Chola Vaughn, I'm coming from the Medical College of Wisconsin in Milwaukee. And I'll be talking about derm conditions and skin of color. I have no disclosures. Our learning objectives. Oh, sorry. Can I get it with the presenter view on here, please? Yay, thank you. So we'll be identifying common vulvar dermatoses in people of color, learning about how to treat them and how to provide the highest level of care across a variety of skin tones. Earlier today when I gave that first lecture, I kind of talked about this algorithm. And I mentioned that I'll be talking more about the white vulva in this talk. And so we are going to talk a lot about lichen sclerosis, lichen simplex chronicus, and vitiligo in the context of skin of color. But vulvar dermatoses in skin of color is more than just that. So I'm going to take a step back and talk about overarching considerations in vulva of color. And to me, those are three. First of all, pattern recognition, understanding the physiology of skin color, and then talking about the distraction of pigment. So first of all, I'll talk about pattern recognition. And I bet if I show this picture to you, most of you within a few seconds know the diagnosis with a fair degree of certainty. But if I show you this picture, you probably have more of a differential and not a knee-jerk answer. Maybe you're thinking, OK, could this be vitiligo? Is it lichen sclerosis? Is it post-inflammatory hypopigmentation? We're not quite sure. And this highlights an issue of pattern recognition in vulva of color. I saw this article a couple of years ago about how trauma nurses have trouble identifying bruises in dark skin. And then it went on to say that the bruises were harder to see in the dark skin. And I think it's very subtle. But when we make this cognitive leap from, I have trouble identifying bruises or erythema, it's harder to see the bruises or erythema than there's this deflection of responsibility onto the patient that I think can be a little dangerous. And of course, in skin of color, there are fundamentals of optics, reflectance, and I understand that. But I think we do have to be careful about using language to excuse ourselves from a failure of pattern recognition. And to illustrate that point, I bet your eyes are drawn to the two familiar faces out of these four. But are any of these women harder to see? No, it's just that our brains are actually attracted to patterns that they recognize. And the root causes of our difficulty go deep. Most of us were not exposed to much, well, someone was just telling me, not really any vulva in their training, much less vulva of color. And so in dermatology, we see papers like this ad nauseum that show the lack of racial representation in textbook and journal images. It's getting better now because this was recognized and people really started to work on it. But still, our dermatology textbooks probably show about 4.5% skin of color at the most recent assessment. And this is how that looks in gynecology textbooks. With medical students, you can see the second from the bottom bar, they get almost no exposure to vulva of color, so much that it actually breaks the graph. It just says value there because they couldn't even calculate it. And then when they do see those images looking at the top section there, you can see that it's predominantly infectious things. So you can imagine that's syphilis and HPV and really little exposure to inflammatory conditions like lichen sclerosis or lichen simplex chronicus in skin of color. So we have to consider not really whether you can see red or white. Can you see darker findings and darker skin? But have you had experience recognizing those patterns? So can you recognize these two images as the same disease, which is lichen simplex chronicus in both cases? The second thing, the second consideration is understanding the physiology of skin color itself. So let's just take a little look into that and how it pertains to the vulva. In training, we all learned some basic differences about pigment. So skin of color has identical melanocyte density, about one melanocyte to every 10 keratinocytes, more on the face and genitals. But the melanosomes in skin of color are larger, darker, meaning they produce more melanin, more stable, transferred individually instead of clusters. But beyond those basics, we're discovering that there may be differences that have direct clinical implications. So darker skin has been found to have a lower pH, lower ceramide content within the stratum corneum, greater cohesion between the keratinocytes and increased mast cells. And then on the left is showing differences in protein expression, including filaggrin, which has implications in atopic dermatitis, and fibroblasts, which are implicated in keloid formation, and then basal layer proteins. And so all of these things probably have clinical relevance. And there really may be some difference in the skin just based on pigment itself. And you can dive deeper into this. Again, I do not recommend. But this is a paper from our blue journal, the Journal of the American Academy of Dermatology, back in 1996, which I found pretty fascinating. It showed racial differences in the transcutaneous penetration of drugs and chemicals, including that fluorescent alone had increased penetration in white skin. And then their cosmetic vehicle had 47% lower penetration in black skin. And when I was reading this and learning, trying to educate myself about this, I really went back and forth about whether this was making something out of nothing and creating divisions where there didn't need to be, whether this was phrenology for a new era. I remember how we used to feel the skulls of the mongoloids and the negroids. And I really struggled with this. But I do think that we are doing a disservice to our patients, of color especially, if we don't acknowledge that our medications might honestly just work differently for them. So I decided to look a little bit more into this with two trainees here. We looked at the inclusion of women of color in lichen sclerosis treatment trials. And this paper was published in the International Journal of Women's Dermatology. It showed that women of color were just not represented in those trials. How we looked at that was we looked at the four major databases from all available years and looked at published studies with adult women diagnosed with vulvar lichen sclerosis and containing a treatment arm using topical corticosteroids. So sometimes that was compared to things like laser, estrogen and testosterone, tacrolimus, whatever. And some only looked at topical steroids at different doses or as they pertain to quality of life. But they all had one treatment arm that looked at our gold standard therapy, topical steroids, for lichen sclerosis. And we found 65 publications that were included. And less than 10% of the studies reported demographic data at all. And white women made up at least 90% of those. So only six papers included racial demographic data. Four of those were from Australia and two of them from the US. And so you can imagine there's already kind of a limited racial and ethnic diversity in the studied patients. And then black women made up at most 3.8% of the sample population. And Latinx women made up at most 5.7% of the population. So in total, mostly white women. And you might be asking yourself, well, why does this matter? You're right. We already know that people of color, there's a lack of diversity in clinical trials overall. And the National Institutes of Health and the Food and Drug Administration in the past were implementing new rules to try to encourage better inclusion and to address this disparity. So that's not new information. But why this particular question matters is because of the risk of squamous cell cancer in lichen sclerosis. So we know that their risk is much higher. And we also know that there are some racial differences in squamous cell cancer outcomes. I included some of those written here. Black patients are reported to have a higher mortality from cutaneous squamous cell cancer due to delays in diagnosis and treatment and also a more aggressive biologic behavior of the malignancy itself. Latinx men with penile SCC are more likely to present with high-risk disease and undergo more aggressive treatment than white patients but have comparable survival. Black men with penile SCC are less likely to undergo surgical management and have higher mortality rates. And so there are racial differences in cutaneous and penile squamous. And you would think that there would be the same in vulvar squamous too. But nobody has officially studied that to know for sure. So the question I had was pretty simple, which is, does vulvar squamous cell behave differently along racial lines? And if so, can we counteract that with topical steroids the same way that we think that we can in white patients from this 2015 seminal paper that showed a statistically significant inverse association between topical steroid treatment adherence and the risk of vulvar squamous. And let me just take a quick detour here to mention, because I think this is really clinically relevant, that the paper that really looked at this, the patients, they kind of divide the patients. The patients who had lichen sclerosis and applied their medicine twice a week minimum, didn't miss, complied fully. And then the patients who sometimes they put it on, sometimes they didn't. When they had more symptoms, they would put it on. But sometimes they might go a couple of months when they were doing pretty well and they would just not put it on. All of the patients who got squamous cell were in that group. And literally zero of the patients that complied two times a week minimum, zero of those patients got cancer. So we know that this is so important. For lichen sclerosis, patients have to be onclobetazole for life, two times a week minimum is the standard. And it's such a powerful thing to be able to say, we can stop vulvar squamous cell cancer by just applying this medicine. But we only know that in this very white group of patients. And so the question is important. Is that true in skin of color as well? It's a potentially life-saving question, but we can't answer it well because we just don't have the data. We also have to learn more about the physiology of itch. But we do know with pretty good certainty that patients of color experience itch differently. And there are several proposed mechanisms for that. One of them is shown here, that increased melanocortin-1 receptor signaling leads to increased tyrosinase enzyme activity and upregulation of TRPV1 on sensory neurons. And that is important in histominergic itch. So a lot of words to say that as the melanocytes are transferring their pigment to the adjacent keratinocytes, that something about the receptors in that transfer actually upregulate the sensation of itch. And so that means that vulva of color then are kind of more prone to itch. But there's also something about being a vulva that makes them more pleasurable to scratch. And I love that somebody studied this thing. If the anogenital skin has higher scratch pleasurability ratings than any other area on the body, I think that makes sense, right? Because if you're like a cave person and something's crawling into your nether parts, you want that to be like, scratch, do something now. So I like this. It makes sense. It is real. Vulva of color then has this double hit based on the physiology, more pleasurable to scratch, more prone to itch. And we do see that play out in clinical practice. You might start to notice that more now that I'm kind of calling it to your attention, which is that patients of color, we might see that they are more prone to things like lichen simplex chronicus of the vulva, pterygonodularis of the vulva. And Sean Quatra is the dermatologist who's kind of leading the national charge on this, really looking at specifically pterygonodularis, which is that disorder where you scratch so much and you get these little nodules on the skin, and some really strong data that there's race-related differences between people who get that disorder. And that's really due to cytokines like Th2, IL-17, IL-22, IL-31. These are all the itch cytokines that those are really upregulated in skin of color. And then the last thing I wanted to talk about is the distraction of pigment itself. So when I look at these two pictures, and I see a lot of vulvas and a lot of vulvas of color, I'm so distracted by the pigment. And then I lose track of the patterns that I know. So things that you would expect to see in lichen sclerosis, like anatomic change, purpura, erythema, things that you see on the left, which is the lichen sclerosis picture, that you don't see on the right, which is vitiligo. And so I think if you focus on the patterns and not on the pigment, you have a better chance of making the correct diagnosis and giving the correct treatment. And I'll talk more about pigment as we get into the specific conditions. And so those are the background information that we need to be able to talk about those conditions. It's just these overarching considerations for all vulva of color. And I wanted to pause here and mention that if you don't see a lot of vulva of color, maybe you don't see that much vulva period, but even less vulva of color, it still is important to think about these considerations and how they might affect your practice in other ways, because we know that so many of these cognitive biases do translate to other areas of practice. With all that said, let's get into some specific conditions. We're going to talk about three, lichen sclerosis, lichen simplex, chromicus, and vitiligo. For lichen sclerosis, again, I trust that you all recognize classic lichen sclerosis in white vulvar skin, because you've seen that a lot. That is what we've all kind of been trained in. But what do we know about it in richly pigmented skin? Almost nothing. And even that is surprising, because it is one of the most studied areas of vulvar dermatology, but we really don't have good data on lichen sclerosis in a diverse population. Much of the lichen sclerosis data, as I mentioned, comes from Australia, and the data from the US and Europe often includes mostly, if not all, white patients. And this made me really start to question, do women of color even get lichen sclerosis? Because I was seeing so much LS in my clinics. I was seeing so many women of color in my clinics, but I wasn't seeing a lot of lichen sclerosis in women of color. And I started to wonder, maybe it's all misdiagnosis. Maybe black women don't get this condition. And so I presented this early on in 2022. I presented my early kind of seedlings of thoughts on this delayed and misdiagnosis in women of color at the ISSVD meeting in Dublin, the International Society for the Study of Vulvovaginal Dermatoses. I presented this and actually won the best presentation award for the talk called Delayed Diagnosis of Vulvar Dermatoses in Skin of Color, which I think just showed at that time that people were really starting to realize how important it was to start asking these questions. This is a case that I shared in Dublin. A 60-year-old black woman who presented with a longstanding history of vulvar pruritus and discoloration. And she had been diagnosed with cutaneous and vulvar psoriasis first, and then subsequently called lichen sclerosis. This is a running theme that I have discovered, which is white and itchy. People just call that lichen sclerosis. And it's not always lichen sclerosis. So she was called lichen sclerosis and kind of unsuccessfully treated for, I think, years. And then when she finally came to see me, what I saw was vaginal erosions, oral Wickham's trie, cutaneous papules. You can see these kind of purple polygonal papules and plaques that we all learn are lichen planus. And she was also starting to have swallowing issues. So we had done an esophageal biopsy, and that did confirm the diagnosis of lichen planus. And so because this was not kind of called early enough, she had a lot of sequelae of her lichen planus that probably could have been avoided if we had diagnosed it earlier. And so flash forward a few years. We published this report last year in the Journal of Lower Genital Tract Disease about the diagnostic accuracy of the ICD-10 code for lichen sclerosis. I wanted to look into patients' charts and say, OK, do, you know, specifically I looked at black women, just to kind of narrow things. Do black women, you know, when it says in their chart that they have lichen sclerosis, do they really have lichen sclerosis, or is it something else? And what we found is that the ICD-10 code really lacked validity, especially for women of color. The way we looked at that is we looked at 167 black women with what was called lichen sclerosis in the chart, and then white controls. And then we coded them by the likelihood that that diagnosis was accurate. And you can go and read the paper and see what we used kind of as our measures of what was high, moderate, or low likelihood. But what we found is that the black women were more likely to be miscoded than the white controls. The black women who were low likelihood, that was about 51% of them. And then their high likelihood was only a quarter of them, 27%, I believe, actually had high likelihood that it really was lichen sclerosis. And in the white controls, that ratio was about flipped. So about a quarter of the white patients were low likelihood, probably didn't have LS, and over half of them were high likelihood, really did have it. Of note, the code doesn't perform that well overall. So at best, we're looking at 68% of the patients who were called lichen sclerosis in the chart actually had lichen sclerosis, but that code was even worse for women of color. And the most common errors are shown here, which is systemic sclerosis, being called lichen sclerosis, totally unrelated disorders, lichen simplex chronicus, and lichen planus. And then here's a case, though, that changed my mind back again. I started to believe, okay, fine, black women can get lichen sclerosis. This is a patient who came to see me, a 66-year-old black woman with over 40 years of vulvar itching and associated with rash. And she had had three biopsies, all showing subacute or chronic inflammation, no actual lichen sclerosis on the slide. Dermatology exam, when I saw her, revealed small labia minora, subtle pallor, focal erosions, kind of left clitoral hood area, and disfigmentation, of course. And so even though she had had three biopsies already, I didn't know where those biopsies had been taken from. I suspected that they were taken from areas of pigment change, and not from areas where the LS was probably active. And so I convinced her to do one more biopsy. We took it from kind of the left clitoral hood area where I felt like there was some activity, and that one was called lichen sclerosis. I still didn't believe it. I asked my derm path to sit and hold the slides. I wanted to sit down at the microscope and see it myself. And I looked at the slides, and it was real. So in hindsight, though, even I was really distracted in that case by the pigment. It's so distracting, and it's easy to forget the pattern recognition that you've learned over time. And one other thing that I didn't put in here, but that is interesting from looking at all of those charts of those women, is that the white women, the reason that they got the diagnosis of lichen sclerosis was usually scarring, anatomic changes. The black women, the reason they got the diagnosis was usually hypopigmentation. So I am saying all the time, like a broken record now, white plus itchy does not equal lichen sclerosis. There are many etiologies of the white vulva. Here are a few. So usually there's two different reasons why a vulva will look white. It's either loss of pigment or it's thickening of the epidermis. So the loss of pigment is in things like lichen sclerosis. Those melanocytes are lost. We don't actually know why that is. In vitiligo, it's an autoimmune destruction of the melanocytes. We'll talk a little bit about that later. And then most commonly, post-inflammatory hypopigmentation. So the melanocytes are burned up in the fire. Of other disorders, things like eczema, seborrheic dermatitis, contact dermoceriosis, so many things can cause this hypopigmentation after the fact. Alternatively, you can get a thickening of the epidermis. So the melanocytes sit at the dermal-epidermal junction, and if the keratinocytes above them are heaped up, then the skin will look paler because your eye has to travel through more cells to get to the pigment. And so that thickening of the epidermis exists in conditions like lichen simplex chronicus, where that chronic itch scratch is thickening the stratum corneum. The things like human papillomavirus, HPV, and then DEVIN. Again, because the wart in HPV is kind of like building a little keratinocyte house around itself, so that's thickening up. And then of course, the neoplastic cells in differentiated vulvae, intraepithelial, neoplasia are growing more keratinocyte cells on top. So those are the reasons why you will get a white vulva. Back to lichen sclerosis specifically, I think some pearls that you might be able to use in your practice. focus on the pattern recognition. Try not to be distracted by the pigment alterations. Things like anatomic distortion, atrophy, purpura, and itch. And we will talk a little bit later about how to tell lichen sclerosis from vitiligo. So stay tuned for that. And then consider changing the potency or vehicle of your topical steroid to something more aggressive when your therapy is not working, especially in patients of color, because it might be that the penetrance or the penetration of the medication is worse because of some byproduct of the skin color, the actual transfer of melanosomes itself. And then be skeptical of the diagnosis. Remember that that code is not working well. If someone comes to you having been called lichen sclerosis, really think about whether that diagnosis is accurate. And then if you're not sure, if there's any question, do a biopsy. This is, you know, lichen sclerosis is such an important diagnosis to make definitively because if it truly is LS, they are monitored for life. Your risk of cancer is always going up. And so the recommendation is twice a week, clobetazole, when things are well controlled, and once a year, check with someone who is comfortable with the vulva and can check for hyperkeratosis or cancers, and that is for life. So, you know, making the diagnosis of LS, I don't take lightly. So if you're not sure, do the biopsy. When performing the biopsy, go for where you're gonna make the diagnosis. So hyperkeratosis, atrophy, purpura, erythema, go for those places, and more so than the pigment change. Similarly, when you're treating it, the pigment will likely be the last thing to get better. Pigment coming back into the skin can take months to years. So we are not really treating for color change in our patients with skin of color who have lichen sclerosis. You're really treating for symptoms and then these other signs like anatomic progression, slowing that down. Next, lichen simplex chronicus. Again, we have the same themes here to consider, which are pattern recognition, delayed diagnosis, and the appropriateness of biopsy. This is a case from the literature of a 55-year-old woman who had a year of itching, and she had been just recommended, you know, avoidance of topical irritants and allergens, some over-the-counter lotion, and then Doxepin, and was not getting better. Finally, had a dermatology referral. They did a wet mount and then prescribed her clobetazole. They didn't think a biopsy was even necessary. They straight called this lichen simplex chronicus clinically and started her on appropriate therapy for that, which is ultrapotent class one steroid, and she was better at six-month follow-up, completely resolved. And sorry, let me just say too, I think that this presentation can be challenging because of the nodularity. Sometimes that like really throws people off. But lichen simplex chronicus is not always kind of like that broad lichenification. Sometimes it is a really nodular form, and that kind of relates to what I was saying before about pterygonodularis and how we do believe that that's more common in skin of color. So seeing these papular and nodular forms is not surprising. And then this is another example of delayed diagnosis where something was called lichen simplex chronicus, but it actually wasn't. This is a 66-year-old woman who had two years of pain and pruritus of the vulva, two years. She had a history of generalized dyscoid lupus, dyscoid lupus erythematosus, DLE, and was on hydroxychloroquine, 200 milligrams daily, and Triamcin alone, 0.1% ointment to this spot and others on her body. When they finally did a biopsy of the vulva, it did show dyscoid lupus. And so they changed her to a more standard dose of hydroxychloroquine, 200 milligrams twice a day, and gave her clobadazole to the vulva. And at six-week follow-up, it was completely resolved after two years of suffering. So another case where delayed diagnosis, biopsy really changes management, and to not assume that we know the diagnosis just by looking. This is a patient, I showed this picture before, this is a woman who came to see me, a 65-year-old black woman who had over a year of vulvar itching and burning. And she had used clotrimazole cream and oral fluconazole without improvement for a presumed vulvovaginal candidiasis. And on exam, you can't tell in this picture, but this is a rock-hard plaque. It is this gray-white confluence. She's sitting on this rock all day. It itched, it burned, I mean, she just cried in the office. Like, it's been a year, no one can help me, I'm miserable, please help me. And you can see, it's everywhere. It's in the interlabial sulci, it's clitoral hood, it's perineum, it's perianally, and this isn't Canada. But she had actually come to me, interestingly, with a biopsy, which didn't change their management for some reason, not sure why. This biopsy had been read as squamous cell hyperplasia without atypia, and that is words that the dermpaths don't really use, so I knew that a dermpath hadn't read it, so I wanted to pull the slides and have us look with my actual dermpaths. And so we sat and reviewed it together. On path, I think that they took this biopsy earlier on because it's not all that impressive, so I think probably it was early on in her course, or they biopsied from an area that wasn't all that active. But you can at least see the pattern, the trends, which are elongated reedy ridges. They're uniform in length, there's no spongiosis here, and really no atypia. And so the reread was mild spongiosis with lichenification. So there was no evidence of lichen sclerosis, no drug eruption, and again, no cancer, which I was worried about because it was so hard. And so I called this lichen simplex chronicus, made the diagnosis, and I was glad because when she'd see me in the clinic, I had done an in-office KOH to just prove that it was not, there was no candida. And when it was negative, I already started injecting her at that first visit with intralesional Kenalog. Not anyone's favorite thing, I always say, nobody likes a needle to the genitals, but she got ILK, and after three rounds of ILK, this completely resolved. And now she just needs to use clobetazole as needed for itching. So some pearls to take away, recognizing the patterns of lichenification in skin of color, which can be hyper or hypopigmented, can be nodular, can be papular. And then if the treatment is not working, consider biopsy, go for the thickest area with your biopsy. If the treatment is working, but the patient keeps relapsing, which might have happened in that patient that I showed, then consider underlying conditions, including pelvic floor dysfunction. I think a lot of times when the skin is fairly normal to start, but they're having a lot of this itching and scratching that leads to lichen simplex chronicus, that is a nerve problem, and that nerve issue is really coming from the pelvic floor. And then the last specific condition that we'll talk about is vitiligo. A lot of you probably know about vitiligo in general already, so we know that it's an autoimmune destruction of the melanocytes. It is recommended that we check a TSH only if there is some positivity on review of systems, so it's not an automatic with vitiligo. And then in the past, it was kind of considered cosmetic. That's really fallen out of favor now. Now it is medically covered. A lot of pharmaceutical companies are getting into the vitiligo game, so we're seeing even more encouragement of treating vitiligo. But what you might not know, what's kind of new in vitiligo is the use of JAK inhibitors, and then the idea of combination therapy. Really quickly, I hate slides like this, so just really quickly, this is the pathogenesis of vitiligo. I know, aren't they terrible? The way that vitiligo works is that the melanocytes are under stress for some reason, so they kind of send out these warning signals, and those are things like heat shock protein. And then the neighboring cells, which are keratinocytes, and which are skin cells, and dendritic cells, which are kind of like the immune system patrollers, they kind of activate the alarms, and that is through things like interferon gamma, the JAK stat pathway, and then CD8T, like natural killer cells, CD8 positive T cells. And then they come in and kill those melanocytes that are under stress, and that is why those melanocytes are gone, and then the skin starts to turn white. What scientists couldn't figure out for a long time is that even when we turn off that signaling, stop the melanocytes from sending off the alarm, stop the keratinocytes and dendritic cells from responding to the signals, the melanocytes wouldn't come back to the depigmented areas. But in the last few years, we're learning more about resident memory T cells, which stay in the depigmented area, and are the reason why people relapse so much with vitiligo. And so we not only need to stop the signaling, but also we need to decrease these resident memory T cells so that the melanocytes will come back into the vitiliginous skin. And this affects a lot of patients with vulvar vitiligo, and for a long time, really what we had was steroids and calcineurin inhibitors like tacrolimus. But now we have a new kid on the block, which is ruxolitinib. The ruxolitinib trials were published in 2022 as TRUV1 and TRUV2, and looked at patients 12 years or older who had non-segmental vitiligo with depigmentation covering 10% or less of total body surface area. The adverse events here are actually important because they pertain to the vulva. Things like acne that they saw on the face pertain to our patients who maybe have folliculitis or hydradenitis in the vulva. Nasopharyngitis or increased risk of infection kind of pertains to candida, recurrent candida or BV in the vagina. And then application site pruritus, itchiness, can really muddy the waters for our patients who maybe have vitiligo and also lichen sclerosis, and also lichen simplex chronicus. So it is important to know that these are common side effects that we can see in patients who are applying ruxolitinib to the vulva. And the limitations of the studies themselves, again, mostly white patients, mostly Fitzpatrick one through three. The lips, scalp, ears, and neck were not included. The vulva was included, but it was kind of lumped in together with trunk, so we don't really have a good way to look back at those studies and tell what the specific response was for the vulva patients. But the biggest practical limitation to getting ruxolitinib is the cost. If it is not covered by insurance, and I think I pulled this just like, you know, right before these slides were due, like this is up-to-date data on how much it is for ruxolitinib if uninsured in my area, over $2,000. I had one patient who was using ruxolitinib for lichen sclerosis, and she decided to pay for it. She was able to get it, she kind of shopped around aggressively, was able to get it for $1,300 somewhere, and when she was doing really bad, for a 30-gram tube, and when she was doing really badly, she would just like, you know, like ration out a little bit of it, and she would use it. And so, you know, we wrote letters to the pharmaceutical company. We were able to get her some samples and stuff. But it is just prohibitively expensive. But the good news is that there is a cousin of ruxolitinib, which is tofacitinib, that you can get from compounding pharmacies for much cheaper. So the compounding pharmacy that I use is Noblesville. You know, they can also, you know, they can compound things with estrogen, they can do a lot of tricks, and Skin Medicinals is another one. So they have tofacitinib in a solution, ointment, or cream, for something that, you know, people would be able to afford. Now granted, it's not the exact same, it doesn't work on the exact same jacks, but, you know, the price is reasonable to give it a try. And then, so those are things that will stop the signaling, but like, as I mentioned, we also have to stop the resident memory T-cells, and to do that, UV light is our best option. The, this study, I'm not sure, I can't see that far up, 2021 that this came out, and it kind of was, you know, talking about how the immunomodulators, like topical steroids, suppress the T-cell destruction of the melanocytes, but UV light is needed for melanogenesis, and they did a meta-analysis looking at calcineurin inhibitor, or tacrolimus monotherapy, and what they saw is that 2.3% of the patients on calcineurin inhibitors alone repigmented, but when you added UV light, that jumped up to 16.1%, so a huge difference with UV light. And after that, a lot of papers started coming out kind of talking about combination therapies, so ruxolitinib with UV light, you know, everything with UV light. So for our vulvar vitiligo patients, you know, going in and having, you know, UV light, you know, phototherapy, UVB phototherapy in the office is probably not ideal, but what you can do is this Dermapal. You can get them a home unit to use, covered by insurance. You have to request it from the manufacturer, which is Davlin, and they kind of get this little wand, and they can use it on the vulva. It is different from, I think that there's some, like, Amazon light, which I don't even know what kind of light that is. It's probably like, what, like LED light. And it's like 300 bucks on Amazon, and people always want to get that. It is not the same thing. Don't waste your money. Don't buy that one. Get their insurance to cover this through the manufacturer, Davlin. And a common struggle that we all have is telling lichen sclerosis from vitiligo, you know, especially in skin of color. It's like white, sometimes itchy, and we're so distracted by the pigment. But there are ways to tell these two apart. These are two examples here, lichen sclerosis on the left, and vitiligo on the right. And you can see lichen sclerosis tends to be more white to violet, whereas vitiligo is kind of stark white that will glow under a wood's lamp. Lichen sclerosis, because the attack, the autoimmune attack is on the dermal layer of skin, and that layer is kind of thinning out, you'll get wrinkling of the overlying epidermis, whereas in vitiligo, there is no, you know, it's just the melanocytes on a cellular level are lost at the dermal-epidermal junction, so there's no skin surface change. In lichen sclerosis, you have petechiae and purpura. The reason for that is because, again, that dermal layer is thinning out, and so the blood vessels that course through it, they're just not supported anymore, so they kind of shear under the skin, and then you get a little bleeding under the skin. That does not happen in vitiligo. And then in lichen sclerosis, as the skin is trying to repair from that dermal attack, it just doesn't always repair it correctly, and so you get scarring, and that doesn't happen in vitiligo. Lichen sclerosis is almost always symptomatic. It almost always has itch. Maybe not now, if they've been living with it for decades, but at the beginning, it is generally an itchy condition, whereas vitiligo tends to be asymptomatic. You can have an inflammatory vitiligo that is a little bit itchy, but in general, usually they didn't even notice that anything was there. You might be the first person to tell them that there's depigmentation, or maybe a sexual partner noticed it. And then lichen sclerosis does not affect the hair follicles, so you won't have poliosis or whitening of the hair, whereas on the right, I love that you can see how in the areas of the vitiligo, the hair follicle has been affected, and so those hairs have turned white as well. And so here's that photo again. Hopefully this time, maybe you're not as distracted by the pigment, and you can see the changes on the left, the anatomic changes, erythema, epidermal change, and things that you don't see on the right for vitiligo. So a couple of pearls for vitiligo. Revisit the conversation with patients who maybe have elected not to treat. Maybe they've had vitiligo for 10 years, and 10 years ago, there weren't as many things to treat this, and now we do have some new things that we can try. Ruxolitinib, 1.5% cream, is FDA approved for vitiligo, so you have a really good chance of getting that covered for your vitiligo patients who have vulvar vitiligo. It's twice daily. The patient that I described only had lichen sclerosis, did not have vitiligo. I'm always hoping that maybe they have overlap, but she didn't, and that's why it was not covered by insurance and so expensive. But if they truly have vitiligo, you can get this approved. And if not, you can try compounded tofacitinib, $75 to $135 a month, and then consider a combination with a handheld phototherapy. Those are things that they might not have known were options for them five, 10 years ago, but now these options are available. And then for the new patients who come in with vulvar vitiligo, avoid framing the issue as cosmetic or unimportant. I think it's really, you know, it's crucial that we tell them that ultimately, there is no long-term medical health risk of having vitiligo, that they can choose not to treat it, but that it is an important issue, and that if they want to treat it, we have treatments available. And I think, especially for patients of color, who sometimes their identity is so wrapped up in skin color, that it's important that we don't just kind of discount this. It is now, you know, it's covered by insurance. It can progress. I think that's something that is important to tell people. We don't know the rate that it's gonna progress at. It's so different for every patient. But yes, if they have vulvar vitiligo, is there a chance that they might start to get it on their face, on their hands? Yes. And for those reasons, I think a three-month trial of a topical steroid or a calcineurin inhibitor, that's pretty low risk. And they can try it for a few months. Repigmentation is a slow process, but they can try it and see if it's a hassle. If they don't care that much about it, if it's not working at all, then maybe that informs their decision of whether or not they want to continue it. And then I just want to finish up with kind of my call to action of things that we can all do to take better care of our vulvar patients of color. The first thing is thinking about images and including more images, putting more images out into the world of skin of color vulva. You can include more images of color in your presentations, like if you're giving presentations like this in front of a group. Go to VisualDx or find an atlas and use a balance of skin of color images. Support publications of vulvovaginal disease and darker skin types. Nina Madnani has an atlas that she published I think two years ago now. And Jasmine Abdul-Qadir has a female genital mutilation guide that kind of compares what the scarring looks like in lichen sclerosis compared to female genital mutilation. And that comes mostly from sub-Saharan Africa, those images. So those are two amazing publications that we can support. And then include images of darker skin in your publications. So if you're doing a case series, maybe try to preferentially choose the picture that is of darker skin, even though it might be more difficult to see in publications, I think it's important to put it out there. And the way to do that in VisualDx, when you search for that condition, there's a button at the top. I love this. Way to go, VisualDx. You can click that skin of color button and it will give you all of those images. You can practice seeing what that looks like on different skin tones. And then you can include some of those pictures. If you're doing a presentation that has like 10 images, make this one or two of those. And then really, in order to have those pictures, we need to go back to our research and make sure that the patients of color are included in that so we can get those pictures in the first place. And then that we're telling the world what kinds of patients we had in our studies. So include skin color information if it's applicable in addition to demographics. I have a kid. He's 13 and he's very white presenting. So I call him a black man, but he's blonde. You know, he's green-eyed. Like you'd think he's a white kid. And so saying that these are black patients isn't always enough. Sometimes you have to really say what the skin color is. You know, brown, light brown, medium brown, dark brown. Consider DEI in your research and publications or maybe just have a team member who's kind of more versatile in it and can at least like make sure that you're talking about DEI throughout the publication, throughout the manuscript in an appropriate way. And then feel free to contact me. Here's my email. I love to partner on things. I love to talk about patients and work on papers together. And we have a Vulvar Dermatoses Research Consortium, the VDRC, which is kind of a multi-institutional group trying to just do more research projects and kind of like assemble more power in our studies by grouping our patients together. And so I would love to work on projects through that group in particular. Tailor your treatments. Consider that vulva of color might respond differently to your topical steroid regimen as we discussed. And then be thoughtful about treatment endpoints. So treating symptoms, treating erythema, and not so much being distracted by the need for repigmentation. Of course, vitiligo, that's what you're treating for. But things like lichen sclerosis, lichen simplex chronicus, weeks, months, years for that pigment to come back. And then finally, being careful about language. So moving away from saying things like it's harder to see erythema in darker skin types to saying I need more practice identifying erythema in darker skin types. Because of course, everybody, I do, everybody does. And so accepting that responsibility. So let me just say really quickly, so we talked about the algorithm. Again, I finished the algorithm with the white vulva. We talked about our overarching considerations in vulva of color. And then we talked about a few specific conditions. LS, LSC, vitiligo. We had some pearls thrown in there. And then finally, that call to action. I hope that this was illustrative for you. Thanks for having me. Thank you, Carissa, for inviting me.

dermatological conditions

vulvar dermatoses

people of color

lichen sclerosis

vitiligo

misdiagnosis

JAK inhibitors

clinical representation