Current Decision Pathway and Guidelines on LDL Management Post-ACS

Following an ACS event, the management of LDL-C levels is a key component of secondary prevention strategies to reduce the risk of recurrent cardiovascular events. Current guidelines emphasize aggressive LDL-C level reduction as an essential part of post-ACS care, reflecting the strong evidence linking lower LDL-C levels to improved outcomes.

Current Guidelines and Standards for LDL-C Management Following ACS:

: According to major clinical guidelines (eg, American College of Cardiology/American Heart Association and European Society of Cardiology), high-intensity statin therapy is recommended for all patients with ACS, unless contraindicated. High-intensity statins, such as atorvastatin at 40 to 80 mg or rosuvastatin at 20 to 40 mg, are aimed at achieving significant LDL-C level reduction, typically by 50% or more.

: The primary goal is to lower LDL-C to levels that have been shown to reduce the risk of recurrent events. Current recommendations advocate for:

 (1.8 mmol/L) for most patients post-ACS.

In patients at very high risk (eg, those with multiple risk factors, diabetes, or additional cardiovascular events), a LDL-C level less than 

 (1.4 mmol/L) is considered an ideal target.

: In certain high-risk patients, if LDL-C levels remain above target despite high-intensity statin therapy, additional lipid-lowering agents such as ezetimibe (a cholesterol absorption inhibitor) or PCSK9 inhibitors may be used to further lower LDL-C levels.

: Post-ACS, LDL-C levels should be closely monitored and therapy adjusted to achieve and maintain the target LDL-C level, ensuring optimal secondary prevention.

These guidelines emphasize that aggressive lipid management with a focus on LDL-C level reduction plays a critical role in reducing the long-term risk of recurrent cardiovascular events following an ACS event. Regular follow-up and adherence to treatment plans are essential in achieving these goals.

Panelists discuss how managing low-density lipoprotein cholesterol (LDL-C) levels through high-intensity statin therapy and additional lipid-lowering agents following an acute coronary syndrome (ACS) event is critical for secondary prevention, with current guidelines recommending aggressive LDL-C level reduction to lower the risk of recurrent cardiovascular events.

Alan S. Brown, MD MHA FACC FAHA MNLA

Skin of Color Savvy: The Art and Science of Treating Patients of Color

Skin of Color Savvy: Diversity in Dermatology Within the Modern Landscape, with Crystal Aguh, MD, and John Harris, MD, PhD

, Crystal Aguh, MD, associate professor of dermatology and director of the Ethnic Skin Program at the Johns Hopkins School of Medicine, and John Harris, MD, the founding Director of the Vitiligo Clinic and Research Center, founding director of the Autoimmune Therapeutics Institute and professor and chair of the Department of Dermatology at UMass Chan Medical School in Worcester, together explored the importance of mentorship, visibility, and leadership among dermatologists and dermatology trainees of different backgrounds.

Hosted by Skin of Color Society (SOCS) leaders, this podcast episode continues to delve into the latest research, clinical insights, and culturally intelligent and responsive care practices in the field of dermatology. Together, Aguh and Harris spoke on a variety of subjects in this area.

Aguh and Harris discussed the importance of diversity in clinical trials and research, emphasizing the need for diverse principal investigators and teams. Harris highlighted his experiences moderating a panel on incorporating diversity into clinical research, noting the challenges and benefits. They discussed the impact of federal regulations on National Institutes of Health (NIH) grants and the necessity of addressing questions about the importance of diversity.

Harris pointed out the challenges of addressing conversations regarding diversity among clinicians and in clinical research within the present political climate, highlighting that some have questioned whether to bring up the conversation at all. Both expressed optimism about the growth and impact of SOCS in advancing research and treatment for patients of color.

As the episode closed, the conversation reinforced the power of mentorship, the importance of role models, and the responsibility of current leaders to cultivate a more equitable future in dermatology. For both those in medical school and those who are current health care providers, the episode offers a compelling look at how connection, advocacy, and shared purpose can drive lasting change within the specialty.

To learn more about SOCS’s mentorship programs and initiatives, visit 

Editor's note: This interview was summarized with the aid of artificial intelligence.

This episode of the SOCS podcast features an in-depth discussion between Crystal Aguh, MD, and John Harris, MD, PhD.

John E. Harris, MD, PhD

Thank you to all 3 of you for participating in this rich discussion. I’d like to give you one last opportunity for any pearl that you might have that you want to share with your colleagues about taking care of patients with atopic dermatitis now, and then what we are going to be doing over the next year or two, as we learn more and continue to add to our therapeutic options. Do you have anything you would like to add?

My advice to my colleagues is for those who aren’t participating locally in journal clubs and meetings, do it because by doing so, you’ll meet incredible providers who share the same passion you do by improving the lives of patients. You’ll find other providers who speak your same language who you get along with and you’ll enjoy collaborating with on care for patients. The second thing is for patients to hang in there. We’re in this together. This is a journey. This isn’t a 1-gene condition. This is complicated, but we’re in it together, and we’re going to find the answers and stick with it until we find the answer that will make our patients become their best selves. I joke that my patients are my Prozac all day long because they give me such a high when they come in and they’re happy. You can see when they’re not happy, but it’s so empowering on my side and it’s a real honor to be in a position to ask them questions that nobody else can ask and to walk side by side with our patients in this journey.

Susan, do you have any words to your colleagues or to your patients or their families?

 It is a partnership, laying out the options treatment wise and weighing the risks and benefits, and all the other extraneous things, costs, and other things that influence the family. It’s also being the empathetic providers that we all are and that the patient knows you’re listening. That’s a huge aspect of any chronic disease, that patients need to feel heard and they need to know that you are listening and that it matters what they’re going through. We know statistically and scientifically all of the things about the diseases, but everybody’s different and not everyone fits into that mold. We need to be able to pull those idiosyncrasies out from the patient, knowing what has failed and helped, and you are there as their provider to get success for their disease and their quality of life and to be able to move forward.

If you have a patient who is not doing well on what we have available, you might want to go to clinicaltrials.gov and look at sites all over the country where children, adolescents, and adults with different types or different levels of atopic dermatitis might be able to participate in a clinical trial to help get the data needed to move forward. 

 The National Eczema Association [NEA] may have information about clinical trials across the country, so they may be a good resource for that as well.

 I encourage my patients to start their own local chapter of the NEA. Patients need to collaborate with each other and relate so they can help each other by sharing stories and know they’re not the only one. It’s insane to me how I’ll go in and see a patient, and they’ll feel so alone, but there are so many people out there suffering from this. They should never feel alone.

They’re going to seek answers through social media or through other online sources. They’re going to be seeking answers, and you can either direct them and give them the proper information, or they’re going to find it on their own, so we have to realize that and try to direct them to places that matter. Thank you for watching this HCPLive® Peer Exchange. If you enjoyed the content, please subscribe to our e-newsletters to receive upcoming Peer Exchange segments and other great content right in your inbox. Thanks to all 3 of you, and we’ll see you again soon.

Clinical pearls regarding the management of patients with atopic dermatitis with newer treatment approaches as the field continues to evolve. 

Optimizing Therapy for Patients With Atopic Dermatitis 

Keri Holyoak, PA-C, MPH, Dermatology Center of Salt Lake 

Mohd Salman, MD, is a specialist in gastroenterology. He obtained his medical degree from ERA Medical College in Lucknow. His clinical and research interests focus on inflammatory bowel disease, advanced endoscopic techniques, and emerging therapies in gastroenterology.

 is a life-threatening condition requiring urgent medical intervention. Over the past decades, advances in corticosteroid therapy, biologics, small molecules, and predictive scoring systems have improved patient outcomes. However, challenges remain in optimizing medical therapy and reducing colectomy rates.

Despite advancements in biologic therapy, colectomy rates within a year of medical salvage therapy remain high (30–50%). Response to corticosteroids within the first week of hospitalization is a key predictor of long-term colectomy risk. In the Oxford cohort study, patients achieving complete response (stool frequency ≤ 3/day, no blood) had a 5% colectomy rate, whereas incomplete responders had a 40% colectomy rate within 9 months.

Additional predictors of colectomy include pre-admission immunomodulator use, which triples the risk of colectomy at 1 year. A combination of serum albumin ≤ 2.5 g/dL and band neutrophil count ≥ 13% at infliximab initiation had a 100% positive predictive value for 90-day colectomy.

Scoring systems incorporating prior biologic exposure, age, and need for salvage therapy further refine risk stratification. 

 also predicts colectomy risk, with a Mayo score of 3 associated with a 91% sensitivity for colectomy within a year. Biomarkers such as CRP/albumin ratio and CRP/lymphocyte ratio outperform traditional indices like the Mayo and Oxford scores in predicting colectomy.

 despite intravenous corticosteroid therapy is a concerning sign of steroid failure and often necessitates early consideration of salvage therapy.

Several challenges remain unresolved in the management of ASUC.

Accelerated or Intensified Infliximab Dosing

An accelerated infliximab regimen (5 mg/kg at weeks 0, 2, and 6, with dose escalation to 10 mg/kg in select cases) has been explored. Observational studies show lower short-term colectomy rates with intensified dosing. However, meta-analyses reveal no significant difference in long-term colectomy rates or complications between standard and intensified regimens.

A recent Australian randomized trial found no difference in clinical response at day 7 between 10 mg/kg and 5 mg/kg dosing. Although intensified dosing may benefit select patients (e.g., those with serum albumin <25 g/L), further studies are needed to refine patient selection.

Janus Kinase (JAK) inhibitors, such as tofacitinib and upadacitinib, have shown promise as alternative rescue therapies in steroid-refractory ASUC. In a phase 4 trial, 58.3% of patients receiving tofacitinib 10 mg twice daily achieved clinical response at day 7, with 45.8% remaining on therapy at 6 months.

Concerns remain regarding thrombotic risks, particularly in patients over 50 with cardiovascular risk factors. While upadacitinib has shown efficacy in case series, large-scale trials are required to establish its role in ASUC management.

Biologics for Maintenance Following Cyclosporine Rescue

Patients achieving remission with cyclosporine require maintenance therapy, traditionally with azathioprine. In patients with prior azathioprine failure, biologics like vedolizumab have been proposed as alternatives. A systematic review showed a 65% colectomy-free survival rate with vedolizumab maintenance following cyclosporine induction. While promising, further studies are needed to confirm its safety and efficacy.

Metabolomic alterations in Ulcerative Colitis

A systematic analysis of metabolomics studies related to UC, mainly from ‘lipids and lipid-like molecules’ and ‘organic acids and derivatives’ superclasses reveal 101 metabolites consistently altered in multiple datasets within the same sample type and 78 metabolites common across different sample types. Of these, 62 metabolites exhibited consistent regulatory trends across various datasets or sample types. Pathway analysis revealed 22 significantly altered metabolic pathways, with 6 pathways being recurrently enriched across different sample types.

The practice of sequential rescue therapy—switching from infliximab to cyclosporine or vice versa—remains controversial. Studies report remission in 33-40% of patients, but significant adverse events, including severe infections and sepsis-related mortality, raise concerns. Given the unclear impact on long-term colectomy risk, sequential rescue therapy is not routinely recommended.

Non-traditional approaches, such as exclusive enteral nutrition (EEN) and hyperbaric oxygen therapy (HBOT), have shown potential.

 An open-label trial found lower steroid failure rates and reduced hospitalization in ASUC patients receiving EEN. HBOT, in a small study, improved remission rates and reduced colectomy risk. However, due to limited evidence, these therapies remain experimental.

Bowel ultrasound is emerging as a non-invasive tool for assessing ASUC severity. Studies indicate that increased bowel wall thickness correlates with steroid failure. A thickness > 6 mm predicts the need for salvage therapy. While promising, ultrasound-based assessments require validation in larger cohorts.

ASUC requires rapid recognition and multidisciplinary management. Corticosteroids remain the first-line therapy, with early identification of non-responders critical for guiding rescue therapy. While infliximab and cyclosporine remain standard salvage therapies, small molecules like tofacitinib and alternative biologics are emerging as potential options. Predictive scoring models and biomarkers aid in risk stratification, but require further validation.

The role of unconventional therapies and imaging techniques like bowel ultrasound is expanding, offering non-invasive monitoring tools. Future research should focus on personalized treatment strategies to optimize ASUC outcomes and reduce colectomy rates.

Vuyyuru, S. K., Nardone, O. M., & Jairath, V. (2024). Predicting outcome after acute severe ulcerative colitis: A contemporary review and areas for future research. 

https://pmc.ncbi.nlm.nih.gov/articles/PMC11312513/

Liu, M., Guo, S., & Wang, L. (2024). Systematic review of metabolomic alterations in ulcerative colitis: Unveiling key metabolic signatures and pathways. 

Therapeutic Advances in Gastroenterology, 17

https://pmc.ncbi.nlm.nih.gov/articles/PMC10981261/

Le Berre, C., Honap, S., & Peyrin-Biroulet, L. (2023). Ulcerative colitis. 

https://pubmed.ncbi.nlm.nih.gov/37573077/

Acute severe ulcerative colitis (ASUC) is a critical condition necessitating prompt intervention. Despite advancements in corticosteroids, biologics, and small molecules, colectomy rates remain significant. Predictive factors for colectomy include corticosteroid response, pre-admission immunomodulator use, and specific biomarkers. Emerging therapies like JAK inhibitors and alternative biologics show promise, though concerns about safety and efficacy persist. Non-traditional therapies and imaging techniques, such as bowel ultrasound, are being explored. Future research should focus on personalized treatment strategies to enhance outcomes and minimize colectomy rates.

Examining recent developments in ASUC management, including predictive markers for colectomy, new treatment approaches, and ongoing challenges.

Advances, Challenges in Managing Acute Severe Ulcerative Colitis 

Mohd Salman, MD

I want to focus in on topicals, given that clinical scenario I outlined. Let’s say you were going to stick with topicals for the in-between patient we talked about. Peter, is there general guidance in terms of body surface area when you’re thinking about topicals? A lot of this ties into earlier discussion on what’s practical for a patient, something they can follow through on. Is there a sweet spot where it works, beyond which it becomes impractical even if it’s mild or mild to moderate disease?

That’s another problem with the way we categorize disease. Frequently, if we’re doing something like an easy score, that takes body surface area heavily into account. But we have patients with very small body surface area, where it’s quite severe. Other times, patients are mild, but it’s overwhelming—like 90% body surface area. Part of the calculation is responsiveness to treatment and feasibility of treatment. For littler kids, you can get away with whole-body application of topicals. When they’re little, it’s easy because they’re portable; the parents can usually do it. But as the kids get older, adolescents in particular, it’s very tough. They get easy burnout and very fatigued about putting on a lot of topicals. For those patients, even small body surface areas might be an issue.

That’s the best way to approach it: on a person-to-person basis. But I always say that everybody’s got to try some topicals. Even when we’re on systemics, almost all our patients on the systemic agent are going to use some topicals; you’re never outside that. It depends on the response. Sometimes I’m confident that this is never going to work, and that when I talk to them next week, they’re going to say they’re worse. I think that they’re going to have to go on to a systemic agent. Then I call them, and they say, “No, it’s great. Pretty much everything is healed. I did most of the body for a few days, everything responded, and I’m focusing on my hands or my ankles. We made it.” Other times it’s small. I said, “Come on. Let’s push hard. We’ll do everything. We’ll do wet wraps.” Then in 2 weeks, they call me and say, “I’ve been using it like crazy, and my hands are still miserable and cracking and bleeding.” Then we have to go to systemics.

Oftentimes, when we’re making that move on the value of step-wise therapy for atopic dermatitis, we’re adding many of those therapies together. It’s not a straightforward discussion of trading in your topical for a systemic. There’s often concurrent use. Matt, when is combination therapy viable for patients? And when do you want to see if monotherapy does its thing? Is there a difference between the 2, or are you doing everything at once and peeling off? Take me through how this works in your practice.

For me—and we all practice this way—every patient who’s on a systemic is on combination therapy. Whenever I’m talking about drugs—let’s say I’m giving a promotional talk for a systemic—I tell the audience to ignore the monotherapy data, because they’re not clinically relevant. I tell them, “Those were data the FDA required, but they’re not clinically relevant.” The data we want to look at are the combination therapy along with topical corticosteroids. That’s what’s always done in the trials. When I put somebody on systemic therapy, I’m telling them, “Use your topical, but hopefully with the systemic that we have, you won’t need to use the topical anymore.” As you get better, you don’t need to keep using it.

That’s the case when I have people on combination therapy. If they need a little topical, I’m not worried about it. It’s not, “Let’s put you on a systemic. Once you’re better, we’ll stop the systemic and see if we can keep you on the topical.” No, it’s, “Let’s start you on a systemic. Assuming the systemic works good, you don’t need to use the topical anymore.” That’s the direction that I’m going in. Part of that is because it’s so hard from an insurance perspective to start and restart the systemics because patients stopped ordering it, or their authorization immediately is revoked.

The other part of it is the experience with the drugs that we have. If you stop the systemic, at some point the disease is going to come back. Peter has published—and I agree with him—that with the biologics, the data show you can give people a long-term remission. If they have done wonderfully and are clear, a lot of times, if they stop and you pick dupilumab, it might be 3 to 6 months or even longer before the disease comes back. But it’s going to come back. I always think in terms of infection risk in these patients. If we wait until the disease starts to flare, and before we restart therapy, they’ve already been through the high-risk period for getting a skin infection that can turn into something serious.

Dr Noor, you’re no stranger to getting many things on board to get someone under control. How does the idea of monotherapy and combination therapies play a role in what you’re doing, especially for someone who’s transitioned up the severity ladder? As Matt told us, combination therapy is the most indicative of what’s happening in the real world. Tell us about your practice.

One thing that’s very consistent with essentially every patient in my practice is that I look them in the face and say, “I’m going to get you better.” I can get you better because I have all these options, and these options are extensive. We have wonderful options, all the way down to cyclosporine and methotrexate, and the ability to combine different treatments. If we can appreciate the data, if we can appreciate the safety, then we can appreciate what to expect that this individual needs.

One thing that I always stand by, and it’s going to sound silly, is that I’m not a vending machine. I don’t do the same thing for each individual. It’s not like you come in, you punch in a button and say, “I have moderate atopic dermatitis,” and out comes your drug. That’s not how it works. Every patient is an individual, and I treat everybody individually to make sure I get the best possible outcome for that individual. Every patient knows that, in every room and in every scenario. If that means that they need to go on a biologic and a topical, like ruxolitinib; a biologic; or even an oral JAK inhibitor, then I’m going to take that situation individually and determine the best option for that patient.

Experts in dermatology share general guidance for use of topicals, switching from topical to systemic treatment, and when combination therapy is an option for patients with atopic dermatitis.

Guidance for Topical Treatment Use Based on BSA in AD

Omar Noor, MD

A pair of authors of a recent scientific statement and the president of the HFSA discuss cognitive impairment in heart failure. 

Role of Screening, Addressing Cognitive Impairment in Heart Failure Management

For some time, the heart failure community has warned of an impending storm brewing under the nose of public health despite their rallying cries and calls for a greater emphasis on management. With the aging US population as a backdrop, the prevalence of 

 is expected to grow in the coming years and, with heart failure fellowships going unfilled at an alarming rate, many in the field are concerned they are heading toward a perfect storm bent on wreaking havoc on public health.

The concern among filling fellowship slots aside, advanced heart failure and transplant specialists currently practicing have been confronting a growing concern associated with the aging population, but that could spell disaster for heart failure in particular: cognitive impairment. In their latest scientific statement, the Heart Failure Society of America has aimed at the issue and how it affects the management of heart failure.

Published on March 12, 2024, the 17-page document cites 142 references and is divided into 5 sections addressing the following subjects: risk factors for cognitive impairment, implications of cognitive impairment, management of cognitive impairment, integration of cognitive impairment into decision-making, and gaps in knowledge and challenges to implementation. In addition to calling attention to the prevalence of cognitive impairment in this patient population, the docuemnt also provides an overview of recommended screening tools and practices based on contemporary literature.

In this HCPLive peer-to-peer discussion, we spotlight perspectives on the subject from 3 subject matter experts in Eiran Gorodeski, MD, MPH, Parag Goyal, MD, MS, and James Fang, MD. In the conversation, Fang, who also serves as the president of the Heart Failure Society of America, acts as a moderator and guides Gorodeski and Goyal, who served as lead co-authors for the statement, through a discussion on the creation process, key takeaways, the complexities of heart failure management in patients with cognitive impairment, and the role of the Heart Failure Society of America and other professional organizations in aiding clinicians with incorporating changes and recommendations within these types of documents.

, director of the Advanced Heart Failure & Transplant Center at Harrington Heart & Vascular Institute in the University Hospitals Health System as well as section head of advanced heart failure in the Division of Cardiovascular Medicine and Professor of Medicine at Case Western Reserve University.

, statement co-author, associate professor of Medicine, the Founding Director of the Heart Failure with Preserved Ejection Fraction Program, and the director of the Cardiac Amyloidosis Program at Weill Cornell Medicine.

 president of the Heart Failure Society of America, chief of Cardiovascular Medicine at the University of Utah School of Medicine, and director of the Cardiovascular Service Line at University of Utah Health Care.

Relevant disclosures for Gorodeski include Dynamed Plus. Relevant disclosures for Goyal include Agepha, Axon, and Sensorum Health. Relevant disclosures for Fang include Amgen, AstraZeneca, Boehringer Ingelheim, Novartis, and 

Bozkurt B, Ahmad T, Alexander KM, et al. Heart Failure Epidemiology and Outcomes Statistics: A Report of the Heart Failure Society of America. 

. 2023;29(10):1412-1451. doi:10.1016/j.cardfail.2023.07.006

Goyal P, DiDomenico RJ, Pressler SJ, Allen LA, Gorodeski EZ. Cognitive Impairment in Heart Failure: A Heart Failure Society of America Scientific Statement. 

. Published online March 12, 2024. doi:10.1016/j.cardfail.2024.01.003

Eiran Gorodeski, MD, MPH, Parag Goyal, MD, MSc, and James Fang, MD, discuss the HFSA's recent scientific statement on the prevalence and impact of cognitive impairment on the management of heart failure. 

The Role of Screening, Addressing Cognitive Impairment in Heart Failure Management

Parag Goyal, MD, MSc

The first question is, what is treatment resistant depression? So, when depression fails to respond to conventional treatment, then we call that treatment resistant depression (TRD). And beyond that very basic definition, it's only natural to ask yourself: “Well, how much treatment does it have to fail before it counts as TRD?” Right. So, if you look for a more precise definition or for a more fleshed out definition, it turns out that the definitions vary. Every place you go to has a different definition of TRD. The point here is that there is no consensus for a specific definition, and there's no universally accepted definition for what TRD is. As you'll see with these examples, there's differences in how many treatment attempts have to fail before you call it treatment resistance. Also, there's differences in parts of the wording [as well]. The definitions really vary.

How common is TRD? We just got through talking about how we don't have a precise definition, so if we don't have a precise definition, we sure don't have a precise percentage. But a very good rule of thumb is that it's roughly one third of patients with major depressive disorder (MDD) have TRD. Different people who have, you know, created estimates in different ways all come in at around that number. So, one out of three is just a very good rule of thumb. So, about a third of the people with MMD have TRD. With that many people with TRD, you know that anyone who practices mental health is going to have lots and lots of patients who they see who have TRD. The situation we see is kind of like this: You know, we see TRD all the time, every day. And I think so often that we hardly notice it sometimes because we're just we're just so used to it. Sometimes this can be the patient who comes in and says, "Oh, I'm doing fine." But when they say "fine," what they really mean is that they're not nearly as suicidal anymore. They are able to get up and go to work even though they're miserable, etc. Sometimes "fine" can still mean very depressed. Some of these people, you can give them a Patient Health Questionnaire (PHQ-9) and find out they're pretty darned depressed. We see these patients all the time who, even if they’re getting excellent care and the patient’s compliant and doing everything they’re supposed to do, [but] they’re doing lousy anyway. Of course, we all see that. Here we see, a lot of my patients just stay depressed: “This is fine.” The reason that this meme is amusing is because it's not fine. It's horrible for every individual with TRD; they are suffering. So, what can we do about it?

If a patient fails conventional treatment, what else can you do? I think the reason that TRD has come into our vocabulary so much more in recent years is that there's more we can do about it. So, it's worth talking about more because we have other things we can do. I'm going to list some of those other things we can do for treatment resistant depression. It's not an exhaustive list by any means, but here's some of the things we can do. One thing we can do for TRD is Transcranial Magnetic Stimulation (TMS). [It is] very safe, very effective. Also, there is Electroconvulsive therapy (ECT). ECT has its advantages and disadvantages. It is certainly has still has a place in psychiatry and it's been around a long time. There's ECT also. And then there's ketamine and esketamine. That's been increasingly used and for good reason. Here I just show the molecules; there's two mirror image molecules. The ketamine is a mixture of those two, esketamine is the one on the left. We have ketamine and esketamine are also good options. There's a lot more things to do. I mean, there's these and then there's, "but wait, there's more." There are psychedelic agents, there's deep brain stimulation, vagal nerve stimulation, direct transcranial current magnetic seizure therapy, [and] probably other stuff too that I don't I didn't remember to put on the slide. There are other options, but the ones I list I think are the main ones. If you can remember one thing from what I'm talking about, it's this: if you have patients who have an inadequate response to what you're doing; you can be doing a great job and your patient can still be doing lousy. If you're in that situation, then what I recommend is this: let's do something different because we've got different stuff. We have other treatments that work very, very well. So as a health care provider, it's our duty to learn as much as we can about these other options so that we can do the very best we can for the patients who trust us with their care.

Transcript was AI-generated and edited for clarity.

Steve Harvey, MD, discusses the challenges of defining treatment resistant depression and provides and overview of treatment options.

Overview of Treatment Resistant Depression

Steve Harvey, MD

) is the third leading cause of cancer-related death despite only accounting for 3% of all new cancer diagnoses.

 Obesity is a well-known risk factor for multiple types of cancer, including PDAC. In fact, there exists a relative risk of PDAC of 1.10 for every 5-unit increment increase in body mass index (BMI).

 While bariatric surgery has been demonstrated to reduce overall cancer incidence and mortality, conflicting data exist regarding the effects of bariatric surgery on PDAC.

We performed a retrospective case-control study utilizing the National Inpatient Sample (NIS) database from October 2015 to December 2020. All adult subjects (age ≥18 years) with a BMI >40 kg/m2 or >35 kg/m2 with ≥1 metabolic comorbidity were identified and stratified into those with and without a history of bariatric surgery (Roux-en-Y gastric bypass or sleeve gastrectomy).

, Tenth Edition Clinical Modification (ICD-10-CM) codes were used to define variables of interest. Baseline characteristics and comorbidities among the 2 groups were compared using chi-squared and Wilcoxon rank-sum tests and logistic regression analysis was performed to assess the risk of PDAC after adjusting for multiple risk factors, including tobacco use, acute and chronic pancreatitis, diabetes mellitus and various stages of obesity.

Over 19 million subjects were included, 1,656,329 of whom had a history of bariatric surgery. Patients with a history of bariatric surgery were significantly younger, more frequently female (75% vs 58%), had higher rates of class 3 obesity (69% vs 52%) and lower prevalence of hypertension, hyperlipidemia, chronic kidney disease, Charlson Comorbidity Index (CCI) ≥3, tobacco use, acute and chronic pancreatitis and pancreatic cancer (0.1% vs 0.2%) while having a higher prevalence of OSA (

 <.001). Additionally, in-hospital mortality (0.5% vs 1.8%), total hospital charges and overall length of stay were lower in the bariatric surgery cohort compared to the nonsurgical cohort (

 <.001). After adjusting for multiple comorbidities and risk factors, history of bariatric surgery was demonstrated to significantly reduce the risk of PDAC on both univariable (odds ratio [OR], 0.50; 95% confidence interval [CI], 0.44 - 0.56) and multivariable analysis (OR, 0.68; 95% CI, 0.61 - 0.77).

This is the largest analysis to date investigating the effects of bariatric surgery on pancreatic cancer risk reduction and serves to clarify previously inconclusive data. We have shown bariatric surgery to exhibit an independently protective effect against PDAC oncogenesis. It is reasonable to suggest that patients at increased risk of PDAC as well as other obesity-related malignancies may be recommended for surgically-assisted weight loss earlier and more frequently.

With advancements in minimally invasive bariatric procedures, expanding patient eligibility and indications for surgery, increasing utilization of bariatric surgery and endoscopic bariatric and metabolic therapies may help alleviate the growing burden of pancreatic cancer.

Surveillance, Epidemiology and End Result (SEER) Program. Surveillance Research Program, National Cancer Institute. 2023 Apr 25. https://seer.cancer.gov.

Aune D, Greenwood DC, Chan DS, et al. Body mass index, abdominal fatness and pancreatic cancer risk: a systematic review and non-linear dose-response meta-analysis of prospective studies. Ann Oncol. Apr 2012;23(4):843-52. doi:10.1093/annonc/mdr398

Schauer DP, Feigelson HS, Koebnick C, et al. Bariatric Surgery and the Risk of Cancer in a Large Multisite Cohort. Ann Surg. Jan 2019;269(1):95-101. doi:10.1097/SLA.0000000000002525

Adams TD, Stroup AM, Gress RE, et al. Cancer incidence and mortality after gastric bypass surgery. Obesity (Silver Spring). Apr 2009;17(4):796-802. doi:10.1038/oby.2008.610

Sjöström L, Gummesson A, Sjöström CD, et al. Effects of bariatric surgery on cancer incidence in obese patients in Sweden (Swedish Obese Subjects Study): a prospective, controlled intervention trial. Lancet Oncol. Jul 2009;10(7):653-62. doi:10.1016/S1470-2045(09)70159-7

Tee MC, Cao Y, Warnock GL, Hu FB, Chavarro JE. Effect of bariatric surgery on oncologic outcomes: a systematic review and meta-analysis. Surg Endosc. Dec 2013;27(12):4449-56. doi:10.1007/s00464-013-3127-9

Bulsei J, Chierici A, Alifano M, et al. Bariatric surgery reduces the risk of pancreatic cancer in individuals with obesity before the age of 50 years: A nationwide administrative data study in France. Eur J Surg Oncol. Apr 2023;49(4):788-793. doi:10.1016/j.ejso.2022.11.013

Fan H, Mao Q, Zhang W, Fang Q, Zou Q, Gong J. The Impact of Bariatric Surgery on Pancreatic Cancer Risk: a Systematic Review and Meta-Analysis. Obes Surg. Apr 05 2023;doi:10.1007/s11695-023-06570-x

Wilson RB, Lathigara D, Kaushal D. Systematic Review and Meta-Analysis of the Impact of Bariatric Surgery on Future Cancer Risk. Int J Mol Sci. Mar 24 2023;24(7)doi:10.3390/ijms24076192

A history of bariatric surgery was associated with up to 50% reduced risk of PDAC among a national cohort.

Bariatric Surgery is Associated with Reduced Risk of Pancreatic Cancer: Analysis of a US National Database

Vibhu Chittajullu, MD

Role of PCPs in Proactively Discussing CRC Screening With Patients

How can primary care providers effectively communicate the importance of colorectal cancer screening and guide patients in selecting the most appropriate option?

What role do patient preferences and adherence play in choosing a colorectal cancer screening method?

What are future innovations in the colorectal cancer space?

Effective communication by primary care providers about colorectal cancer screening involves clear, empathetic discussions that emphasize the importance of early detection and personalized risk assessment. Providers should guide patients in selecting the most appropriate screening option by considering individual risk factors, preferences, and potential barriers to adherence. Patient preferences and adherence significantly influence the choice of screening method, as they impact the likelihood of completing the screening process. Future innovations in colorectal cancer screening may include advancements in non-invasive testing, improved risk stratification tools, and personalized screening schedules.

Vivek Kaul, MD, discusses how primary care providers can effectively communicate the importance of colorectal cancer screening and guide patients in selecting the most suitable option, and the significant role of patient preferences and adherence in this decision-making process, while also addressing future innovations in screening methods.

First Line Care in CRC

Vivek Kaul, MD 

 What I’m hearing from you guys is that it’s important to educate your patients, to provide informed tools for them to make an informed decision based on their specific scenario. For our last question, I’m going to ask all of you: sickle cell disease has been around for over 100 years, and we’re still dealing with organ damage, acute exacerbations, quality-of-life issues, fatigue, difficulty finding a mate, difficulty finding work. What are your concerns around health equity and access to care that are persistent? What would be the 1 thing that if you could fix about sickle cell disease if you had a magic wand or a genie bottle? I’m going to have Dr Desai start, then Dr Shah and Dr Smith.

 I’m going to make the first wish. It’s to get every patient connected to some care—having somebody who will care and talk about these things, to say “I don’t know” sometimes and walk through life with them. We’ve talked about how complicated it is; they can’t do it by themselves. Everybody needs that advocate, they need the person that understands the disease. Even if they don’t understand, they’re willing to take that extra step. I wish everybody had a place that they could be connected to care.

 Excellent. Dr Shah, what’s your 1 wish from the genie bottle or magic wand?

 For wish No. 2, I have a 2A and 2B; they’re connected. The 2A is a big shift in mindset about therapies, from being reactive to prophylactic. We have drugs that are reactive because they’re anemic or because they have pain. But why do they have to be anemic or in pain? Why can’t we move more toward prophylactic? But because therapies are expensive, there’s so much out there, and not all patients are in centers that can give you those therapies, when we get to those therapies being prophylactic, they must be accessible, easy to take, and cost-effective. Not a drug that’s so expensive that a payer isn’t going to want to support that across the country. We have patients who aren’t plugged in to care, don’t have access to health care, and don’t have insurance. Why aren’t they getting the same therapy as another patient in an area that has a comprehensive sickle cell center? So there are 2 arms: better prophylactic medications with access to as many patients as possible.

 Public health. We don’t know how many patients have sickle cell disease in the United States, but Brazil does. Brazil is supposed to be an emerging nation. That’s a travesty. If we knew how many patients had sickle cell disease in every state in the United States, then we could more appropriately advocate for resources to do everything you just heard. We can know just by having somebody snap their finger and make each state share their newborn screening registry with each other; we could do that. Eleven states are already doing it, according to the CDC [Centers for Disease Control and Prevention]. My 1 wish is to get all 50 states to do that so we can talk intelligently about how many patients have the disease. We can then make health care allocation decisions for not just doctors but community health workers, hospitals with drugs, and community-based organizations and resources to help these patients.

 Thank you so much. My 1 wish is that all 3 of your wishes—or 3½ to 4 wishes—come true. If we get there, then each individual with sickle cell disease should be able to live to be 99 years old, get to lose all their teeth, and use a walker. Having a quality of life and a quantity of life that equals that of their peers is the ultimate goal.

I want to thank you, Dr Desai, Dr Shah, and Dr Smith. Thank you for this very informative session, for all your knowledge, and for sharing your experiences. This is a transformational period in sickle cell disease care. I look forward to more drugs being approved, I look forward to a lot more research, and I look forward to the 50 states being connected and for every patient to have access to the right type of care. Thank you very much, everyone.

Concluding their discussion on sickle cell disease management, expert panelists share key unmet needs and hopes for the future.

Authors