I spoke to a patient, a 63-year-old woman who immigrated to the United States from Central America in 1978, about her experience living with liver disease. She is now an 

 NAFLD patient advocate who was diagnosed with autoimmune hepatitis and NAFLD in 2005. After experiencing the devastation of her diagnosis, she has managed to learn to live with the disease and wants to help others achieve better quality of life.

Our patient had been diagnosed with autoimmune hepatitis for several years and doing well. She developed pain in her upper right abdomen and saw three specialists. They assumed she was an alcoholic even though she told them she didn’t drink. She talked to her primary care physician who sent her to a liver specialist. 

The doctor spent 90 minutes talking to her and, based on blood work every three months and ultrasounds every six months, determined that her autoimmune hepatitis medication- prednisone, was causing fatty liver. It took three liver biopsies to confirm the diagnosis of NAFLD on top of autoimmune hepatitis.

Helpful Tips About Healthy Diet and Finding Support

This woman has made huge changes to her lifestyle. Sheexercises regularly, meditates, drinks plenty of water and has changedher eating habits by following a healthy diet and avoiding sugary drinks, such as soda and concentrated juice drinks. She prepares her own food and only takes medicine prescribed by a physician, who do so with caution because she has been at the last stage of liver cirrhosis for the last three years.

Though difficult, she has learned to avoid greasy foods found in fast food restaurants, eats abundant greens, incorporates fruit into her breakfast and vegetables for lunch. She’s learned to prepare food in different ways by sautéing, baking or grilling her food using olive oil. She does not fry her food, which she may have done previously. She avoids additives and salt, relying instead on herbs and spices.

Before trying new foods, she and her caregivers research its possible impact on the liver. When she buys groceries, she avoids red meat, high fructose corn syrup and anything with more than five ingredients. She also practices portion control and learned that the palm of your hand is the amount of meat you should eat, which for her is mostly fish, chicken and occasionally lobster.

She advises people tofollow their doctors’ orders and, once diagnosed, find a support group to learn and share information with others living with the same disease. People can find information online from organizations, such as the 

, and Facebook groups, such as Living with Cirrhosis, Living with Fatty Liver/NASH.

She is a true reflection of what it is to live with chronic liver diseases and how changing in your lifestyle can improve liver health and overall health.

This article is the final installment of four articles exploring the epidemic of liver disease called nonalcoholic fatty liver disease and its more severe form, nonalcoholic steatohepatitis.

The Multiple, Complex Challenges of Living with and Managing Liver Disease

Amreen Dinani, MD

Experts discuss the recent use of biosimilars like inolimomab as treatment for ulcerative colitis (UC).

Biosimilar Treatment Options for Patients With UC

David P. Hudesman, MD

Frank Diamond

Geoffrey Grammer, MD closes this series highlighting the administration options of esketamine, its safety profile, and the importance of monitoring patients using this treatment.

Esketamine Safety Mechanisms and Bioavailability

Geoffrey Grammer, MD

Current Therapeutic Guidelines for Managing Resistant Hypertension

Video content above is prompted by the following:

Briefly, what are the current therapeutic guidelines for managing resistant hypertension?

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 resistant hypertension management requires a structured approach combining lifestyle modifications, optimal doses of multiple drug classes, and the identification of underlying causes such as sleep apnea.

John M. Flack, MD, MPH, FASH

Focusing in on Novel Oral Systemic Therapies for Moderate Plaque Psoriasis: Medcast Video

03:15 The role of APP’s in getting patients access to dermatological care.

06:06 Managing patients with suboptimal controlled plaque psoriasis

13:05 Breaking down barriers to access new treatments for plaque psoriasis.

20:23 Deciding between oral and injectable systemic therapies.

24:25 The mechanism of action of TYK-2 inhibitors

28:24 The safety profile of deucravacitinib

33:14 Monitoring your patients with plaque psoriasis

Lauren Miller, MPAS, PA-C, leads an expert discussion surrounding exciting developments in the treatment landscape of plaque psoriasis.

Kristine Kucera, PA-C, MPAS, DHS

We’ve had a great conversation about treating atopic dermatitis. We all see a lot of patients. What I’d like to do is ask each of you: In your practice in dealing with these patients, do you have some kernels of truth that you’ve relied on that have helped set your patients up for success, or something you can give our audience that they can take back and utilize to have the best possible outcomes? Matt, I’m going to start with you.

 Linda, I’m going to give you the spiel that I give a patient once I’ve gotten through disease education and we’re now selecting therapy. I’m a believer that setting them up for success means shared decision-making so that they’re not taking what I think they should be on, they’re taking what they think they should be on. It can be really simple. I believe that shared decision-making needs to be really simple: 2 options, at most 3 bullet points per option.

Here’s my spiel: “Luckily for you, we have great options now, they’re not steroids, you’re going to stay on them long term. I’m going to give you some choices, and you’re going to tell me which one sounds better. First, we can treat you with a pill. It’s going to start working in 2 or 3 days, but it does weaken your immune system. Or we could give you a shot that starts working in a week or two but does not weaken your immune system. You have to keep giving yourself a shot every 2 weeks or once a month. So again, a pill works that in a couple days, no shots but weakens your immune system, or a shot every 2 weeks that starts working in a week or two and does not weaken your immune system. Which one sounds better to you?”

Most patients have a very clear either, “I couldn’t imagine giving myself a shot” or “I wouldn’t want to do anything that might weaken my immune system.” If they say pill, then I’m going to talk about the boxed warning. “I do have to tell you it’s going to have some things that sound really scary.” The advice I have for everybody is when you’re talking about the boxed warning, don’t start with heart attack, stroke, death, and cancer. Start with, “Some things sound really scary. The data we have about this medication haven’t shown an increased rate of these things. But the FDA wants you to know about them because a different medication used in people who don’t have eczema that’s distantly related to this medication did slightly increase the chances of these scary things. But again, for this medication, none of the information we have about it has shown an increased rate.”

I do want you guys to know and our viewers, I didn’t say it doesn’t increase the rate. I said the information we have has not shown any increased rate. I said scary things a couple of times. I’ve said distantly related medication, people who don’t have eczema. Then I say, “The scary things, just so you’re not surprised when you get it, are things like heart attacks, strokes, and blood clots, and cancer. But again, all the information we have about this medication has not actually shown an increased rate of those things happening.” That makes people more comfortable with the JAK [inhibitors], and I don’t feel like I’ve said anything inaccurate. If that was taped and played in court, everything I said was right, and I stand behind everything I said. My pearl is shared decision-making and how I talk about the JAK boxed warnings.

 It makes me think about a quote that is often attributed to Confucius. It might be apocryphal because people attribute a lot of quotes to Confucius. But it’s, “Because the newer treatments are good, it does not follow that the old ones were bad. For if our worshipful and honorable ancestors had not recovered from their ailments, you and I would not be here today.” But they are really nice, and to have some new treatments and be able to talk about these with our patients has changed the game. I think this is the beginning of a new era in atopic dermatitis. We can now promise things and deliver in a way that we’ve never been able to before. I’m really excited about this, and also excited to see where it’s going.

 I would add that the patients who present to our office who are most undertreated are still those moderate patients. I would say my pearl would be looking, as we’ve all said today, at the patient holistically, not just the BSA [body surface area] of that patient on one day and time but considering other factors like the impact of itch. Sometimes I look at something called the BSA of itch, where you’re saying, “Your skin disease is 5% today, but where are you itchy? How is this impacting your life?” The moderate patients are as impacted quality of life-wise by their disease as our severe patients, if you look at the studies. So, make sure you are presenting your options.

I like what Aaron said, even when you have a mild patient in the office, I often say, “You look good today, but I want to show you the runway, which is very different than it was 5 or 10 years ago. If your disease control is to change, if your satisfaction about your treatment or something about your life is to change, if your disease is to change in some ways, I want you to know that other treatments exist.” Because for so many years for these patients, they didn’t. Still, I think there’s lack of awareness of our advanced therapies for atopic dermatitis. It’s capturing the moderate patients, it’s getting all of our patients to higher levels of disease control. I agree with Peter, I feel so lucky to take care of these patients in the year 2023, and I think we’ll only feel that amplified in the years to come.

This has been a fantastic discussion. I think we’ve all learned from each other. I want to thank each of you for this informative discussion. And I want to thank you all for watching this 

. If you’ve enjoyed the content, please subscribe to our e-newsletters to receive upcoming peer exchanges and other great content right in your inbox. Thanks so much.

Experts in dermatology share practice pearls and takeaways for treatment of atopic dermatitis.

Pearls for Atopic Dermatitis Management

Matthew Zirwas, MD

Another case, case number 2. We’ll have Sheetal run this one. A 26-year-old female coming in with a near history of pain in multiple joints. Pain started in the knees with some mild intermittent swelling, a fairly insidious onset of pain, and then over the next 2, 3 months, it migrated to involve the symmetric ankles, elbows, feet, and shoulders. She complained of some persistent inflammatory low back pain—so they actually call out inflammatory low back pain—associated with morning stiffness going on for about 2 hours. Then for the past month before coming, she has developed these lesions that seem to spare the face, the palms, and the soles. She complained of some fever and fatigue. On exam, she had some mild knee tenderness with some mild swelling, MCP [metacarpophalangeal joints], PIP [proximal interphalangeal joint], pretty diffuse involvement. They don’t talk much about the skin exam, but we’ll assume that the lesions are where they said they were. Routine blood testing, the CBC [complete blood count], comprehensive metabolic panel were normal. CRP [c-reactive protein], SED [erythrocyte sedimentation] rate was elevated, RF [rheumatoid factor] was negative. The only imaging result we have thus far is a hand radiograph that showed right second PIP erosion, and then right fifth PIP fixed flexion deformity. We have intermittent history of exam here, but that being said, initial impressions, testing, then of course looking at the fatigue part of this as well. Give me some thoughts on how you would start approaching this patient.

: If I’m pretending a fellow is presenting this patient and coming out of the room, I would say, it’s a young female, 26-year-old, around the age that we would see psoriatic arthritis about, close to 30 years old, 30 to 50, 1 to 1. Even though the last case was female and she’s female, we see it with equivalent levels in both men and females. The arthritis has been going on for some time. We have a chronic arthritis that has an inflammatory component, symmetric polyarticular arthritis, like the old Moll and Wright criteria would be RA [rheumatoid arthritis] -like in this situation. She also has inflammatory back pain with prolonged morning stiffness. This patient has psoriasis only over the last month, but I guess she’s had a year history of inflammatory arthritis. I would focus on how psoriasis does precede the majority of patients who get psoriatic arthritis approximately 70% of the time, but in a minority of patients, 15% of them, the psoriasis and the arthritis can present simultaneously, and then in another 15%, you can get the psoriasis after they have the inflammatory arthritis.

She has significant fatigue. She is CR negative, rheumatoid factor, has elevation in her inflammatory markers, and after 1 year of disease, she has an erosion seen on radiograph, and has ankylosis. It’s concerning to me that this is somewhat of a rapid progressor with significant polyarticular symmetric psoriatic arthritis with a good amount of progression. I would feel comfortable with the diagnosis of psoriatic arthritis here. For further testing, I’d recommend some imaging of her sacroiliacs, of her spine if she complains of any other areas like cervical disease just to get an idea if we can find inflammation and finding sacroiliitis.

When it comes to the treatment regimen we would recommend, it would be reviewing the domains involved. Her domains involved are her peripheral arthritis, she has axial involvement, she has skin involvement. She has no mention, at least in this stem that I’m reading right here, of dactylitis or enthesitis, although I find that unless you go looking, you won’t find it. I find the more I look for enthesitis, the more I find enthesitis. But currently, the domains based on the stem we have are peripheral joint, axial inflammation, and skin. There’s no mention made of nail changes. It would be going along the lines of agents that would work in these areas. Because we have axial involvement, we would be straying away from the conventional synthetic DMARDS [disease modifying anti-rheumatic drugs]. In this patient we would be looking at a combination of, for her arthritis, possibly NSAIDs [nonsteroidal anti-inflammatory drugs] plus a biologic, but for her skin disease, it would be the biologic. The biologics that I would consider here, I’m not reading any concerning features of demyelination as a comorbidity or inflammatory bowel disease symptoms, but we do need to ask them if they have any diarrhea, mucus, or blood in their stools on a frequent basis. If she doesn’t, then I would be open to anything along the lines from a TNF [tumor necrosis factor] or an IL-12/23, an IL-23, IL-17. There’s nothing that’s stopping me from consideration. One would argue that given her axial involvement, though, maybe we would put the TNF and possibly even the IL-23 family a bit higher than the other families.

: They call out the fatigue as well. There’s some consideration, but they all do a good job. It’s interesting that they call that out.

: Right, this is how I think through it. It’s nice that we have some data on the IL-23 MOA [mechanism of action] with the guselkumab [Tremfya] with fatigue. My hope, as Len said, that we’ll start to look at some of these more patient important metrics in the future clinical trials in PsA [psoriatic arthritis].

: This case is nice because it asks the question of how would you differentiate her pain and fatigue from fibromyalgia? This is important. This patient, this woman clearly has inflammatory disease. She has clinically inflamed joints, she has elevated inflammatory markers, I would say that even if she has overlapping fibromyalgia, this is not so relevant because it’s not going to influence my choice of therapy. It can complicate measuring improvement down the road, but I don’t think that this would be particularly relevant at the first visit because she would also be in pain and fatigued due to her active disease.

: Thank you for highlighting that, Ana-Maria. I agree with you. In this situation, differentiating the pain and fatigue from her inflammatory conditions vs fibromyalgia is clearer because she has a clear inflammation that becomes much grayer when they don’t have much inflammation on exam and then they have these metrics and you’re trying to figure out what it is. Len, were you saying something?

: Yes. I would only add, in fact I agree with everything, it’s a first visit and you know how you’re going to start this therapy. She probably has fibromyalgia and that may become more important down the line as Ana-Maria said. I would get more aggressive earlier in sorting out this inflammatory back pain and whether this is like the pseudo fibromyalgia of spondyloarthritis that we’re trying to understand in young women. Maybe she has a mixed picture of this. Obviously, we’d start with a pelvis film and maybe somewhere down the line, if it was negative, get MR [magnetic resonance] imaging of this. But I agree with everything otherwise. Right now, she has clearly inflammatory disease and needs to be treated.

: First off, sometimes when you see this much of inflammation in a particularly young patient, female or male for that matter, and they do describe IBP, inflammatory back pain, that well, I start believing it more, which is not necessarily fair. You almost start reading into the most subtle changes on the radiograph that you might not otherwise. But, with what’s going on peripherally, we need to be thinking fast that she’s going to be needing something beyond just most likely a conventional DMARD. But I agree, there’s a lot on the checklist to do that first visit, but, at a minimum, getting a radiograph of the sites.

Sheetal Desai, MD, leads the discussion on a real-world case scenario of a 26-year-old woman with polyarticular symmetric psoriatic arthritis and shares her approach to treatment.

Case 2: 26-Year-Old Woman With PsA

Sheetal Desai, MD

Sorana Segal-Maurer, MD, offers clinical insights on treating patients with HIV who have viral mutations, including M184V, highlighting guideline recommendations.

HIV: Treating Patients with Viral Mutations

Video content above is prompted by the following questions:

Patients with viral mutations, including 

, require a different and more tailored therapeutic approach to manage their disease.

Can you share your treatment approach for a patient with a viral mutation, such as 

What are the current treatment guideline recommendation on this?

Sorana Segal-Maurer, MD

Professor Stephen Nicholls is a world-renowned cardiologist, and leads the Victorian Heart Hospital (VHH) at Monash University.

New findings from the KRAKEN trial highlight the potential of muvalaplin, an oral treatment, for lowering lipoprotein (a) [Lp(a)] levels in adults with elevated Lp(a) and high cardiovascular risk.

American Heart Association (AHA) Annual Scientific Sessions 2024

, the trial represents the first evidence of an oral agent for lowering Lp(a), according to trial sponsor Eli Lilly and Company.

“High levels of Lp(a) have been shown to be a significant risk factor for atherosclerotic cardiovascular disease, affecting over one billion adults globally," said principal investigator Stephen J. Nicholls, MBBS, PhD, director of the Victorian Heart Hospital and Institute, and professor of cardiology at Monash University, Australia. "Current cholesterol-lowering therapies are not approved to lower Lp(a) levels, highlighting an unmet need for people living with cardiovascular disease. These data represent a needed scientific advancement with the potential to reduce the risk of cardiovascular events such as heart attacks or strokes with a once-daily pill."

A 12-week, double-blind, placebo-controlled, phase 2, 233-patient trial conducted in 43 sites across 5 countries, KRAKEN was designed to assess the efficacy and safety of muvalaplin at doses of 10 mg/d, 60 mg/d, or 240 mg/d. The trial’s primary endpoint, placebo-adjusted percentage change in Lp(a) levels, was assessed using intact Lp(a) and apolipoprotein(a)-based assays.

For inclusion in the trial, patients were required to have Lp(a) levels of at least 175 nmol/L and a history of atherosclerotic cardiovascular disease, diabetes, or familial hypercholesterolemia.

At 12 weeks, placebo-adjusted reductions in Lp(a) using the intact assay were 47.6% (95% CI, 35.1% to 57.7%), 81.7% (95% CI, 78.1% to 84.6%), and 85.8% (95% CI, 83.1% to 88.0%) with muvalaplin 10 mg, 60 mg, and 240 mg doses, respectively. Using the apo(a)-based assay, the corresponding reductions were 40.4% (95% CI, 28.3% to 50.5%), 70.0% (95% CI, 65.0% to 74.2%), and 68.9% (95% CI, 63.8% to 73.3%). Secondary endpoints showed reductions in apolipoprotein B levels, while high-sensitivity C-reactive protein remained unchanged.

For more on the trial and the potential of muvalaplin, check out our interview with Nicholls from the floor of AHA 2024.

 HCPLive Nicholls KRAKEN AHA 24

Relevant disclsoures for Nicholls include Amgen, Eli Lilly, Novartis, Sanofi-Regeneron, Silence Therapeutics, and others.

Nicholls SJ, Ni W, Rhodes GM, et al. Oral Muvalaplin for Lowering of Lipoprotein(a): A Randomized Clinical Trial. 

 Published online November 18, 2024. doi:10.1001/jama.2024.24017

Eli Lilly and Company. Lilly’s muvalaplin lowered lipoprotein(a) levels in adults with high risk for cardiovascular events by up to 85% at highest tested dose. Eli Lilly and Company. November 18, 2024. Accessed November 18, 2024. https://investor.lilly.com/news-releases/news-release-details/lillys-muvalaplin-lowered-lipoproteina-levels-adults-high-risk.

Muvalaplin, an oral treatment, shows promise in reducing lipoprotein (a) [Lp(a)] levels in high cardiovascular risk patients, as demonstrated in the KRAKEN trial. This phase 2 trial, presented at the AHA Annual Scientific Sessions 2024, is the first to provide evidence of an oral agent effectively lowering Lp(a). Conducted across 43 sites, the trial involved 233 patients and revealed significant placebo-adjusted reductions in Lp(a) levels with muvalaplin doses of 10 mg, 60 mg, and 240 mg. Secondary endpoints indicated reductions in apolipoprotein B levels, with no change in high-sensitivity C-reactive protein.

Stephen Nicholls, MBBS, PhD, provides additional insight into KRAKEN trial data and the potential of muvalaplin.

Authors