The Workup Before Initiating a JAK Inhibitor for Alopecia, With David Cotter, MD, PhD

Before prescribing a patient with alopecia areata a JAK inhibitor, what should you do? At the 

2025 Society of Dermatology Physician Assistant (SDPA) annual summer meeting

, an assistant clinical professor at the University of Nevada, on the workup before initiating a JAK inhibitor for 

, key safety concerns for JAK inhibitors, and his perspective on JAK inhibitor use in younger patients.

“I hope that when people leave my talk that they have some tools to use when they get back to [the] clinic on Monday, [and] they feel comfortable prescribing JAK inhibitors,” Cotter said. “There's nothing wrong with reaching for them. It's so easy. You check some baseline labs… [and] if everything looks good at baseline, you start the medicine, and you can see your patient back in 4to 12 weeks and recheck labs. Usually by the 12-week mark, you're high-fiving because there's really clinically meaningful hair regrowth.”

For Cotter, the workup before initiating a JAK inhibitor for alopecia areata consists of a Comprehensive Metabolic Panel (CMP), fasting lipids test, checking for latent TB infection and hepatitis B serologies, and QuantiFERON gold. Patients may also receive a pregnancy or an HIV test. In Cotter’s practice, he also checks for varicella zoster (VZD) virus antibody titers.

“That's outside of the JAK guidelines, but I like to know if my patients are already immune to VZD, because when I think about all of the side effects of a JAK inhibitor, that keep me up at night,” Cotter said.

Cotter also recommends that individuals get a single vaccine. Still, he checks their baseline titers to see if they are immune to shingles at baseline, so he is aware of the odds of shingles reactivation.

Even after completing the proper workup before initiating JAK inhibitors, Cotter emphasized the importance of follow-up with repeat labs in a period of 4 – 12 weeks.

“What we do in our practice is we check patients at the 12-week mark, and we'll recheck their blood counts by ordering a CBC with [differential],” Cotter said. “We'll check liver function tests and fasting lipids. If everything is normal at the 12-week mark, we'll space those labs out to anywhere from Q6 to Q12 months, depending on the patient's baseline risk. So, a healthy 14-year-old who has no other medical complications, we'll check those labs annually, but say an 80-year-old chain smoker with cardiovascular risk factors, we're going to be checking those labs every 3 months.”

Cotter, D. Hair Loss Track: JAK-ing Up Alopecia Areata. Presented at the 2025 SDPA annual summer meeting 2025 on June 27th.

 David Cotter, MD, PhD

HCPLive Five at SLEEP 2025 

 SLEEP 2025, the 39th annual meeting of the Associated Professional Sleep Societies,

 from June 9 – 11th in Seattle, Washington, to share new sleep medicine data.

As a part of HCPLive’s on-site coverage, the editorial team conducted > 15 interviews on various topics, from new pharmacotherapy treatments for OSA and AI in sleep medicine to changes to the restless legs syndrome (RLS) guidelines and the association between napping and mortality risk in older adults.

In this edition of the HCPLive Five, the team captured the top 5 interviews at the meeting, featuring research on a VeNS device for insomnia and PTSD, latest pharmacotherapy developments for sleep apnea, new RLS guidelines, the link between naps and mortality risk, and AD109 for obstructive sleep apnea (OSA).

VeNS Device Improves PTSD, Insomnia Symptoms in RCT, with Peter Colvonen, PhD

Peter Colvonen, PhD, an associate clinical professor at the University of California, San Diego, presented results from a randomized controlled trial showing that vestibular nerve stimulation (VeNS) significantly improved PTSD and insomnia symptoms. The 12-week trial involved over 380 adults with PTSD, many of whom face years-long waits for 1-on-1 therapy.

VeNS, a non-invasive, at-home device, led to significantly greater reductions in PTSD and Insomnia Severity Index scores compared to a sham. Colvonen emphasized its potential as an interim solution for patients stuck on long waitlists, highlighting VeNS as a scalable option to stabilize symptoms until gold-standard care becomes available.

Latest Pharmacotherapy Developments for Sleep Apnea, with Danny Eckert, PhD

Danny Eckert, PhD, a professor at Flinders University, highlighted emerging pharmacotherapies for obstructive sleep apnea (OSA), addressing both anatomical and non-anatomical causes. The FDA-approved GLP-1 agonist tirzepatide helps reduce OSA in obese patients through weight loss.

For non-obese individuals, AD109, a combination of aroxybutynin and atomoxetine, showed promise in a phase 3 trial, resolving OSA in 25% of patients. Eckert also discussed potassium channel blockers that reset airway reflexes and acetazolamide, which lowers loop gain and reduces OSA severity. These advances mark a shift toward personalized, drug-based OSA treatments, especially for patients who struggle with traditional therapies like CPAP.

RLS Guidelines Advise Against Dopamine Agonists, With John Winkelman, MD, PhD

John Winkelman, MD, PhD, chief of the sleep disorders clinical research program at Massachusetts General Hospital, discussed the AASM’s updated restless legs syndrome (RLS) guidelines, which now advise against routine use of dopamine agonists due to high augmentation risk. Up to 50% of patients on these drugs may experience symptom worsening over five years. The guidelines recommend iron therapies and alpha-2-delta ligands (gabapentin, gabapentin enacarbil, pregabalin) instead.

Winkelman emphasized identifying and managing exacerbating factors like antidepressants, antihistamines, or sleep apnea. He advises a slow, careful taper of dopamine agonists over 6–12 months, warning patients of temporary worsening but long-term improvement once off the medication.

Naps at Noon Linked to Mortality Risk in Older Adults, with Chenlu Gao, PhD

Chenlu Gao, PhD, from Massachusetts General Hospital and Harvard Medical School, presented findings linking longer, irregular, and early afternoon naps to increased all-cause mortality in middle-to-older adults. Using UK Biobank data from over 86,000 participants, the study found that greater nap duration, high day-to-day variability, and naps between 11 am–3 pm were associated with higher mortality risk over an 8-year follow-up.

Gao emphasized the study was observational and not causal—napping patterns may reflect underlying health issues like sleep disorders or chronic illness. She advised clinicians to address root causes of excessive napping rather than eliminating naps entirely.

AD109 Improves OSA in Phase 3 SynAIRgy Trial, With Patrick Strollo, MD

Patrick Strollo, MD, from the University of Pittsburgh Medical Center, presented phase 3 SynAIRgy trial results showing that AD109, a once-daily oral neuromuscular modulator, significantly improved obstructive sleep apnea (OSA). In the 26-week trial of 646 participants intolerant of CPAP, AD109 reduced apnea-hypopnea index (AHI) by 55.6% and improved oxygenation measures. More than half of participants had reduced OSA severity, and 22.3% achieved full disease control (AHI < 5).

AD109, a first-in-class combination of aroxybutynin and atomoxetine, works by enhancing upper airway muscle tone during sleep. Apnimed plans to submit an FDA application in early 2026, with additional phase 3 data expected later in 2025.

Sleep experts gathered at SLEEP 2025 to discuss advancements in sleep medicine, including new treatments and guidelines. Key topics included a VeNS device for PTSD and insomnia, pharmacotherapy for sleep apnea, updated RLS guidelines, and the link between napping and mortality risk. The VeNS device showed promise in reducing PTSD and insomnia symptoms, while new pharmacotherapies like AD109 and tirzepatide offered hope for OSA patients. Updated RLS guidelines advised against dopamine agonists, and research linked irregular naps to increased mortality risk, emphasizing the need to address underlying health issues.

Check out the top 5 interviews from SLEEP 2025.

Danny Eckert, PhD

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

Optimizing Treatment Outcomes in Retinal Vein Occlusion

Optimizing Treatment Outcomes in Retinal Vein Occlusion (RVO)

Hong-Uyen Hua, MD

The Landscape and Future of Ocular Rheumatology, with Jacob Lang, OD

2025 American Optometric Association Conference

 in Minneapolis, MN, Jacob Lang, OD, medical director of dry eye services and director of Associated Eye Care’s ocular disease residency program, presented his lecture on the current landscape of 

Ocular rheumatology encompasses a variety of eye diseases, from simple inflammation to papilledema and uveitis. Recent movements towards a general universal terminology structure, which has streamlined the field significantly and allowed for more rapid advancements in treatments and methodology.

Lang spoke on the status of the eye as an immune privileged site susceptible to a variety of conditions and interactions, as well as its direct linkage to the immune system.

“As we look at different eye diseases, we’re learning more and more about how inflammation affects the eye,” Lang told 

. “Really, inflammation is the enemy of every eye care doctor. And so, if we’re thinking about treating and managing inflammation as eye doctors, we’re really thinking about it from a systemic perspective, and that’s rheumatology.”

Lang expressed excitement for the future of ocular rheumatology, noting a variety of upcoming drugs which may facilitate more specificity in treatment and targeting.

“We’re seeing that in rheumatology with all the biologics, and eye care is no different,” Lang said. “We’re going to see more tailored therapies, more specific therapies, that’ll treat eye disease in a better, more productive, safer way for our patients. We’re seeing that with biologics and ocular surface disease, we’re seeing that in thyroid disease.”

Lang also noted significant advancements with teprotumumab for thyroid eye disease, a monoclonal antibody that targets insulin-like growth factor 1 receptors to reduce inflammation.

Additionally, Lang spoke on treating inflammation at large and the paradigm shift that he believes is necessary to prioritize what is increasingly appearing as a common ground for various eye diseases.

“Ocular surface disease and eye diseases are anchored in inflammation, and there can be systemic conditions that might be affecting that,” Lang said. “We need to understand holistically how we’re treating these patients and how we can best manage inflammation within the eye.”

In closing, Lang discussed his expectations for the field through the rest of 2025.

“I think there’s a lot of new drugs that’ll be launching this fall; I think we’re seeing more specific medications for our patients,” Lang said. “I’m also really excited about optometry taking a bigger role in integrated care: working as a team to take care of our patients, whether that be with rheumatologists, internal medicine doctors, endocrinologists, the village that it takes to take care of these complex patients.”

Lang reports the following disclosures: Alcon, Aldeyra, Dompe, Horizon, Kala, Novartis, and others.

Lang J, McGee S. Ocular Rheumatology; An Anterior Segment Perspective. Presented at the 2025 American Optometric Association Conference in Minneapolis, MN, June 25-28, 2025.

Ragusa E, Salvarani C, Cimino L. Through the eyes of an ocular immunologist: The interdisciplinary ophthalmology-rheumatology approach. Saudi J Ophthalmol. 2025;39(1):1-4. Published 2025 Mar 24. doi:10.4103/sjopt.sjopt_81_25

Lang discusses his expectations and excitement for upcoming developments in the field and encourages clinicians to work together to better treat complex patients.

Jacob Lang, OD

Ken reports on medical innovations and advances in practice and edits presentations for news and professional education publications. He previously taught and mentored pharmacy and medical students, and provided and managed pharmacy care and drug information services. He regularly contributes to Contagion Live, HCP Live, and Neurology Live.

Kenneth Bender, PharmD

Maddy Pontius is a Master’s Student in Forensic Psychology at the University of Denver with interests in rehabilitation psychology, health psychology, and neuropsychology. She is hoping to work within the overlap of offender rehabilitation and healthcare in the future.

Maddy Pontius, BA

Discussions about migraine treatment often revolve around a single topic: triggers. Patients with migraine are always eager to learn about factors that activate migraine in order to avoid them. Tracking and avoiding triggers is often one of the few means of control migraine patients feel they have over an otherwise unpredictable disease. However, this is an oversimplification. In practice, trigger avoidance is usually ineffective, and sometimes even detrimental to patients. That’s because:

Many supposed “triggers” are not triggers at all, but rather are premonitory symptoms signaling an attack is already underway.

Rarely does a single trigger produce a migraine attack.

Avoiding triggers can erode patients’ quality of life, since it can lead to avoidance of enjoyable activities

 as well as feelings of helplessness and self-blame.

Migraine Triggers Versus Prodromal Symptoms

Research has confirmed several triggers of migraine attacks:

 are perhaps the most common migraine trigger among women. The drop in estrogen levels just prior to menses is likely the cause.

, including for religious reasons such as Ramadan

 Links between chronic stress, pain, migraine, and catastrophic thinking have been demonstrated by many studies.

 However, removing a stressful situation alone is unlikely to improve migraine. In fact, the abrupt cessation of stress is often itself a migraine trigger.

Many environmental factors may affect migraine (such as altitude, lightning, and barometric pressure changes) but the effects are relatively mild and in some cases nonsignificant.

It’s important to emphasize that rarely does any single trigger invariably produce a migraine attack. Much depends upon the patient’s own migraine threshold, which fluctuates over time. For example, sudden changes in daily activity or environment increase migraine susceptibility,

 making triggers more potent than usual. This can be disorienting for patients, who may find that activities that were tolerable one day become triggering the next.

Further confusing for patients is the difficulty figuring out which of the events or symptoms that preceded a migraine attack was the trigger. This has led to a plethora of reported triggers, most of which have not been borne out by research. Rather, data supports the idea that many of these symptoms are actually premonitory, or prodromal symptoms,

 which occur 2 to 48 hours prior to the headache phase of a migraine attack.

 Seen in this light, such symptoms are not triggers that can be avoided; rather, they signal to the patient that an attack is already underway.

Common premonitory symptoms often confused for triggers include:

Chocolate is probably the best example of a food craving misunderstood as a trigger. Although patients rank chocolate number one of all food-based triggers, placebo-controlled studies have failed to show that chocolate triggers migraine.

 The same can be said of caffeine, an oft-cited food “trigger” that 

Prodromal symptoms are individual to each patient. Identifying their prodromal symptoms can help a patient with migraine recognize that the headache phase is imminent, lessening the element of surprise and allowing them to take mitigation steps such as leaving work early, seeking out a dark room, notifying caregivers, or obtaining childcare for during the attack.

Reframing Triggers for Effective Migraine Treatment

Asking patients to avoid triggers does not appear to be effective, based on studies comparing the practice to a control group that didn’t change their behaviors. Trigger avoidance was also found less effective than cognitive therapy or an approach of learning to cope with triggers.

 Avoiding stress, for example, has been found less effective for chronic pain than coping or adaptive strategies and may lead to anxiety, increased disability, and catastrophic thinking.

Focusing extensively on migraine triggers during an office visit is not only an ineffective use of provider-patient time, but it may also have a host of negative consequences on the person with migraine’s quality of life:

Patients can feel blamed or self-blame for a migraine attack (e.g., “This is my fault because I drank wine”).

A patient may find it impossible to identify their triggers, especially in those with very frequent attacks (where everything can appear to be a trigger) or infrequent attacks (where it’s difficult to find consistent patterns).

The triggers identified may not be avoidable, such as stress or weather.

Focusing on triggers can increase anxiety or lead to anticipation of attacks. It may even pave the way to more migraine attacks. Nocebo is a major problem in headache, both in clinical trials and practice.

 Studies of other pain disorders have shown that increased pain expectations cause an increase in symptoms

; the suggestion that a specific trigger will cause a migraine attack may create similar expectancy mechanisms.

It does not address the underlying cause of the disorder.

With all this in mind, here are a few strategies when advising patients on triggers.

 Maintaining a regular diary or calendar eliminates recall bias and focuses on overall migraine control. It may also allow the discovery of unrecognized triggers amenable to treatment, such as caffeine withdrawal on weekends or menstrual migraine. In addition to tracking attacks, ask patients to write down strategies that worked, both preventively and abortively (medical and non-medical), to reduce their migraine symptoms.

Focus on healthy lifestyle choices that raise migraine threshold. 

Rather than trigger avoidance, focus on engaging in proactive behaviors that, done consistently, raise patients’ threshold for migraine triggers. Those include good sleep, regular nutrition patterns, regular exercise, and stress management techniques.

For further practical details on healthy lifestyle changes that improve migraine, see my colleagues’ Stephen Silberstein, MD and William Young, MD’s article “Lifestyle Changes for Migraine: Practical Tips for the Neurologist & PCP.”

To help patients understand the concept of threshold and their ability to raise their own migraine resistance level, try this patient-centric article from Ctrl M Health.

Recognize and treat “cephalgiaphobia.” 

Ask patients if they worry about migraine when they are headache-free or restrict activities due to fear of migraine. Fear of migraine between attacks is an important predictor of chronification and medication overuse.

 Finding effective acute medication may reduce the risk of chronification.

 Cognitive behavioral therapy can be particularly effective.

 Patients with very frequent migraine—for whom triggers appear to be everywhere—may benefit from effective preventive medication.

Expect that patients will be new to the idea of replacing trigger-avoidance strategies with proactive behaviors. They will need encouragement and guidance to follow through. Until recently, evidence-based, expert-reviewed programs to help patients with lifestyle change for migraine were rare. That is a guiding reason why we at the Jefferson Headache Center and Thomas Jefferson University Hospital have partnered with Ctrl M Health, whose app-delivered program makes this information widely accessible.

Providers have the ability to help patients redirect their efforts into the factors within their control that are shown to actually make a difference. I find patients also benefit from the empowerment this behavioral approach brings, making them more confident in their ability to manage migraine. Those gains, in turn, allow them to continue making progress in reducing migraine frequency and severity, improving their quality of life.

The Jefferson Headache Center and Thomas Jefferson University have partnered with Ctrl M Health to create comprehensive, evidence-based programming and support for people with migraine. For free provider resources, best practice tips, and patient handouts, visit their For Providers page.

1. Martin PR. Managing headache triggers: think ‘coping’ not ‘avoidance.’ Cephalalgia. 2010;30(5):634–7. DOI: 10.1111/j.1468-2982.2009.01989.x

2. Loder EW. Menstrual migraine: pathophysiology, diagnosis, and impact. Headache. 2006;46(Suppl 2):S55–60. DOI: 10.1111/j.1526-4610.2006.00555.x

3. Abu-Salameh I, Plakht Y, Ifergane G. Migraine exacerbation during Ramadan fasting. JHeadache Pain. 2010;11(6):513–7. DOI: 10.1007/s10194-010-0242-z

4. Drescher MJ, Elstein Y. Prophylactic COX 2 inhibitor: an end to the Yom Kippur headache. Headache. 2006;46(10):1487–91. DOI: 10.1111/j.1526-4610.2006.00609.x

5. Meng ID, Cao L. From migraine to chronic daily headache: the biological basis of headache transformation. Headache. 2007;47(8):1251–8. DOI: 10.1111/j.1526-4610.2007.00907.x

6. Kunz M, Chatelle C, Lautenbacher S, Rainville P. The relation between catastrophizing and facial responsiveness to pain. Pain. 2008;140(1):127–34. DOI: 10.1016/j.pain.2008.07.019

7. Lipton RB, Buse DC, Hall CB, Tennen H, Defreitas TA, Borkowski TM, et al. Reduction in perceived stress as a migraine trigger: Testing the “let-down headache” hypothesis. Neurology. 2014;82(16):1395–401. DOI: 10.1212/WNL.0000000000000332

8. Marmura MJ, Hernandez PB. High-altitude headache. Curr Pain Headache Rep. 2015;19(5):483. DOI: 10.1007/s11916-015-0483-2

9. Prince PB, Rapoport AM, Sheftell FD, Tepper SJ, Bigal ME. The effect of weather on headache. Headache. 2004;44(6):596–602. DOI: 10.1111/j.1526-4610.2004.446008.x

10. Martin VT, Behbehani MM. Toward a rational understanding of migraine trigger factors. The Medical clinics of North America. 2001;85(4):911–41. DOI: 10.1016/S0025-7125(05)70351-5

11. Schulte LH, Jurgens TP, May A. Photo-, osmo- and phonophobia in the premonitory phase of migraine: mistaking symptoms for triggers? J Headache Pain. 2015;16:14. DOI: 10.1186/s10194-015-0495-7

12. Becker WJ. The premonitory phase of migraine and migraine management. Cephalalgia. 2013;33(13):1117–21. DOI: 10.1177/0333102412437390

13. Maniyar FH, Sprenger T, Schankin C, Goadsby PJ. Photic hypersensitivity in the premonitory phase of migraine—a positron emission tomography study. Eur J Neurol. 2014;21(9):1178–83. DOI: 10.1111/ene.12451

14. Pavlovic JM, Buse DC, Sollars CM, Haut S, Lipton RB. Trigger factors and premonitory features of migraine attacks: summary of studies. Headache. 2014;54(10):1670–9. DOI: 10.1111/head.12468

15. Marcus DA, Scharff L, Turk D, Gourley LM. A double-blind provocative study of chocolate as a trigger of headache. Cephalalgia. 1997;17(8):855–62. DOI: 10.1046/j.1468-2982.1997.1708855.x

16. Martin PR, Reece J, Callan M, MacLeod C, Kaur A, Gregg K, et al. Behavioral management of the triggers of recurrent headache: a randomized controlled trial. Behav Res Ther. 2014;61:1–11. DOI: 10.1016/j.brat.2014.07.002

17. Ramirez-Maestre C, Esteve R, Lopez-Martinez A. Fear-avoidance, pain acceptance and adjustment to chronic pain: a crosssectional study on a sample of 686 patients with chronic spinal pain. Ann Behav Med. 2014;48(3):402–10. DOI: 10.1007/s12160-014-9619-6

18. Volders S, Boddez Y, De Peuter S, Meulders A, Vlaeyen JW. Avoidance behavior in chronic pain research: a cold case revisited. Behav Res Ther. 2015;64:31–7. DOI: 10.1016/j.brat.2014.11.003

19. Peris F, Donoghue S, Torres F, Mian A, Wober C. Towards improved migraine management: determining potential trigger factors in individual patients. Cephalalgia. 2017;37(5):452–63. DOI: 10.1177/0333102416649761

20. Becker WJ. The premonitory phase of migraine and migraine management. Cephalalgia. 2013;33(13):1117–21. DOI: 10.1177/0333102412437390

21. Peres MF, Mercante JP, Guendler VZ, Corchs F, Bernik MA, Zukerman E, et al. Cephalalgiaphobia: a possible specific phobia of illness. JHeadache Pain. 2007;8(1):56–9. DOI: 10.1007/s10194-007-0361-3

22. Giannini G, Zanigni S, Grimaldi D, Melotti R, Pierangeli G, Cortelli P, et al. Cephalalgiaphobia as a feature of high frequency migraine: a pilot study. J Headache Pain. 2013;14:49. DOI: 10.1186/1129-2377-14-49

23. Lipton RB, Fanning KM, Serrano D, Reed ML, Cady R, Buse DC. Ineffective acute treatment of episodic migraine is associated with new-onset chronic migraine. Neurology. 2015;84(7):688–95. DOI: 10.1212/WNL.0000000000001256

24. Grazzi L, Andrasik F. Non-pharmacological approaches in migraine prophylaxis: behavioral medicine. Neurol Sci. 2010;31(Suppl 1):S133–S5. DOI: 10.1007/s10072-010-0306-5

Forget what you think you know about red wine or chocolate ‘activating’ migraine. Many commonly accepted “triggers” aren’t triggers at all.

Helping Your Patients Avoid the Migraine Trigger Trap

Michael Marmura, MD

Ryan Oakley, MD, takes a closer look at the recent history of ketamine in depression. He also explores the differences between ketamine and esketamine.

Ketamine for the Treatment of MDD

 I'm going to be talking about the interventional options that move a little bit away from direct electrical stimulation, using a more advanced neurochemical intervention. I would be surprised if most of you haven't at least heard of ketamine at this point as being used for mental illness in some way. It's all over the news, it's being marketed for a lot of different things. We're going to discuss a little bit about what it has actual evidence for and clear some of that up, including talking about what the FDA just released to combat some of that marketing. We're also going to talk about the evolution and the creation of the FDA-approved insurance-covered form of ketamine, which is esketamine, and how we use that in our clinics as an intervention.

So, what's special about ketamine, why is this being developed as an interventional treatment? First, to understand where ketamine is right now what it's been used for, its primary use is the procedural anesthetic and medicine. It started being explored for depression specifically based on some animal studies that showed that, when intervening on the glutamate system, the animals depressed behaviors improved, also based on some human clinical studies with medications that act on the glutamate system, like lamotrigine or alprazolam, also found to have some antidepressant activity. So then, a group decided to see if we could intervene directly on the glutamate system with an NMDA antagonist, like ketamine, to see what kind of effect would that have on depression. This group did a study, a randomized controlled trial, double-blind crossover study, and showed that it did, in fact, have a pretty dramatic, rapid, and sustained antidepressant activity. It was then explored a lot more as a treatment for depression.

We talked about ketamine a little bit. Esketamine was developed later. Essentially, ketamine is a combination of two different mirror images of a molecule. Esketamine is one of those mirror images of the molecule that they've designed and created to be delivered intranasally in an office setting, which sort of improves its scalability (ie, how easily we can deliver this treatment). So that's where esketamine is. “Es” is actually the name of the mirror image of ketamine, [and] this how it gets its name.

So, breaking down the difference between ketamine and esketamine, the biggest one is which one's actually insurance-based, which one has approval. Ketamine is not approved by the FDA for any kind of mental health treatment at this point. It's also not covered by insurance. Esketamine is approved by the FDA for treatment-resistant depression or major depression with suicidal ideation. The FDA recently put out a warning on compounded ketamine, because ketamine is getting marketed almost like a snake oil treatment for all the different types of mental illness where there's not a lot of evidence to support it (except for in depression, IV formulation, and a specific way of delivery). Whereas esketamine has evidence, we have a well-defined means of how to deliver it.

[What are] other differences between them? Ketamine, the drug itself or the medication is actually quite inexpensive. Esketamine, the drug, is actually quite expensive. However, insurance covering esketamine actually makes it more affordable for patients, whereas ketamine treatments, you're not just paying for the medication, you're paying for staff, you're paying for monitoring, paying for IV, all these things. It actually becomes less affordable for the patient, whereas esketamine is a very affordable option for people with treatment and depression. Other things to note is that there's no federally mandated program that tells us how to use ketamine. There are no guidelines for it. Esketamine does have guidelines. Ketamine doesn't have a risk evaluation mitigation system. So, we don't have a place where we can find out more about the side effects of how safe ketamine actually is, whereas esketamine does have that. We're continually monitoring how safe it is, and also able to update information for patients to make sure we deliver it the most safe way possible.

Transcript was AI-generated and edited for clarity. 

Ryan Oakley, MD

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

Skin of Color Savvy: Live at RAD 2025 with Tiffany Mayo, MD, and Raj Chovatiya, MD, PhD

In this special on-site episode of Skin of Color Savvy: The Art and Science of Treating Patients of Color, by the 

, dermatologists Raj Chovatiya, MD, PhD, and Tiffany Mayo, MD, engage in a wide-ranging discussion on atopic dermatitis in skin of color, recorded live from the 

2025 Revolutionizing Atopic Dermatitis (RAD) Conference

 in Nashville, Tennessee. Together, the 2 leading voices in dermatology examine diagnostic challenges, patient communication, and the future of topical therapy—offering both clinical insights and actionable strategies for improving care across diverse skin tones.

The conversation begins with an exploration of diagnostic disparities in atopic dermatitis. Mayo highlights how historical underrepresentation of skin of color in dermatologic imagery, along with erythema being a primary clinical feature, contributes to delayed diagnosis in patients with richly pigmented skin. Chovatiya echoes this, noting the visual bias in dermatology and the importance of rethinking severity grading in atopic dermatitis, which often relies on erythema not easily visible in darker skin. Both clinicians emphasize that postinflammatory pigment alteration—especially hyperpigmentation—is not only common in patients of color but often more distressing to patients than the disease itself.

The episode stresses the importance of eliciting patient priorities during consultation. Mayo urges clinicians to directly ask, “What bothers you most?” as pigment changes may be more concerning to patients than active eczema. She also outlines counseling strategies to clarify that medications aren’t the cause of pigment alteration, but rather the disease itself, helping to maintain treatment trust and adherence.

The discussion transitions into clinical pearls for differentiating atopic dermatitis from its mimickers—particularly in darker skin tones. Mayo shares her use of dermoscopy to enhance diagnostic accuracy in cases where morphology is subtle, while Chovatiya recommends palpation as a basic but powerful tool. Both caution against under-recognizing active disease in richly pigmented skin and recommend incorporating validated patient-reported outcome measures like POEM scores to capture disease burden when visual cues are misleading.

As the discussion turns to treatment, the hosts spotlight the growing role of targeted, nonsteroidal topical therapies. Mayo outlines her real-world use of agents such as tapinarof, roflumilast, and ruxolitinib, citing their long-term safety, tolerability, and usefulness across diverse presentations. She emphasizes that simple regimens, monotherapy when possible, and flexible formulations (such as foams) are key to promoting adherence, especially among patients with textured hair, facial involvement, or sensitive skin.

Chovatiya highlights the inclusivity of recent clinical trials, particularly for tapinarof, noting their deliberate enrollment of racially diverse participants and design parameters that more closely mimic real-world behavior. Data from long-term extension studies show that even with intermittent use, patients can maintain control of their disease—an important message for busy individuals who struggle with daily application. Roflumilast and ruxolitinib offer similarly flexible maintenance strategies, supporting proactive or as-needed regimens that match the heterogeneity of atopic dermatitis in the real world.

The episode closes with a mutual call for “intentionality” in atopic dermatitis care: in diagnosis, treatment selection, trial design, and patient communication. Mayo reminds listeners that patients of color may not exhibit textbook signs, making it essential to gather layered diagnostic data and engage patients around their lived experiences. Chovatiya reinforces that clinicians must recognize the multidimensional nature of atopic dermatitis—its signs, symptoms, comorbidities, and psychosocial burden—and approach every patient with individualized, culturally responsive care.

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

Editor’s note: This podcast summary was edited through the use of artificial intelligence tools.

Leading experts discuss managing atopic dermatitis in skin of color in a live recording from the 2025 Revolutionizing Atopic Dermatitis Conference. 

Tiffany Mayo, MD, FAAD

In approximately 1 in 1000 women worldwide over the age of 40 and in the US, as many as 65 out of every 100,000 women are diagnosed with a rare, autoimmune disease that can cause significant liver damage and potentially lead to liver failure if left untreated.

 This disease is known as primary biliary cholangitis (PBC).

 Although PBC is more common in women, we now know that more men than previously thought also have this disease.

Many people may not experience symptoms in the early stages of the disease.

 If this chronic liver disease is left untreated, it can progress to cirrhosis.

The journey to a PBC diagnosis can be long and challenging, especially when there may not be any signs of the disease that others can see.

 For many patients, the path to a PBC diagnosis can involve numerous testing and procedures.

First-line and second-line treatment options are available to patients. After 1 year on first-line therapy, one’s health care provider will assess treatment goals by looking at biochemical response.

 Some patients don’t meet treatment goals—this is known as an inadequate response to therapy. In such cases, several second-line treatments are available for appropriate patients who qualify.

Routine liver blood tests can reveal abnormalities.

 If PBC is suspected by one’s doctor, an antimitochondrial antibody (AMA) test is generally used to confirm a PBC diagnosis.

 For people living with PBC, some treatment goals include normalizing or improving a protein called alkaline phosphatase (ALP) and managing symptoms of the disease, such as pruritus.

 A treatment plan that helps sustain ALP levels and more effectively manages symptoms may help improve disease outcomes.

Symptoms can range from mild to severe and can develop slowly over 5 to 20 years.

 As the disease progresses, there is an increased risk of inflammation of the bile duct and scarring of the liver that may cause serious complications.

More than half of people diagnosed with PBC are asymptomatic and not all symptoms of PBC are visible.

 The symptoms that commonly appear—such as pruritus (chronic itch) and fatigue—are often invisible to others and may negatively affect daily life.

 The debilitating itchy skin that may be associated with PBC can have a profoundly negative impact on a person’s daily life and those around them and may also be associated with sleep disturbance, fatigue, and depression.

For patients living with PBC, it is important to connect with others who have similar experiences who can provide crucial support, in addition to support from loved ones.

 It is also important to have a supportive care team that listens attentively, thoroughly explains the treatment process, and presents all available options.

As research and awareness of PBC continue to grow, there is hope for those living with the disease.

 Advancements in medical science aim to improve both the understanding and management of PBC, offering patients new avenues for care and support.

After receiving a PBC diagnosis, it’s essential for patients to maintain close communication with their care team. Regular check-ins with healthcare providers ensure that any changes in symptoms are promptly addressed and that the treatment plan is continually optimized.

 Beyond medical management, discussing ways to improve the patient’s daily life is key. Consider lifestyle adjustments for the patient, such as adopting a healthy diet and engaging in regular physical activity, along with treatment, which can help mitigate the progression of PBC.

By having the patient be proactive and informed, they can work alongside their care team to manage PBC effectively.

This content is sponsored by Gilead Sciences.

European Association for the Study of the Liver. EASL clinical practice guidelines: the diagnosis and management of patients with primary biliary cholangitis. 

 2017;67(1):145-172. doi:10.1016/j.jhep.2017.03.022

American Liver Foundation. Primary biliary cholangitis. Accessed September 30, 2024. Available at: https://liverfoundation.org/liver-diseases/autoimmune-liver-diseases/primary-biliary-cholangitis-pbc/

Levy C, Bowlus CL, Carey E, et al. A real-world observational cohort of patients with primary biliary cholangitis: TARGET-primary biliary cholangitis study design and rationale. 

. 2018;2(5):484-491. doi:10.1002/hep4.1173

Shaker M, Mansour N, John BV. Primary biliary cholangitis in males: pathogenesis, clinical presentation, and prognosis. 

 2022;26(4):643-655. doi: 10.1016/j.cld.2022.06.008

Bernal RB, Ferrigno B, Morales EM, et al. Management of primary biliary cholangitis: current treatment and future perspectives. 

 2023;34(2):89-100. doi:10.5152/tjg.2023.22239

Laschtowitz A, de Veer RC, Van der Meer AJ, Schramm C. Diagnosis and treatment of primary biliary cholangitis. 

. 2020;8(6):667-674. doi:10.1177/2050640620919585

Mayo Clinic. Primary biliary cholangitis diagnosis. Accessed September 17, 2024. Available at: https://www.mayoclinic.org/diseases-conditions/primary-biliary-cholangitis/diagnosis-treatment/drc-20376880

Bonder A. Current and emerging treatment options for primary biliary cholangitis. 

Sivakumar T, Kowdley KV. Anxiety and depression in patients with primary biliary cholangitis: current insights and impact on quality of life. 

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