Dr. Jared Gardner's Dermatopathology Lecture: Case Study Review

Hi, I'm Dr. Jared Gardner. I'm here today with my awesome dermatology residents and DermPath fellows, and we're going to do some random DermPath unknowns. They have not had time to see these or preview them before. They're just some slides I pulled out of my study collection to show them cold. So the challenge is more intense this time, guys. All right, so here's a case, and I wish I had... I'm going to get this scanned because it would be better to see from... from low power. But this was a draining nodule on the trunk that looked like a cyst. There's kind of a cystic space in the middle but no lining. What's this right here? Does anyone... Like granulation tissue? Very good. Granulation tissue. So important to recognize. It's a common kind of simple thing. But man, granulation tissue can look really wild sometimes. And it definitely, starting out, I remember thinking it looked pretty scary. Because it's very busy, right? Got big, plump endothelial cells in these vessels. And then all this inflammation mixed in. Neutrophils. And, uh, and, uh. In this case, a lot of eosinophils mixed in here. Histiocytes, lymphocytes, all blended together. And then there's a bunch of fibrin lining this central space here, but no actual cyst lining. Tons of eos. Hmm. Well, the key here is not in the middle of the cyst, but out here. Now, what is going on? Can anyone figure this out? It is not human. It is not human. Right. We have an alien invader here. A non-human life form of some sort. Wow, it's quite pretty, isn't it? I don't know what all those parts are, but they're not human parts. I can tell you. What are those cells? Or structures. They look like giant cells at first. I don't even know what's going on here. Oh, that I recognize. What's that? Muscle. Skeletal muscle. Look at that. And then here we have an outer wall, an exoskeleton. And little bits here and there of that yellowish-orange stuff called chitin, right? Here's some more. And look, sometimes... This is an arthropod, right? The question is which one? Sometimes arthropod exoskeletons have these very jagged little ridges or lines. Again, I'm sure an entomologist could tell me all about these things, but I can only have enough time to learn so many things and derm path and soft tissue is more than enough for a lifetime for me. So in any case, does anyone know what this is? What kind of arthropod we're dealing with here? Myiasis, like a fly. Myiasis, bot fly. Yeah, this is a maggot. a fly larva way prettier microscopically than they looked the naked eye, which is true of pretty much everything in pathology. It all looks pretty under the microscope, even if it looks awful and nasty in real life. So this whole thing is the maggot, the fly larva, and it used to live inside this little burrow here in the skin. So the fly lays the egg in the skin and it turns into the little larva, the maggot, and it's got a little... hole that it breathes through from the skin surface and the body is none too pleased with having this maggot growing in its skin. And I know maggot makes it sound grosser, but that's what it is. It is a pretty nasty little infection or infestation rather, excuse me. And then the body is creating granulation tissue and granulomatous, I mean it's not much granuloma here, but a granulation tissue response sometimes with granuloma and with a bajillion eosinophils. Eosinophils can be seen in lots of settings, but one of those settings that you particularly see it is when you have Helmets like worms in the skin of different sorts like larvae migrants or in the setting of botfly or other things So rarely do I get to see these other things that you could think of if you just had this because here we're just getting It kind of fragmented piece of the arthropod You could think about a tick if this were on the skin surface because it's about this about the size honestly a bit bigger than most ticks I've seen. But if that were like clinging to the skin surface, you could think, oh, maybe a tick. If this were right underneath the stratum corneum, kind of pushed down from the epidermis and it was on the foot, you could think of tongue ependotrans, tongue gaiasis. There may be some special features of the organism that can let you tell them apart. But really, I have to tell you, basically, once I see a piece of arthropod, I use the size and the location to guide me and then the clinical scenario to guide me to which of the... the different arthropod forms or species are most likely going on in the patient. So that's how I kind of do it, is based on the size of the organism and whether it's on top of the skin, in the epidermis, down underneath, and then put that together with the clinical. Alright, so bot fly. Okay, I'll let you tell me the history, because the path is pretty darn classic here. Anyone do it from 2x? So, tender, thymidous nodules on the lower extremities. Tender erythematous nodule in the lower extremities. Absolutely. Any young woman who recently started oral contraceptives, right? That's the classic like test question. So yeah, this is what then? Eno-dosim. Yeah, erythema no dosim. So paniculitis, the paniculitis I think are confusing because we talk a lot about septal versus lobular. And I feel like in real life, there's often a lot of overlap. But one of the ones that holds the most true to the septal. versus lobular I think is you know do some it really is a predominantly septal process and for any any of you guys who are beginners what that means is that the lobules the subcutaneous fat lobules have relatively minimal inflammation or involvement by inflammatory cells and the septa in between the fat lobules, which are normally present but very thin. If you look at normal subcutis, there are thin little bands of collagen that divide the lobules of mature fat. And those get inflamed and fibrotic and then because of that they widen and get really thick. So even from low power you can see that the lobularity of the subcutis is very dramatically highlighted for us because the septal areas are so thickened and widened. And when you go look closer in those, and it depends on the stage, early erythema nodosum can be more richly inflammatory and less fibrotic. You can have some hemorrhage and neutrophils. And then as it kind of progresses on and gets chronic, that tends to turn into kind of fibrosis with a granulomatous reaction. So histiocytes, sometimes giant cells. I feel like you often see EOs, lymphocytes, and you know, you get a little bit of involvement of the fat. Again, septal paniculitis versus lobular paniculitis, in my experience, not. It's not a perfect clear cut line, but it works the most here. So this is a nice example of the changes you'll see in the septa of the fat in urethema nodosum. And I think some of these little granulomas here, I think people have called them Miescher's radial granulomas. If you like buzzwords, I don't know if that's really the best example, but there's like a little granuloma right here. So that's nice erythema nodosa. There were some giant cells. Really good example and a really awesome biopsy. Look at that. Because see, a regular punch, if you just did one punch and got down to here, I wouldn't be able to tell you anything on that. So if you're lucky enough to get, I mean, that's amazing to get a punch intact all the way down here. It's wonderful. But in real life, if you're biopsying for paniculitis, as I think you guys all know, Do a double punch if you need to punch once and go back down into the punch biopsy hole and take another piece down Into the fat. I know it's hard because it bleeds a lot a wedge or elliptical incisional, you know ellipse excision, excuse me incision So doing like a wedge biopsy is the best thing but obviously that that does take more time and is more involved And so I understand that it's not always feasible and practical to do but that is the ideal scenario for diagnosing paniculitis, but in a pinch, a double punch boxy will do just fine, in most cases. So there you go, erythema nodosum. This is a plaque on the trunk of a 25 year old patient, no skin. Just look around here. Kind of a lot of different stuff going on. It looks very heterogeneous, right? It's a hard case. I struggled when I saw my first one of these two, and I've struggled again with them since, but I was really baffled by this. So I'll tell you, the pitfall here is to look at this thing and see spindly kind of tumor with fat trapping, right? Honeycomb fat entrapment, and to think DFSP. It'd be understandable. The thing that would be a little weird for DFSP is that it's not just like fat trapping. It's like way down here mixed in with the subcutaneous tissue. Look, there's all these like big vessels that it's like wrapped around and like kind of intervened between. And while yes, DFSP is infiltrative and can do that, this is not like as, I don't know, something about it's almost like too patchy down in here. I don't know how to explain that really. The other thing is that in this case, the cytology is not. Quite right for DFSP. Yes, it's bland and monotonous, but it's not, some of it's spindled, but a lot of it's more like little oval or round nuclei, right? See? Very bland, very, very benign appearing, but so is DFSP, which is, that's where the pitfall, because this tumor is actually more often like bland spindle cells that look very much like dermatofibrosarcoma protuberans, and that's why it's an important pitfall to know about. See here, it's more spindled. Blan spindle cells with fat trapping. So these are Wagner-Meissner-Meissner bodies. They're little little structures that are recapitulating Meissner's corpuscles. Like each one it looks kind of similar to a to Meissner's corpuscle. Right see like here's like one little circle here's another one. Here's another one, another one. They're like all clustered together. This tumor is S100 and SOX10 positive and CD34 positive. This is a diffuse neurofibroma in a patient with neurofibromatosis. And they can have spindled, bland spindles, like that, that look more like neurofibroma. But this is tricky because... In diffuse neurofibroma, there are two things. Number one, you often get lots of infiltration or intermingling with the fat. It's not aggressive growing like a DFSP. It's just intermingling with the background fat that's there. I mean, they can be very, they're not aggressive, rapidly growing tumors, but they can be very large and disfiguring in patients with neurofibromatosis. So they are benign, but they can cause significant morbidity, okay, when they're large. But because of the fat entrapment, And because the fact that neurofibroma is usually CD34 positive, they can closely mimic dermatofibrosarcoma protuberans, okay? The other thing is that the diffuse form of neurofibroma, in contrast to the more conventional types of neurofibroma that we see as little, like the little nodular form we see in the skin, that the cells tend to be more rounded, oval to round nuclei, than spindle. They can be spindled, but you'll often see kind of a more rounding. And because of that, sometimes they can get kind of cellular, almost sheet-like areas that are more cellular than this and made of round cells. to the point that I've seen some and they reminded me of like a round blue cell tumor except that they had like no mitoses and nothing to indicate malignancy but I was very perplexed when I first saw one of these in fellowship and thought how are there all these round cells and then Dr. Meissner explained that in diffuse neurofibroma that you tend to have kind of more rounded cells so it when you're lucky you'll find Wagner-Meissner-Meissner bodies look they're everywhere here we got them here here here so Wagner-Meissner-Meissner bodies are typically seen. They're kind of the classic finding in the diffuse type of neurofibroma, although you don't always see them. And remember that neurotized nevi can get things that look just like Wagner-Meissner Meissner bodies as well, although they're not going to be so big and deep, but this thing is way down in the subcues. The other thing is I've seen this a couple of times now where you have this kind of unusual, like striped kind of tiger stripe pattern. Maybe it's actually better from lower power. Isn't that interesting? It's like, it's like, uh, lining up in these kind of rows that makes this like kind of stripey Tigroid sort of pattern. I don't know. I don't know maybe that's been described, but I don't remember reading about it But I've just I've noticed it at least I think this case in one other if I recall correctly where I had this kind of unusual like row like orientation So it's kind of a fascinating tumor, but just the take-homes remember that diffuse neurofibroma and traps fat totally normal It can mimic DFS P and neurofibroma CD 34 positive so do s100 socks 10 If you're having any problems because DFSP almost never expresses those. I have seen one, only one example of fibrous sarcoma. It is DFSP that had patchy, real S100 expression. And it totally blew my mind. Only one case ever. So in... As a general rule, DFS-P should be negative for S100 and SOX10. Of course, if we do this long enough, we'll find weird exceptions to all the rules eventually. And there's more of those Wagner-Meissner-Meissner bodies. And there's some more kind of spindly area of the neurofibroma. Ah, skin! You guys are feeling the relief of seeing some epidermis. But don't get too relieved, because it's still a spindle cell tumor. I know spindle cell tumors are hard. I did a fellowship in it, and I've been doing this for almost 10 years, and I still struggle with them all the time. What's this? Is that kind of like the story form pattern? Oh, that is exactly like the story form pattern. This is the story form to break all other story forms. Like, oh, I just, I gotta go home now. I know it's only like 7.50 in the morning, but I can't do any more work today. It's such an incredible pattern. And so, so fascinating to look at. So you can use a hundred different words to describe story form, but the only way to really learn it is just look at that. That's the picture. That's what story form is. It's swirling, whirling, stirred with a spoon, cartwheeling, pinwheeling. People have tried so many different ways to describe it because no word captures this really fascinating pattern where the cells are all stacked up in little lines that kind of then whirl and swirl around each other. Very bland, thin, elongated spindle cells, right? And sometimes I kind of think that the way that these cells are is that they're kind of like a plate. That if you look at them on one surface, they're very thin and narrow. But if you flip them 90 degrees, then they look more like an oval, right? So they're like flat like pancakes, okay? Kind of like oval-shaped pancakes. So several different tumors can do that, where you can have kind of a story form pattern, and you can have cells that are very thin or are kind of more oval. So what do you guys think this is? I'll go back to lower power. There's more of that story form. Yeah, that's like really the most perfect example of story form. I mean, one of the best I've ever seen. And then here's the... A DFSP. So what's this? This is DFSP, Dermatofibrosarcoma for two brands. No tricks here. And when you see this, that last case I showed you, it doesn't really look much like a DFSP, but I promise you, I have seen some where it would be real easy to make a mistake because of the extensive fat trapping and more spindly-looking diffuse neurofibromas with fat entrapment can very much look like this. I've not seen diffuse neurofibromas make good story-form pattern, like striking story-form pattern like this. They can swirl a little bit, but this is pretty dramatic. Now the other thing, so what other things might come in the differential here for DFSP? I'm sorry, let me say the features first. Blan spindle cells, often with a story form pattern, and entrapment, honeycomb pattern of fat entrapment like this. And it's very clean, right? The fat is like just imprisoned within the DFSP cells, and there's not really much inflammation or fat necrosis or anything. This is the very classic example of how DFSP invades. It just fills in the fat. And look. The fat entrapments not only happen in there. It's all of this. This all used to be pristine subcutaneous You know real estate here was all fat all the way up to here, right? Like right there is where the dermis ends right around here and the subcutis begins And if you're not sure about it, you go and look for the eccrine glands because eccrine coils They reside at the deep and the deep dermis or the superficial subcutis at the dermal subcu junction, right? So Wherever you find your eccrine coils, that's right around where the subcutis should have started. And so you can see evidence of it right there. And so even though this area here might have almost no fat in it, this all used to be fat. So that is one of the tricky things. Sometimes DFSP can extensively infiltrate the fat to the point that almost no fat remains. It just wipes it all out. And only at the very edge will you see a few little islands of entrapped adipocytes. So like right here, right? So even though that doesn't look honeycomb, oh, that's great for DFSP because you know that this area should be all fat based on what the stuff I just showed you. But it's not fat. It's been totally overrun by spindle cell tumor. OK, so in this case, it's very it's very good because we do have honeycomb down here. But I've definitely seen multiple DFSPs where you'll only find like like this, a couple little islands of stranded fat. And that confused me when I first saw that. So that's why I'm pointing it out. Okay. So what other things can come in the differential with DFSP? Dermatofibroma. Yeah, dermatofibroma. Now, usually it's pretty easy to tell dermatofibroma and DFSP apart. On H&E only, you can use stains if you want. CD34 will be strong, diffuse positive in the vast majority of DFSPs, with some rare exceptions. And when there's higher grade fibrosarcomatous transformation, those sometimes lose. 34 expression. They don't have to. But otherwise, dermatofibromas tend to have epidermal hyperplasia over them and acanthosis or induction of the epidermis, whereas DFSP usually does not have that, although I've seen some that did, and those are confusing. Dermatofibromas tend to have more plump, larger cells with more abundant cytoplasm, more rounded nuclei, sometimes with some atypia. So paradoxically, if you see scattered atypia, that points to dermatofibroma rather than DFSP. DFSPs should be bland, monotonous, very elongated, thin spindle cells like that because it's a translocation sarcoma, right? And so all the cells look the same, okay? And the other thing is that you often find hemorrhage or blood-filled spaces, hemocitarin, foam cells, multinucleated giant cells, including two-ton giant cells. All of those things are features of dermatofibroma, not DFSPs. You can see pigment in DFSPs sometimes, but it's not hemocitarin. It's melanin usually. And what is that? call it a DFSP with melanin pigment with pigmented dendritic like melanocytic looking cells in them. Yeah, that's called a bednar tumor, which is just a pigmented variant of a melanin pigmented DFSP. It's just a fancy name for us as pathologists to recognize. Doesn't mean anything different clinically to my knowledge. Okay. Another thing I didn't talk about is collagen trapping, which is a common finding in dermatophibroma, but you can't rely on it because, look, we've got some nice collagen trapping in this dermatophibra sarcoma protuberans. Really good. Usually, DFSP doesn't quite trap collagen like this. This is the type of collagen trapping we usually see in dermatophibroma, but you can sometimes see it in dermatophibra sarcoma protuberans. So it is a common finding of DF, but do recognize that it can be seen in... Dfsp also I find the other features the blood hemocytin foam cells and fatter plumper nuclei with atypia To be the most helpful things all of those are really good pointers towards dermatofibroma and away from Dfsp and again in hard cases you can do a CD 34 you can also use factor 13a I don't personally like it for spindle cell tumors really I Basic I rarely use factor 13a. I personally don't find it very helpful It will stain a lot of dendritic cells in the midst of a dermatified broma and is usually pretty negative in the middle of a DFSP. But I find it a lot not very specific. It stains lots of different things. If you're watching this at home and you use factor 13A, that's okay. But don't think that everything that's factor 13A positive is a dermatified broma. That is definitely not true. So, okay. So that's one differential. Any other differentials that we can come up with? And also I told you diffuse nerve fibroma. Can mimic DFSP sometimes. Anything else? Like a hemangio. Well, I'll tell you another one. Hemangio pericytoma. Go say it. Yeah. Solitary fibrous tumor, which used to be called hemangio pericytoma, can sometimes, it usually doesn't have quite, like it has kind of more of a. a patternless pattern. I mean, the spindle cells are just kind of haphazard, but occasionally it can make little fascicles or have some areas that get a little swirly. The important thing to know about why those can look alike is that DFSP often has dilated ectatic vessels. Here we have some dilated vessels here, but sometimes they can be dilated and branching and give that staghorn appearance, which is the classic vascular pattern seen in solitary fibrous tumor, um, and which it's called the hemangio-pericytic vascular pattern because that is what SF SFT used to be called. And they both express CD34. So solitary fiber tumor is very, very rare in the skin. Most of the cases I've seen are in the deep soft tissue, but it can rarely present in the skin. It usually, almost all of the ones that I've seen are very circumscribed and not infiltrated, but sometimes there is a variant of SFT that has fat in it. It makes its own fat. It's like called lipomatous SFT. And I've never seen one of those in the skin, but I could see that easily being mistaken for DFSP and because they kind of similar cytology to some extent that cells of SFT are usually a little more plump and not quite so thin and stretched out but I've seen some exceptions and then the what's a good solution does anyone know a specific marker for solitary fibrous tumor because CD 34 is a great marker for certain things very sensitive for certain entities like DFSP but it's not specific right CD 34 stains lots of lots of things Many, many different fibroblastic tumors will be CD34 positive. And also, of course, most vascular tumors with some exceptions. So it works, but you have to know exactly what your differential is and to remember that many things express CD34. So what's a more specific marker for solitary fibrous tumor that would be negative in DFSB? So STAT6, okay, S-T-A-T-6. And that's because solitary fibrous tumor is also a translocation tumor. It's not a sarcoma. There's both low-risk, medium-risk, and high-risk variants of SFT. It doesn't really fit neatly into a benign versus malignant box. So... There's a way we, again, this is probably outside the scope of what you guys need to know, but there's a risk stratification method that we can use based on the age of the person, the size, how many mitoses, and if it has necrosis. And then there are ones that fall into the low-risk group, basically usually act benign. And then the ones in the high-risk group act like sarcomas. And then the intermediate group is kind of in between. So that's kind of a newer model, even since I was in training. But I actually like that for solitary fibrous tumor. So if you ever have one of these in practice, they should get removed with negative margins. and someone should be giving you a risk scoring. If they don't, you probably should get a consult to make sure. But STAT6, their translocation is NAB2-STAT6 gene fusion or balanced translocation. And this is one of those times where actually the immunostain STAT6 works better than the fish. My understanding is that when the fish rearranges, the loci are very close to their original location, so it's harder to see the break apart. I'm not a fish expert, but basically the immunostain works beautifully. It's a strong nuclear stain, and it's... pretty specific. I mean nothing's perfect but it's pretty specific for solitary fibrous tumor and be negative in DFSP. The other thing that I would point out as being and there are a handful of others we won't go all the way into them but the other thing to remember is perineuromas also can look quite like a DFSP because the whirling Swirling growth of perineuroma can look a lot like the story form pattern of Dermatofibrosarcoma protuberans. Perineuromas can express CD34. They will express perineurial markers, EMA, GLUT1, and CLAUD1. The problem is they often are kind of finicky, patchy, weak staining perineuromas. So I find all of those markers, none of them work totally perfectly. EMA particularly, I've had really a hard time. Like it's the classic marker that should be positive in all perineuromas, but it's very difficult to work. It works great on epithelioid tumors, but on spindly tumors like perinurioma, I find it to be very wispy and weak and difficult to interpret a lot of times, at least in my hands. I've heard that it's something to do, I think, with different levels of antigen retrieval. There's something in the laboratory you can do to tweak it, but I've not experimented with that personally. But I've heard from some people that they've gotten their EMA to work better by, I think, doing a different type of antigen retrieval. I can't remember the details, but someone told me that not long ago. Anyway... The thing about that though is that sometimes perineurium and DFSP can have overlap because DFSPs occasionally can have some focal EMA expression or can have some staining that's a little bit like perineurium. If there's any doubt, you can do FISH. And of course, you guys know what's the translocation here. 1722. And what are the genes involved? 1722. I think it's PDGF-beta and collagen 1A1. Yeah, collagen 1A1, PDGF-B. B as in boy, B as in beta. And then more recently, it's been discovered the vast majority have that fusion. But recently, in the past few years, we've discovered it's been reported that there is an alternate fusion involving the PDGFD, D as in delta, and fused with a couple of different partner genes. And I've seen one of those in practice, and we're actually in the process of writing that up as a case report. So hopefully that'll be out in the near future. So just to know that it's the... Collagen 1A1 PDGFB is really important, but there is a new fusion PDGFD that's been described, and I imagine that now that we know that exists, we'll find more and more of those over time. I only do the FISH in really difficult cases. This case is classic, and you probably could sign that out on H&E, honestly. Here's our low power. Okay, what do you think? I'm wondering about M. I feel like there's some large, dark, kind of angulated glimpse up in the epinephrine. Look at that, little crinkly, wrinkly. I mean, that's cerebriform, right? Now, I always joke, I promise you I can find you a cerebriform cell in pretty much any biopsy if you give me enough time. But, I mean, honestly, that really looks cerebriform. And there's also a lot of tagging, right? We have a lot of lymphocytes along the basal layer here. I mean... very concerning because they've got little halos around them. They're tagging along the epidermis. And in this area here, we don't really see any interface or much spongiosis. So we've got too many lymphocytes for too little sponge. So that always makes us think of mycosis fungoides. But let me go back to low power again. Where do you think we are in the body? What are these? Apocrine glands. Yeah, apocrine glands, right? They've got that abundant granular orange, I'm sorry, pink cytoplasm with these little refractile. bodies up here i'm not exactly sure what they are but they're usually there and then the nuclei are really big and round they have like a prominent nucleolus they look like a little eyeball staring at you someone on instagram once said they look like minions like the little one-eyed minion uh from the the minions movie and i was like oh it's so true they do so i like that so african glands so where so there's that and then what do we see in the dermis little smooth muscle bundles Breast could be. Breast will have smooth muscle and sometimes can have African glands. And the genital area, exactly. So in this case, we're actually in the vulva, okay? In the nipple, usually the muscle bundles are thicker and bigger. And in the vulva or scrotum, they usually are really small. But admittedly, that is a somewhat subjective thing, but just to know. And also, I feel like usually African glands are more abundant in the genitals. And whereas you can rarely see them around the nipple areola, so they can be in both places. Yeah, this ended up being from the fall, I believe. And then what about this? Yes, we've got atrophic epidermis, a band of homogenized eosinophilic, almost pale. So you can see that it's collagen here. You can see the fibers when we flip the condenser, but it's kind of pale sclerotic. So sometimes that happens in lichen sclerosis. You get this band of sclerotic collagen, and sometimes it can get edema in there that makes it look really, really pale, almost white. And then below it, you've got a band of... histiocytes that are kind of trickling between the collagen. You sometimes get this kind of, it almost looks a little like interstitial GA. So we wrote a paper about that a couple years ago, Sarah Shalin and I and our colleagues, we wrote a paper about this kind of interstitial granulomatous pattern. This interstitial pattern, it looks like interstitial GA that you see down under the sclerotic band in lichen sclerosus. You tend to see that more often in extra genital lichen sclerosus than in genital, but you can see it in both. And then sometimes there will also be a band of lymphocytes in here too. But you can have either lymphocytes or this kind of interstitial histiocytes or both. Okay. So in this case, this was clinically lichen sclerosus and did not fit for mycosis fungoides. So this is an example of one of the mimics of mycosis fungoides that in lichen sclerosus, you can have really prominent epidermotropism of lymphocytes that really mimic, strongly mimic mycosis fungoides. cutaneous T cell lymphoma. Pretty scary. So this is another reminder of why we don't make the diagnosis of mycosis fungoides on path alone in isolation. It's got to fit clinically because there are a variety of entities that can have what looks like tagging of lymphocytes in the epidermis or epidermotropism and yet is not mycosis fungoides. So this is lichen sclerosis mimicking with a kind of pseudo-M appearance. And you can see that there's a whole long list in the DermPath textbooks of things that can do that. that but you can see it sometimes lichenoid keratoses can have a prominent areas that look like mf you can sometimes see it overlying pigmented purpura and a variety of other things too but this one is pretty scary because not only does it have all the tagging with the halos around the lymphs but it's also got the little cerebriform crinkly looking nuclei pretty scary huh so lichen sclerosis and here's kind of this is it would be harder when you have this right Because here you can't really see that homogenized collagen very well. You're beginning to see it right here. But in the earlier kind of inflammatory phase of lichen sclerosis, as it's just starting out, it starts as kind of usually as an interface dermatitis. This case is a little strange because it's got all these lymphs in the epidermis, but not really much in the way of vacuolar change or dying keratin sites like you'd normally expect. So kind of weird. I mean, it is very, you could easily take a picture of that. I'm sorry, I'm trying to, slides a little sticky on the back. and of course there's a wrinkle right where I wanted to show you but that's okay I mean you could take a picture of some of those cells and put that in a book and say this is classic mycosis fungoides right scary all right so low power and clinical wins the day like in sclerosis at a trophic is if you like This is also vulva. And this patient, there's diffuse scar here from a previous surgical operation. And this patient has a known history of lichen sclerosis also, although I don't really have a great area to show you on this particular section of the lichen sclerosis. But they did have known lichen sclerosis, and they previously had a surgery. the best area. So here's kind of their not totally normal but more normal looking epidermis right it's kind of atrophic because it gets over a scar right but that's just to give you an idea that's what their normal skin for this area looks like. Sorry trying to get the lighting level just right okay and then let's go over to this thicker area that's acanthotic in the middle. This area has got acanthosis come on here we go. acanthosis, hypergranulosis here, and the nuclei are a good bit larger and even a bit more atypical. See, look at those guys. Now you know Atypia is in the eye of the beholder to some extent, but I mean those to me look more enlarged and hyperchromatic. I'm sorry, I have to keep flipping it. The disadvantage of glass slides is that in digital slides the lighting is usually just perfect and in glass slides not so much. This is a very difficult and controversial area, but I thought it's probably good to make you aware of it. Because we do have to deal with this and we encounter this from time to time. And I found it very challenging. But here we have hypergranulosis, but no HPV change, no like real coelocytes, right? These little vacuoles here, that's not a coelocyte, right? That vacuole artifact is a totally normal thing to see around keratinocytes. Those nuclei are really tiny. Coelocytes will be up there in the granular and will have vacuoles a lot of times, but much bigger nuclei. The nuclei should be really large, like paradoxically larger at the top than you'd expect. So if it were high-grade dysplasia and had HPV positive, that would be H-cell, high-grade squamous intrapithelial lesion. Usually the thing about H-cell is that H-cell is going to be full thickness atypia, or at least like two-thirds to full thickness atypia. And usually the cells are very blue and basaloid because they have large, dark, hyperchromatic nuclei without much pink. keratin in them. So here though, we have very like abundant pink, right? Like it's abundant keratinization of the cytoplasm. You can see like the keratin filaments really prominent there, right? So usually that's why the H-cell usually has a very blue basaloid look to it and usually very atypical nuclei. This is much more subtle atypia to me. I mean, in the range that you could wonder, is this really atypical or is it reactive? So in the setting of... lichen sclerosus, when I see areas of acanthosis with basal layer atypia, I start wondering about a different type of dysplasia, which is called DVIN, which stands for differentiated vulvar intrepidial neoplasia. So VIN, vulvar intrepidial neoplasia, VIN 1, 2, and 3, right, is the kind of older terminology that now corresponds to L-CIL for low-grade squamous intrepidial lesion or which I basically almost never use that term in the volvop personally, or H-cell, which is the squamous situ, basically, that's HPV-driven, high-risk HPV-driven. So now we say L-cell and H-cell, which corresponds to the older VIN system. And you can still use both, but the most modern terminology from the last criteria, the last terminology system, the lower anogenital squamous terminology, which is what stands for last, L-A-S-T, is L-A-S-T. L-cell and H-cell. Okay. And if this is 2021, I'm making this video. So if you're watching this many years in the future on YouTube, go and look it up because these systems tend to change over the years and new terminologies come up. So, but this is a different kind of VIN, vulvar intracerebral neoplasia, that's not HPV related. It falls outside of the H-cell L-cell system. And this is called differentiated VIN because it's differentiated in the fact that it's not that ugly basaloid looking cells like you see in H-cell, but instead it's very ugly. kind of glassy eosinophilic keratin producing cells with just some kind of subtle basilar atypia. Okay and this type of VIN is important because it arises in the setting of lichen sclerosus usually and it has a significant risk of progressing into invasive squamous cell carcinoma. Okay in fact my understanding is that the risk of invasive squamous cell carcinoma is higher in this form of of dysplasia than in the H cell, okay? I mean, it can happen to both, but I feel like these are the ones that seem to have more of a risk of becoming invasive squamous. Even though they don't look that bad, H-cell looks way uglier than this. I should have pulled an H-cell to show you, but I didn't have one handy. I'm sorry. So in any case, these are not driven by HPV. What happens here is that P53 is abnormal. And if you do a P53 immunostain, you'll see diffuse staining along the basal aspect of this area compared to the background epidermis, which should just have kind of... patchy, what we call wild type staining. I've also seen some examples that had null type P53, where P53 was completely wiped out in the D-Vin area and the background normal skin had some patchy staining. So in any case, whenever I see lichen sclerosis, I'm always on the lookout for areas where I'm getting acanthosis, where I'm seeing basal atypia. Sometimes I've seen cases where they had scattered high level dying keratinocytes. I'm not sure if that's a specific feature, but I have noticed that before. So all those things make me, when I see that in the setting of... patient with LS, then I start thinking about D-VAN. Oh, this case, look, this case had some dying keratinocytes up behind the arrows. And then I'll do P53 or Key 67 also to see the proliferative activity here. Neither of those things are perfect. I think they're kind of tricky to interpret. And usually in these cases, I show my gynecologic pathology colleagues to get help because I find this very subtle and difficult to diagnose. I think the literature on it, from what I've read, it's still the criteria for how exactly to diagnose it are correct. are not perfect, somewhat vague and subjective. I hope I'm not offending any of the authors of those papers. And I'm certainly not the world's expert on this, but just know that there's a form of dysplasia that occurs in lichen sclerosus, and it can progress to invasive squam. And it's called differentiated VIN, D-VIN. I wish I had the P53 stain handy, but it worked really beautifully in that case. It was diffuse staining in the D-Vin area there. Okay. I know that's a hard one, but I wanted to make sure you guys knew about it. And this is also from the anagenital area. Yeah, this is a perfect condoloma from low power. It's a, you know... warty, multi-lobulated warty looking lesion. And instead of the finger-like papillae of a typical verruca vulgaris, usually condyloma, cumulonatum, genital warts, usually have kind of that more rounded papillary surface that looks kind of more knuckled instead of finger-shaped, more like knuckle-shaped. So that's what people like to say. But other than that, the features of condyloma are very similar to the features of a regular verruca. You have parakeratosis alternating with orthokeratin. The para tends to be kind of down in these cleft areas between the papillae sometimes. And you often have dilated vessels in the papillary dermis, like here. And ideally, I want to see coilocytes. And this particular case is loaded with coilocytes. And the coilocytes usually are located in the upper spinous or the granular layer. And see, look, not only do they have pale or vacuolated cytoplasm, but they have really large nuclei. And sometimes they're like two nuclei sitting together inside one space, like you can kind of see right here in this guy. He's like a binucleated one. The cytoplasm can be kind of grayish or can be truly clear and vacuolated. But the nuclei are... big. So for real coelocytes, that's what I want to see. These almost look kind of bubbly in this case. It's interesting. And sometimes you'll see large granules in the coelocytes. It's like actually the granular layer cells that are showing the HPV change. So we call this coelocytes or HPV viral cytopathic effect. It means the same thing basically. And for me, I... And ideally, to definitively make a diagnosis of condyloma, I like to see some good coelocytes, just to be sure. I mean, because even though condyloma is not malignant, it is a sexually transmitted infection. And I don't want to label someone unnecessarily with that because there are sometimes social ramifications of that. And so we always want to think about not just benign and malignant, but about all of those factors and make sure we get the diagnosis right and not cause problems for people in that way. So if I have a lesion that I'm suspicious about... condoloma that's not I mean this is as good as you could actually ever ask for. It's like the most perfect condyloma ever. But if I have lesions where I'm not sure, sometimes I'll do HPV in situ hybridization, which if positive is really helpful to support condyloma. If negative, it does not totally exclude it because depending on what kind of issue you use, the one I currently use I think has 6 and 11 in it. I can't remember if it has any extras besides that, but it has a mixture of low risk. But there are many, many types of HPV, right? Not every ish in situ hybridization will have probes for all of the different types that could possibly cause genital warts or other types of verruca. So again, there's good condyloma. And once you see condyloma, you always want to look around and make sure there's no high-grade dysplasia H-cell. And so if I started seeing really blue basaloid, atypical areas, then that would be worrisome for H-Cyl. Because you can have H-Cyl arise in the background of condyloma. Alright, and there's more coalescites. So, condyloma. This is incredible. Is that a hair shaft that's loaded with fungus? Indeed, a hair shaft loaded with fungus. And not just one, but two, three. All the hair shafts are just completely overwhelmed by fungus. They've got little canidia spore forms on the outer surface. The inner surface, what used to be a hair shaft, is now like a fungal shaft, right? It's like... completely replaced with vertical parallel fungal hyphae. And you can see a little bit of brown melanin. That's from the hair shaft itself, I think, in this case. Because, you know, the hair shaft has pigment in it. That's why hair has color. And the hair shaft has been completely consumed by fungus. It's like a zombie hair shaft. It's all overwhelmed and controlled by the fungus. So what is this? This on the scalp. Yeah, tinea capitis. And you can see this pattern, which has been called both, you can have endothrix, which is when the hair shaft is filled with fungus, and ectothrix when the shaft is surrounded by fungus. In my experience, I often see kind of both together, like what looks like endothrix and ectothrix pattern together. Neither of those are actually a fungal type, right? They're just a pattern of fungal involvement of the hair shaft. And so usually you see this in the setting of tinea capitis, but I've also seen it like on the forearm or other sites on the body where someone had dermatophytosis that involved their follicles. And when it did, it got colonized like this. And so these are caused by dermatophyte fungi. And what's the most common one that causes tinea capitis? It varies by geographic location. Is that right? Okay, so trichophyte and rubrum in the U.S. overall, but some areas maybe microsporum canis. Microsporum, right, for M? Yeah. Okay, good. Just want to make sure I didn't get that wrong. Okay. And then here, this is an awesome case because here we can actually see it coming out of the surface. Isn't that amazing? I mean, if you don't like that, I just can't help you. I mean, that's fantastic. Just a cut to see hair coming out of the surface of the skin where it's cut perfectly like that is something we don't see that often. Like it's got to be the perfect cut, right, to split the hair down the middle. But to see three hair shafts in a row, all loaded with fungus. Swooned. It's too good to be true. Here's what it looks like more often or if you get like a alopecia style punch, right? you're going to see more like this, right? Where you get a cross section of the hair shaft that's got fungus. And if you get this and it ruptures, right? And you get inflammation and a little abscess around it, then you could say it's Miyake's granuloma, right? And in my experience, when I've seen things that clinically fit for Miyake's granuloma and I find fungus, I, you know, I was always taught that the fungus should be in the dermis outside the follicle in the middle of the abscess. I feel like I almost never see that. I feel like I'll see the abscess and the perifollicular inflammation. that's giving that myakis, that kind of more indurated myakis granuloma appearance clinically, but the fungus usually I don't find in the dermis itself. But anyway, this is important to remember. And sometimes when you have endothrix, ectothrix, sometimes the fungus is only in the hair shafts or down in the follicles. But other times you will find it on the surface too. So always make sure when you're doing a PAS that you do check around your follicles. And also if you're thinking of myococcus or of tinea capitis. Make sure to check on the surface too for fungus with your GMS or PAS stain, whichever you like to use, whichever works better in your lab. Really great, excellent example of that. I don't get to see that biopsy very often because tinea capitis is often in kids and it's often recognized by the dermatologist or the pediatrician or whoever and then treated. So I don't see it biopsied that often. So it's kind of a rare treat for me. So there's the skin up here and then here is, is or was the subcutis. Now there's something going on here. This reminds me of like encapsulated fat necrosis. And it reminds you of encapsulated fat necrosis because that is precisely what it is. It's actually like the... best example ever. It's so fantastic because you can see, A, because we can see the skin, like it was beautifully removed by a very skilled dermatologist. And they took the skin and then popped the nodule out from underneath. And the nodule is perfectly circumscribed and encased by a wall of fibrosis and a bit of inflammation, right? You can see here's this kind of peripheral wall of fibrosis making a band. And then if you look on the outside, that's their normal living happy fat. relatively happy, and then next to it, not happy fat, and that the fat can have a range of like fat necrosis with foamy histiocytes like here. If we flip the condenser, we can see the bubbly foamy a little bit better. Xanthomatous cells, right? Fat necrosis is a thing worth studying because it can look kind of weird and wild sometimes. Not here, it's really easy because we can see that it's a nodule. But sometimes on a small biopsy, you can really struggle with what's all the cellularity going on here. And then sometimes the actual adipocytes where there used to be adipocyte is rimmed around by histiocytes, right? See the histiocytes are surrounding the empty space that used to be a dead fat cell. And then the other areas here are more like sheet-like. Like everything here is just dead fat, right? It doesn't have as much histisite. It's all just wiped out, like kind of almost mummified. you know, a sheet of totally ghosted out dead fat where the nuclei are almost all gone, right? Sometimes you can see that arabesque pattern, lipomembranous change in encapsulated fat necrosis. And I feel like these, my understanding is that usually this is like a post-traumatic thing, like post-traumatic fat necrosis sometimes basically gets a totally dead nodule and then gets walled off by scar. or fibrosis like we saw in this case, and then it presents this nice nodule of kind of dead and mummified eventually fat that is walled off and doesn't get resorbed by the body and it can persist I understand for like sometimes for years and be there for a long time because it's encased in the fibrosis so that it never like gets cleaned up by the by the rest of the immune system and the histiocytes right it's all just walled off here like like the nuclear reactor at Chernobyl, right? It's just in like a little sarcophagus. So I just made that up today. We'll see if that sticks. If it does, then I'll cite this video in the future and say that I coined it here today on 9-2-2021. Okay, just kidding. Wait, I'll wait. the Nobel Committee. I hope you guys are giving me a pity laugh from home. Thank you. In any case, here's another slice from the same case. So in these, as you guys know, these sometimes are mobile and these little nodules can like move around and the patient can like push it around like a little marble under the skin, which is really pretty crazy and wild. And I'll see if I can. get access to a video of that to include or upload at some point in the future. Because it's pretty cool. If I find a video, I'll check, if you're watching this on YouTube, check the video description down below for links. I usually put links and stuff in video descriptions on my videos. Oh, I got it. I'm getting some sunlight coming through my window there. See that little, uh, this little, uh, light there? That's the sun reflecting through the ocular of my microscope. When I cover it, it goes away. So... Looks like a... Yeah, there are granulomas here. There's kind of these pale nodules. Or gout that maybe is kind of feathery in the lighter areas. Okay. Gout looks like something that's very, very light. Yeah, good. This looks very much like gout, right? It's multiple nodules of pale, light, feathery, fluffy, like cloud-like substance. And if you go close, you kind of get the impression that maybe there used to be little thin needle-shaped crystals there. And then it's surrounded by a wall of histiocytes, right? See there, look at that needle shape right here. But, as you guys know, that during the... processing of the tissue and staining, the urate crystals get washed away, right? So, and I was always taught it was because of formalin fixation, but from some other papers I've read and some experience I've actually, it seems like maybe some of it gets dissolved by formalin, but the bigger thing seems to be the processing and then the H&E stain itself actually. So, the best way to see the crystals of course is to do a fresh smear and or to submit an alcohol, but you can just submit it fresh. and then say please smear for looking for gout, and then we can see the urate crystals. So this looks great for gout, but this is interesting. This is like a nodule on the foot. But then we got areas like this. And here, this is like very dark purple, and some of it looks kind of needle-shaped but is purple, kind of like calcium sort of look. And when we flip the condenser, Yes, some are long and needle-shaped, but others, can you see them right in here? They're like diamond or square or what we say rhomboid-shaped, right? Like, oh there, that's better. See them there? Way bigger, thicker, and chunkier than gout crystals. Also, they're easily visible here on a formal and fixed H&E section, and many of them are purple, which is not the color that gout should be. So this is slightly unfair because this is something that I don't think I've ever seen actually in the skin. But this is from the foot, and I think soft tissue things in the foot can be close enough to the skin that they can come up and get sampled and sent to DermPath potentially. So it's fair to at least know about this. And I would say that even in the hands and feet, I've only rarely seen this in the hands and feet. Usually I see this in big joints, deep joints, like the knee, or I often see it in the spine, like in intervertebral disc specimens from spine fusion surgeries. Let me see if I can get the polarizing to work. I'm going to try. Sometimes it's a little difficult to catch on camera because of the light adjustment. Let's see if I can get it. One second. Turn the auto adjust off. There we go. See them? And so they glow and are birefringent under polarized light examination. You can really see that rhomboid shape now. So does anyone know what this is? Yes, this is pseudogout, calcium pyrophosphate deposition disease, right? Which again, usually is there almost always when I see it there. clusters of purple, dark purple, because they're calcium. So they're staining purple on H&E. And then when you go closer, the crystals are preserved and they're rhomboid shaped. Although occasionally I've seen ones like this that have both rhomboid and kind of longer needle shaped ones. So the question in this case, usually just on H&E, gout and pseudogout look very different and are easy to tell apart. But this case is hard because that stuff looks perfect for calcium pyrophosphate. But over here, I thought it looked perfect for real, true gout monosodium urate. So my suspicion is that this patient may actually have had gout and pseudogout both mingled together here. Now, I don't, unfortunately, have proof of that because I don't have a smear to go with this. But if you would have just given me this area, I would have signed this out. Gout. Done. I wouldn't have even, like... questioned it or said we need to get a smear, I would have said this looks perfect for gout. That looks exactly like what gout is supposed to look like. But then we have all of these purple rhomboid polarizable crystals in here too. And this is really extensive. It's everywhere. So I suspect, I think this is definitely pseudogout, but also I suspect that there may be some intermingled monosodium urate deposition in the midst of it. So kind of a fascinating and interesting case. And again, I rarely see pseudogout in the hands and feet, but occasionally I've seen it near the small joints in the hands and feet where it can push up close to the skin surface potentially. But like I've never seen it like in the dermis itself. Okay. Oh, if you don't like that, I don't know what I can do to make you happy. Oh, it's perfect. Look at that. They clinically, they said bright red papule. Rule out cherry angioma. Good. Yeah. Even from 2X. Virtually, you guys instantly know clear cell acanthoma, it's elongated, reedy, really acanthomatous, or very acanthotic, excuse me, a sharp cut off from the surrounding epidermis, right? The cells aren't really clear despite the name, they're more like pale. Cytoplasm, also with a bunch of spongiosis in between and both those things together give this lesion its pallor, its pale look. It's a sharp, discreet line delineating it from the surrounding epidermis. And occasionally I've seen ones that are kind of multifocal that'll have a zone. and then back to normal epidermis, then another zone. So, you know, they're not perfectly round. And this one's also great because it has the classic finding we're supposed to have of neutrophils, right? So there's neutrophils scattered in the midst of this thing, trickling through the epidermis, and they're on their way up to the stratum corneum where they mingle in to the para. So you have lost the granular layer, parakeratosis with neutrophils. In many ways, a lot of similar things here to what we see in psoriasis, right? The surface aspect of a clear cell acanthoma has, I mean, there's a lot of stuff that's like psoriasis, even the little dilated vessels down here, right? So that is a perfect example of a clear cell acanthoma. And they're usually a solitary lesion. The leg is a common site. And then I think I've mentioned before, but occasionally I've seen a few other things that can kind of mimic clear cell acanthoma. And I've seen trichylamomas that kind of look a little like this and also inverted follicular. keratoses can sometimes have some overlap. Not like this particular case, but I've seen ones where where there were those three entities, clear cellulite canthoma, IFK, and trichelomoma, can have a little bit of overlap. And also poro keratosis, I'm sorry, poroma, excuse me, poroma can do this sharp cut off here at the edge. So otherwise this doesn't look really like a poroma, but poroma does that sharp cut off. So that's another thing that can overlap here. And I have had one case earlier in my career that on a shave biopsy, I thought was actually because it was really glassy and it was a little atypical. I thought it was going to be a squame. And I think I called it a squame, superficially sampled. And then when they went back to re-excise it, it was actually a clear cell eukaryothoma instead. So I had never thought about this as mimicking squamous cell. But on that particular case, it was a superficial shave biopsy and it was glassy and pushing down. And I thought it was enough to call a squame. And once I saw the whole lesion, I realized, ah, no, it's not. So. That's how we learn things. Really good example, just classic. What pattern do we have here? with superficial and deep perivascular dermatitis pattern, right? We've got a brisk infiltrate around the superficial and the deep vessels. We also have infiltrate that goes around the adnexal structures, right? Around the pilosovatius unit, around the eccrine coils. So we can see that pattern in a lot of things. The first thing we need to see, though, is is there any epidermal change, right? Because if you have this pattern alone versus this pattern with epidermal changes, it can change what's going on. Epidermis looks relatively normal here, really. No good vacuolar interface, very minimal spongiosis. There's a bit of hemorrhage in the dermis here, but I didn't see any vasculitis. And there is also... It's sometimes hard to see eosinophils when there's a lot of erythrocyte extravasation because it makes everything look kind of like an EO from low power and then you go closer and you're like, oh, it's not an EO, that's blood. So I find that I have to hunt a little closer at higher power to see if there are EOs when blood is present in the background, okay, when we have leaky vessels. And I did not see eosinophils. I looked for a while and didn't find eos here. And then right here, I don't know if it will transmit well in the video, but we'll try. Right in here. We've got some bluish mucin and Patrick, one of my Dermpat fellows, told me the other day that this looks like this little pattern of like wispy mucin with little tiny speckles on it, that it looks like dew on the spider webs, like you know spider webs on the grass that get the like morning dew on them. But he said that that was our colleague Dr. Wells Chandler actually. I had told him that and so I thought I love those cool visual analogies and I really like that one So I don't know if dr. Chandler invented that or if someone else did and you know Like many of these things we hear them from mentors We modify them and then we pass them on to our trainees and it's like the circle of life in Pathology teaching but anyway, there's mucin there right and so mucin can be very subtle sometimes and yeah looking for those little speckled dots This is high powers. I can get I'm sorry. It's helpful also There's a little bit of elastic fiber here. Sometimes in people with a lot of solar elastosis, it's really difficult to tell if there's mucin. So I go down and look deeper in the dermis. Don't look up right under the epidermis. Come down deeper and see if you can find mucin. And also one last thing when we're talking about mucin, ignore mucin around the eccrine coils. You're going to find mucin around, not in this case, but... many times you will see mucin around eccrine coils, okay? And it doesn't seem to mean anything. Sometimes, especially like in the distal extremities, I feel like I see lots of mucin around the eccrine coils, like near the hands and feet. I assume it's some sort of a reactive phenomenon, but I see it very commonly and it doesn't seem to have any significance to my knowledge. All right, so what do we do with this? No epidermal change, superficial and deep, and peri-adnexal, and mucin. So what's a good diagnosis here? And no EOs. Yeah, I think this is tumid lupus and this would be a plaque on the chest of a young or middle-aged female adult. That would be the classic story. I think this case was like from the shoulder or somewhere. So in any case, that is tumid lupus. I think fits very nicely. And as you guys know, tumid lupus oftentimes is just localized and not, is usually not associated with systemic lupus. Although if I start seeing interface change up here, then I start thinking about like. regular lupus erythematosus. Clinical of tumid lupus is kind of distinct in that it tends to be one or a few plaques like on the chest. And there are some other entities that you guys have probably heard of like REM, reticular erythematous mucinosis, which is I think of as kind of like tumid lupus with more abundant mucin. But I feel personally like it's probably on a spectrum, although I'm not an expert on this and I'm sure there are some people who disagree. You know, there's lumpers and splitters and derm path. And then also, um, jessners it's like basically a kind of more abundant lymphoid rich thing that i think is on the spectrum with tubal lupus personally and it can be so so much inflammation that it can mimic a lymphoma so that's those are two things to think of that i feel like exist in this spectrum and in this case even though i didn't see vasculitis there does seem to be like some vascular damage like the vessels are leaking the endothelial cells like a little swollen so i wonder if we have kind of a lymphocytic vasculitis going on here which is kind of a bit of a controversial topic but sometimes when we have dense lymph lymphocyte infiltrator on vessels without neutrophils, we do see blood leaking out of the vessels and maybe some fibrin. And in connective tissue diseases, you can have some vascular damage and even can have like actual leukocytoclastic vasculitis in some cases. So I thought that probably we do have some leaking of the vessels in this particular case here. And if you would have shown me this and not told me the history and then put some eosinophils in it, I think this would be great for an arthropod bite reaction too. In fact, at low power, when I first put this down, I was like, oh, maybe this would be a bug bite because Bug bites often get some hemorrhage with them. But then I didn't find any EOs. And then once I saw the clinical and the mucin, I thought, oh, no, I think this is good for tumid lupus instead. But in arthropod bite reactions, I often see period nexil, particularly around the eccrine coils in arthropod bite. All right. So there's tumid lupus. And then let's see to finish up here. Okay. We'll just end on one last simple case. What's this? Yeah, Bowen's disease, squamous situ, and I just wanted to show you this one because look at how wild the pleomorphism can be in squamous situ. Like, you can see those cells from outer space, like even from 2x. They're ginormous. You can see them from way up here at like cruising altitude. And some of the most bizarre pleomorphism in the body, I see like in pleomorphic sarcomas, particularly like pleomorphic liposarcoma, has some insane pleomorphism. And the other place I see insane pleomorphism, squamous cell carcinoma and cytobowens disease. some reason they just get dramatically ugly and yet the prognosis is usually very good right i mean occasionally these can invade and be more aggressive but i feel like most of the bowens i see likes to hang out in the epidermis and the adnexa it likes to stay in situ um and and i don't see invasion in bowens that often. It happens, but I feel like it's those glassy keratinocytic looking or keratin producing squames that I see invading more. And these ugly bluish bowen looking ones tend to be more in situ. But that's just an example of how crazy the pleomorphism is. And you can also get crazy weird atypical mitoses that look like all sorts of unusual shapes. in Bowen's disease squamous situ. All right guys, there's a little review of a potpourri of cases. I hope you enjoyed and for those watching at home, thanks for watching. Have a great day.

All right, so here's a case, and I wish I had... I'm going to get this scanned because it would be better to see from... from low power.

But this was a draining nodule on the trunk that looked like a cyst. There's kind of a cystic space in the middle but no lining. What's this right here?

Does anyone... Like granulation tissue? Very good.

Granulation tissue. So important to recognize. It's a common kind of simple thing.

But man, granulation tissue can look really wild sometimes. And it definitely, starting out, I remember thinking it looked pretty scary. Because it's very busy, right?

Got big, plump endothelial cells in these vessels. And then all this inflammation mixed in. Neutrophils. And, uh, and, uh.

In this case, a lot of eosinophils mixed in here. Histiocytes, lymphocytes, all blended together. And then there's a bunch of fibrin lining this central space here, but no actual cyst lining. Tons of eos.

Hmm. Well, the key here is not in the middle of the cyst, but out here. Now, what is going on? Can anyone figure this out?

It is not human. It is not human. Right. We have an alien invader here. A non-human life form of some sort.

Wow, it's quite pretty, isn't it? I don't know what all those parts are, but they're not human parts. I can tell you.

What are those cells? Or structures. They look like giant cells at first. I don't even know what's going on here.

Oh, that I recognize. What's that? Muscle.

Skeletal muscle. Look at that. And then here we have an outer wall, an exoskeleton.

And little bits here and there of that yellowish-orange stuff called chitin, right? Here's some more. And look, sometimes... This is an arthropod, right?

The question is which one? Sometimes arthropod exoskeletons have these very jagged little ridges or lines. Again, I'm sure an entomologist could tell me all about these things, but I can only have enough time to learn so many things and derm path and soft tissue is more than enough for a lifetime for me.

So in any case, does anyone know what this is? What kind of arthropod we're dealing with here? Myiasis, like a fly. Myiasis, bot fly. Yeah, this is a maggot.

a fly larva way prettier microscopically than they looked the naked eye, which is true of pretty much everything in pathology. It all looks pretty under the microscope, even if it looks awful and nasty in real life. So this whole thing is the maggot, the fly larva, and it used to live inside this little burrow here in the skin.

So the fly lays the egg in the skin and it turns into the little larva, the maggot, and it's got a little... hole that it breathes through from the skin surface and the body is none too pleased with having this maggot growing in its skin. And I know maggot makes it sound grosser, but that's what it is. It is a pretty nasty little infection or infestation rather, excuse me. And then the body is creating granulation tissue and granulomatous, I mean it's not much granuloma here, but a granulation tissue response sometimes with granuloma and with a bajillion eosinophils.

Eosinophils can be seen in lots of settings, but one of those settings that you particularly see it is when you have Helmets like worms in the skin of different sorts like larvae migrants or in the setting of botfly or other things So rarely do I get to see these other things that you could think of if you just had this because here we're just getting It kind of fragmented piece of the arthropod You could think about a tick if this were on the skin surface because it's about this about the size honestly a bit bigger than most ticks I've seen. But if that were like clinging to the skin surface, you could think, oh, maybe a tick. If this were right underneath the stratum corneum, kind of pushed down from the epidermis and it was on the foot, you could think of tongue ependotrans, tongue gaiasis.

There may be some special features of the organism that can let you tell them apart. But really, I have to tell you, basically, once I see a piece of arthropod, I use the size and the location to guide me and then the clinical scenario to guide me to which of the... the different arthropod forms or species are most likely going on in the patient.

So that's how I kind of do it, is based on the size of the organism and whether it's on top of the skin, in the epidermis, down underneath, and then put that together with the clinical. Alright, so bot fly. Okay, I'll let you tell me the history, because the path is pretty darn classic here.

Anyone do it from 2x? So, tender, thymidous nodules on the lower extremities. Tender erythematous nodule in the lower extremities. Absolutely.

Any young woman who recently started oral contraceptives, right? That's the classic like test question. So yeah, this is what then? Eno-dosim. Yeah, erythema no dosim.

So paniculitis, the paniculitis I think are confusing because we talk a lot about septal versus lobular. And I feel like in real life, there's often a lot of overlap. But one of the ones that holds the most true to the septal. versus lobular I think is you know do some it really is a predominantly septal process and for any any of you guys who are beginners what that means is that the lobules the subcutaneous fat lobules have relatively minimal inflammation or involvement by inflammatory cells and the septa in between the fat lobules, which are normally present but very thin. If you look at normal subcutis, there are thin little bands of collagen that divide the lobules of mature fat.

And those get inflamed and fibrotic and then because of that they widen and get really thick. So even from low power you can see that the lobularity of the subcutis is very dramatically highlighted for us because the septal areas are so thickened and widened. And when you go look closer in those, and it depends on the stage, early erythema nodosum can be more richly inflammatory and less fibrotic. You can have some hemorrhage and neutrophils. And then as it kind of progresses on and gets chronic, that tends to turn into kind of fibrosis with a granulomatous reaction.

So histiocytes, sometimes giant cells. I feel like you often see EOs, lymphocytes, and you know, you get a little bit of involvement of the fat. Again, septal paniculitis versus lobular paniculitis, in my experience, not. It's not a perfect clear cut line, but it works the most here. So this is a nice example of the changes you'll see in the septa of the fat in urethema nodosum.

And I think some of these little granulomas here, I think people have called them Miescher's radial granulomas. If you like buzzwords, I don't know if that's really the best example, but there's like a little granuloma right here. So that's nice erythema nodosa. There were some giant cells.

Really good example and a really awesome biopsy. Look at that. Because see, a regular punch, if you just did one punch and got down to here, I wouldn't be able to tell you anything on that.

So if you're lucky enough to get, I mean, that's amazing to get a punch intact all the way down here. It's wonderful. But in real life, if you're biopsying for paniculitis, as I think you guys all know, Do a double punch if you need to punch once and go back down into the punch biopsy hole and take another piece down Into the fat.

I know it's hard because it bleeds a lot a wedge or elliptical incisional, you know ellipse excision, excuse me incision So doing like a wedge biopsy is the best thing but obviously that that does take more time and is more involved And so I understand that it's not always feasible and practical to do but that is the ideal scenario for diagnosing paniculitis, but in a pinch, a double punch boxy will do just fine, in most cases. So there you go, erythema nodosum. This is a plaque on the trunk of a 25 year old patient, no skin. Just look around here. Kind of a lot of different stuff going on.

It looks very heterogeneous, right? It's a hard case. I struggled when I saw my first one of these two, and I've struggled again with them since, but I was really baffled by this. So I'll tell you, the pitfall here is to look at this thing and see spindly kind of tumor with fat trapping, right? Honeycomb fat entrapment, and to think DFSP.

It'd be understandable. The thing that would be a little weird for DFSP is that it's not just like fat trapping. It's like way down here mixed in with the subcutaneous tissue.

Look, there's all these like big vessels that it's like wrapped around and like kind of intervened between. And while yes, DFSP is infiltrative and can do that, this is not like as, I don't know, something about it's almost like too patchy down in here. I don't know how to explain that really.

The other thing is that in this case, the cytology is not. Quite right for DFSP. Yes, it's bland and monotonous, but it's not, some of it's spindled, but a lot of it's more like little oval or round nuclei, right? See?

Very bland, very, very benign appearing, but so is DFSP, which is, that's where the pitfall, because this tumor is actually more often like bland spindle cells that look very much like dermatofibrosarcoma protuberans, and that's why it's an important pitfall to know about. See here, it's more spindled. Blan spindle cells with fat trapping.

So these are Wagner-Meissner-Meissner bodies. They're little little structures that are recapitulating Meissner's corpuscles. Like each one it looks kind of similar to a to Meissner's corpuscle. Right see like here's like one little circle here's another one. Here's another one, another one.

They're like all clustered together. This tumor is S100 and SOX10 positive and CD34 positive. This is a diffuse neurofibroma in a patient with neurofibromatosis. And they can have spindled, bland spindles, like that, that look more like neurofibroma. But this is tricky because...

In diffuse neurofibroma, there are two things. Number one, you often get lots of infiltration or intermingling with the fat. It's not aggressive growing like a DFSP. It's just intermingling with the background fat that's there.

I mean, they can be very, they're not aggressive, rapidly growing tumors, but they can be very large and disfiguring in patients with neurofibromatosis. So they are benign, but they can cause significant morbidity, okay, when they're large. But because of the fat entrapment, And because the fact that neurofibroma is usually CD34 positive, they can closely mimic dermatofibrosarcoma protuberans, okay?

The other thing is that the diffuse form of neurofibroma, in contrast to the more conventional types of neurofibroma that we see as little, like the little nodular form we see in the skin, that the cells tend to be more rounded, oval to round nuclei, than spindle. They can be spindled, but you'll often see kind of a more rounding. And because of that, sometimes they can get kind of cellular, almost sheet-like areas that are more cellular than this and made of round cells. to the point that I've seen some and they reminded me of like a round blue cell tumor except that they had like no mitoses and nothing to indicate malignancy but I was very perplexed when I first saw one of these in fellowship and thought how are there all these round cells and then Dr. Meissner explained that in diffuse neurofibroma that you tend to have kind of more rounded cells so it when you're lucky you'll find Wagner-Meissner-Meissner bodies look they're everywhere here we got them here here here so Wagner-Meissner-Meissner bodies are typically seen. They're kind of the classic finding in the diffuse type of neurofibroma, although you don't always see them.

And remember that neurotized nevi can get things that look just like Wagner-Meissner Meissner bodies as well, although they're not going to be so big and deep, but this thing is way down in the subcues. The other thing is I've seen this a couple of times now where you have this kind of unusual, like striped kind of tiger stripe pattern. Maybe it's actually better from lower power.

Isn't that interesting? It's like, it's like, uh, lining up in these kind of rows that makes this like kind of stripey Tigroid sort of pattern. I don't know. I don't know maybe that's been described, but I don't remember reading about it But I've just I've noticed it at least I think this case in one other if I recall correctly where I had this kind of unusual like row like orientation So it's kind of a fascinating tumor, but just the take-homes remember that diffuse neurofibroma and traps fat totally normal It can mimic DFS P and neurofibroma CD 34 positive so do s100 socks 10 If you're having any problems because DFSP almost never expresses those.

I have seen one, only one example of fibrous sarcoma. It is DFSP that had patchy, real S100 expression. And it totally blew my mind.

Only one case ever. So in... As a general rule, DFS-P should be negative for S100 and SOX10. Of course, if we do this long enough, we'll find weird exceptions to all the rules eventually.

And there's more of those Wagner-Meissner-Meissner bodies. And there's some more kind of spindly area of the neurofibroma. Ah, skin! You guys are feeling the relief of seeing some epidermis. But don't get too relieved, because it's still a spindle cell tumor.

I know spindle cell tumors are hard. I did a fellowship in it, and I've been doing this for almost 10 years, and I still struggle with them all the time. What's this?

Is that kind of like the story form pattern? Oh, that is exactly like the story form pattern. This is the story form to break all other story forms.

Like, oh, I just, I gotta go home now. I know it's only like 7.50 in the morning, but I can't do any more work today. It's such an incredible pattern.

And so, so fascinating to look at. So you can use a hundred different words to describe story form, but the only way to really learn it is just look at that. That's the picture. That's what story form is. It's swirling, whirling, stirred with a spoon, cartwheeling, pinwheeling.

People have tried so many different ways to describe it because no word captures this really fascinating pattern where the cells are all stacked up in little lines that kind of then whirl and swirl around each other. Very bland, thin, elongated spindle cells, right? And sometimes I kind of think that the way that these cells are is that they're kind of like a plate.

That if you look at them on one surface, they're very thin and narrow. But if you flip them 90 degrees, then they look more like an oval, right? So they're like flat like pancakes, okay? Kind of like oval-shaped pancakes.

So several different tumors can do that, where you can have kind of a story form pattern, and you can have cells that are very thin or are kind of more oval. So what do you guys think this is? I'll go back to lower power.

There's more of that story form. Yeah, that's like really the most perfect example of story form. I mean, one of the best I've ever seen.

And then here's the... A DFSP. So what's this?

This is DFSP, Dermatofibrosarcoma for two brands. No tricks here. And when you see this, that last case I showed you, it doesn't really look much like a DFSP, but I promise you, I have seen some where it would be real easy to make a mistake because of the extensive fat trapping and more spindly-looking diffuse neurofibromas with fat entrapment can very much look like this. I've not seen diffuse neurofibromas make good story-form pattern, like striking story-form pattern like this. They can swirl a little bit, but this is pretty dramatic.

Now the other thing, so what other things might come in the differential here for DFSP? I'm sorry, let me say the features first. Blan spindle cells, often with a story form pattern, and entrapment, honeycomb pattern of fat entrapment like this.

And it's very clean, right? The fat is like just imprisoned within the DFSP cells, and there's not really much inflammation or fat necrosis or anything. This is the very classic example of how DFSP invades. It just fills in the fat. And look.

The fat entrapments not only happen in there. It's all of this. This all used to be pristine subcutaneous You know real estate here was all fat all the way up to here, right? Like right there is where the dermis ends right around here and the subcutis begins And if you're not sure about it, you go and look for the eccrine glands because eccrine coils They reside at the deep and the deep dermis or the superficial subcutis at the dermal subcu junction, right? So Wherever you find your eccrine coils, that's right around where the subcutis should have started.

And so you can see evidence of it right there. And so even though this area here might have almost no fat in it, this all used to be fat. So that is one of the tricky things. Sometimes DFSP can extensively infiltrate the fat to the point that almost no fat remains.

It just wipes it all out. And only at the very edge will you see a few little islands of entrapped adipocytes. So like right here, right?

So even though that doesn't look honeycomb, oh, that's great for DFSP because you know that this area should be all fat based on what the stuff I just showed you. But it's not fat. It's been totally overrun by spindle cell tumor.

OK, so in this case, it's very it's very good because we do have honeycomb down here. But I've definitely seen multiple DFSPs where you'll only find like like this, a couple little islands of stranded fat. And that confused me when I first saw that.

So that's why I'm pointing it out. Okay. So what other things can come in the differential with DFSP?

Dermatofibroma. Yeah, dermatofibroma. Now, usually it's pretty easy to tell dermatofibroma and DFSP apart. On H&E only, you can use stains if you want. CD34 will be strong, diffuse positive in the vast majority of DFSPs, with some rare exceptions.

And when there's higher grade fibrosarcomatous transformation, those sometimes lose. 34 expression. They don't have to.

But otherwise, dermatofibromas tend to have epidermal hyperplasia over them and acanthosis or induction of the epidermis, whereas DFSP usually does not have that, although I've seen some that did, and those are confusing. Dermatofibromas tend to have more plump, larger cells with more abundant cytoplasm, more rounded nuclei, sometimes with some atypia. So paradoxically, if you see scattered atypia, that points to dermatofibroma rather than DFSP.

DFSPs should be bland, monotonous, very elongated, thin spindle cells like that because it's a translocation sarcoma, right? And so all the cells look the same, okay? And the other thing is that you often find hemorrhage or blood-filled spaces, hemocitarin, foam cells, multinucleated giant cells, including two-ton giant cells. All of those things are features of dermatofibroma, not DFSPs. You can see pigment in DFSPs sometimes, but it's not hemocitarin.

It's melanin usually. And what is that? call it a DFSP with melanin pigment with pigmented dendritic like melanocytic looking cells in them.

Yeah, that's called a bednar tumor, which is just a pigmented variant of a melanin pigmented DFSP. It's just a fancy name for us as pathologists to recognize. Doesn't mean anything different clinically to my knowledge.

Okay. Another thing I didn't talk about is collagen trapping, which is a common finding in dermatophibroma, but you can't rely on it because, look, we've got some nice collagen trapping in this dermatophibra sarcoma protuberans. Really good.

Usually, DFSP doesn't quite trap collagen like this. This is the type of collagen trapping we usually see in dermatophibroma, but you can sometimes see it in dermatophibra sarcoma protuberans. So it is a common finding of DF, but do recognize that it can be seen in... Dfsp also I find the other features the blood hemocytin foam cells and fatter plumper nuclei with atypia To be the most helpful things all of those are really good pointers towards dermatofibroma and away from Dfsp and again in hard cases you can do a CD 34 you can also use factor 13a I don't personally like it for spindle cell tumors really I Basic I rarely use factor 13a. I personally don't find it very helpful It will stain a lot of dendritic cells in the midst of a dermatified broma and is usually pretty negative in the middle of a DFSP.

But I find it a lot not very specific. It stains lots of different things. If you're watching this at home and you use factor 13A, that's okay. But don't think that everything that's factor 13A positive is a dermatified broma. That is definitely not true.

So, okay. So that's one differential. Any other differentials that we can come up with?

And also I told you diffuse nerve fibroma. Can mimic DFSP sometimes. Anything else?

Like a hemangio. Well, I'll tell you another one. Hemangio pericytoma.

Go say it. Yeah. Solitary fibrous tumor, which used to be called hemangio pericytoma, can sometimes, it usually doesn't have quite, like it has kind of more of a. a patternless pattern.

I mean, the spindle cells are just kind of haphazard, but occasionally it can make little fascicles or have some areas that get a little swirly. The important thing to know about why those can look alike is that DFSP often has dilated ectatic vessels. Here we have some dilated vessels here, but sometimes they can be dilated and branching and give that staghorn appearance, which is the classic vascular pattern seen in solitary fibrous tumor, um, and which it's called the hemangio-pericytic vascular pattern because that is what SF SFT used to be called. And they both express CD34. So solitary fiber tumor is very, very rare in the skin.

Most of the cases I've seen are in the deep soft tissue, but it can rarely present in the skin. It usually, almost all of the ones that I've seen are very circumscribed and not infiltrated, but sometimes there is a variant of SFT that has fat in it. It makes its own fat.

It's like called lipomatous SFT. And I've never seen one of those in the skin, but I could see that easily being mistaken for DFSP and because they kind of similar cytology to some extent that cells of SFT are usually a little more plump and not quite so thin and stretched out but I've seen some exceptions and then the what's a good solution does anyone know a specific marker for solitary fibrous tumor because CD 34 is a great marker for certain things very sensitive for certain entities like DFSP but it's not specific right CD 34 stains lots of lots of things Many, many different fibroblastic tumors will be CD34 positive. And also, of course, most vascular tumors with some exceptions. So it works, but you have to know exactly what your differential is and to remember that many things express CD34.

So what's a more specific marker for solitary fibrous tumor that would be negative in DFSB? So STAT6, okay, S-T-A-T-6. And that's because solitary fibrous tumor is also a translocation tumor. It's not a sarcoma.

There's both low-risk, medium-risk, and high-risk variants of SFT. It doesn't really fit neatly into a benign versus malignant box. So... There's a way we, again, this is probably outside the scope of what you guys need to know, but there's a risk stratification method that we can use based on the age of the person, the size, how many mitoses, and if it has necrosis. And then there are ones that fall into the low-risk group, basically usually act benign.

And then the ones in the high-risk group act like sarcomas. And then the intermediate group is kind of in between. So that's kind of a newer model, even since I was in training.

But I actually like that for solitary fibrous tumor. So if you ever have one of these in practice, they should get removed with negative margins. and someone should be giving you a risk scoring.

If they don't, you probably should get a consult to make sure. But STAT6, their translocation is NAB2-STAT6 gene fusion or balanced translocation. And this is one of those times where actually the immunostain STAT6 works better than the fish.

My understanding is that when the fish rearranges, the loci are very close to their original location, so it's harder to see the break apart. I'm not a fish expert, but basically the immunostain works beautifully. It's a strong nuclear stain, and it's...

pretty specific. I mean nothing's perfect but it's pretty specific for solitary fibrous tumor and be negative in DFSP. The other thing that I would point out as being and there are a handful of others we won't go all the way into them but the other thing to remember is perineuromas also can look quite like a DFSP because the whirling Swirling growth of perineuroma can look a lot like the story form pattern of Dermatofibrosarcoma protuberans.

Perineuromas can express CD34. They will express perineurial markers, EMA, GLUT1, and CLAUD1. The problem is they often are kind of finicky, patchy, weak staining perineuromas. So I find all of those markers, none of them work totally perfectly.

EMA particularly, I've had really a hard time. Like it's the classic marker that should be positive in all perineuromas, but it's very difficult to work. It works great on epithelioid tumors, but on spindly tumors like perinurioma, I find it to be very wispy and weak and difficult to interpret a lot of times, at least in my hands.

I've heard that it's something to do, I think, with different levels of antigen retrieval. There's something in the laboratory you can do to tweak it, but I've not experimented with that personally. But I've heard from some people that they've gotten their EMA to work better by, I think, doing a different type of antigen retrieval.

I can't remember the details, but someone told me that not long ago. Anyway... The thing about that though is that sometimes perineurium and DFSP can have overlap because DFSPs occasionally can have some focal EMA expression or can have some staining that's a little bit like perineurium. If there's any doubt, you can do FISH. And of course, you guys know what's the translocation here.

1722. And what are the genes involved? 1722. I think it's PDGF-beta and collagen 1A1. Yeah, collagen 1A1, PDGF-B.

B as in boy, B as in beta. And then more recently, it's been discovered the vast majority have that fusion. But recently, in the past few years, we've discovered it's been reported that there is an alternate fusion involving the PDGFD, D as in delta, and fused with a couple of different partner genes.

And I've seen one of those in practice, and we're actually in the process of writing that up as a case report. So hopefully that'll be out in the near future. So just to know that it's the... Collagen 1A1 PDGFB is really important, but there is a new fusion PDGFD that's been described, and I imagine that now that we know that exists, we'll find more and more of those over time. I only do the FISH in really difficult cases.

This case is classic, and you probably could sign that out on H&E, honestly. Here's our low power. Okay, what do you think?

I'm wondering about M. I feel like there's some large, dark, kind of angulated glimpse up in the epinephrine. Look at that, little crinkly, wrinkly.

I mean, that's cerebriform, right? Now, I always joke, I promise you I can find you a cerebriform cell in pretty much any biopsy if you give me enough time. But, I mean, honestly, that really looks cerebriform.

And there's also a lot of tagging, right? We have a lot of lymphocytes along the basal layer here. I mean...

very concerning because they've got little halos around them. They're tagging along the epidermis. And in this area here, we don't really see any interface or much spongiosis. So we've got too many lymphocytes for too little sponge. So that always makes us think of mycosis fungoides.

But let me go back to low power again. Where do you think we are in the body? What are these? Apocrine glands. Yeah, apocrine glands, right?

They've got that abundant granular orange, I'm sorry, pink cytoplasm with these little refractile. bodies up here i'm not exactly sure what they are but they're usually there and then the nuclei are really big and round they have like a prominent nucleolus they look like a little eyeball staring at you someone on instagram once said they look like minions like the little one-eyed minion uh from the the minions movie and i was like oh it's so true they do so i like that so african glands so where so there's that and then what do we see in the dermis little smooth muscle bundles Breast could be. Breast will have smooth muscle and sometimes can have African glands.

And the genital area, exactly. So in this case, we're actually in the vulva, okay? In the nipple, usually the muscle bundles are thicker and bigger.

And in the vulva or scrotum, they usually are really small. But admittedly, that is a somewhat subjective thing, but just to know. And also, I feel like usually African glands are more abundant in the genitals.

And whereas you can rarely see them around the nipple areola, so they can be in both places. Yeah, this ended up being from the fall, I believe. And then what about this? Yes, we've got atrophic epidermis, a band of homogenized eosinophilic, almost pale. So you can see that it's collagen here.

You can see the fibers when we flip the condenser, but it's kind of pale sclerotic. So sometimes that happens in lichen sclerosis. You get this band of sclerotic collagen, and sometimes it can get edema in there that makes it look really, really pale, almost white. And then below it, you've got a band of... histiocytes that are kind of trickling between the collagen.

You sometimes get this kind of, it almost looks a little like interstitial GA. So we wrote a paper about that a couple years ago, Sarah Shalin and I and our colleagues, we wrote a paper about this kind of interstitial granulomatous pattern. This interstitial pattern, it looks like interstitial GA that you see down under the sclerotic band in lichen sclerosus.

You tend to see that more often in extra genital lichen sclerosus than in genital, but you can see it in both. And then sometimes there will also be a band of lymphocytes in here too. But you can have either lymphocytes or this kind of interstitial histiocytes or both. Okay. So in this case, this was clinically lichen sclerosus and did not fit for mycosis fungoides.

So this is an example of one of the mimics of mycosis fungoides that in lichen sclerosus, you can have really prominent epidermotropism of lymphocytes that really mimic, strongly mimic mycosis fungoides. cutaneous T cell lymphoma. Pretty scary.

So this is another reminder of why we don't make the diagnosis of mycosis fungoides on path alone in isolation. It's got to fit clinically because there are a variety of entities that can have what looks like tagging of lymphocytes in the epidermis or epidermotropism and yet is not mycosis fungoides. So this is lichen sclerosis mimicking with a kind of pseudo-M appearance.

And you can see that there's a whole long list in the DermPath textbooks of things that can do that. that but you can see it sometimes lichenoid keratoses can have a prominent areas that look like mf you can sometimes see it overlying pigmented purpura and a variety of other things too but this one is pretty scary because not only does it have all the tagging with the halos around the lymphs but it's also got the little cerebriform crinkly looking nuclei pretty scary huh so lichen sclerosis and here's kind of this is it would be harder when you have this right Because here you can't really see that homogenized collagen very well. You're beginning to see it right here.

But in the earlier kind of inflammatory phase of lichen sclerosis, as it's just starting out, it starts as kind of usually as an interface dermatitis. This case is a little strange because it's got all these lymphs in the epidermis, but not really much in the way of vacuolar change or dying keratin sites like you'd normally expect. So kind of weird. I mean, it is very, you could easily take a picture of that.

I'm sorry, I'm trying to, slides a little sticky on the back. and of course there's a wrinkle right where I wanted to show you but that's okay I mean you could take a picture of some of those cells and put that in a book and say this is classic mycosis fungoides right scary all right so low power and clinical wins the day like in sclerosis at a trophic is if you like This is also vulva. And this patient, there's diffuse scar here from a previous surgical operation.

And this patient has a known history of lichen sclerosis also, although I don't really have a great area to show you on this particular section of the lichen sclerosis. But they did have known lichen sclerosis, and they previously had a surgery. the best area. So here's kind of their not totally normal but more normal looking epidermis right it's kind of atrophic because it gets over a scar right but that's just to give you an idea that's what their normal skin for this area looks like. Sorry trying to get the lighting level just right okay and then let's go over to this thicker area that's acanthotic in the middle.

This area has got acanthosis come on here we go. acanthosis, hypergranulosis here, and the nuclei are a good bit larger and even a bit more atypical. See, look at those guys. Now you know Atypia is in the eye of the beholder to some extent, but I mean those to me look more enlarged and hyperchromatic. I'm sorry, I have to keep flipping it.

The disadvantage of glass slides is that in digital slides the lighting is usually just perfect and in glass slides not so much. This is a very difficult and controversial area, but I thought it's probably good to make you aware of it. Because we do have to deal with this and we encounter this from time to time.

And I found it very challenging. But here we have hypergranulosis, but no HPV change, no like real coelocytes, right? These little vacuoles here, that's not a coelocyte, right? That vacuole artifact is a totally normal thing to see around keratinocytes.

Those nuclei are really tiny. Coelocytes will be up there in the granular and will have vacuoles a lot of times, but much bigger nuclei. The nuclei should be really large, like paradoxically larger at the top than you'd expect.

So if it were high-grade dysplasia and had HPV positive, that would be H-cell, high-grade squamous intrapithelial lesion. Usually the thing about H-cell is that H-cell is going to be full thickness atypia, or at least like two-thirds to full thickness atypia. And usually the cells are very blue and basaloid because they have large, dark, hyperchromatic nuclei without much pink. keratin in them.

So here though, we have very like abundant pink, right? Like it's abundant keratinization of the cytoplasm. You can see like the keratin filaments really prominent there, right?

So usually that's why the H-cell usually has a very blue basaloid look to it and usually very atypical nuclei. This is much more subtle atypia to me. I mean, in the range that you could wonder, is this really atypical or is it reactive?

So in the setting of... lichen sclerosus, when I see areas of acanthosis with basal layer atypia, I start wondering about a different type of dysplasia, which is called DVIN, which stands for differentiated vulvar intrepidial neoplasia. So VIN, vulvar intrepidial neoplasia, VIN 1, 2, and 3, right, is the kind of older terminology that now corresponds to L-CIL for low-grade squamous intrepidial lesion or which I basically almost never use that term in the volvop personally, or H-cell, which is the squamous situ, basically, that's HPV-driven, high-risk HPV-driven.

So now we say L-cell and H-cell, which corresponds to the older VIN system. And you can still use both, but the most modern terminology from the last criteria, the last terminology system, the lower anogenital squamous terminology, which is what stands for last, L-A-S-T, is L-A-S-T. L-cell and H-cell. Okay.

And if this is 2021, I'm making this video. So if you're watching this many years in the future on YouTube, go and look it up because these systems tend to change over the years and new terminologies come up. So, but this is a different kind of VIN, vulvar intracerebral neoplasia, that's not HPV related. It falls outside of the H-cell L-cell system.

And this is called differentiated VIN because it's differentiated in the fact that it's not that ugly basaloid looking cells like you see in H-cell, but instead it's very ugly. kind of glassy eosinophilic keratin producing cells with just some kind of subtle basilar atypia. Okay and this type of VIN is important because it arises in the setting of lichen sclerosus usually and it has a significant risk of progressing into invasive squamous cell carcinoma. Okay in fact my understanding is that the risk of invasive squamous cell carcinoma is higher in this form of of dysplasia than in the H cell, okay? I mean, it can happen to both, but I feel like these are the ones that seem to have more of a risk of becoming invasive squamous.

Even though they don't look that bad, H-cell looks way uglier than this. I should have pulled an H-cell to show you, but I didn't have one handy. I'm sorry.

So in any case, these are not driven by HPV. What happens here is that P53 is abnormal. And if you do a P53 immunostain, you'll see diffuse staining along the basal aspect of this area compared to the background epidermis, which should just have kind of... patchy, what we call wild type staining. I've also seen some examples that had null type P53, where P53 was completely wiped out in the D-Vin area and the background normal skin had some patchy staining.

So in any case, whenever I see lichen sclerosis, I'm always on the lookout for areas where I'm getting acanthosis, where I'm seeing basal atypia. Sometimes I've seen cases where they had scattered high level dying keratinocytes. I'm not sure if that's a specific feature, but I have noticed that before. So all those things make me, when I see that in the setting of... patient with LS, then I start thinking about D-VAN.

Oh, this case, look, this case had some dying keratinocytes up behind the arrows. And then I'll do P53 or Key 67 also to see the proliferative activity here. Neither of those things are perfect.

I think they're kind of tricky to interpret. And usually in these cases, I show my gynecologic pathology colleagues to get help because I find this very subtle and difficult to diagnose. I think the literature on it, from what I've read, it's still the criteria for how exactly to diagnose it are correct. are not perfect, somewhat vague and subjective. I hope I'm not offending any of the authors of those papers.

And I'm certainly not the world's expert on this, but just know that there's a form of dysplasia that occurs in lichen sclerosus, and it can progress to invasive squam. And it's called differentiated VIN, D-VIN. I wish I had the P53 stain handy, but it worked really beautifully in that case. It was diffuse staining in the D-Vin area there. Okay.

I know that's a hard one, but I wanted to make sure you guys knew about it. And this is also from the anagenital area. Yeah, this is a perfect condoloma from low power. It's a, you know...

warty, multi-lobulated warty looking lesion. And instead of the finger-like papillae of a typical verruca vulgaris, usually condyloma, cumulonatum, genital warts, usually have kind of that more rounded papillary surface that looks kind of more knuckled instead of finger-shaped, more like knuckle-shaped. So that's what people like to say.

But other than that, the features of condyloma are very similar to the features of a regular verruca. You have parakeratosis alternating with orthokeratin. The para tends to be kind of down in these cleft areas between the papillae sometimes.

And you often have dilated vessels in the papillary dermis, like here. And ideally, I want to see coilocytes. And this particular case is loaded with coilocytes. And the coilocytes usually are located in the upper spinous or the granular layer.

And see, look, not only do they have pale or vacuolated cytoplasm, but they have really large nuclei. And sometimes they're like two nuclei sitting together inside one space, like you can kind of see right here in this guy. He's like a binucleated one.

The cytoplasm can be kind of grayish or can be truly clear and vacuolated. But the nuclei are... big.

So for real coelocytes, that's what I want to see. These almost look kind of bubbly in this case. It's interesting. And sometimes you'll see large granules in the coelocytes. It's like actually the granular layer cells that are showing the HPV change.

So we call this coelocytes or HPV viral cytopathic effect. It means the same thing basically. And for me, I... And ideally, to definitively make a diagnosis of condyloma, I like to see some good coelocytes, just to be sure. I mean, because even though condyloma is not malignant, it is a sexually transmitted infection.

And I don't want to label someone unnecessarily with that because there are sometimes social ramifications of that. And so we always want to think about not just benign and malignant, but about all of those factors and make sure we get the diagnosis right and not cause problems for people in that way. So if I have a lesion that I'm suspicious about...

condoloma that's not I mean this is as good as you could actually ever ask for. It's like the most perfect condyloma ever. But if I have lesions where I'm not sure, sometimes I'll do HPV in situ hybridization, which if positive is really helpful to support condyloma. If negative, it does not totally exclude it because depending on what kind of issue you use, the one I currently use I think has 6 and 11 in it. I can't remember if it has any extras besides that, but it has a mixture of low risk.

But there are many, many types of HPV, right? Not every ish in situ hybridization will have probes for all of the different types that could possibly cause genital warts or other types of verruca. So again, there's good condyloma.

And once you see condyloma, you always want to look around and make sure there's no high-grade dysplasia H-cell. And so if I started seeing really blue basaloid, atypical areas, then that would be worrisome for H-Cyl. Because you can have H-Cyl arise in the background of condyloma. Alright, and there's more coalescites. So, condyloma.

This is incredible. Is that a hair shaft that's loaded with fungus? Indeed, a hair shaft loaded with fungus. And not just one, but two, three.

All the hair shafts are just completely overwhelmed by fungus. They've got little canidia spore forms on the outer surface. The inner surface, what used to be a hair shaft, is now like a fungal shaft, right? It's like... completely replaced with vertical parallel fungal hyphae.

And you can see a little bit of brown melanin. That's from the hair shaft itself, I think, in this case. Because, you know, the hair shaft has pigment in it. That's why hair has color.

And the hair shaft has been completely consumed by fungus. It's like a zombie hair shaft. It's all overwhelmed and controlled by the fungus.

So what is this? This on the scalp. Yeah, tinea capitis.

And you can see this pattern, which has been called both, you can have endothrix, which is when the hair shaft is filled with fungus, and ectothrix when the shaft is surrounded by fungus. In my experience, I often see kind of both together, like what looks like endothrix and ectothrix pattern together. Neither of those are actually a fungal type, right? They're just a pattern of fungal involvement of the hair shaft.

And so usually you see this in the setting of tinea capitis, but I've also seen it like on the forearm or other sites on the body where someone had dermatophytosis that involved their follicles. And when it did, it got colonized like this. And so these are caused by dermatophyte fungi. And what's the most common one that causes tinea capitis?

It varies by geographic location. Is that right? Okay, so trichophyte and rubrum in the U.S. overall, but some areas maybe microsporum canis.

Microsporum, right, for M? Yeah. Okay, good.

Just want to make sure I didn't get that wrong. Okay. And then here, this is an awesome case because here we can actually see it coming out of the surface.

Isn't that amazing? I mean, if you don't like that, I just can't help you. I mean, that's fantastic.

Just a cut to see hair coming out of the surface of the skin where it's cut perfectly like that is something we don't see that often. Like it's got to be the perfect cut, right, to split the hair down the middle. But to see three hair shafts in a row, all loaded with fungus.

Swooned. It's too good to be true. Here's what it looks like more often or if you get like a alopecia style punch, right? you're going to see more like this, right? Where you get a cross section of the hair shaft that's got fungus.

And if you get this and it ruptures, right? And you get inflammation and a little abscess around it, then you could say it's Miyake's granuloma, right? And in my experience, when I've seen things that clinically fit for Miyake's granuloma and I find fungus, I, you know, I was always taught that the fungus should be in the dermis outside the follicle in the middle of the abscess.

I feel like I almost never see that. I feel like I'll see the abscess and the perifollicular inflammation. that's giving that myakis, that kind of more indurated myakis granuloma appearance clinically, but the fungus usually I don't find in the dermis itself.

But anyway, this is important to remember. And sometimes when you have endothrix, ectothrix, sometimes the fungus is only in the hair shafts or down in the follicles. But other times you will find it on the surface too.

So always make sure when you're doing a PAS that you do check around your follicles. And also if you're thinking of myococcus or of tinea capitis. Make sure to check on the surface too for fungus with your GMS or PAS stain, whichever you like to use, whichever works better in your lab. Really great, excellent example of that. I don't get to see that biopsy very often because tinea capitis is often in kids and it's often recognized by the dermatologist or the pediatrician or whoever and then treated.

So I don't see it biopsied that often. So it's kind of a rare treat for me. So there's the skin up here and then here is, is or was the subcutis.

Now there's something going on here. This reminds me of like encapsulated fat necrosis. And it reminds you of encapsulated fat necrosis because that is precisely what it is. It's actually like the...

best example ever. It's so fantastic because you can see, A, because we can see the skin, like it was beautifully removed by a very skilled dermatologist. And they took the skin and then popped the nodule out from underneath.

And the nodule is perfectly circumscribed and encased by a wall of fibrosis and a bit of inflammation, right? You can see here's this kind of peripheral wall of fibrosis making a band. And then if you look on the outside, that's their normal living happy fat.

relatively happy, and then next to it, not happy fat, and that the fat can have a range of like fat necrosis with foamy histiocytes like here. If we flip the condenser, we can see the bubbly foamy a little bit better. Xanthomatous cells, right? Fat necrosis is a thing worth studying because it can look kind of weird and wild sometimes.

Not here, it's really easy because we can see that it's a nodule. But sometimes on a small biopsy, you can really struggle with what's all the cellularity going on here. And then sometimes the actual adipocytes where there used to be adipocyte is rimmed around by histiocytes, right?

See the histiocytes are surrounding the empty space that used to be a dead fat cell. And then the other areas here are more like sheet-like. Like everything here is just dead fat, right? It doesn't have as much histisite. It's all just wiped out, like kind of almost mummified.

you know, a sheet of totally ghosted out dead fat where the nuclei are almost all gone, right? Sometimes you can see that arabesque pattern, lipomembranous change in encapsulated fat necrosis. And I feel like these, my understanding is that usually this is like a post-traumatic thing, like post-traumatic fat necrosis sometimes basically gets a totally dead nodule and then gets walled off by scar.

or fibrosis like we saw in this case, and then it presents this nice nodule of kind of dead and mummified eventually fat that is walled off and doesn't get resorbed by the body and it can persist I understand for like sometimes for years and be there for a long time because it's encased in the fibrosis so that it never like gets cleaned up by the by the rest of the immune system and the histiocytes right it's all just walled off here like like the nuclear reactor at Chernobyl, right? It's just in like a little sarcophagus. So I just made that up today.

We'll see if that sticks. If it does, then I'll cite this video in the future and say that I coined it here today on 9-2-2021. Okay, just kidding. Wait, I'll wait. the Nobel Committee.

I hope you guys are giving me a pity laugh from home. Thank you. In any case, here's another slice from the same case.

So in these, as you guys know, these sometimes are mobile and these little nodules can like move around and the patient can like push it around like a little marble under the skin, which is really pretty crazy and wild. And I'll see if I can. get access to a video of that to include or upload at some point in the future.

Because it's pretty cool. If I find a video, I'll check, if you're watching this on YouTube, check the video description down below for links. I usually put links and stuff in video descriptions on my videos. Oh, I got it. I'm getting some sunlight coming through my window there.

See that little, uh, this little, uh, light there? That's the sun reflecting through the ocular of my microscope. When I cover it, it goes away. So...

Looks like a... Yeah, there are granulomas here. There's kind of these pale nodules.

Or gout that maybe is kind of feathery in the lighter areas. Okay. Gout looks like something that's very, very light.

Yeah, good. This looks very much like gout, right? It's multiple nodules of pale, light, feathery, fluffy, like cloud-like substance. And if you go close, you kind of get the impression that maybe there used to be little thin needle-shaped crystals there. And then it's surrounded by a wall of histiocytes, right?

See there, look at that needle shape right here. But, as you guys know, that during the... processing of the tissue and staining, the urate crystals get washed away, right?

So, and I was always taught it was because of formalin fixation, but from some other papers I've read and some experience I've actually, it seems like maybe some of it gets dissolved by formalin, but the bigger thing seems to be the processing and then the H&E stain itself actually. So, the best way to see the crystals of course is to do a fresh smear and or to submit an alcohol, but you can just submit it fresh. and then say please smear for looking for gout, and then we can see the urate crystals. So this looks great for gout, but this is interesting.

This is like a nodule on the foot. But then we got areas like this. And here, this is like very dark purple, and some of it looks kind of needle-shaped but is purple, kind of like calcium sort of look. And when we flip the condenser, Yes, some are long and needle-shaped, but others, can you see them right in here?

They're like diamond or square or what we say rhomboid-shaped, right? Like, oh there, that's better. See them there? Way bigger, thicker, and chunkier than gout crystals. Also, they're easily visible here on a formal and fixed H&E section, and many of them are purple, which is not the color that gout should be.

So this is slightly unfair because this is something that I don't think I've ever seen actually in the skin. But this is from the foot, and I think soft tissue things in the foot can be close enough to the skin that they can come up and get sampled and sent to DermPath potentially. So it's fair to at least know about this. And I would say that even in the hands and feet, I've only rarely seen this in the hands and feet.

Usually I see this in big joints, deep joints, like the knee, or I often see it in the spine, like in intervertebral disc specimens from spine fusion surgeries. Let me see if I can get the polarizing to work. I'm going to try. Sometimes it's a little difficult to catch on camera because of the light adjustment.

Let's see if I can get it. One second. Turn the auto adjust off. There we go.

See them? And so they glow and are birefringent under polarized light examination. You can really see that rhomboid shape now. So does anyone know what this is?

Yes, this is pseudogout, calcium pyrophosphate deposition disease, right? Which again, usually is there almost always when I see it there. clusters of purple, dark purple, because they're calcium.

So they're staining purple on H&E. And then when you go closer, the crystals are preserved and they're rhomboid shaped. Although occasionally I've seen ones like this that have both rhomboid and kind of longer needle shaped ones. So the question in this case, usually just on H&E, gout and pseudogout look very different and are easy to tell apart.

But this case is hard because that stuff looks perfect for calcium pyrophosphate. But over here, I thought it looked perfect for real, true gout monosodium urate. So my suspicion is that this patient may actually have had gout and pseudogout both mingled together here.

Now, I don't, unfortunately, have proof of that because I don't have a smear to go with this. But if you would have just given me this area, I would have signed this out. Gout.

Done. I wouldn't have even, like... questioned it or said we need to get a smear, I would have said this looks perfect for gout.

That looks exactly like what gout is supposed to look like. But then we have all of these purple rhomboid polarizable crystals in here too. And this is really extensive. It's everywhere.

So I suspect, I think this is definitely pseudogout, but also I suspect that there may be some intermingled monosodium urate deposition in the midst of it. So kind of a fascinating and interesting case. And again, I rarely see pseudogout in the hands and feet, but occasionally I've seen it near the small joints in the hands and feet where it can push up close to the skin surface potentially. But like I've never seen it like in the dermis itself. Okay.

Oh, if you don't like that, I don't know what I can do to make you happy. Oh, it's perfect. Look at that.

They clinically, they said bright red papule. Rule out cherry angioma. Good. Yeah.

Even from 2X. Virtually, you guys instantly know clear cell acanthoma, it's elongated, reedy, really acanthomatous, or very acanthotic, excuse me, a sharp cut off from the surrounding epidermis, right? The cells aren't really clear despite the name, they're more like pale.

Cytoplasm, also with a bunch of spongiosis in between and both those things together give this lesion its pallor, its pale look. It's a sharp, discreet line delineating it from the surrounding epidermis. And occasionally I've seen ones that are kind of multifocal that'll have a zone.

and then back to normal epidermis, then another zone. So, you know, they're not perfectly round. And this one's also great because it has the classic finding we're supposed to have of neutrophils, right? So there's neutrophils scattered in the midst of this thing, trickling through the epidermis, and they're on their way up to the stratum corneum where they mingle in to the para.

So you have lost the granular layer, parakeratosis with neutrophils. In many ways, a lot of similar things here to what we see in psoriasis, right? The surface aspect of a clear cell acanthoma has, I mean, there's a lot of stuff that's like psoriasis, even the little dilated vessels down here, right?

So that is a perfect example of a clear cell acanthoma. And they're usually a solitary lesion. The leg is a common site. And then I think I've mentioned before, but occasionally I've seen a few other things that can kind of mimic clear cell acanthoma. And I've seen trichylamomas that kind of look a little like this and also inverted follicular.

keratoses can sometimes have some overlap. Not like this particular case, but I've seen ones where where there were those three entities, clear cellulite canthoma, IFK, and trichelomoma, can have a little bit of overlap. And also poro keratosis, I'm sorry, poroma, excuse me, poroma can do this sharp cut off here at the edge. So otherwise this doesn't look really like a poroma, but poroma does that sharp cut off.

So that's another thing that can overlap here. And I have had one case earlier in my career that on a shave biopsy, I thought was actually because it was really glassy and it was a little atypical. I thought it was going to be a squame.

And I think I called it a squame, superficially sampled. And then when they went back to re-excise it, it was actually a clear cell eukaryothoma instead. So I had never thought about this as mimicking squamous cell. But on that particular case, it was a superficial shave biopsy and it was glassy and pushing down.

And I thought it was enough to call a squame. And once I saw the whole lesion, I realized, ah, no, it's not. So.

That's how we learn things. Really good example, just classic. What pattern do we have here? with superficial and deep perivascular dermatitis pattern, right? We've got a brisk infiltrate around the superficial and the deep vessels.

We also have infiltrate that goes around the adnexal structures, right? Around the pilosovatius unit, around the eccrine coils. So we can see that pattern in a lot of things. The first thing we need to see, though, is is there any epidermal change, right?

Because if you have this pattern alone versus this pattern with epidermal changes, it can change what's going on. Epidermis looks relatively normal here, really. No good vacuolar interface, very minimal spongiosis.

There's a bit of hemorrhage in the dermis here, but I didn't see any vasculitis. And there is also... It's sometimes hard to see eosinophils when there's a lot of erythrocyte extravasation because it makes everything look kind of like an EO from low power and then you go closer and you're like, oh, it's not an EO, that's blood. So I find that I have to hunt a little closer at higher power to see if there are EOs when blood is present in the background, okay, when we have leaky vessels. And I did not see eosinophils.

I looked for a while and didn't find eos here. And then right here, I don't know if it will transmit well in the video, but we'll try. Right in here.

We've got some bluish mucin and Patrick, one of my Dermpat fellows, told me the other day that this looks like this little pattern of like wispy mucin with little tiny speckles on it, that it looks like dew on the spider webs, like you know spider webs on the grass that get the like morning dew on them. But he said that that was our colleague Dr. Wells Chandler actually. I had told him that and so I thought I love those cool visual analogies and I really like that one So I don't know if dr. Chandler invented that or if someone else did and you know Like many of these things we hear them from mentors We modify them and then we pass them on to our trainees and it's like the circle of life in Pathology teaching but anyway, there's mucin there right and so mucin can be very subtle sometimes and yeah looking for those little speckled dots This is high powers. I can get I'm sorry. It's helpful also There's a little bit of elastic fiber here.

Sometimes in people with a lot of solar elastosis, it's really difficult to tell if there's mucin. So I go down and look deeper in the dermis. Don't look up right under the epidermis.

Come down deeper and see if you can find mucin. And also one last thing when we're talking about mucin, ignore mucin around the eccrine coils. You're going to find mucin around, not in this case, but... many times you will see mucin around eccrine coils, okay? And it doesn't seem to mean anything.

Sometimes, especially like in the distal extremities, I feel like I see lots of mucin around the eccrine coils, like near the hands and feet. I assume it's some sort of a reactive phenomenon, but I see it very commonly and it doesn't seem to have any significance to my knowledge. All right, so what do we do with this? No epidermal change, superficial and deep, and peri-adnexal, and mucin. So what's a good diagnosis here?

And no EOs. Yeah, I think this is tumid lupus and this would be a plaque on the chest of a young or middle-aged female adult. That would be the classic story. I think this case was like from the shoulder or somewhere.

So in any case, that is tumid lupus. I think fits very nicely. And as you guys know, tumid lupus oftentimes is just localized and not, is usually not associated with systemic lupus.

Although if I start seeing interface change up here, then I start thinking about like. regular lupus erythematosus. Clinical of tumid lupus is kind of distinct in that it tends to be one or a few plaques like on the chest. And there are some other entities that you guys have probably heard of like REM, reticular erythematous mucinosis, which is I think of as kind of like tumid lupus with more abundant mucin.

But I feel personally like it's probably on a spectrum, although I'm not an expert on this and I'm sure there are some people who disagree. You know, there's lumpers and splitters and derm path. And then also, um, jessners it's like basically a kind of more abundant lymphoid rich thing that i think is on the spectrum with tubal lupus personally and it can be so so much inflammation that it can mimic a lymphoma so that's those are two things to think of that i feel like exist in this spectrum and in this case even though i didn't see vasculitis there does seem to be like some vascular damage like the vessels are leaking the endothelial cells like a little swollen so i wonder if we have kind of a lymphocytic vasculitis going on here which is kind of a bit of a controversial topic but sometimes when we have dense lymph lymphocyte infiltrator on vessels without neutrophils, we do see blood leaking out of the vessels and maybe some fibrin. And in connective tissue diseases, you can have some vascular damage and even can have like actual leukocytoclastic vasculitis in some cases. So I thought that probably we do have some leaking of the vessels in this particular case here.

And if you would have shown me this and not told me the history and then put some eosinophils in it, I think this would be great for an arthropod bite reaction too. In fact, at low power, when I first put this down, I was like, oh, maybe this would be a bug bite because Bug bites often get some hemorrhage with them. But then I didn't find any EOs. And then once I saw the clinical and the mucin, I thought, oh, no, I think this is good for tumid lupus instead.

But in arthropod bite reactions, I often see period nexil, particularly around the eccrine coils in arthropod bite. All right. So there's tumid lupus.

And then let's see to finish up here. Okay. We'll just end on one last simple case. What's this?

Yeah, Bowen's disease, squamous situ, and I just wanted to show you this one because look at how wild the pleomorphism can be in squamous situ. Like, you can see those cells from outer space, like even from 2x. They're ginormous. You can see them from way up here at like cruising altitude. And some of the most bizarre pleomorphism in the body, I see like in pleomorphic sarcomas, particularly like pleomorphic liposarcoma, has some insane pleomorphism.

And the other place I see insane pleomorphism, squamous cell carcinoma and cytobowens disease. some reason they just get dramatically ugly and yet the prognosis is usually very good right i mean occasionally these can invade and be more aggressive but i feel like most of the bowens i see likes to hang out in the epidermis and the adnexa it likes to stay in situ um and and i don't see invasion in bowens that often. It happens, but I feel like it's those glassy keratinocytic looking or keratin producing squames that I see invading more.

And these ugly bluish bowen looking ones tend to be more in situ. But that's just an example of how crazy the pleomorphism is. And you can also get crazy weird atypical mitoses that look like all sorts of unusual shapes. in Bowen's disease squamous situ.

All right guys, there's a little review of a potpourri of cases. I hope you enjoyed and for those watching at home, thanks for watching. Have a great day.

Transcript for:Dr. Jared Gardner's Dermatopathology Lecture: Case Study Review

Transcript for:
Dr. Jared Gardner's Dermatopathology Lecture: Case Study Review