. Alter describes improvements in muscle mass, fat distribution, bone health, and cardiovascular markers following GH therapy. Patients — especially those with severe GHD — typically show excitement and marked improvement with treatment. The panel also tackles the nuanced case of a short child with a normal height velocity but a much taller mid-parental target height. Dr. Alter notes that growth genetics are complex (over 180 genes involved) and a comprehensive workup including extended family history is warranted. Treatment decisions must also factor in family preferences, as some families decline GH therapy even when medically indicated. The episode closes with discussion of broader GH indications beyond GHD, including idiopathic short stature (ISS) and other genetic syndromes qualifying for GH therapy. In the next episode, “Diagnosing Growth Hormone Deficiency in Children — Testing, Tools, and Decision-Making,” the panel outlines the step-by-step diagnostic approach to suspected pediatric GHD, including the role of IGF-1, stimulation testing, and imaging.

Recognizing Growth Hormone Deficiency — Symptoms, Presentation, and Quality of Life

This episode focuses on how GHD presents clinically in pediatric patients across different age groups and the quality-of-life implications of missed or delayed treatment.

Dr. Alter explains that in newborns and infants, GHD often manifests as hypoglycemia — since both growth hormone and cortisol maintain blood glucose — and, in male infants, microphallus. Beyond the first few years, GHD typically presents later, most commonly between ages 10 and 13, and the severity of presentation tends to correlate with age of onset. Younger patients are more likely to have organic or structural causes.

The panel discusses the challenge of distinguishing true GHD from physiologic pre-pubertal growth deceleration. Dr. Yang notes that in the U.S., there is a tendency to treat borderline cases, whereas European colleagues may take a watch-and-wait approach. Data suggests that roughly half of these pre-pubertal patients may self-correct once puberty begins and retest as normal.

When GHD is genuine and left untreated, consequences extend beyond height. Dr. Alter describes improvements in muscle mass, fat distribution, bone health, and cardiovascular markers following GH therapy. Patients — especially those with severe GHD — typically show excitement and marked improvement with treatment.

The panel also tackles the nuanced case of a short child with a normal height velocity but a much taller mid-parental target height. Dr. Alter notes that growth genetics are complex (over 180 genes involved) and a comprehensive workup including extended family history is warranted. Treatment decisions must also factor in family preferences, as some families decline GH therapy even when medically indicated.

The episode closes with discussion of broader GH indications beyond GHD, including idiopathic short stature (ISS) and other genetic syndromes qualifying for GH therapy.

Diagnosing Growth Hormone Deficiency in Children — Testing, Tools, and Decision-Making

,” the panel outlines the step-by-step diagnostic approach to suspected pediatric GHD, including the role of IGF-1, stimulation testing, and imaging.

Endocrinology experts compare pediatric and adult growth hormone deficiency—causes, testing, MRI use, and transition care tips to improve outcomes.

Welcome back to another HCP Live Peer Exchange series. In this episode titled “Unraveling Growth Hormone Deficiency — Etiology and Prevalence,” moderator Dr. Joshua Yang discusses growth hormone deficiency with Dr. Craig Alter, Dr. Jose Garcia, and Dr. Nidhi Agrawal. In this opening episode, the panel introduces the HCP Live Peer Exchange series focused on Managing Growth Hormone Deficiency Across the Continuum of Care. Dr. Joshua Yang sets the stage by outlining the program’s scope, which encompasses diagnosis, treatment decision-making, transition of care, and real-world clinical challenges across both pediatric and adult populations. Dr. Yang begins by discussing the prevalence of GHD in children. Worldwide, GHD affects approximately 1 in 4,000 to 1 in 10,000 children, though in the U.S. the rate is closer to 1 in 3,000 — likely because American clinicians tend to treat milder and moderate cases, and use a higher GH peak cutoff of 10 ng/mL versus the European standard of 7 ng/mL. Dr. Garcia adds that adult GHD is estimated at 1 in 50,000 to 1 in 100,000 individuals, though emerging data suggests higher prevalence — with up to 10–15% of patients with prior head trauma also harboring GHD. The panel then explores etiologies. In children, causes are often congenital (midline defects, pituitary genetic mutations) or idiopathic. Dr. Alter stresses that the primary clinical priority is always accurate diagnosis before treatment — illustrated by a case of a craniopharyngioma initially presenting only as delayed puberty. For adults, structural causes dominate: pituitary adenomas, craniopharyngiomas, radiation, surgery, stroke, or trauma. The episode closes with a discussion of idiopathic pediatric GHD patients — often mild or moderate cases — and the question of whether they carry GHD into adulthood. The consensus is that retesting is essential, and that IGF-1 alone is not reliable enough to confirm or exclude adult GHD. In the next episode, “Recognizing Growth Hormone Deficiency — Symptoms, Presentation, and Quality of Life,” the panel explores how GHD presents at different ages in children and the long-term consequences of undiagnosed or undertreated GHD.

Unraveling Growth Hormone Deficiency — Etiology and Prevalence

Welcome back to another HCP Live Peer Exchange series. In this episode titled “Unraveling Growth Hormone Deficiency — Etiology and Prevalence,” moderator Dr. Joshua Yang discusses growth hormone deficiency with Dr. Craig Alter, Dr. Jose Garcia, and Dr. Nidhi Agrawal.

In this opening episode, the panel introduces the HCP Live Peer Exchange series focused on Managing Growth Hormone Deficiency Across the Continuum of Care. Dr. Joshua Yang sets the stage by outlining the program’s scope, which encompasses diagnosis, treatment decision-making, transition of care, and real-world clinical challenges across both pediatric and adult populations.

Dr. Yang begins by discussing the prevalence of GHD in children. Worldwide, GHD affects approximately 1 in 4,000 to 1 in 10,000 children, though in the U.S. the rate is closer to 1 in 3,000 — likely because American clinicians tend to treat milder and moderate cases, and use a higher GH peak cutoff of 10 ng/mL versus the European standard of 7 ng/mL.

Dr. Garcia adds that adult GHD is estimated at 1 in 50,000 to 1 in 100,000 individuals, though emerging data suggests higher prevalence — with up to 10–15% of patients with prior head trauma also harboring GHD.

The panel then explores etiologies. In children, causes are often congenital (midline defects, pituitary genetic mutations) or idiopathic. Dr. Alter stresses that the primary clinical priority is always accurate diagnosis before treatment — illustrated by a case of a craniopharyngioma initially presenting only as delayed puberty. For adults, structural causes dominate: pituitary adenomas, craniopharyngiomas, radiation, surgery, stroke, or trauma.

The episode closes with a discussion of idiopathic pediatric GHD patients — often mild or moderate cases — and the question of whether they carry GHD into adulthood. The consensus is that retesting is essential, and that IGF-1 alone is not reliable enough to confirm or exclude adult GHD.

,” the panel explores how GHD presents at different ages in children and the long-term consequences of undiagnosed or undertreated GHD.

Experts compare pediatric vs adult growth hormone deficiency—causes, testing, MRI use, and why retesting matters during transition to adult care.

Baba Inusa, MBBS, is a Consultant Paediatrician in the School of Life Course & Population Sciences at King's College London.

Study investigator Inusa explains the gap in sickle cell disease findings from SWAP, a multinational survey. 

Hematology

Sickle Cell

Sickle Cell condition center page, resources on the topics of medical news and expert insight into sickle cell disease can be found. Content includes articles, interviews, videos, podcasts, and breaking news on sickle cell research, treatment, and drug development.

Increased Sickle Cell Pain Burden in Sub-Saharan Africa Despite Younger Patients

Diana Isaacs, PharmD, is an endocrine clinical pharmacist, director of Education and Training in Diabetes Technology, and codirector of Endocrine Disorders in Pregnancy at the Cleveland Clinic.

Isaacs covers the range of AID devices currently available and approved for T2D, providing suggestions for implementation and continuous glycated hemoglobin monitoring.

Endocrinology

The HCPLive endocrinology page is a comprehensive resource for clinical news and insights on endocrine system conditions. This page consists of interviews, articles, podcasts, and videos on the research, treatment and development of therapies for diabetes, hormonal disease, and more.

Type 2 Diabetes

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Strategic Alliance Partnership

Implementing Automated Insulin Delivery in Type 2 Diabetes, With Diana Isaacs, PharmD

In this Q&A interview, Bhatia discusses the FDA's recent acceptance of BLA for imsidolimab for generalized pustular psoriasis (GPP).

Plaque Psoriasis

The HCPLive plaque psoriasis page is a resource for medical news and expert insights on psoriasis. This page features expert-led coverage, articles, videos and research on the therapies and development of treatments for psoriatic disease, and more.

Q&A: Discussing Imsidolimab for Generalized Pustular Psoriasis, With Neal Bhatia, MD

Andrea Cipriani, MD, PhD, from the University of Oxford.

Study showed the PETRUSHKA decision-support tool reduced antidepressant discontinuation, supporting personalized treatment approaches.

Psychiatry

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PETRUSHKA Tool Improves Antidepressant Persistence in MDD, With Andrea Cipriani, MD, PhD

Victoria Johnson joined MJH Life Sciences in 2020 and has written for NeurologyLive, CGTLive, and is now an assistant managing editor for HCPLive and RheumatologyLive. She doesn’t have enough time for her numerous hobbies. You can reach her at vjohnson@mjhlifesciences.com.

The FDA has approved budesonide/glycopyrrolate/formoterol fumarate as the first single-inhaler triple therapy for asthma.

FDA News

Asthma

The HCPLive asthma page is a comprehensive resource for clinical news and insights on asthmatic disease. This page consists of interviews, articles, podcasts, and videos on the research, treatment and development of therapies for allergic and severe asthma, and more.

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Infectious Disease condition center page is a comprehensive resource for clinical news and insights on respiratory health. This page consists of interviews, articles, podcasts, and videos on the research, treatment and development of therapies for asthma, COPD, interstitial lung disease, COVID-19, and more.

FDA Approves BGF Triple Therapy for Asthma in Patients 12 and Older

Tim Smith joined the MJH Life Sciences team in 2022 and is currently an associate editor for HCPLive. He is also the executive producer of two podcasts: Skin of Color Savvy and The Medical Sisterhood. Previously, he was the producer of the Lungcast podcast. He graduated from UC Berkeley and worked in multimedia journalism as a staff writer prior to joining MJH. You can contact him at tsmith@mjhlifesciences.com.

AbbVie submitted an sNDA to the FDA seeking approval of upadacitinib for severe alopecia areata in adults and adolescents.

Alopecia

Upadacitinib sNDA Submitted to FDA for Severe Alopecia Areata

Yao Wei Lu, PhD, assistant professor of medicine and member of the Hastings Center for Pulmonary Research at the Keck School of Medicine of USC

yao wei lu.jpeg

Lu explains findings that link PCBP1 to the pathogenesis of AARS2-related cardiomyopathy. 

Cardiology

Cardiology condition center page is a comprehensive resource for clinical news and insights on cardiovascular and cardiometabolic diseases. This page consists of interviews, articles, podcasts, and videos on the research, treatment and development of therapies for heart disease and cardiovascular events, as well as associated diabetes, renal failure, and more...

New Target Emerges for AARS2-Related Cardiomyopathy With Early-Life Mortality

Ryan Livingston joined the MJH Life Sciences team in March of 2025, shortly after graduating from TCNJ with a bachelor’s degree in English. He enjoys creative writing, reading, and scuba diving. He can be reached at rlivingston@mjhlifesciences.com.

The FDA granted Fast Track Designation to coramitug, an investigational anti-TTR antibody designed to clear existing amyloid deposits in ATTR cardiomyopathy.

Cardiomyopathy

FDA Grants Fast Track to Coramitug for ATTR-CM, Supporting Amyloid-Clearing Phase 3 Trial

Abigail Brooks is an assistant managing editor for 

She joined MJH Life Sciences in August 2023 shortly after graduating from Monmouth University where she earned her BA in Communication with a concentration in Public Relations/Journalism and later an MA in Interactive Digital Media. She enjoys traveling, running, and reading books. She can be reached at abrooks@mjhlifesciences.com.

The FDA has accepted bepirovirsen's NDA for Priority Review and granted Breakthrough Therapy designation, with a PDUFA date of October 26, 2026.

FDA Grants Bepirovirsen Breakthrough Therapy Designation, Priority Review for Chronic Hepatitis B

The phase 3 trials enrolled frequent exacerbators regardless of eosinophil count or smoking status.

COPD

COPD condition center page, resources on the topics of medical news and expert insight into chronic obstructive pulmonary disease can be found. Content includes articles, interviews, videos, podcasts, and breaking news on COPD research, treatment, and drug development.

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