Neal, what are some of the unmet needs that we see with these patients with psoriatic disease?

 We talked about this before a little, and I’ll still divide it between the unmet needs of the patients and the unmet needs of the dermatologist. Because in the patients, we’re learning more about that in pediatrics now that a lot of pivotal trials are done, and we’re hearing about patients of color. Obviously, there are comorbidities that go along with skin and joints. We’re collaborating with rheumatologists. That’s still on the rise, and the unfortunate part of that is we’re heavily reliant on pharma dollars to bring us those data, which require our support, for not only participating but also supporting them in some of their endeavors and bringing that education to us. The bigger equation is that there are a lot of dermatologists who don’t feel as if they’re part of the biologics conversation. They feel like the immunology is above their head. They don’t write enough, nor do they want to. Their access to information is often limited to promotional programs from the industry or meetings that they don’t feel as if they’re a part of because they hear the same voices and see the same faces talking about biologics. They think there’s some club of which they are not a part. Something is going on with dermatologists, because these are some of the smartest people around, yet they’re the first ones putting their hands up and saying, “I don’t want to write these voices.”

I don’t understand what it’s going to take to open some eyes and say, “I understand what’s going on. We’re treating the big picture for these patients.” One of the biggest unmet needs is for dermatologists to drop their guard, get involved a little more, and understand. George and I were part of an initiative that took on the question and reversed the script that said, why are dermatologists not writing biologics? What are the fears? What are the misconceptions? What are the obstacles? We hear so much about why you should you write X biologic for whatever reason. We don’t have enough conversations about why you’re not writing biologics. If you see what it’s doing to the patients who don’t get access to the drugs because we’re not putting pen to paper—not because insurance companies aren’t paying for them but for whatever reason—that’s probably the biggest unmet need: getting dermatologists out of their own way and starting to understand the process of what’s best for the patients in the long run.

Erin, do you see other unmet needs in the setting of psoriatic disease?

Yes, there are a few, 1 of which is something that I’d like to see explored: what do we do with our patients who have a malignancy or who have had a malignancy? All the studies that we have that get these drugs to market involve excluding patients with a history of any malignancy for 5 years. They’re over it, but you have a patient on a biologic, and they’re going to get a malignancy—maybe it’s age related, or maybe it’s gender related, like prostate or breast cancer, or maybe it’s not related to the fact that they are on a biologic. What do we do with those patients? Nobody will do those studies because they don’t want to go there. I don’t know how we would obtain those data, but it would be interesting to find out what we can use in terms of patients who’ve had a malignancy and if it gets treated. Can you put them back on a biologic?

The other unmet need is similar but not malignant: pregnancy. Patients get pregnant and have terrible arthritis along with their psoriasis. Heretofore, we’re supposed to stop the biologic for the whole time that they’re pregnant. Well, untreated psoriasis is a much worse comorbidity for a pregnant woman than being on a biologic because that degree of systemic inflammation causes small birth-size babies and other problems with pregnancy, but we don’t have good data on that. We have 1 anti–TNF [tumor necrosis factor] that looks at it in vitro for the most part. We rely on registry data, mainly from GI [gastrointestinal] medicine and other fields like rheumatology, to say what may or may not be safe. Those are areas where I’d like to have answers to questions because I don’t know what to do. I’m winging it, and it’s a big area because people are older and people get this disease and malignancies in particular. What can we say about them?

 Our oncology partners don’t necessarily have a lot to say either, and they’re pretty much in the dark as well.

They don’t even know the name of the drug, let alone what the adverse-effect profiles are.

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A group of specialists discusses unmet needs in psoriatic disease including physician education about biologics and research about treatment options for pediatric patients, patients with malignancies, and patients who are pregnant.

Unmet Needs in the Treatment of Psoriatic Disease

Erin Boh, MD, PhD, FAAD

The panel concludes by discussing the long-term outcomes for patients treated for hypercortisolism.

Long-Term Outcomes for Patients Treated for Hypercortisolism

The panel concludes by discussing the long-term outcomes for patients treated for hypercortisolism, emphasizing the need for further studies and data, and sharing their final thoughts on the disease and its future management.

Honey East, MD

Joseph, do you have any final thoughts about, or takeaways from, this discussion?

Education is important for everybody. Many health care providers, including myself, always had this feeling about FMT [fecal microbiota transplant]. Is it dangerous? Will patients wind up getting sick? Where does the stool come from? Is it a mix of donors or a single donor? How much will it cost? And the whole idea of a colonoscopy with bowel prep and propofol, which I mentioned before, seems like a lot. We need to change the way we think about the natural course of 

 infection [CDI]. Hopefully, people will and explore all treatment options that are available at this point.

As far as education with the practitioners, it is about educating the patients as well. If they happen to be frequent fliers for, let’s say, as you mentioned, UTIs [urinary tract infections]. Or they go to their physician, and they say, “I have a cold,” and they’re given an antibiotic. You have to explain to patients as you’re seeing them come into your practice that it’s not important to get an antibiotic every time you go to your physician’s office. And to educate them and not to try to doctor-shop and get an antibiotic if they don’t get the right answer from their primary care physician [PCP] or whomever. It’s important not only for practitioners, but for patients or potential patients for 

 Certainly, we’re going to continue to need patient education, and I appreciate that comment. Andrew?

I am cautiously optimistic now, at this point, as to where we’re headed with CDI treatment, as we have the first FDA-approved FMT product at this point right now with seemingly more on the way. We’ve got the first one through the door, and it’s going to be a matter of seeing where things go from here. As you mentioned earlier, maybe hopefully in the next 10 years we’ll have narrowed it down to which key microorganisms are essential for restoring the microbiota. And if we see these improvements, then hopefully the treatments will continue to become more effective into the future as well.

Appreciate that. I have to say that I’ve considered myself in the past a drug pusher, if you will, in the good sense of the term. But I am excited the fact that there is now an FDA-approved fecal microbiota replacement and that’s a nice, good step forward with assurance that it’s screened and safe, for the most part. And that’s a major step for managing patients with recurrent 

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Experts provide practice pearls for educating patients on and using FMTs for the management of CDI.

Key Takeaways on FMTs in the Treatment of CDI

Joseph Reilly, BS, PharmD, BCGP

Celiac disease is a gluten-sensitive enteropathy, with a global pooled prevalence of 1.4%, which is increasing. Injury to the small bowel results in loss of absorptive surface area that translates into malabsorption of fat-soluble vitamins, iron, folic acid, and vitamin B12, which result in gastrointestinal and systemic symptoms. Here, we will review the updated recommendations of the American College of Gastroenterology (ACG) guidelines on the evaluation and management of celiac disease.

Patients with symptoms and signs of malabsorption, including chronic diarrhea with steatorrhea, weight loss, abdominal pain, and bloating, should be considered for celiac disease testing. The new guidelines suggest that those with a first-degree family member with confirmed diagnosed of celiac disease should also be considered for testing, regardless of whether they have symptoms. Screening in the general population is not recommended.

A combination of positive celiac serologies and small-bowel biopsies showing villous abnormalities are required to make the diagnosis of celiac disease. The sensitivity and specificity of tissue transglutaminase IgA (TTG-IgA) for untreated celiac disease is 95%, making it the serologic testing of choice. Because the prevalence of IgA deficiency in patients with celiac disease is as high as 2 - 3%, it is advisable to measure total IgA levels at the beginning of testing. If the levels of IgA are insufficient, an IgG-based test like deamidated gliadin peptide IgG or TTG-IgG would be the preferred serologic testing. For diagnosis, it is important to confirm that patients are incorporating gluten in their diet, as antibody-based testing is grounded on the intake of gluten.

For patients with positive serologies, EGD with duodenal biopsies is required to confirm the diagnosis.Those with a high clinical probability of celiac disease (>5%) and negative serology should undergo upper endoscopy with duodenal biopsies due to the possibility of seronegative celiac disease and for evaluation of other enteropathies. Obtaining 1 or 2 biopsies from the duodenal bulb and at least 4 biopsies from the post-bulbar duodenum is important for an adequate diagnosis as celiac disease can be patchy. The diagnosis is confirmed based on the presence of villous blunting, intraepithelial lymphocytosis, and crypt hyperplasia per the Marsh or simplified Corazza classification. Intraepithelial lymphocytosis (≥25/100 epithelial cells) alone is not specific for celiac disease, hence alternative diagnoses should be considered.

In cases of serology and histology discordance, testing for high-risk HLA haplotypes of celiac disease is helpful to clarify the diagnosis. If HLA-DQ2 and HLA-DQ8 are negative, the diagnosis of celiac disease can be safely ruled out. HLA-DQ2 and HLA-DQ8 also play a role when patients have already started a gluten-free diet on presentation. In those who are positive, a gluten challenge can be pursued.

In the case of children, a combination of elevated TTG IgA and a positive endomysial antibody (EMA) in a second blood sample is recommended to confirm the diagnosis. This approach is also reasonable for adult patients foregoing EGD, although the diagnosis would be deemed possible, instead of confirmed. For children younger than 2 years, the guidelines recommend a combination of TTG-IgA and deaminated gluten peptide (DGP)-IgG, as EMA IgA is less accurate in this population.

The only effective therapy for celiac disease is gluten-free diet (GFD). Due to the importance of adherence to a gluten-free diet, consultation with a dietitian is recommended after diagnosis. About 80% of individuals with celiac disease who are on a GFD will have a negative serology after 6 to 12 months. Although clinical improvement and normalization of antibodies suggest adherence to GFD, intestinal mucosal healing should be one of the end-point goals of therapy. As healing can take time, particularly in adults, the guidelines suggest a follow-up endoscopy with biopsy after 2 years of following a GFD. Lack of mucosal healing correlates with lymphoproliferative malignancy, bone disease, and refractory celiac disease. In the case of asymptomatic children following a GFD, follow-up biopsies are not recommended.

Although multiple tools to detect gluten in food have come to the market recently, data is lacking about their impact on clinical outcomes and adherence to GFD. Hence, the guidelines suggest against gluten detection devices.

Although dysbiosis is present in patients with celiac disease, there is not enough data to support the use of probiotics. Although oat consumption is safe in most patients with celiac disease, some might react to the oat protein itself, and there is risk of contamination with wheat. Hence, the guidelines suggest consuming gluten-free oats.

Patients with celiac disease are at higher risk of pneumococcal infections compared with the general population, which is due to functional hyposplenism. Hence, the ACG guidelines recommend vaccination against pneumococcus after diagnosis as part of the preventative care of patients with celiac disease. For adults without previous vaccination, the ACG suggests 1 dose of PCV20 (pneumococcal conjugated vaccine 20) alone or 1 dose of PCV15, followed by 1 dose of PPSV23 (pneumococcal polysaccharide vaccine 23).

Measurement of bone density with dual-energy X-ray absorptiometry should also be considered.

The updated guidelines provide new recommendations about considering testing asymptomatic first-degree relatives of confirmed individuals with celiac disease, correlation between serologic and endoscopic diagnosis in children and adults, the role of mucosal healing, the lack of evidence of tools to detect gluten, and probiotics. It also highlights the importance of preferring gluten-free oats, and of preventative immunization and measurement of bone density. As research evolves in this field that affects an increasing number of individuals, more data will be available to facilitate their diagnosis, adherence to gluten-free diet, and preventative care.

Rubio-Tapia, Alberto MD1; Hill, Ivor D. MD2; Semrad, Carol MD3; Kelly, Ciarán P. MD4; Greer, Katarina B. MD, MS5; Limketkai, Berkeley N. MD, PhD, FACG6; Lebwohl, Benjamin MD, MS7. American College of Gastroenterology Guidelines Update: Diagnosis and Management of Celiac Disease. The American Journal of Gastroenterology 118(1):p 59-76, January 2023. | DOI: 10.14309/ajg.0000000000002075

An expert reviews the updated recommendations of the American College of Gastroenterology guidelines on the evaluation and management of celiac disease.

Celiac Disease ACG Guidelines Update

Lady Katherine Mejía Pérez, MD

PRECISION trial

Video content above is prompted by the following:

The PRECISION trial was a phase 3, multicenter, randomized study of aprocitentan, a dual ERA, in patients with a systolic blood pressure of 140 mm Hg or higher despite taking 3 antihypertensive drugs, including a diuretic.

Difficult-to-treat hypertension is a condition where blood pressure remains uncontrolled despite the use of three or more antihypertensive medications, including a diuretic. This condition is distinct from resistant hypertension, which is more common and involves blood pressure that is not controlled with three medications but may not include a diuretic. Difficult-to-treat hypertension is less frequent, affecting a smaller subset of patients with high blood pressure. It often requires a more comprehensive approach, including lifestyle modifications and potential secondary causes evaluation, to achieve optimal management.

Panelists discuss how the PRECISION trial evaluated aprocitentan, a dual endothelin receptor antagonist (ERA), in patients with resistant hypertension taking 3 antihypertensive medications including a diuretic.

Manesh R. Patel, MD

Troum discussed the AGILE study and how DECT scanning helped visualize improvements in uncontrolled gout.

Orrin Troum, MD: Accurately Imaging Gout With DECT Scanning

 of pegloticase (Krystexxa; Amgen) may reduce the treatment burden for patients with uncontrolled gout in new research which found 1-hour infusions to be well-tolerated.

Orrin Troum, MD, clinical professor of medicine, Keck School of Medicine, University of Southern California, and director, clinical rheumatology research, Providence St John's Hospital, Santa Monica, California, presented data from the phase 4 AGILE study evaluating shortened infusions at last month’s 

can College of Rheumatology (ACR) Convergence 2024

 spoke with Troum to learn more about gout management and how shortened infusion times can help reduce patients’ treatment burdens. He also discussed autoimmune investigations he is involved in at Providence St John's, including indications such as lupus, Sjogren disease, and psoriatic arthritis.

Troum emphasized the value of dual-energy computed tomography (DECT) scans in managing gout and the importance of expanding the access of use of DECT scans, which are not available for rheumatologists in all areas.

“By DECT scanning, you can get a very clear picture with over 90% accuracy with being specific and sensitive to identifying urate crystals, and that has been a big help to me, because it helps us in targeting patients, specifically with tophaceous gout that we can measure… and by the end of Krystexxa therapy, they don't have anymore. So that's really a very good outcome for me that I've used… Not everybody has access to it, but [it’s been a] very useful tool for me,” Troum said.

Relevant disclosures for Troum include AbbVie/Abbott, Amgen, Bristol-Myers Squibb, Eli Lilly, Genentech, GlaxoSmithKlein, Novartis, Roche, and UCB.

Troum O, Botson J, Fang F, et al. Safety, Tolerability and Efficacy of Pegloticase Administered with a Shorter Infusion Duration in Subjects with Uncontrolled Gout Receiving Methotrexate: Primary Findings of the AGILE Open-label Trial. Presented at: Presented at: ACR Convergence 2024; November 14-19; Washington, DC. Abstract 2012.

Orrin M. Troum, MD

 What else is out there? We have hydroxyurea. We have voxelotor, crizanlizumab, Endari, transfusions. What’s next? There’s a plethora of treatment options to treat the variety of patients who have who have sickle cell disease. We’re stuck with 4 or 5 options. What else is in the pipeline to treat sickle cell disease?

 If we had this conversation 5 years ago, it wouldn’t be much of a conversation. It’s a good time to be in sickle cell, and the future is bright. Gene therapy, despite the issues, is there. There are many ways to do that. As someone had mentioned, science will prevail with time. The curative options are there, but it’s important to recognize that they’re not going to be there tomorrow, and they’re not going to be there next year for the masses.

There are a number of other therapies out there. Fetal hemoglobin is out there. Fetal hemoglobin is a good target. We know about BCL11A. There are groups trying to make fetal hemoglobin higher using a medication that is in development, and I’m sure there are many ways that’s being tried. There’s a class of medications, called PKR activators, that were designed for pyruvate kinase deficiency. It’s is a very small population, but they can be repurposed to reduce hemolysis in sickle cell disease in ways not too unsimilar to voxelotor. Crizanlizumab is medicine that targets P-selectin.

Several other medications in that class are in development or are being repurposed to see if they can address pain. Because even though we’re trying to address the root cause, when a patient comes with pain, what can you do to abort that pain? We have nothing, except for opiates, which are not the solution. It’s a tough battle, but there are efforts trying to do that with P-selectin and all selectins, and many ways with inflammation. But there are many classes. This is a bigger conversation than it could have been even a couple of years ago. It’s an exciting time, and we’ll get to a point where sickle cell disease treatment is a cocktail approach. You take a couple of things, and as long as we can work on it, if we can address things from different angles, then we’ll make our patients have better lives.

Absolutely. Well, thank you so much. This has been an amazing conversation. I want to thank Abdullah, Wally, and Pat. Before we close, tell the audience your 1 big dream, or 1 final thought, that you want everybody who sees or hears or takes care of patients with sickle cell disease to know as a takeaway message from this conversation. I’m going to start with Abdullah. Your 1 final word that you want them to know about?

As you said, this has been a really exciting conversation. Wally, you, and Pat contributed greatly. Considering this discussion, there are 2 things. It’s important, scientifically, to pursue curative options like gene therapy. I’ll repeat that science will prevail. We will have to overcome the risks, understand them better, and remedy them. That’s 1 thing. 

Coming back to Wally’s point, we need more disease-modifying agents that we can use in Africa or India. The typical approach would be—I agree with Pat—new F-inducing agents or a combination of F-inducing agents. Maybe a combination of F-induction with some downstream modifications like anti-inflammatory or antiadhesion therapies. These are going to be important, and I believe these have to be pursued in sickle cell, along with these high-tech, higher-source modalities. This includes swallowing a pill, which can easily be conveyed to Africa or low-resource countries.

Thank you so much, Abdullah. I’m going to follow up with Wally. Wally, what are your 1 or 2 big-picture, take-home thoughts?

 I’d like to put my public health hat on. I want our audience to know about a report that came out in November from the National Academies of Sciences, Engineering, and Medicine. Ify, you and your colleagues did wonderful preparing 512 pages about all that is wrong in sickle cell care in the United States and what needs to be done to make sickle cell care better. There were 7 pillars that you pointed out, and they had to do with education and social policy. They had to do with patient empowerment and disparities. You declared sickle cell to be a disparities disease, as Pat said earlier. They had to do with therapy as well. But it wasn’t just therapy that you focused on. You focused on social determinates of health, you focused on policy, racism, and changes in the fabric of the health care system, especially for adults with sickle cell. We don’t even have an adult sickle cell disease health care system. We have a shack instead of a home for adults with sickle cell disease. That’s the 1 thing I want to take away. None of this discussion we just had will matter is there’s nobody to care for the patients. And in many parts of the country, there’s nobody—doctor, nurse, or other—to care for these patients.

Very well said. Thank you so much, Wally. 

I’m going to add to that because it’s so important. The names of the medicines don’t matter. Whether you live in Cincinnati, or Angola, or India, if we have good therapies, they should be available. We need to leverage that equity to global treatment of sickle cell disease. Hydroxyurea was developed in the 1980s and ’90s and is only now becoming available in Africa. Not really, even. I don’t want to give a talk when I’m retiring in a few decades telling patients about all these new therapies that we’re using in the United States and how sickle cell disease is history, except in Africa, where 90% of kids are still dying before they’re adults. That can’t happen. As these therapies are developed, by Bill Gates or whomever, we’re going to need a lot of people. We need to be sure that these are truly equitable in a timely manner, or we’re doing a huge disservice to the global sickle cell community.

Thank you so much. I’m going to give my thoughts. The first thing I want the audience to recognize is that sickle cell disease is a lifetime genetic disorder. It doesn’t go away when you become a teenager or when you leave pediatrics. It doesn’t disappear when you get married. It’s there for the rest of your life. It does shorten your life span. 

The second thing is pain with sickle cell disease. It’s important, but it’s not the only important thing. Organ damage, that chronic, slow slump of devastation to the organs is a reality, and no patient will die because of pain. They will die from strokes, kidney disease, pulmonary hypertension, infection, heart problems, lung problems. It’s important to look at them as treating not just pain but the entire person. That entire person will also involve their quality of life. Ask them how they’re doing, how are they functioning. Do they get up and go to work? If not, why not? When you’re giving treatment, look at the impact of treatment. Not just on their pain, as we talked about, but on their overall quality of life. 

We talked about screening for sickle cell disease at birth, screening for complications following the guidelines, and early intervention. For example, retinopathy picked up early can prevent blindness, treating hyposthenuria early prevents ESRD [end-stage renal disease], and picking up pulmonary hypertension can prolong life by putting the right treatment in place. But there’s also supportive care. And let’s not forget the role of the primary care provider. The last time I checked, having sickle cell disease does not protect you from getting breast cancer, colon cancer, high blood pressure, diabetes, or diverticulitis, or any other thing that anybody else gets. My patients have all this, and they deserve whole care—not sickle cell care but all-around holistic medical care.

Thank you so much for watching this HCPLive® Peer Exchange. If you enjoyed the content, please subscribe to the e-newsletter to receive upcoming Peer Exchanges and other great content right in your in-box.

Experts look into what is next for sickle cell disease and provide key thoughts on the space. 

What’s Next and Final Thoughts in SCD 

Patrick McGann, MD, MS, Cincinnati Children’s Hospital  

Future Outlook for Atopic Dermatitis Treatments

Please share final thoughts on the future of atopic dermatitis treatment with oral systemic agents.

The future of atopic dermatitis treatment with oral systemic agents is promising, with ongoing research and development of novel therapies. Advances in understanding the pathophysiology of atopic dermatitis have led to the identification of new therapeutic targets, resulting in the development of more effective and targeted treatments. These agents aim to provide better disease control, reduce side effects, and improve patient quality of life. The integration of personalized medicine approaches and biomarkers may further enhance treatment outcomes, offering tailored therapies based on individual patient profiles and disease characteristics.

Medical experts share their final thoughts on the future of atopic dermatitis treatment with oral systemic agents.

Raj Chovatiya, MD, PhD

 Looking forward, how do you envision implementing therapies in a more aggressive fashion? I’m going to go to each of you to share some clinical pearls about how you envision the heart failure world getting its arms around the need to take a chemotherapy-like approach to our patients in getting them on therapy. Since you were the last to speak Muthiah, I’ll ask you to be the next to speak.

I’m going to jump forward, I’m going to look to the future. I think we are looking at an environment in which these drugs are going to be accessible, affordable, easy to administer, and I think we should start to engage our patients and have patients have a more active role in the initiation and titration of these drugs. We can envision a system much like insulin titration, in which at least some patients who are engaged in their care could modulate dosing, could initiate new drug therapy, in their home environments with relatively limited monitoring structures.

We’ve got a cancer analogy, now we have an endocrinology analogy, that’s great. Rob, what do you think? What does the future hold in structuring rapid titration and getting patients to target?

I’m really hopeful on a couple of fronts. One is that we strike this term “consider.”“We’ll consider starting ARNI [angiotensin receptor-neprilysin inhibitor] at follow up.” We’ve got to eliminate that from our vernacular, that can’t be in a discharge summary. We need to start these therapies in the hospital, and I think it’s all as others have highlighted, this multidisciplinary team. We’ve learned about the tremendous success of having a pharmacist who can help a case manager if there’s paperwork and other financial limitations. So the future is multidisciplinary teams, it’s rapid sequence. We’ve got to do better for our patients.

Javed, what do you think? At Baylor Scott and White [Health], how are you thinking about this?

No, I don’t have much to add on top of what Muthiah and Rob said. Let me just take a moment and make a plea to all our listeners. Symptoms should be targets of therapy in heart failure, not a guide for therapy. Things like high blood pressure, diabetes, lipids, these diseases by definition are asymptomatic. We have many cancers that are diagnosed on screening, and that comes as a surprise to patients, they are asymptomatic. We would never leave these patients alone because their symptoms are OK. You treat the biology of the disease. Heart failure is the same thing. Whether you have a lot of symptoms or you have few symptoms, we need to target the underlying biology and treat them aggressively with appropriate indicated therapies. Just because somebody says they’re doing OK is not a reason to not treat them appropriately.

Absolutely, an important take-home message from Dr Javed Butler. At our institution at [Massachusetts General Hospital], we recognize the need for infrastructure for rapid sequence initiation and titration, even before STRONG-HF trial data came out. We have a clinic called the GDMT [guideline-directed medical therapy] clinic, and it is in existence for one job, which is education, initiation, and titration of GDMT. We’ll either start outpatients or we will take patients who have just been discharged in continuity to get them to target. It’s a 12-week process or shorter. We utilize many of the tools Dr Vaduganathan mentioned, not only education, but home-based titration, including virtual care, virtual laboratory testing as well, in order to get patients to target, because by and large that’s really the most important monitoring piece in this process. Blood pressure matters to be sure, but provided patients are not symptomatically hypotensive, we will continue titrating. We get patients in the office periodically, however, we have a nurse practitioner-based approach but we also have a pharmacist, as Dr Mentz mentioned. In our patients in our GDMT clinic, we are achieving quadruple therapy in over 90% of our patients, with nearly 90% on sacubitril/valsartan, and over 60% on target doses of all 4 drugs.

We’ll close with the point, Rob, in the CHAMP-HF Registry, how many patients were at target dose?

 This is striking, you can count it on a couple of hands.

It was single digits. The point is that it can be done. GDMT works for our patients, it reduces morbidity and mortality. We should not wait for initiating and titrating, getting patients feeling better and living longer. Four drugs, 5 pathways, 6 years of extra survival.

Thanks to all of you for this rich and informative discussion, and thank you for watching this peer exchange. If you enjoyed the content, please subscribe to our e-newsletters to receive upcoming peer exchanges and other great content right in your inbox. I’m Jim Januzzi, thanks for watching.

Drs James Januzzi, Javed Butler, Robert Mentz, and Muthiah Vaduganathan share practice pearls for treating patients with heart failure, focusing on the future of treatment.

Clinical Pearls for the Treatment of Heart Failure

Robert J. Mentz, MD

Pediatric Lipid Screening

Can you describe the importance of pediatric lipid screening? What are the current recommendations, and are they being implemented?

Are there practical strategies you could recommend to improve the uptake of pediatric lipid screening?

Pediatric lipid screening is crucial for early detection and management of dyslipidemia, which can prevent cardiovascular diseases later in life. Current guidelines recommend universal lipid screening for children between ages 9-11 and 17-21, with selective screening for those with risk factors. However, implementation remains inconsistent due to barriers such as lack of awareness and time constraints in clinical practice. To improve uptake, strategies include integrating screening into routine pediatric visits, utilizing electronic health records for reminders, and educating healthcare providers and families about the importance and benefits of early lipid screening.

Panelists discuss how pediatric lipid screening remains underutilized despite current recommendations and explore practical strategies to increase screening rates and identify cardiovascular risk factors early in childhood.

Authors