This has been a great program. I’ve learned a lot. We covered lots of ground about antithrombotic therapy, coronary artery disease [CAD], and peripheral artery disease [PAD] in general. Let me turn to our distinguished panel for some closing thoughts. I’ll start with you, Manesh. Any final points [that] you want to make for the audience?

Deepak, it’s been fun and exciting. It’s fun to talk to people about evidence for the things we see. We’ve learned over the last decade is that vascular disease unfortunately is still the leading cause of cardiovascular mobility issues and mortality. As we have more options, which is a good thing, we have to get the right dose for the right patient at the right time. Some of that is understanding the risk and the risk benefits that we’ve talked about. Concerning patients with polyvascular disease, patients with broad thrombotic risk, it’s important to understand how you can make them have better outcomes. We’ve talked about that today. Hopefully it’s something that people will take home.

 I agree. It’s been a wonderful panel. I’m thrilled to be part of this. My take-home message would be to focus on identifying these polyvascular patients. Because they’re such high-risk patients, it’s important not to be focused on the coronary artery disease. But if patients have coronary artery disease and vascular disease in another territory, then that’s the pinnacle of our risk. Diabetes on top of that is going to be at that highest cardiovascular risk, so we need to talk with our patients about the fact that they’re at a higher risk and how that guides our recommendations for changing medications. Oftentimes patients can be resistant, understandably, to wanting to add another medication. But part of patient-centered decision-making is educating them that this is why that goes a long way.

We need to educate the medical community about those risks that identify polyvascular disease, diabetes is a real risk amplifier. Great points. Eric, any closing thoughts?

 This was a fantastic discussion. For everyone watching this, it’s important for us to not be fearful of making a change in our practice. We’ve been set in our ways for a long time, but we’ve had these accumulating data. It’s time for us to be open-minded about making changes that benefit our patients. We’ve heard today that there are many agents that can optimize long-term cardiovascular and limb-related risk outcomes and improve the care for our patients, so it was a great discussion.

Absolutely agree and Sahil, any final thoughts?

 That’s really important. What Eric just said is that we’ve been in this mode of using dual-antiplatelet therapy for extended amounts of time with very little evidence, particularly in the PAD population, which is the predominant part of my practice. It’s great that we have strong evidence to support the use of dual-pathway inhibition. We need to get the message out to our referring doctors and our patients that this is the way forward to optimize the risk.

Terrific. Marc, you’ll get the final word.

 It’s been an honor to be part of this panel. We’ve learned that we have a gap in terms of the evidence and how we treat our patients. Part of that is that we have a lot of patients to see. We’re all very busy clinicians. Everyone wants to do their best. But understanding who the highest-risk patient is and what the best evidence is needs to be at the top of your mind as you see your clinic patients, and polyvascular disease resonates. I learned that term from you, Deepak, many years ago. It has been shown in every study to be such a potent marker of risk and beneficial for some of these strategies and other things like diabetes. We need to take that into the clinic and start treating our patients better.

I couldn’t agree more. Hopefully the audience found this exchange of ideas informative, interesting, and educational. Hopefully these are things you can take this into your practices. As I mentioned, I learned a lot. A final point I’ll make is that when you’re thinking about coronary artery disease, think about the whole patient. For that patient you’re seeing for 1 specific condition, that might be the issue in the office for that day. But they may have other risk factors. They may have plaque in other arterial territories. We talked a lot in this session about polyvascular disease, but keep in mind that CAD, PAD, and cerebrovascular disease can coexist. Even though the patient might be seeing you for angina in that office visit or hospital encounter, think about all those associated risks. If you identify those associated risks, you realize that it’s a very high-risk patient, the sort of patient for whom we want to do everything possible to reduce their risk, including intense lifestyle modification. Beyond that, in many cases pharmacotherapy, polypharmacy with wisdom and caution, and in some cases procedural care are all complementary approaches, not competitive approaches.

Thanks to all of you on our panel and to our audience for this rich and informative discussion. If you enjoyed the content, please subscribe to our e-newsletters to receive upcoming 

 and other great content right in your in-box.

A panel of expert cardiologists share their concluding thoughts on management of polyvascular disease in clinical practice.  

Concluding Thoughts

Amy Pollak, MD

Monitoring and Setting Treatment Expectations With JAK Inhibitors in Alopecia Areata

How do you decide whether a JAK inhibitor is an appropriate treatment option for a patient?

A panelist discusses how they determine the appropriateness of a Janus kinase (JAK) inhibitor for patients by evaluating disease severity, duration, prior treatment failures, patient comorbidities, risk factors, and laboratory results and engaging in detailed benefit-risk discussions while setting realistic expectations about treatment outcomes and potential adverse effects.

Brett King, MD, PhD

Conan Tu, MD, is chief of Adult Primary Care, Eastern Long Island for Optum NY/NJ.

Diabetes Dialogue: Addressing America's Shortage of Diabetes Care Providers, with Jay Shubrook, DO, & Conan Tu, MD

85th Scientific Sessions of the American Diabetes Association (ADA 2025)

, hosts Diana Isaacs, PharmD, and Natalie Bellini, DNP, welcome Jay Shubrook, DO, and Conan Tu, MD, to explore the mission and momentum of the 

The conversation centers on addressing the national shortage of diabetes specialists. Shubrook, a primary care diabetologist and founding figure in diabetology training, details the evolution of fellowship programs dating back to 2004, with the current infrastructure supporting 11 programs and plans for further expansion. Tu, an internist from New York, shares his personal journey into diabetology, emphasizing the increasing demand for diabetes-focused care in primary settings and the transformative impact of timely, expert-level interventions.

The guests outline how the American College of Diabetology is building a standardized, certified workforce through board certification, with an emphasis on team-based care. The College is also actively expanding to include pharmacists, nurse practitioners, and other healthcare professionals in its educational and certification efforts, helping to equip interdisciplinary teams to manage diabetes more effectively.

Additional discussion highlights include the importance of continuity of care—particularly during the transition from pediatric to adult diabetes services—the integration of cardiometabolic risk management, and the critical need for scalable models of care. The speakers advocate for diabetologists to serve not only as direct providers but as in-house experts, mentors, and system-level educators capable of elevating care across large networks.



Learn more about the American College of Diabetology.

Relevant disclosures for Isaacs include Eli Lilly and Company, Novo Nordisk, Sanofi, Abbott Diabetes Care, Dexcom, Medtronic, and others. Relevant disclosures for Bellini include Abbott Diabetes Care, MannKind, Sanofi, and others. Relevant dislcures for Tu include AstraZeneca, Eli Lilly and Company, and Optum. Relevant disclosures for Shubrook include Abbott, AstraZeneca, Bayer, Eli Lilly and Company, and Novo Nordisk.

Explore the urgent need for diabetes specialists and the American College of Diabetology's efforts to enhance care through education and certification.

Conan Tu, MD

Treatment and Outcomes of Coats’ Disease with David Abramson, MD

2025 New York State Ophthalmological Society (NYSOS) Annual Meeting

, David H. Abramson, MD, an ophthalmologist at Memorial Sloan Kettering Cancer Center, presented the results of, and his findings from, a pediatric surgery on a patient with 

Coats’ disease, historically defined by telangiectatic, exudative retinal vessels with peripheral capillary dropout, remains a diagnostic and therapeutic challenge, particularly in its advanced stages. While early-stage, localized disease—limited to approximately 90 degrees of the retina—can often be managed effectively with laser photocoagulation, more extensive cases typically progress to subretinal exudation, retinal detachment, neovascular glaucoma, and loss of the eye.

Abramson noted that anti-VEGF agents, despite widespread success in other exudative retinal pathologies, have shown limited effectiveness in Coats’ disease. Successes have been rare and unpredictable. Notably, however, this case involved combination therapy with laser and anti-VEGF and resulted in a successful outcome. Abramson hypothesizes a potential link between treatment responsiveness and underlying telomere biology disorders, though this remains speculative.

“I’ve had a suspicion – but I don’t really have anything more than a suspicion – that it’s the patients who have the telomere biology disorders causing Coats’ who are the ones that actually do respond to anti-VEGF agents,” Abramson told 

Surgical management for total retinal detachment in Coats’ disease is technically straightforward but often ineffective due to the viscous nature of chronic subretinal exudate, which Abramson likens to honey. The high rate of surgical failures has led many experienced pediatric retinal surgeons to advocate for conservative management in such scenarios. Steroid use has shown anecdotal promise, but consistent replication of positive outcomes remains elusive.

Additionally, existing treatments are prone to subfoveal, submacular, and subretinal scarring, which result in profound vision impairment. Abramson notes the necessity of this damage.

“Success here is not determined as getting good vision,” Abramson said. “Success is keeping the eye and, of course, identifying what [the disease] is.”

Abramson’s genetic findings will further complicate and enrich general understanding of Coats’ disease. Though long considered a unilateral condition, widefield fluorescein angiography now reveals bilateral involvement in many cases. Moreover, genetic studies have implicated mutations in genes such as LTBP2, though many cases remain genetically unexplained. These findings support a broader systemic context, which Abramson categorized as "Coats’ plus”, characterized by multi-organ involvement—cardiac, hepatic, pulmonary, dermatologic, neurocognitive, and hematologic—including risks of malignancy and bone marrow failure.

While no gene-targeted therapies for Coat’s disease exist to date, recognizing these systemic associations enables earlier multidisciplinary interventions and more comprehensive patient care. Ultimately, Abramson underscores the importance of evolving beyond outdated clinical paradigms, integrating both modern imaging techniques and genetic diagnostics to improve outcomes and guide long-term management strategies.

Abramson, DH. Coats' Disease: A New Gene and a New Finding. Presented at the 2025 New York State Ophthalmological Society Annual Meeting. May 16, 2025. New York, NY.

Abramson discusses the potential benefits and limitations of treatment methods for Coats’ disease and further discusses the genetic component of its pathology.

David H. Abramson, MD

 (managing medications when not eating or drinking) are frequently applied in medicine. 

It is routine to adjust medications when patients are ill or undergoing procedures, but the ‘formal’ adoption of 

 is unusual in the US. However, outpatient 

 are common in Canada, Australia, New Zealand, and many European countries. The local pharmacist often adjusts outpatient medications to decrease acute kidney injury (AKI) incidence.

 When sick day guidelines were originally conceived in 2013, they were part of a worldwide effort to decrease the incidence of AKI.

 Yet, as is often the case in medicine, there are more nuances to 

The National Institute for Health Care Excellence (NICE) convened an international expert panel in late 2022 to develop a consensus on 

 The panel included a multidisciplinary group of 26 experts from 4 countries and 10 medical disciplines. The panel listed 42 specific recommendations: 5 that are signs or symptoms of dehydration (Chart 1), 6 that require immediate medical interventions (Chart 2), and 14 scenarios for patient self-management (Chart 3). Although some scenarios had less than 100% agreement, most recommendations were close to unanimous. The expert panel also agreed on which medications qualify under the ‘

Educating and involving patients in adjusting medications to fit circumstances is essential for successful self-management. Up to 50% of Americans are estimated to have at least chronic disease, which requires management and, often, medication adjustment.

 Self-management techniques have proved to be successful for patients with diabetes, asthma and hypertension.

 represent a new frontier in medication management. The guidelines establish categories for intervention based on severity ranging from complete self-management to a 911 call. While most sick day guidelines focus on diabetes management, the newer guidelines include SGLT2 inhibitors, anti-hypertensive medications, and diuretics. The focus is to address complications related to either volume depletion, hypo or hyperglycemia, or ketoacidosis.

Any guideline has its supporters and detractors; however, the concept of holding medications while 

 is postulated to decrease the incidence of iatrogenic AKI and thus save nephrons. However, only time will tell.

National Institute of care and Excellence (NICE) Acute kidney injury: prevention, detection and management, NICE guideline. December 18, 2019, 

, guideline 1.2.13 pg 12. Accessed June 17, 2023

Lea-Henry TN, Baird-Gunning J, Petzel E, Roberts DM. Medication management on sick days. 

Sick day guidance - think kidneys. Think Kidneys NHS. January 2018. Accessed June 17, 2023. https://www.thinkkidneys.nhs.uk/aki/wp-content/uploads/sites/2/2018/01/Think-Kidneys-Sick-Day-Guidance-2018.pdf.

Watson KE, Dhaliwal K, Robertshaw S, et al for PAUSE (Preventing Medication Complications During Acute Illness Through Symptom Evaluation and Sick Day Guidance) Medication Safety Advisory Panel. Consensus Recommendations for Sick Day Medication Guidance for People With Diabetes, Kidney, or Cardiovascular Disease: A Modified Delphi Process. 

Watson KE, Dhaliwal K, McMurtry E, et al. Sick Day Medication Guidance for People With Diabetes, Kidney Disease, or Cardiovascular Disease: A Systematic Scoping Review. 

Kwong YD, Tuot DS. Optimizing Self-Management Programs in Kidney Disease: Implementation of Sick-Day Protocols. 

In their latest column, Kim Zuber, PA-C, and Jane Davis, DNP, break down the concept of "sick day rules" and what this means for providers caring for those with kidney disease. 

Sick Day Rules in Nephrology, with Kim Zuber, PA-C, and Jane Davis, DNP

Kim Zuber, PA-C

Lily Dara, MD, is a physician-scientist, hepatologist, and assistant professor of medicine at the University of Southern California.

Distinguishing Drug-Induced vs Classic Autoimmune Hepatitis, with Lily Dara, MD

Drug-induced autoimmune-like hepatitis (DI-ALH)

 is a rare subtype of idiosyncratic drug-induced liver injury (DILI) that closely mimics autoimmune hepatitis (AIH). While their presentation is similar, their management is not, underscoring the importance of differentiating between the two.

While distinguishing DI-ALH from classic AIH is critical for appropriate diagnosis and management, doing so is no easy feat – both conditions share nearly identical serological markers and histological features.

“It's really important to distinguish drug-induced autoimmune-like hepatitis from autoimmune hepatitis. Because if the patient is on nitrofurantoin and you stop it and the numbers come down, you really don't need immunosuppression,” Lily Dara, MD, a physician-scientist, hepatologist, and assistant professor of medicine at the University of Southern California, explained to 

She notes that in the case of persistent liver injury, immunosuppression is finite and patients can generally come off of prednisone within 4-6 months. If the patient does not relapse, Dara says this defines that it was drug-induced. If the patient relapses or continues to have injury, she says this indicates underlying idiopathic or classic AIH.

“Once you have autoimmune hepatitis in the differential, you still go down that pathway of diagnosis, which requires a liver biopsy,” Dara explained. “If you suspect it's a drug, you immediately stop the drug, and you watch the liver enzymes closely. If they don't come down, you start immunosuppression.”

She stresses the importance of long-term monitoring of these patients, noting that if it is a bout of AIH that was caught and treated quickly, patients can still relapse 1-2 years later. Accordingly, Dara says patients should be monitored for 5 years to ensure they do not manifest as having classic AIH.

She also highlights that some drugs known to trigger DI-ALH can be substituted for safer alternatives. Specifically, she cites the use of alpha-methyldopa for pregnancy-related hypertension and notes nifedipine or labetalol are guideline-recommended options that may be safer.

Dara goes on to discuss research into genetic predisposition, referencing studies from the Drug-Induced Liver Injury Network that explore HLA phenotypes and genetic markers associated with DI-ALH. However, due to small sample sizes, she says more extensive studies are needed to identify potential biomarkers and distinguish it from classic AIH.

Editors’ note: Dara has no relevant disclosures.

Tan CK, Ho D, Wang LM, Kumar R. Drug-induced autoimmune hepatitis: A minireview. World J Gastroenterol. doi:10.3748/wjg.v28.i24.2654

Dara explains the importance of distinguishing DI-ALH from classic AIH, how their management differs, and where research in this field is heading.

Lily Dara, MD

Panelists discuss how to effectively onboard patients to Janus kinase (JAK) inhibitors through transparent risk discussions, early follow-up visits at 4 weeks, and personalized treatment approaches that consider patient-reported outcomes and the “3 Cs” (cancer, cardiac disease, clotting disease) while emphasizing the anti-inflammatory benefits and quality-of-life improvements these therapies provide.

Personalized Strategies for Sequencing Therapies in Atopic Dermatitis

Video content above is prompted by the following: 

Patient onboarding for JAK inhibitor therapy requires comprehensive counseling focused on realistic expectations and anticipatory guidance. Clinicians should provide transparent discussion of the boxed warning while contextualizing risks within the atopic dermatitis–specific safety data. The “3 Cs” assessment framework—evaluating patient history of cancer, cardiac disease, and clotting disorders—helps guide appropriate patient selection while recognizing that many patients with comorbidities can safely receive JAK inhibitors based on current evidence.

Effective patient communication emphasizes the anti-inflammatory properties of JAK inhibitors, drawing parallels to familiar medications such as ibuprofen to contextualize safety concerns. Early follow-up at 4 weeks demonstrates physician commitment and allows for treatment optimization, as JAK inhibitors typically show rapid efficacy that often exceeds patient expectations. Continued emphasis on fundamental atopic dermatitis skin care principles remains essential even with systemic therapy success.

The evolving landscape of atopic dermatitis treatment now enables truly personalized approaches based on patient-reported outcome measures and quality-of-life impacts. Current treatment guidelines support switching therapies when patients don’t achieve moderate improvement within 3 to 6 months, moving away from stepwise approaches and toward optimization of individual patient outcomes. This patient-centric model recognizes that JAK inhibitors address multiple symptom domains simultaneously—including itch, sleep disruption, and psychosocial impacts—making them suitable for diverse patient presentations while maintaining the core principle of treating patients as family members deserving optimal care.

Lindsay S. Ackerman, MD, FAAD

Expert hepatologists discuss future developments in HCV.

The Future and Resources in HCV Care

 Mark, are you looking into the future? Are you excited about anything in whether treatment of hep[atitis][hepatitis] C or management of hep[atitis][hepatitis] C? Is there anything down the line that's got you excited?

Certainly, it's a very exciting time. I mean, we've got opportunity in front of us to really for the first time eliminate hep[atitis][hepatitis] C's[in] public health. We can't lose sight of that. I think it's easy to lose sight of that as we struggle with some of the barriers that we've talked about today. So, what do we need to do? Some of you've heard here, we need to increase access to medications. And although tThese medications are highly cost effective, if not [a form of] cost savings, in a relatively short period of time, meaning society will spend less money over a brief period, say five 5 years, if we treat everyone. Despite that, there's there are still barriers to accessing medication. So, tThe first thing we're excited about is removing those barriers. Nancy mentioned and prior authorization forms. I'm working on one now that's 37 patient pages long. Six months we've been back and forth. I'll leave that where it is because there’s not much more I can say. But [the important point is] ensuring we have access. And tThen to pick up on people'sTipu’s point, it's bringing the medications to the patient. And tThere we really need point-of-care testing. So, the second thing I'm excited about is point-of-care PCR [polymerase chain reaction] testing, or antigen testing is another possibility. We mentioned the antibody shows that your immune system has seen hep[atitis][hepatitis] C, but when you cure someone, they remain antibody-positive. So, it [the testing] becomes less effective as we cure more people.. So gGo into a community,[and do] a point-of-care test, a rapid result that shows they're actively affected. Then you've got access. So, yYou reach into the backpack, pull out the medication, hand them a medication, follow that minimal mileage to actually get their phone number, although I'll make another plug for using social media like WhatsApp because they can lose their phone, but they’ll still have the same access. So tThat's the second thing, is point of care. And you say, well, what about people with bad livers? Well, bBring a mobile elastography or fiber scan machine. And iIf your their score is low, you they don't have liver failure. So, point of care. The third thing I'm excited about is actually the potential to develop long-acting therapies. And iIn the HIV space that I've alluded to a couple of times, they now have medications that can be given at that last eight 8weeks. Huh, eight 8 weeks. Well, iIf we had a hep[atitis][hepatitis] C medication that sustained in the liver for eight 8 weeks after a single injection, that would be a one-shot cure. And tThat is being worked on as we speak., Sso, it's not without the realm of possibility. And give me one more.: It's vaccine. And wWe've talked a lot about trying to treat our way out of the hep[atitis][hepatitis] C epidemic, but this is an incredibly transmissible pathogen. We saw that with healthcare–worker needle sticks. We see that with populations and networks of people who inject drugs,. [It’s]incredibly transmissible. So yYes, we should be treating everybody and taking the path of treatment prevention, but vaccine is essential. And tThere's now a lot of excitement around vaccine development and what's called human challenge studies. That's where you take a volunteer with the appropriate informed consent, you intentionally give them hepatitis C, and vaccinate some and see if the vaccine can clear the infection. And then oOf course, you've got treatment to rescuethem,…those who don't clear. It sounds a bit crazy, but they do this with malaria, they do this with dengue, they do this with shigella, diarrhea, and they did this with COVID-19, intentionally affecting [infecting] people. And wWhy would you do that? Because it allows you to test vaccine candidates very quickly. If they don't work, move on. So tThose are the things I'm excited about as we work our way to 2030. It's only seven 7years away, so we've got a lot of work to do.

 So sSome exciting things [are] on the horizon potentially. For some of our viewers who might not be aware, iIt's really an exciting time around Hep[atitis][hepatitis] C. We have a relatively newly announced federal elimination plan that has been brought forward. This is something that's obviously very fluid and dynamic, but it's in development. . [There are] [It has] the three 3 key components,: iIt would fast track point-of-care tests like Mark has described. It would open access to medications, hopefully eliminating a lot of the barriers that we've discussed. And it would also provide funding for the infrastructure needed to actually carry this work out. So sStay tuned for all of this, there is a lot that'’s happening. We'’ve covered a lot of ground. Nancy, if providers, if viewers [patients] are looking for more information, do you have any go-to sites that they can access to get more infoit?

Well, aAbsolutely. There are tons of them. So I think that Hep[atitis][Hepatitis] CP Live actually has great tools, the American Liver Foundation, [and] you cannot go wrong with things like the CDC or the World Health Organization. Also, I wouldn't discount your industry partners, especially once you [patients] know the agent that you're[they’re] being started on. There are really great resources on those websites when [they] you know what you're[they’re] going to be taking. But I think that misinformation is also prevalent. So yYou want to make sure that you're talking to your patients about what their fears are. There still are websites out there that say that Hep[atitis][hepatitis] C treatment is intolerable, that you're going to end up with depression or some of the interferon-related side [adverse] effects, [or] that you won't be able to work through things, or that these are still experimental. I mean, tThese are not experimental therapies anymore. And so, yYou want to make sure that you're using a tool that's vetted and up-to -date, not archaic.

 YeahYes, hcv.com is also another great resource.— A alot of information there, practical information about implementation, and tons of great educational content. Thanks to all of you for this rich and informative discussion. And thank you, our viewers, for joining us during this HCP Live Peer Exchange. If you enjoyed today's content, please subscribe to our e-news letters to receive information regarding upcoming peer exchanges and other great content right to your inbox. Thank you very much.

Transcript was AI-generated and edited for clarity.

Expert hepatologists discuss future developments in HCV that they are excited about and provide resources for new providers to get started on delivering HCV care.

Mark Sulkowski, MD

 is managed with corticosteroids; however, approximately 30 - 40% of patients are refractory to corticosteroids and require medical or surgical rescue therapy.

Corticosteroid refractoriness may be attributed to genetics as well as expression of pro-inflammatory cytokines. Downstream signaling of interleukin 2 (IL-2) prevents glucocorticoid receptor translocation, but this may be dampened by Janus kinase (JAK) inhibition. Singh et al. conducted a single-center, prospective, double-blind randomized controlled trial in India to determine if the addition of tofacitinib, a JAK1 and JAK3 inhibitor, to corticosteroids was superior to corticosteroids alone in hospitalized patients with ASUC.1

The study randomized patients with ASUC to tofacitinib 10 mg 3 times daily (n = 53) versus placebo (n = 51) plus hydrocortisone 100 mg every 6 hours. An intention-to-treat analysis after 7 days of clinical assessment revealed patients in the tofacitinib group had higher responses to therapy, defined by a decline in Lichtiger index >3 points and an absolute score <10 for 2 days (difference, 24.2%; odds ratio [OR], 3.42; 95% CI 1.37 - 8.48; 

= .007), and lower need for rescue therapy (difference, -20.1%; OR, 0.27; 95% CI 0.09 - 0.78; 

Following the 7 days, patients and investigators were unblinded. The probability of infliximab or total colectomy up to 90 days was found to be significantly lower in the tofacitinib responders who were continued on tofacitinib and a prednisone taper compared to non-responders who were continued on 5-ASA or azathioprine and a prednisone taper (

Despite these positive outcomes, adverse effects were relatively high amongst the tofacitinib (24.5%) and placebo (13.7%) groups. In the tofacitinib group, most of these adverse events were not major (hair loss, acne, upper respiratory tract infections, etc.). However, 1 death and 4 deaths were noted in the tofacitinib and placebo groups, respectively. Deaths were attributed to mostly severe disease phenotype, but also systemic toxicity (n=2) and hemorrhagic venous infarct (n = 1). One venous thromboembolism event, a dural venous thrombus, occurred in a patient in the tofacitinib group.

This novel study suggests that tofacitinib plus corticosteroids may be a first-line therapy that supplements the limited options available for patients with ASUC. Limitations include external validity, objective measures of disease activity, and the non-conventional duration of 7 days of corticosteroids that may hinder clinical applicability in the US.

Future studies to personalize this approach, limit generalizability, optimize dosage and duration of up-front therapy, and further delineate adverse event rates are required to further support the use of JAK inhibition for ASUC.

Singh A, Goyal MK, Midha V, et al. Tofacitinib in Acute Severe Ulcerative Colitis (TACOS): A Randomized Controlled Trial. Official journal of the American College of Gastroenterology | ACG 9900:10.14309/ajg.0000000000002635.

Findings from a novel study supports the JAK inhibitor tofacitinib as a potential first-line therapy for ASUC.

Tofacitinib in Acute Severe Ulcerative Colitis (TACOS): A Randomized Controlled Trial

Ravi Shah, MD

Sammy Saab, MD, MPH, is a professor in the departments of medicine and surgery at the David Geffen School of Medicine at UCLA, medical director of the UCLA Adult Liver Transplant Program, medical director of the Pfleger Liver Institute, and the chief of transplant hepatology.

Unmet Needs in Wilson Disease, with Sammy Saab, MD, MPH

, also known as hepatolenticular degeneration, is a genetic disorder of copper metabolism that leads to the accumulation of copper in the liver and other tissues, including the brain.

With an estimated prevalence of 1 case per 30,000 live births in most populations, Wilson disease is rare but serious, with gradual damage from the accumulation of copper resulting in hepatic, neurologic, and 

 manifestations. With effective treatment options available, early detection and intervention are critical for preventing disease progression, mitigating symptoms, and maintaining quality of life.

In an interview with HCPLive, Sammy Saab, MD, MPH, a professor in the departments of medicine and surgery at the David Geffen School of Medicine at UCLA, medical director of the UCLA Adult Liver Transplant Program, medical director of the Pfleger Liver Institute, and the chief of transplant hepatology, explains unmet needs in Wilson disease, describing how affected patients often present with nonspecific symptoms and are not easily diagnosed due to the need for a combination of laboratory work, genetic testing, urinary testing, and histology to make a diagnosis. He highlights the need for a more simplified approach to identify affected patients.

Saab also calls attention to a current lack of data on long-term Wilson disease management and how to know whether a patient is being over-treated. He notes many patients do not come back for follow-up, which further complicates their disease management.

“We have a long way to go,” Saab said. “We've come a long way with medications, but we still have a way to go in terms of having simplified tests.”

Editors’ note: Saab has relevant disclosures with Gilead Pharmaceuticals, AbbVie, Takeda, Salix, Ipsen, Madrigal, Mallinckrodt, Ipsen, and Cymabay.

UpToDate. Wilson disease: Epidemiology and pathogenesis. Jun 19, 2024. Accessed March 21, 2025. 

https://www.uptodate.com/contents/wilson-disease-epidemiology-and-pathogenesis

Saab describes historical and ongoing unmet needs in Wilson disease, highlighting recent progress but also the need for a streamlined diagnosis.

Authors