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Infographic: Doctors Who Enter the Entrepreneurial World
Infographic: Doctors Who Enter the Entrepreneurial World

Medscape

timea day ago

  • Business
  • Medscape

Infographic: Doctors Who Enter the Entrepreneurial World

Nearly 4 of 10 doctors surveyed were already involved in an entrepreneurial venture apart from their primary medical job or considering one. One in four of those physicians aimed to eventually spend 100% of their time on the outside venture. They frequently were confident of eventual success and profitability, according to a new Medscape report. This infographic presents key findings from a new report profiling doctors who feel the entrepreneurial urge. To learn more, check out the Medscape Physicians as Entrepreneurs Report 2025. Medscape Physicians as Entrepreneurs Report 2025

Episode 5: Lupus Rashes: What to Spot, What to Shield
Episode 5: Lupus Rashes: What to Spot, What to Shield

Medscape

timea day ago

  • Health
  • Medscape

Episode 5: Lupus Rashes: What to Spot, What to Shield

This transcript has been edited for clarity. For more episodes, download the Medscape app or subscribe to the podcast on Apple Podcasts, Spotify, or your preferred podcast provider. Maureen A. McMahon, MD, MS: Hello. I'm Dr Maureen McMahon. Welcome to the Medscape InDiscussion podcast series on systemic lupus erythematosus. Today we'll discuss the dermatologic aspects of lupus with our guest, Dr John Edminister. Dr Edminister is a board-certified dermatologist and assistant professor at Wake Forest University School of Medicine. He specializes in complex medical dermatology, with clinical and research interest in autoimmune skin diseases such as dermatomyositis, lupus, and pemphigus vulgaris. Thank you for joining us today. John R. Edminister, MD: Happy to be here. McMahon: It's great to have you here. I'm excited to have a dermatologist so I can pick your brain a little bit. Edminister: Absolutely. It's one of my favorite topics to talk about. I love learning about lupus — seeing it, treating it, and talking with other colleagues about it in nondermatology specialties. McMahon: One of the things that we're always talking about, with the fellows and when we see patients in clinic, is making sure that when we are calling something a malar rash, that it really is a malar rash and not other common things we see, such as rosacea. I was wondering if you had any tips for us. Edminister: Yes, so this is the age-old question. It's a great place to start our discussion. The malar rash is the characteristic prototypical rash of acute cutaneous lupus. When you break down how lupus affects the skin, there's ACLE, which is acute cutaneous lupus erythematosus. There's subacute cutaneous lupus. That is more of a polycyclic; these annular lesions sometimes can even be psoriasiform. And then there are other, more chronic cutaneous lesions that I am sure you and the fellows have come across, like discoid lesions. And rosacea is one of the things that often can be misdiagnosed. I'll admit it's quite hard. Rosacea in particular is a chronic inflammatory facial rash that is often photoaggravated, but it's persistent. It can be characterized by that. We call it an erythematous telangiectatic appearance with flushing, for example. But one of the features it has that can differentiate it is that the rash can have acne, papular pustular lesions. The presence of these acne-like papules would not be expected in lupus. That's not to say that someone with the ACLE malar rash can't have acne, to completely try to throw you off, but there are a few other things that can sort of hint you toward one way or the other. Classically with rosacea you may have flushing, which is transient and extends past the nasal labial fold and onto the upper cutaneous lip. That is one of those other classic hints. McMahon: I think that's helpful. I find it can be challenging because even patients with established lupus can also have rosacea. So, trying to help distinguish between a flare and background rosacea as well can be challenging. Edminister: Very true. And it leaves you in situations where you're considering, well, do I have to do a punch biopsy on this young woman's face? Not exactly a cosmetically insensitive area to do a procedure, but we do do them. When I see patients with a new facial rash that even has the slightest possibility of being the malar rash or the acute cutaneous lupus, I will often first check the chart to see if there's a CBC, something with the recent leukopenia cytopenias. Because if a 22-year-old woman has a malar-like rash, new-onset fatigue, joint pain, and white blood count of 2.9, then I have no qualms deferring the biopsy and just getting an (antinuclear antibody testing (ANA) and doing a laboratory-based workup pending that result. I think you can make the diagnosis without a biopsy. What I teach my residents in dermatology is that we need to look on the other side and see how rheumatologists define and categorize a diagnosis of lupus. So I teach them the ACR and EULAR criteria because if you can spare someone an extra procedure, if the first procedure didn't yield much, then the complement is low and they come back with a Smith [positive for anti-Smith antibodies] or whatever it might be, you've done your job in securing a diagnosis of SLE, based on how the lab results come back. McMahon: I think that's helpful. Then hopefully we can help those patients reach both of us for management, on both the rheumatologic and the dermatologic side, too. You mentioned biopsy, and I think that's something else that, as rheumatologists, we're not quite as comfortable with as I assume that you are in the dermatology world. When do you find it helpful to get biopsies in these patients? Are there any tips that we should look for on the biopsy reports, as far as distinguishing between lupus and dermatomyositis? Edminister: Yes, biopsying can be complex. There are a few different situations where it's helpful. Lupus and dermatomyositis can show almost the exact same reaction pattern on histology. That's usually something we call a vacuolar interface dermatitis pattern. There can be mucin deposition. Some dermatopathologists might comment that the interface change is a little more subtle in dermatomyositis, and perhaps there can be epidermal atrophy. But overall, if you probably blinded the dermatopathologist and showed them lupus or dermatitis, many of them might just sign it out as compatible with a connective tissue disease. There are certain eruptions of the skin that are associated with systemic lupus, where it is helpful to have a biopsy that has features of lupus. These are rare, but I'll give you an example. You can actually have a Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN)-like eruption of ACLE or heralding a diagnosis of SLE. I had that in a case where somebody had basically what looked like SJS, but we were able to use laboratory tests and then a biopsy to also confirm histologically that they had cutaneous lupus in addition to necrotic epidermal lesions that were more SJS-like. There are other overlapping conditions. There's an overlap of pemphigus vulgaris and lupus, which is called pemphigus erythematosus. Biopsy would be helpful there because you're going to have direct immunofluorescence findings that support a pemphigus blister, but then you can also have findings that demonstrate a vacuolar interface dermatitis, and you're kind of clinching that dual overlapping diagnosis. The same thing can be said with Rowell syndrome. That's known as an overlap of erythema multiforme-like lesions with cutaneous lupus as well. The list goes on. I've recently seen a great case of bullous SLE. The bullous eruption of SLE is a tense, blistering eruption. It kind of looks like pemphigoid, meaning we get these intact blisters. And for that, it's nice to have that histologic confirmation of that blister that may, for example, show a subepithelial blistering lesion where ideally you want to get an ELISA test. If you have some other proof that the patient might have SLE, that's helpful, whether that's on a skin biopsy of another lesion they have that could be compatible with cutaneous lupus or through laboratory testing. McMahon: Are there any other clinical features that would distinguish a bullous lupus? Edminister: That is something we run into, for example, with epidermolysis bullosa acquisita (EBA). That is another acquired autoimmune blistering disease that does not have to do with lupus. It is a tense subepithelial blistering disease. The antibody — or the epitope, I should say — which the antibody is directed against is collagen VII, which is the same one in bullous lupus. But the distribution is different. If you have more oral mucosal involvement, affecting the vermilion lips, that's assigned toward bullous lupus, whereas EBA can have different variations; but it can even be mechanobullous, meaning it's overlying the dorsal hands and other areas. This is sort of like children who are born with epidermolysis bullosa as opposed to this acquired autoimmune, blistering disease. That kicker for a recent case I had was the presence of oral mucosal involvement and extending onto the vermilion lips, blistering. It was a slam-dunk type VII collagen, SLE diagnosis, anti-Smith, anti-double-stranded DNA — very, very elevated. But it was previously thought to be EBA. McMahon: That's a great case and a great tip, and something to keep in mind. One of the other things that I think has been a challenge is the differences between detecting rashes and managing rashes, and patients who have more white skin compared to darker skin. I was wondering if you have any tips for us on that front. Edminister: Yes, this is very important. Erythema is going to be the most important discussion point on that. Erythema, even in a sort of clinical trial scoring system, signifies active damage. It's trying to tell us that there's active lupus that could lead to damage, rather than the damage is atrophy and the depigmentation, for example. The sequelae of a chronic discoid lesion, when they're active in bright red, you're assuming that now's a good time to treat, to prevent that damage. The problem with erythema is that there's a potential for it to be miscategorized or even underrecognized by clinicians and researchers. In Black patients, erythema was actually more often described as pink, vs in White patients, where it was described as red using a CLASI (Cutaneous Lupus Erythematosus Disease Area and Severity Index) scoring system. This was in a good write-up in JAMA Dermatology just at the end of 2024. That's concerning because with the pink designation of erythema, would it be assigned a lower rating? At that point, you're talking about the perceived activity being lower and the associated scoring being lower, which can affect clinical trial eligibility. In skin of color, erythema can even look gray, purple, or brown. Take-home point: Look for these various hues of erythema. Take good clinical photos before you start a new systemic treatment. This is important if you are looking at all for skin changes as a parameter of improvement. And the other thing — this is calling back on our malar rash discussion. It would be remiss of me not to mention the heliotrope rash of dermatomyositis and how that differs. While not entirely reliable, if you haven't done it, you can search for a picture of the heliotrope flower; it's purple. A heliotrope rash is historically described as a purplish eruption on the eyelids in patients who are White or have very fair skin. I've seen it look bright red, bright pink — very, very noticeable. But for patients with skin of color, it could just look like a little eyelid dermatitis or even postinflammatory hyperpigmentation, because that purplish hue doesn't stand out as much. I know we're talking mostly about lupus, but given that it's in the differential diagnosis, periorbital edema is something that can be quite impressive in dermatomyositis. If there is rash there, it tends to hug the sides of the nodes a little bit more. So, it's very medially based, as compared to the malar rash. That's just a way to sort of round out how you might approach the malar rash vs rosacea vs the heliotrope rash and consider the underlying skin tones as well. McMahon: I think those are helpful points to remember and critical when we're initially evaluating these patients and making our initial diagnoses. Moving on to thinking about how we manage patients with lupus. I know one of the first things we talk about with patients who have skin involvement, and especially photosensitive skin involvement, is the importance of sun protection. I know when I talk to patients, I probably just give them a general 'use sunscreen' talk. I would love to get your take on what you tell your patients and some of the tips that you give them. Edminister: Absolutely. You would think that as a dermatologist, this would be the majority of the time of the visit, but there are so many things we have to talk about in such a short amount of time. These visits feel like they could go for hours and you could talk about photoprotection for 20 minutes; it's something that is so important, and I try to stress it. As an example, let's pretend that I'm having this discussion with a Black woman who has maybe some postinflammatory hyperpigmentation from some old rash. If she has lupus, we have to consider that we need to cover both UVA and UVB. UVB is mostly blocked when we're talking about windows. However, a certain amount of UVA can come through, even through car windows. There have been some individuals who, depending on their degree of photosensitivity or even occupation, may go far as installing tinted windows. Depending on what state you live in, you might require medical clearance for that. It does move beyond UVA and UVB because in phototesting studies, they've shown that a lot of lupus patients also have sensitivity, even to visible light, which is fascinating and scary. How do you avoid that? How do you avoid visible light — aside from the sun being a huge source of it — all these indoor bulbs? There is someone smarter out there than me who could talk about the different light bulbs and how they can affect lupus. But that conversation exists. Apparently, LED lighting, light-emitting diode bulbs, are preferred. They don't emit any ultraviolet radiation, whereas the CFLs, compact fluorescent lamps, or even the halogen bulbs, reportedly can emit low levels of UV radiation and enough that might even cause a little bit of erythema. So, I mean, you can get in the weeds. These are not conversations I have regularly with my patients. McMahon: But in a refractory patient, it might make a difference. Edminister: It may, that's correct. If we want to talk about general things, there's always photoprotective clothing. It is much better these days. A lot of these outdoor stores nowadays have good options. I don't fish, but I have a lot of fishing gear now. I walk my dog here in North Carolina at 1:00 PM over my lunch break, and the UV index is like 12. I will burn out there in like 15 minutes. Rather than wait 15 minutes for the sunscreen to rub into my skin and be activated, I just throw on one of these long-sleeved shirts and then a wide-brimmed hat, and I'm pretty protected. I tell my patients to have readily available clothing that is loose and comfortable to wear, even on a hot July day. For some of these conditions, like lupus, dermatomyositis, it doesn't take that much exposure. Joe Jorizzo, who founded our department at Wake Forest, always says a short walk through the parking lot can be all it takes. And there's probably some truth to that. I've seen patients flare from spending way too much time in the sun, but it can even be just a short dose. McMahon: We face that in Southern California as well. Edminister: To bring it down to the very basics, now there's sunscreen. We've talked about how lupus patients potentially are sensitive to UVA, UVB, and visible light. What's going to cover those three? The answer is going to be a broad-spectrum mineral-based sunscreen with something like iron oxide in it. The added iron oxide is giving you some of that visible light coverage; the original zinc oxide formulations are more just broad-spectrum UVA. Going back to our example, say we have a young Black woman. What's great about these sunscreens is they can now match your skin tone, all the way from Fitzpatrick 6 down to someone who's 2 or 1. You can choose one of these mineral-based sunscreens that have a zinc oxide tint and find one that will rub into your skin without leaving a cast that looks unsightly or something you don't like to see. McMahon: Finding something that patients can incorporate into their daily life and then forget about it is probably the most helpful thing. Edminister: That's right. It goes the other way, too. When I go on runs outside, I wear the store-brand chemical sunscreen because I know it's going to be hot and I don't need some elegant sunscreen for my face. But it's also cheap. And adherence matters. Ultimately, I walk patients through the benefits and the annoying parts of different sunscreens. I have them adopt a way of using sunscreen that fits with their life. McMahon: I was wondering if you have any tips on, when you use topical corticosteroids, which potencies you use. Edminister: Certainly the most important word that will come back again here, and this is showing who I trained with — Dr Steve Feldman, a dermatologist here at Wake Forest — is adherence . We can talk about potencies, and I will. But ultimately, perhaps the most important thing to talk about with patients is what they want to put on their skin. Some people like greasy ointments. They think they feel soothing. Some people find it the most annoying thing in the world. Some people just prefer a certain feel on their skin, and whatever they prefer is what they're going to keep using. If you give someone over-the-counter hydrocortisone and they like using it, that's going to work better than giving them clobetasol, thousands of times stronger, that they don't like using. Ultimately, that's something to consider. Two prescription corticosteroids are always going to be safe to use on facial rashes or lesions when they are there. What I tell patients is steroids are not moisturizers, but when you have a rash, it's perfectly safe to use once to twice daily, and that would be your hydrocortisone 2.5% cream, lotion, ointment — whatever you want to do. Then there's desonide, and that's a 0.05% formulation. Perfectly safe to use on facial rashes. The flip side of steroids is that it's going to be your topical calcineurin inhibitors, like tacrolimus ointments. Those work great on the face and they don't have long-term overuse issues. At the very center, some of the discoid lesions already have atrophy, so do you want to be using something that could add to that? Just to add a point to this conversation, you could give a tacrolimus ointment and not worry about long-term overuse side effects. The dirty secret is, I know dermatologists who have used clobetasol on their face. So, I will say that steroids on the face can cause acne, steroid acne, and that's not good. But as far as the whole atrophy thing goes, clobetasol might be a stretch, but if you use a potent or a very potent steroid ointment on a very active discoid lesion on the face, like a fluocinonide 0.05%, under supervision and when it's there, that's going to be fine. As long as it's not prolonged use for months on end. It comes down to: Do you have enough time to explain that? Is the patient trustworthy to follow those instructions? But that's just something to consider. Last thing I'll say is that for discoid cicatricial and scarring lesions on the scalp, ointments work great. We have a lot of patients who don't mind using greasy ointments on discoid lesions on the scalp. Whereas others might prefer a clobetasol solution, like a liquid that sort of rubs in and evaporates just due to that alcohol component. Then, lastly, there is an oil-based one, fluocinolone oil, which is great for scalp lesions and also conchal-bowl discoid lesions. There's an otic formulation of those drops. So, to prescribe, you would look up fluocinolone oil in an otic drop formulation. McMahon: I'm thinking somewhat along those same lines. When do you move to oral agents in place of, or in adjunctive treatment with, topicals? Edminister: When someone has an SLE diagnosis, your access to therapies is very expanded. If from a skin perspective, they just have a few discoid lesions. Honestly, for their sake and just to be a steward of the system, I'm not going to do anifrolumab infusion if their joints are fine and their kidneys are beautiful and they feel well otherwise, but they've got a couple of skin lesions. If it's localized, a few lesions, you should be able to use a combination of topical therapies, or they could come into the office and I could inject a little bit of intralesional triamcinolone. Something to consider with DMARDs and hydroxychloroquine is some of that data suggesting that — and I know I'm sort of bouncing back, but if someone has isolated cutaneous lupus, I think there was a recent study I read and some other versions of this idea that using an antimalarial can sort of delay the progression to eventually develop SLE. Some of our patients with isolated cutaneous disease might still have antibodies for SSA. That SSA has implications for pregnancy and other things. I would want to be on an antimalarial, probably, if I were them. I just wonder with those circulating antibodies, they probably have some systemic autoimmune interferon-based disease going on, even if it's really just manifesting mostly in their skin. I think for hydroxychloroquine, that's going to be your first line. We've all had that discussion where we accidentally freak out a patient about the retinal monitoring. And then you quickly explain, "I want you to take a baseline eye exam." I always try to walk it back by saying, "Listen, that's just a baseline exam." But the real monitoring begins after 5 years of taking hydroxychloroquine, according to the societies. And you might not even be on this for 5 years. And then there are other drugs, like dapsone, reserved mostly in my experience for bullous lupus. Some people will use retinoids for different lupus lesions, discoid lesions. Methotrexate, mycophenolate — they all have their own things that, again, sometimes I have to walk back. Some package inserts scare people. I understand that the medicines can have serious side effects and can make people feel quite unwell, and they all have their adverse effects. But I always try to explain that, in some of our cases, at least when I'm prescribing some of these drugs, we're using more anti-inflammatory dosing of methotrexate. McMahon: And not the anticancer dosing that the product labels are based off of. Edminister: Yes. So, there are those discussions. McMahon: And certainly, I think that those agents are used even more commonly when we have patients having other systemic manifestations. I know we always are in dialogue with our dermatologists to see what might be the best medication to kind of catch all aspects of their lupus activity. Edminister: I love working with our rheumatologists here at Wake Forest. They're an awesome department, and we refer back and forth to each other all the time. It feels like we're always sending messages on the patient portal to each other. And a discussion that we've have often is, when should the patient get belimumab and when should they get anifrolumab? I can't speak for every dermatologist, and I just hope this is, maybe, helpful for any rheumatologist listening. Maybe this is just like my sector of the world, or only my opinion, but it feels like most dermatologists who see lupus these days prefer, and are more impressed with, anifrolumab when it comes to skin response. Whereas I know that the underlying systemic lupus and extracutaneous manifestations might drive the rheumatology team to be like, hmm, maybe belimumab given the nephritis, or whatever it may be. There might not be enough data on anifrolumab. McMahon: Right. Exactly. I do think it is always kind of a back-and-forth, and again, taking about the overall picture, what might be the best combination to capture all the disease manifestations that are going on. Edminister: Absolutely. And, of course, I want the skin to be as good as it can. But the kidneys are pretty important too. So, ultimately, it's that discussion, seeing the patient's goals, how all the consulting physicians feel, and what is determined to be important to protect the patient. McMahon: Thank you. I think we have had a lot of great tips today. I want to thank Dr Edminister for being here today. Edminister: It was a pleasure. Thank you so much for inviting me. McMahon: Thank you for joining us today. Please take a moment to download the Medscape app to listen and subscribe to this podcast series on systemic lupus erythematosus. This is Dr Maureen McMahon for the Medscape InDiscussion podcast. 2019 European League Against Rheumatism/American College of Rheumatology Classification Criteria for Systemic Lupus Erythematosus Interface Dermatitis: Delineating the Diagnosis With Adaptive Immune Markers Rowell Syndrome: A Controversial Entity Subtype and Racial Erythema Variation for Cutaneous Lupus Trials Integrating Skin Color Assessments Into Clinical Practice and Research: A Review of Current Approaches Overview on Desonide 0.05%: A Clinical Safety Profile Efficacy of Topical Tacrolimus for Treating the Malar Rash of Systemic Lupus Erythematosus Cicatricial Alopecia: Discoid Lupus Erythematosus Fluocinolone Acetonide Topical Oil for Scalp Psoriasis Early Initiation of Hydroxychloroquine in Cutaneous Lupus Erythematosus to Prevent Progression to Systemic Lupus Erythematosus: A Long-Term Follow-Up Study The Autoantibody Response to Ro/SSA in Cutaneous Lupus Erythematosus Monitoring for Retinal Toxicity in Patients Taking Hydroxychloroquine and Chloroquine

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