Retina specialists discuss treatment and adherence strategies for patients with nAMD and DME. future

Promoting Treatment Adherence in nAMD and DME

 Through this discussion today, we haven’t talked about treatment adherence. This can be a significant challenge. We know from [results of] many studies [that] 50% of patients discontinue anti-VEGF therapy within the first 3 years. [Findings from] some studies have said within the first year, 30% to 40% of patients may discontinue therapy depending on the practice environment. And we know that adherence is an issue. First, I’d like to hear your strategy on keeping patients adherent to therapy. And with the change in this durability, do you think adherence would change as well and potentially improve?

[Diabetes] and neovascular AMD [age-related macular degeneration] are slightly different because the adherence for treatment with [patients with diabetes] has traditionally been worse, likely because these patients are more active, they’re working, it’s harder for them to take off work. But for both populations, AMD and DME [diabetic macular edema], having the patients understand what is happening and why they’re coming is big for me. Showing them their OCT [optical coherence tomography] [scans] and telling them, “These are what I’m looking at; these are the findings that I see improving” and explain[ing] to them why we’re changing things, whether in terms of the number of weeks or the drug, [so that] they’re being brought in and not being passive in the process has been the most successful for me.

And [to] the second part of your question about [whether] extended intervals improve adherence, in some ways, yes, [it’s] fewer visits, [it’s] easier for people to take off time and have it [be] more predictable. Once every 4 months [is something] people can plan for. Once every 6 weeks gets tough, depending on the type of job you’re in, and for caregivers, we need to bring [in] some of our older patients [with] neovascular AMD [nAMD]. So extended interval duration will help with adherence. On the flip side, I don’t want to go too long because sometimes if patients forget about “I have my eye doctor or my retina specialist appointment,” that can be a little bit of a drop-off. And when you’re at the end of an extended treatment interval, that’s when I’m worried that if they go maybe 2 or 3 weeks longer, I don’t want something terrible happening [such as] a hemorrhage. So finding a happy medium where they have an expected appointment once every 4 months, for example, [and] it might not go much longer than that, simply keep[s] them in the fold and keep[s] them in our scheduling processes.

 I agree. There are so many things we could do to improve adherence. We have to talk to them about missed appointments and getting back in right away, not wait until the next interval appointment, try to give them encouragement on the OCT [optical coherence tomography] [scans], [and] show them pictures…to say that they are getting better. I like to show them a graph of their OCT [scan]. They show them the central subfoveal thickness over time, which our software does very well, show them the benefits of their incredible adherence to therapy and what’s happening over time. Overall, we have to encourage this because we know there’s a huge dropout rate with these patients over time. Getting them to come back and keep their appointments in high fidelity is important for us to be able to do this in a good way. Let’s touch a little bit on future treatments. What excites you? What do you think is interesting? You know the space very well. Is there something that you look at and say, “That’s going to make our patients have a great durable option with [fewer] injections and potentially [fewer] complications”?

Much has been spoken about gene therapy options and how we deliver them surgically or in the office with suprachoroidal therapy. If we do have treatments that we can do in the office with every-4-months durability, that’s tough to beat. So the suprachoroidal delivery of gene therapy is interesting. That’s office based, which most people can get their head around, and doesn’t require going in the operating room, which has its own risks. If that can be delivered at scale with durability as good as our current drugs or perhaps longer, that has the potential to change my mind in terms of how I would approach treatment in these patients. So office-based [therapy] with extended durability is what could work at scale. And the suprachoroidal option is potentially promising. There are data being presented at our current meetings, and everyone will look forward to the full trial data for those delivery options. But gene therapy delivered in the office is another paradigm shift that can happen.

 I would agree with you. I would also add tyrosine kinases to the mix there. That’s been a burgeoning area of understanding of the new MOA [mechanisms of action] that tyrosine kinases can offer. And I agree with you on gene therapy; surgical delivery of this is probably impractical. And office-based delivery of gene therapy may be the best approach to suprachoroidal delivery platforms. Tyrosine kinases at least offer another ability, which is that they affect all isoforms of VEGF, not only VEGF-A but other isoforms of VEGF, including downstream effects of inhibiting ANG2. So it can have a synergistic effect alongside some of the other drugs that we’ve had in clinical practice so far.

 I agree. It’s going to be a busy few years with clinical trial results coming out but exciting nonetheless.

We have so much promise that’s happening and so many great opportunities in our field in the next few years. I want to thank you all for joining this 

Extending Treatment Intervals for Durable Therapies for Neovascular AMD and Diabetic Macular Edema

. Thank you again for watching, and thank you, Dr Khan, for participating.

Transcript is AI generated and edited for clarity and readability.

Retina specialists discuss treatment and adherence strategies for patients with nAMD and DME. They also comment on the future of nAMD and DME management.

Ali Khan, MD, FACS, FASRS

Bob Ross, PA-C is the co-owner of Triad Diagnostic Technologies.

The APAC Recap: Peripheral Artery Disease at CAPP Live 2024 with Bob Ross, PA-C  

, host Laura Ross, PA-C, president of the Academy of Physician Associates in Cardiology (APAC), is joined by Bob Ross, PA-C, chair of APAC’s vascular medicine committee and a leading expert in 

, to discuss updates on PAD from the inaugural CAPP Live 2024 conference.

The discussion centered on recent updates in PAD diagnosis and management, including key takeaways from Ross’ conference presentation, which highlighted symptoms and risk factors for PAD based on new guidelines from the American College of Cardiology and the American Heart Association. Emphasizing the importance of early detection, Ross offered actionable insights, such as testing those over 50 with diabetes or on statin therapy for PAD and conducting ankle-brachial index (ABI) tests on high-risk patients.

Ross also introduced a validated 9-question screening tool he has been utilizing for more than 25 years, to identify PAD risk factors and symptoms before they become clinically apparent. By implementing such tools, he noted providers can catch PAD earlier and initiate preventative care. Ross also shared practical tips on performing ABIs without advanced equipment and leveraging diagnostic codes for reimbursement, stressing that early intervention can prevent serious complications.

The conversation also explored disparities in PAD care, such as underutilization of statins and aspirin in vulnerable populations, and highlighted educational opportunities through the Society for Vascular Medicine’s annual conference. Ross and Ross concluded by celebrating the critical role PAs play in advancing vascular health and ensuring patients receive comprehensive, preventative care.

All episodes of The APAC Recap will be available on HCPLive.com and our 

For more PAD screening resources from APAC, view the below PAD questionnaire. For more on the Society for Vascular Medicine 2025 course, check out the below information. 

The discussion focused on recent advancements in peripheral arterial disease (PAD) diagnosis and management, emphasizing early detection and intervention. Key insights included testing high-risk individuals, such as those over 50 with diabetes or on statin therapy, and using ankle-brachial index (ABI) tests. A validated 9-question screening tool was introduced to identify PAD risk factors early. The conversation also addressed disparities in PAD care, particularly the underutilization of statins and aspirin in vulnerable populations, and highlighted educational opportunities for healthcare providers to improve vascular health outcomes.

Bob Ross, PA-C, shares expert insights on early PAD detection, updated guidelines, and practical tools to improve vascular health outcomes from CAPP 2024.






Bob Ross, PA-C

3:28 Topline findings for semaglutide in the SELECT trial

8:54 Perspectives on cost-benefit for GLP-1 in obesity

16:44 Considerations for using GLP-1 agonists

20:54 Need to address inequity in access to obesity medications

26:44 Investigational therapies for obesity with potential for CV benefits

30:00 Combination therapy for obesity and CV risk

Dhiren Patel, PharmD, and Bob Busch, MD, interview Fatima Cody Stanford, MD, MPH, MPA, an obesity medicine specialist, to examine the cardiovascular (CV) impact of obesity and delve into the potential benefits of newer weight loss medications in mitigating CV risk and heart failure.

Mitigating Cardiovascular Risk In Obesity

Fatima Cody Stanford, MD, MPH, MPA

James Chalmers, MBChB, PhD, is Asthma and Lung UK Chair of Respiratory Medicine at the School of Medicine, University of Dundee.

As brensocatib is currently under Priority Review with the 

, it could end up becoming the first treatment for patients with non-cystic fibrosis bronchiectasis and the first approved dipeptidyl peptidase 1 (DPP1) inhibitor—a new mechanism of action that could help clinicians to manage an array of neutrophil-mediated inflammatory conditions.

New findings from the ASPEN study suggest that brensocatib showed consistent efficacy as well as safety across 3 subgroups of patients.

 To address these data and their significance, James D. Chalmers, MBChB, PhD, professor of respiratory research at the University of Dundee, spoke with HCPLive at the 

American Thoracic Society (ATS) International Conference

Subgroup Findings on Brensocatib for Non-Cystic Fibrosis Bronchiectasis, with James D. Chalmers, MBChB, PhD

“ASPEN was a phase 3, double-blind, randomized placebo-controlled trial of brensocatib at 2 doses, 25 milligrams and 10 milligrams, against placebo,” Chalmers explained. “It was a global trial, and it's by far the largest trial ever conducted in patients with bronchiectasis. Patients were randomized 1:1:1 to either 25 milligrams brensocatib, 10 milligrams brensocatib, or placebo, and patients were followed up for 52 weeks. The primary outcome was the frequency of exacerbations. That's the most clinically relevant endpoint for people with bronchiectasis.”

Chalmers highlighted key secondary endpoints as well, which included time to first exacerbation, the proportion of patients that were shown to be free of exacerbations, lung function, and symptoms measured by a validated quality of life questionnaire.

In adolescents, both doses of brensocatib (10 mg and 25 mg) were shown by Chalmers and coauthors to have reduced exacerbation rates and helped preserve lung function compared to those in the placebo arm.

 The medication was also effective regardless of maintenance macrolide utilization, with lower exacerbation rates and less FEV₁ decline across the subgroups. Brensocatib also showed consistent benefits across blood eosinophil levels, with reductions observed in exacerbations, lung function preservation, and improved quality of life.

“You may know that bronchiectasis has been a neglected disease,” Chalmers said. “It's really a very recent phenomenon that people have started to try to do trials in this space, and very much a recent phenomenon that people are trying to target this particular type of pathology. So recognizing bronchiectasis as an inflammatory disease has been a key step forward, and therefore targeting this disease with anti-inflammatories, rather than repeatedly treating patients with antibiotics, is going to be a major step forward for how we treat these patients.”

“The safety data was also very reassuring, with very similar rates of adverse events between the brensocatib groups and the placebo groups,” Chalmers added.

He later touched on a variety of specific findings highlighted among the 3 subgroups, noting in particular several points related to 1 particular subgroup.

“Bronchiectasis is predominantly a neutrophil-driven inflammatory disease,” Chalmers explained. “There is also a type of inflammation called T2 inflammation, which is often associated with asthma. About 20% of patients with bronchiectasis have raised T2 biomarkers, like raised blood eosinophils. So there's a question: Will an anti-neutrophil approach work in people who have this other type of inflammation? What we've shown, which is consistent with some of our pre-clinical work, is that patients don't have neutrophilic or T2 inflammation separately; most people with bronchiectasis who have T2 inflammation also have neutrophilic inflammation.”

Consequently, Chalmers noted, the investigators demonstrated with these sub-analyses that patients respond to brensocatib the same regardless of the presence of raised blood eosinophils.

“That will be very useful clinically, because some guidelines, for example, from Australia and New Zealand, are recommending different treatment approaches for patients with high blood eosinophil counts in bronchiectasis,” Chalmers said. “And our data here suggests that for brensocatib, blood eosinophil shouldn't influence your decision to prescribe or not.”

For any additional information on this data, view the full interview segment posted above. To find out more about late-breaking data covered at ATS, view our 

The quotes used in this summary were edited for the purposes of clarity.

Johnson V. Brensocatib, Potential First Treatment for Non-CF Bronchiectasis, Gets Priority Review. HCPLive. Feburary 6, 2025. Accessed May 21, 2025. 

https://www.hcplive.com/view/brensocatib-potential-first-treatment-non-cf-bronchiectasis-priority-review

Brensocatib Shows Consistent Efficacy and Safety Across Three Prespecified Subgroups in New Data from Landmark ASPEN Study. Insmed Incorporated. May 21, 2025. 

https://www.prnewswire.com/news-releases/brensocatib-shows-consistent-efficacy-and-safety-across-three-prespecified-subgroups-in-new-data-from-landmark-aspen-study-302462008.html?tc=eml_cleartime

This interview highlights the subgroup analysis findings of the ASPEN trial, specifically on brensocatib for non-cystic fibrosis bronchiectasis.

James D. Chalmers, MBChB, PhD

Dual Agonists and Upstream Obesity Treatment with Kausik Ray, FMedSci

 in Philadelphia, PA, Kausik Ray, FMedSci, the immediate past president of the European Atherosclerosis Society, director of the Imperial Centre for Cardiovascular Disease Prevention and the Imperial Clinical Trials Unit-Global, and professor of public health and honorary consultant cardiologist at the Imperial College London, discussed the future of dual receptor agonists in treating 

Dual receptor agonists, such as glucagon-like peptide-1 (GLP-1) receptor agonists, have become wildly popular in both the medical and consumer field. With obesity prevalence rapidly increasing in the US, more dual agonist treatments are being developed to target every stage of the disease, from lipid production to glycemia and metabolism regulation. Dual receptor agonists are now being repurposed in an attempt to prevent the causes of obesity rather than the effects.

Ray discussed the various approaches currently in use to treat everything from abnormal lipid counts to obesity insulin resistance and metabolic syndrome. In the past, clinicians have typically employed a “downstream” method of treatment, targeting triglyceride abnormalities. Ray also acknowledged the diminishing returns that this method provides.

“So, we know, for example, that if you change triglycerides, you lower them by about 25%, and let’s say that doesn’t result in APOV or LDL lowering, then you’re not changing clearance, you’re just remodeling, and that doesn’t reduce cardiovascular outcomes,” Ray told 

. “So, people have moved towards using newer agents, like ANGPTL3.”

These dual receptor agonists, a category that also includes GLP-1 receptor agonists, typically target the APOV pool. As a result, they have an effect on VLDL particles and can influence many of the outcomes of obesity in addition to its symptoms.

“So, we showed, for example, that if you target ANGPTL3 with a drug called solbinsiran, for example, you reduce not only those anthrogenic lipids, but you actually also reduce fatty liver,” Ray said. “I’m mentioning that because we know that fatty liver, MASLD, is associated with obesity and insulin resistance.”

This, Ray suggests, is the alternative “upstream” treatment by which clinicians can take out the underlying cause of these diseases – insulin resistance – and thereby treat the mechanism for obesity and all its related conditions.

“So, what we think that these drugs probably do is improve insulin sensitivity, to reduce the LDL production,” Ray said. “And then also through maybe changing ANGPTL3 and some of these other regulatory proteins in the triglyceride pathway, they probably then help that remodeling to a favorable lipid profile.”

Ray also spoke about upcoming dual agonists in the pipeline and their chances of breaking the cycle between obesity and dyslipidemia. Ray explained that most give a roughly 20% weight loss.

“We saw this trend with the single agonist, but they have less weight loss,” Ray said. “And so, it’s possible that you need a much bigger weight loss to try and break that cycle. And then we have the triple agonist coming down the pipeline, which gives an even bigger opportunity to test this.”

Ultimately, Ray expressed an interest in future trials, possibly combining dual receptor agonists with other medications to expand the impact on lipids.

“I think what I’d be interested in is to see what the effect is of combination therapy with an ANGPTL3 and one of these dual agonists on fatty liver disease, on lipids, for example,” Ray said. “Is it a gain of a doubling, for example? Because if that is the case, we’ve got some really powerful treatments for these people.”

Ray K. Obesity and Dyslipidemia – Can We Finally Break the Cycle with Dual Agonists. Presented at the 9

 Annual Heart in Diabetes Conference in Philadelphia, PA, June 6-8 2025.

Rodriguez R, Hergarden A, Krishnan S, et al. Biased agonism of GLP-1R and GIPR enhances glucose lowering and weight loss, with dual GLP-1R/GIPR biased agonism yielding greater efficacy. Cell Rep Med. Published online May 30, 2025. doi:10.1016/j.xcrm.2025.102156

By targeting insulin resistance at its source, dual receptor agonists may have a more efficient method of tackling the growing obesity problem, as well as its cardiovascular effects.

Kausik Ray, FMedSci

Michael Walsh, MD, is an associate professor of Medicine at McMaster University.

62nd European Renal Association (ERA 2025) Congress

 indicate use of spironolactone, a mineralocorticoid receptor agonist, did not significantly reduce the risk of cardiovascular death or heart failure hospitalization in patients undergoing 

, despite earlier hypotheses that mineralocorticoid receptor blockade could provide cardioprotective benefits in this high-risk population.

Adding to data from previous trials, such as ALCHEMIST, results of the study suggest the primary composite outcome of cardiovascular death or hospitalization for heart failure occurred in 20.5% of patients in the spironolactone group versus 21.6% in the placebo group (HR, 0.92; 95% CI, 0.78 to 1.09; 

“So far, very few interventions appear to actually be effective, so there's a lot of hope around any intervention that will actually reduce cardiovascular mortality,” explained lead investigator Michael Walsh, MD, of McMaster University in an interview with HCPLive at ERA 2025. “Aldosterone has been pretty heavily implicated, with a high risk ratio for those who have elevated aldosterone and, in fact, aldosterone is elevated in most dialysis patients. So it seemed like it would be a widespread target to be able to try and treat and in previous small studies, there was a very large signal for risk reduction of cardiovascular mortality, like up to 60% reduction in cardiovascular mortality probably too good to be believed, which is why we felt like we needed to do a large, high quality study.”

The trial included 2532 patients randomized after an open-label run-in phase confirming tolerability of spironolactone 25 mg daily. Participants were assigned to receive either spironolactone or placebo, with a median follow-up designed to assess major cardiovascular outcomes.

Rates of secondary outcomes—including cardiac death, vascular death, all-cause mortality, and all-cause hospitalizations—were also similar between groups. However, severe hyperkalemia occurred more frequently in the spironolactone group (6.6%) compared with placebo (4.5%), representing a 44% increased risk (HR, 1.44; 95% CI, 1.03 to 2.01). Sensitivity analyses,  including per-protocol and expanded heart failure hospitalization definitions, produced similar findings.

To hear more on the trial’s outcomes, limitations, and the path forward in cardiovascular risk reduction for dialysis patients, watch our full interview with Walsh from the floor at ERA 2025.

ACHIEVE: Spironolactone Fails to Reduce Cardiovascular Risk in Dialysis Patients

Relevant disclosures for Walsh include Otsuka, GSK, Bayer, Novo Nordic, and Hansa Pharma.

Walsh M, Collister D, Gallagher M, et al. Spironolactone in patients undergoing maintenance dialysis: the ACHIEVE trial. Presented at: 62nd European Renal Association Congress. June 04 – 07, 2025. Vienna, Austria.

The ACHIEVE trial found use of spironolcatone was not associated with a statistically significant reduction in cardiovascular death or hospitalization for HF.

Michael Walsh, MD

Richard Lafayette, MD, is a professor of medicine and director of the Glomerular Disease Center at Stanford University Medical Center.

Counting down the biggest news from major medical meetings, it's the HCPLive Five!

HCPLive Five at European Renal Association (ERA) Congress 2025

European Renal Association (ERA) Congress

 is a medical conference bringing together world-renowned experts, researchers, and practitioners in nephrology. ERA Congress 2025 was hosted in Vienna, Austria, and saw more than 10,000 participants from  91 countries around the world, with a record 2835 abstract submissions. This year’s conference was centered around the theme “Game Changers in Nephrology” with the slogan “Beyond Nephrology,” boasting a comprehensive and innovative program exploring the latest advancements and transformative ideas in nephrology.

As part of HCPLive’s on-site coverage, the editorial team conducted expert interviews and reported on timely topics across therapeutic advances, pipeline updates, new renal clinical trial data, and more. In this edition of the HCPLive Five, the team highlights key conversations on pegcetacoplan in 

 and idiopathic immune-complex membranoproliferative glomerulonephritis (IC-MPGN), a trio of 

 drugs in clinical development, and the potential benefits of simultaneous initiation of finerenone (Kerendia) and empagliflozin (Jardiance) in patients with 

Pegcetacoplan Sustains Proteinuria Reductions in C3G, IC-MPGN at 52 Weeks

Extended data from the phase 3 VALIANT trial were presented at ERA 2025 and support the sustained efficacy and safety of pegcetacoplan (Empaveli) in patients with C3G or IC-MPGN, including adolescents and adults with native or transplanted kidneys. The 52-week results show continued proteinuria reduction and eGFR stabilization in both treatment-naïve and crossover groups, reinforcing 26-week data presented at the American Society of Nephrology’s 2024 Scientific Sessions.

In this on-site interview at the meeting, Fadi Fakhouri, MD, PhD, co-lead principal investigator for the VALIANT study and a professor of nephrology at CHUV Lausanne, Switzerland, describes pegcetacoplan’s long-term potential in C3G and IC-MPGN and how the data presented at ERA could shift treatment strategies.

Understanding Zigakibart's Potential in IgA Nephropathy, with Jonathan Barratt, MD, PhD

100-week data from the phase 1/2 ADU-CL-19 trial presented at ERA suggest zigakibart, an APRIL inhibitor under development by Novartis, offers durable reductions in proteinuria and maintains a favorable safety profile in patients with IgAN. In the study, patients experienced a mean 60% reduction in proteinuria from baseline, with 55% achieving proteinuria below 500 mg and 31% below 300 mg, as described by Jonathan Barratt, MD, PhD, the Mayer Professor of Renal Medicine at the University of Leicester, in this interview. Additionally, serum IgA and pathogenic Gd-IgA1 levels dropped by 74%, building on earlier 52-week data showing reductions in IgA, IgM, and IgG of 67%, 78%, and 35%, respectively.

Kidney Compass: CONFIDENCE Trial at ERA 2025, with Rajiv Agarwal, MD, MS

Simultaneous initiation of finerenone (Kerendia) and empagliflozin (Jardiance) in patients with CKD and type 2 diabetes was well-tolerated and resulted in significantly greater reductions in urinary albumin-to-creatinine ratio (UACR) than either agent alone, according to results from the CONFIDENCE trial. During ERA, Kidney Compass host Brendon Neuen, MBBS, PhD, a senior research fellow with the George Institute for Global Health and the director of the Kidney Trials Unit with Royal North Shore Hospital, held a discussion with trial investigators Rajiv Agarwal, MD, Professor Emeritus at Indiana University School of Medicine, about the study results and what they mean for CKD management landscape in real-world settings.

Phase 3 ORIGIN Sets Stage for Atacicept in IgA Nephropathy, with Richard Lafayette, MD

Just days before the ERA 2025, the nephrology community welcomed and celebrated new positive data for atacicept in IgAN in the form of topline results from the phase 3 ORIGIN trial. Announced by Vera Therapeutics on June 02, 2025, the data indicate the trial met its primary endpoint of reduction in proteinuria at week 36, with the atacicept group achieving a 46% reduction from baseline and a statistically significant 42% reduction compared to placebo at week 36.

’s coverage of ERA, we sat down with Lafayette to discuss how this latest data adds to our understanding of atacicept and its potential role in the management of IgAN if it were to receive FDA approval.

Kidney Compass: Sibeprenlimab and the VISIONARY Trial, with Vlado Perkovic, MBBS, PhD, at ERA 2025

, hosts Brendon Neuen, MBBS, PHD, and Shikha Wadhwani, MD, MS, are joined by Vlado Perkovic, MBBS, PhD, dean and scientia professor of Medicine at UNSW Sydney, as he dives into one of the meeting’s most anticipated releases—

. Less than 2 weeks prior to the presentation, Otsuka Pharmaceutical Co. announced the US Food and Drug Administration had granted priority review for their BLA and the application has been given a target action date of November 28, 2025.

These 5 represent only some of the data the 

 team covered at this year's meeting! Check out more KOL insight and our full conference coverage on our 

From new data for potential IgAN treatments to the use of combination initiation therapy for type 2 diabetes and CKD, here are 5 key updates from the annual meeting.

Richard Lafayette, MD

A panel of ophthalmologists discuss strategies for improving patient outcomes in retinal vein occlusion with anti-VEGF and other therapies.

Optimizing Treatment Outcomes in Retinal Vein Occlusion

Optimizing Treatment Outcomes in Retinal Vein Occlusion (RVO)

Sruthi Arepalli, MD

2025 American Academy of Allergy, Asthma, & Immunology (AAAAI) 

annual meeting in San Diego from February 28 – March 3, 

 spoke with Timothy Craig, DO, about his session, “Exploring Hereditary Angioedema: Diagnosis, Prophylaxis and Treatment Strategies.”

During the interview, he shared mechanisms behind 

, early recognition of HAE, treatment options, and the importance of cross-specialty care.

Hereditary Angioedema Diagnosis Challenges, with Timothy Craig, DO

 What are the key genetic and inflammatory mechanisms behind HAE, and how do these contribute to the clinical manifestations of the disease?

That’s a really interesting disease, hereditary angioedema. It is genetic. It is a dominant disease, meaning you only have 1 abnormal gene.

If you have that abnormality, you don't make enough C1 inhibitor protein. Without c1 inhibitor protein, there's an activation of factor 12, and then factor 12 activates [kallikrein]. [Kallikrein] causes high molecular weight to fragment [into]… bradykinin [which] binds to the receptor [and] generates cyclic GMP, prostacyclin, and nitric oxide. If you look at the cells [in] the endothelial [lining] in the vessels, you can see the tight junctions between those cells dissolve, and there's little microfilaments of myosin that develop inside the cell, pulling that cell inward, almost like a muscle [does] on your body.

You can see why, then, the fluid would shift from the intravascular space into the interstitial space because of that lack of the tight junction and the cells we treat from each other. It’s a really interesting disease because it's all generated by bradykinin.

The problem, too, is that it takes a long time for that fluid to build up and then also to resolve. Some of these people have 3 days, even 5 days, of swelling. If it's in your stomach, that means you're vomiting. If it's in your hand, maybe you won't be able to type. If it's in your foot, you may not be able to walk. If it's in your neck, you may go to heaven… because asphyxia or upper airway swelling can lead to asphyxia and death.

What are some of the challenges in diagnosing HAE?

One of the major limitations of this disease is recognition. Prior to [diagnosis], it's often [for patients to] receive poor health care. If you go [in] for belly attack, [often] emergency room physicians will think you're seeking narcotics… Some of these people end up getting unnecessary surgery if they get [swelling in] the face. The ER doctors are more likely to say, ‘I know how to treat this. You treat it with antihistamines and steroids and epinephrine,’ but hereditary angioedema swelling is resistant to those

Once the diagnosis occurs, [which] can take up to 3 to 5 doctors in 7 to 10 years… [the patient gets] proper treatment. The doctor understands the disease, [and uses] shared decision-making. It really is a paradigm shift once the diagnosis is made.

Hives usually don't occur in this disease, but you can have hives associated, just like [anyone could]. If you get that swelling without hives, and you have a family history [of] abdominal pain, that makes the diagnosis very likely. You should [assess the] c1 esterase inhibitor level…you rarely ever need genetic testing.

Could you discuss the current treatment strategies for managing HAE?

There has been an evolution of care [with] more people on prophylaxis. The reason is [that] we know that prophylaxis increases quality of life, decreases anxiety, decreases depression.

In research now…we're looking at some [treatments] that may be a pill… instead of…an injection. Some of the other medications we're looking at right now can [be injected] maybe once every six months, so maybe once every three months. We now have some medications that are in research that don't have irritation when they're injected [into] the patient, and so that's good, and they'll probably lead to better compliance.

We’re also looking at prophylactic medications, [which is] one pill a day to keep the symptoms away, and so all that's really important, but those are all for type 1 and type 2, hereditary angioedema. The problem with type 3 hereditary angioedema, which is best to call HAE with normal C1 inhibitor, [is that] in those people, we're not sure what kind of therapy [works]. There are 8 different genetic abnormalities we know that can cause it…. but the problem is, most [cases of] normal, C1 inhibitor HAE [have unidentified genetic abnormalities.

In those cases, we don't know what the best drugs are. I think the best drug for rescue is icatibant because that's at the terminal end where bradykinin binds to the receptor, and that's where icatibant binds. Maybe tranexamic acid…I don't know that's very difficult. Long-term prophylaxis [is] very difficult in these people because they're not homogeneous. It's probably many different types that we haven't discovered yet.

How can healthcare providers collaborate with specialists across different fields to ensure a comprehensive approach to managing the condition?

A lot of doctors know nothing about HAE. We've done well on [educating] allergists [but] most other doctors in the world know little or never even heard of the disease.

As allergists, we have to do a couple things. We have to make sure we educate our emergency room physicians, our primary care physicians. We have to make sure that we give information to the patients that they can share with their physicians. We have to remember to make guidelines so we can help other specialties maybe develop skill sets and hereditary angioedema. We have to make sure we're using therapies correctly, and making sure that the patient understands how to use their therapies so that they can teach their primary care physicians and ER doctors how to use those medications,

There's not enough specialists to really handle all…HAE patients in the country, but I think what you can do is make sure you're available to answer questions [from] doctors around the country. On a regular basis, doctors call me up and say, ‘Hey, what would you do in this case?’ I think that's important if you're calling yourself a specialist in HAE only because [of] the lack of information most doctors have.

Relevant disclosures for Craig include CSL Behring, Takeda Pharmaceuticals USA, Grifols USA, BioCryst Pharmaceuticals, Genentech, BioMarin Pharmaceutical Inc, Blueprint Medicines Corporation, Novartis Pharmaceuticals Corporation, Dermavant Sciences, Amgen Inc, and GlaxoSmithKline.

Giavina-Bianchi P, Craig T, and Zaitoun F. 2306 - Exploring Hereditary Angioedema: Diagnosis, Prophylaxis and Treatment Strategies. Presented at AAAAI 2025 in San Diego on March 1 at 10:45 a.m.

Hereditary angioedema (HAE) is a genetic disorder characterized by insufficient C1 inhibitor protein, leading to bradykinin-mediated swelling. Diagnosis is often delayed due to misrecognition, with patients frequently receiving inappropriate treatments. Current management strategies emphasize prophylaxis to improve quality of life, with ongoing research into more convenient administration methods. Type 3 HAE remains challenging due to unidentified genetic abnormalities. Cross-specialty collaboration is crucial, as many healthcare providers lack awareness of HAE. Education and guideline development are essential to ensure comprehensive care and effective treatment utilization.

At AAAAI 2025, HCPLive spoke with Craig about recognizing and treating hereditary angioedemia.

Timothy Craig, FAAAAI, DO

William Scherer is board certified by the American Board of Foot and Ankle Surgery and is the Senior Podiatric Medical Advisor to Bako Diagnostics.

2025 SDPA Annual Summer Dermatology Conference

 in Washington, DC, William Scherer, DPM, MS, spoke in a session about strategies for clinicians to improve their ability to identify interdigital foot skin infections.

Scherer, known for his role as a Senior Podiatric Medical Advisor for Bako Diagnostics, spoke with the 

 team about foot web space infections, methicillin-resistant Staphylococcus aureus (MRSA), fungal versus bacterial infections, and more. In this segment of his interview, Scherer was asked about his talk’s portion on erythrasma and yeast infections, 2 underrecognized conditions that clinicians may require additional consideration to avoid missing.

Clues to Notice When Diagnosing Foot Infections in Dermatology Settings, with William Scherer, DPM, MS

“Well, the simplest thing is really old-school, especially with erythrasma, where you can use something known as a ‘Wood's lamp,’ Scherer said. “When you take the Wood’s lamp, and those maybe are $10, you can shine that on the foot, and if it fluoresces a coral red color, then that's pretty diagnostic for Corynebacterium or erythrosma. Again, taking a scraping and sending it off to the lab, doing PCR testing, is diagnostic. But the Wood's lamp is one of those old school tests, and I think almost every dermatologist in the country has a Wood's lamp.”

Despite the Wood’s lamp test’s longstanding use, Scherer noted that the test still stands the test of time. Scherer also discussed yeast infections.

“The yeast, a lot of times, will have a whitish color,” Scherer explained. “So sometimes in the interdigital space, you'll see something white, not too scary looking. A lot of times, that's your Candida or your yeast fungal infection. So one is bacteria that you can see with the Wood’s lamp. The other is going to be fungal, and for that you do visual identification and also a scraping, because a lot of times a yeast or a tenipedis or dermatophyte can clinically look very similar.”

Scherer was asked what he hopes clinicians, including physician associates viewing his talk at SDPA, will most remember from his session’s takeaways.

“The key thing is first and foremost, identification,” Scherer said. “A web space infection is relatively common during the summer months, is relatively common in younger patients, but in an older population, it can be a chronic condition. So it's really about increasing your awareness of the importance, [and knowing] that this is not just a simple fungal infection that you can treat with an over the counter product. A lot of patients try, and it fails, and they will come into your office.”

For more from Scherer and his session highlights, view the full segment posted above. To find out more about topics highlighted at SDPA, view the 

The quotes used in this summary were edited for clarity.


This interview segment with Scherer highlights additional takeaways from his SDPA 2025 talk, covering clues for clinicians to identify different interdigital foot infections.

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