So, today we are having an external guest, part of our Distinguished Speaker series. It's Dr. Lucia Sobrin. She is the Charles Edward Whitton Professor of Ophthalmology at Massachusetts Eye and Ear at Harvard Medical School. There, she also holds the position of Associate Director of the Retina Service. And she's also Associate Chief for Clinical Data Science at the Harvard Department of Ophthalmology. I also mentioned that she directs the Morse Laser Center and co-directs the Ocular Immunology and UV-Eitis Fellowship at Massachusetts Eye and Ear. Dr. Sobrin obtained her medical degree from the University of Miami and she completed a residency in Ophthalmology at the Bascom Palmer Eye Institute. She followed her residency with two fellowships, one in Retina at Mass Eye and Ear, and the other in Ocular Immunology and UV-Eitis at Massachusetts Eye Research and Surgery Institute. She also holds a master's degree in public health. Dr. Sobrin is internationally recognized as a clinical clinician scientist. She has made tremendous contribution to our understanding of diabetic retinopathy and UV-Eitis. Her work on UV-Eitis is directed towards improving diagnosis and treatment of this disease and identifying protective factors for non-infection UV-Eitis, among other things. When it comes to diabetic retinopathy, she has led several international studies, one of which includes multi-ethnic genome-wide association studies. These have greatly improved understanding, led to significant discoveries, actually, on the genetic architecture of diabetic retinopathy. And the strength of her work has come from her ability to leverage genetic methods to gain insight into ocular diseases with important implications from pharmacogenetic studies. Dr. Sobrin has received many awards and honors, including a senior achievement award from the American Academy of Ophthalmology and the Harvard Ophthalmology Excellence in Mentoring Award, which demonstrates her dedication to training junior faculties. She's an associate editor and executive editor for UV-Eitis for the American Genital Ophthalmology, and she's an editorial board member of Ophthalmology Science. Please join me in welcoming Dr. Sobrin here, and we very much look forward to her talk. Thank you very much for the introduction. I'll first just start saying that I have a cold and it is not COVID, and I will ask for your patience. If I have a coughing fit, I have cough mints, orange juice, tissues, and Purell up here to help me through the talk. And so I don't want to be that visiting lecturer that gave everyone a cold here in Utah, so thank you for your patience if that happens during this talk. So I will, the research seminar will focus a lot on my research, the genetics and pharmacogenetics of various eye diseases. But my Grand Rounds talk really is about one disease that I've been working on and struggling with in my academic career. And I wanted to share what I've learned with you. I have no financial interests or relationships to disclose. So autoimmune retinopathy, although it is a rare disease, I think it's important for everyone to know a little bit about it because it could present to anyone. These patients really have very vague symptoms and often very few findings on exam, and I even get referrals directly from general ophthalmologists who pick up on this and send them to me. So I think it's important for everyone to realize it because these patients tend to have a long delay in diagnosis because it's so hard to diagnose. I'm going to spend most of the talk talking about the challenges in diagnosis. And in particular, I'm going to emphasize the pitfalls of antiretinal antibody testing and the importance of ruling out other mimicking diseases. And I'll do this through a series of clinical vignettes about patients. And then I'll end on a shorter amount of time talking about the challenges in treatment. Most of you will not end up treating these. Some of you will, but most of you will not. But I'll talk to you about the struggles we've had deciding what to treat them with and then how to follow them to figure out if they're actually getting any better. So this disease was first recognized in 1976 in this paper. And the quote is that this is a blindness caused by photoreceptor degeneration as a remote effect of cancer. And indeed, the first diagnosis was in the setting of cancer. I took out this quote from the paper. Visual disturbances associated with cancer are ordinarily caused by METS, metastasis to the brain, meninges, optic nerve orbit, foridoretina. This report documents blindness caused by retinal degeneration of obscure pathogenesis in three patients with cancer. I think it summarizes it quite well. And although we've gotten to know the pathogenesis a little bit more, it makes me smile that back then it's obscure. And today it's still a little bit obscure for us as I'll show you. These are those three patients. So they all had advanced cancer. They all had ring-like scatomas. Their arterioles were narrow. Their optic discs more or less look normal, but their ERG, if they had one, was flat or they had extensive night blindness. And then on autopsy, when their eyes were removed, all of them had total degeneration of the retinal cells. Now it took about another 20 years in 1995 for there to be more insight into why this happens. This paper recognized one particular protein, recovering, which is a photoreceptor specific calcium binding protein, was expressed on the tumor of a patient who had cancer associated retinopathy. And in figure one, you see that patient, Sarah, binding to a human retina and lighting up the photoreceptor cells. So in their blood, these patients have antibodies to recovering. The reason they have antibody to recover is presumably because their body is trying to fight off their cancer and the cancer expresses recovering. But as a side effect, the antibodies also bind the recovering in the retina and lead to cell death. And then for further evidence in figure three, you'll see in lanes one, two and three, all these patients are patients who have car.  And the 23 KD band that lights up is because is their tissue incubated with against the Sarah of the first patient who had antibodies. Maybe I'll show it on the screen. So. And then what they also proved is in lane eight, you don't see that band at the 23 marker on the Western block. That's a patient who has cancer, but doesn't have cancer associated retinopathy. So they're showing that it's present in multiple patients with cancer and cancer associated retinopathy and in patients without cancer who don't express this specific protein in their blood or on their tissue. They do not have a reaction. And then finally just showing a direct pathophysiology. If you inject anti-recoverant antibodies into a rat eye, it induces what looks like cancer associated retinopathy where the ERG goes to a very low amplitudes. So this is great in car. We kind of understand what causes a disease. There's molecular mimicry between tumor antigens and retinal proteins, but car is actually a really small part of autoimmune retinopathy. Autoimmune retinopathy, the two major categories are perineoplastic, which car is a part of. And then the other well defined subtype of that is Mar melanoma associated retinopathy. But there is a whole other type of air that is non-perineoplastic where we can't find an underlying cancer, but for all intents and purposes, the what we see in the eye is the same, which is widespread retinal degeneration. And that's the one we really don't understand. And that's the one we struggle with the most. So in non-perineoplastic air, this molecular mimicry might be against an unknown antigen, possibly an infection. Also possibly regress malignancy. We often worry that patients who present to us with air and we can't find a cancer in their body that they're actually, their immune system is doing so well at controlling the cancer. We can't find the cancer, but it's still having the side effect of causing the autoimmune retinopathy. And I have had patients who initially we don't find a cancer and eventually they do get diagnosed with a cancer over time. So this is a real concern also when it comes to treatment. And I'll talk a little bit about that. So why is it so difficult to diagnose these patients? Their complaints are very vague. Most commonly, it's going to be Phytopsia, Scutomas, or Nectalopia. And then the fundus really looks on a quick look, totally normal. You'll see sometimes some vascular attenuation, but really not much else. And it's easy to overlook it and call the exam normal. So really it has to you have to have a high clinical suspicion and patient who has vision loss, a normal exam, or only some mild vascular attenuation and visual field alterations. And the real way to start on the path to making the diagnosis is to next get an electro retinogram, which usually shows significant depression. To help us in this difficult task of diagnosing these patients, there was a consensus panel that came together and created these criteria. And we'll go through how these criteria play out. But they are electro retinogram abnormality, the presence of serum antiretinal antibodies. And I'll put an asterisk for that because some people this is quite controversial. Some uveitis and retina specialists don't even order antiretinal antibodies and we'll talk about why in a little bit. The absence of evidence of a retinal generation or dystrophy, other causes need to be ruled out as the reason for their visual function abnormality. And then the absence of overt inflammation, which would indicate a uveitis instead of autoimmune retinopathy. So we're going to spend a lot of time talking about the serum antiretinal antibodies. So here is a list of all the serum antiretinal antibodies that have been reportedly told to be associated with autoimmune retinopathy. I can tell you that the only one on this list that really has strong evidence that it's actually pathogenic is recovering, which we've already talked about. For melanoma associated retinopathy, there's also a protein called Trimp1, which is well characterized. And but apart from that, there's really more evidence that any of these other antibodies have any role in pathophysiology. Moreover, there are a lot of issues with the testing for antiretinal antibodies. In this paper, which was published in 2021 by John Chen and his collaborators, they actually found that 93% of patients whose blood they sent off for antiretinal antibody testing was positive for these antibodies. So 93% of people walking around totally fine, no eye problems have these detectable in their blood. So you can see it's a very poor marker for disease. We also did a study where we sent it to two different laboratories to see if we could get the same result from those two laboratories. And only 60% of the time did the two laboratories even agree that they were antibodies present or not, and only 36% of the time that they agree on the specific antibody. So there's a lot of variability in testing. The test has a high false positive rate. And so you can see why a lot of people feel like this is a somewhat useless test in autoimmune retinopathy. The other thing that's really important for the diagnosis is excluding other things. And this is where a lot of people, this is a trap that we can all fall into. And the thing to remember is that air is a diagnosis of exclusion. You really need to rule out many other things. And the things that are important to rule out are retinal toxicity. This is especially true in patients who present with CAR because some of the chemotherapy agents they're receiving are actually toxic to the retina. And sometimes this is really difficult. And the only clues you might have that it's the agent is that the timing with the start of that agent correlates well with the vision loss. But sometimes that's hard to distinguish. Vitamin A deficiency, especially in patients with bariatric surgery or liver disease can look a lot like autoimmune retinopathy. The big one we struggle with and we're fortunate with the state of genetic testing now that we're a little bit better off is inherited retinal degeneration which can look almost exactly like autoimmune retinopathy. And then occult posterior uveitis. And for this reason I get a fluorescent angiogram and an indecide angiography on every patient to rule these things out when I'm thinking autoimmune retinopathy. So we're gonna go through a couple of few cases to show you how these things play out. So my first patient is a 40 year old radiologist. And he says a few weeks, I've had a few weeks of peripheral vision loss in both eyes, my left eye is a little bit sore and both are sensitive to lights. And I noticed when I was playing soccer I just lost sight of the ball. So visual field loss. He has a family history of glaucoma retinal attachment because multiple people are nearsight in his family and lung cancer and some family members that smoked.  So we had exam showing his exam was normal and actually his visual field was normal for several years. No other important history. And this is his eye exam. So if you looked at this eye quickly, it looks totally normal. There was a little bit of anterior vitria cell. His anterior segment exam was normal. His vision was 2020. His cup to disc is enlarged. That's why he's a glaucoma suspect. And then really the subtle finding is vascular attenuation, but it's pretty subtle. A lot of people would say he has a normal retina and not, and just say everything's fine and come back if you don't get better. But if you do the OCT, what you'll see is that there's loss of the outer retinal layers or indistinguishing of the outer retinal layers, especially temporally here. And this was the clue to his diagnosis. I told you I get diet testing to make sure they don't have retinal vasculitis. And you can see here that he had a pretty unremarkable fluorescein angiogram. It is normal in some patients to have a little bit of end vessel leakage. You can see that in the temporal far periphery of the left eye. And that doesn't mean they have retinal vasculitis. They can just have a little bit of leakiness from their blood vessels. And the same thing's true in inherited retinal degenerations. But this is his visual field. So a marked departure for what he had previously in both eyes and his ERGs were suppressed. So we did the workup. He had no signs of underlying causes of UVitis. He had normal vitamin A and chest X-ray was normal. He did have anti-retinal antibodies. So recovering the one that we hang our hat on was negative. And he had two other ones that were positive. I don't know if it would have changed my management very much that these were positive. If they were all negative, I may have still diagnosed him with autoimmune retinopathy eventually. Really the clinical picture was pointing in that direction. The most important thing was to rule out a genetic cause of his disease and that was negative. So he has a autoimmune retinopathy at this point based on the criteria we went through.   I usually do skull base to pelvis, but this gentleman was a radiologist at Mass General Hospital and he changed his order to scalp to toes. I think he wanted to be extra sure he didn't have cancer anywhere. It was also the fastest PET CT I ever got, got the next day after ordering it. So it's helpful to have a radiologist as a patient. So he meets everything. He's got ERG abnormalities. He's got some anti-retinal antibodies. We can't find any cause for retinal degeneration or distra-free minimal inflammation. He's the closest thing that I can show you to non-perinatal plastic autoimmune retinopathy. Now the asterisks is that the genetic panels that we have, they're pretty good. They cover about 60% of the IRDs that we know about. There are mutations out there we don't know about. He could have one, but the rapid onset of his disease, the good documentation we had previously that he had normal visual fields for years, I think this is about as good of a diagnosis, strong of a diagnosis as I can make for this patient. So now I'm gonna show you a couple of other patients who might've gone down this autoimmune retinopathy diagnosis path but ended up having something else. So the first one is a 66 year old man and he needs a flashlight to walk around his house. So in March of 2021, he had foggy vision and they attributed that to his cataracts and he had cataract surgery. And this is a very common path in autoimmune retinopathy patients because you don't see anything on exam. They do have some cataracts. So they get cataract surgery and things don't get better. Actually, his vision worsened after cataract surgery. So he sees a retina specialist who looks at him and diagnosis him with dry AMD. But it's a little bit of funny picture and so they send the patient to see our inherited retinal degeneration specialist. His ERG is depressed. His visual field shows central scatomas. They have a plan to send a genetic testing panel. He's 66, so a little bit unusual to be presenting with this at this time, but they're gonna do it for completion. And then they send him to me to consider autoimmune retinopathy as well. So the most notable thing about his history is that he has longstanding severe Crohn's disease. No family history of retinal degeneration. And he's feeling totally fine. Here's his fundus. Again, if you looked at it quickly, maybe some Druzen yellow deposits in the periphery, but not much going on there. Central vision is mildly decreased, but no signs of inflammation. And on his OCT, I think you can appreciate there is just some mild indistinction of the outer retinal bands here similar to the first patient, the radiologist. He gets a fluorescein and ICG that are normal and he gets antiretinal antibodies and they're staining on immunohistochemistry. His serum causes a reaction with photoreceptors in a human retina. So he meets the ERG, he has the antibodies. We've tried to rule out retinal degeneration and he doesn't have any inflammation. So does he have a non-perineoplastic autoimmune retinopathy potentially? So the other thing we did was a vitamin A level and it was less than five. And so I've had several patients come to me to rule out autoimmune retinopathy and the reason that they actually had the depression and changes on OCT was just a vitamin A level. So I just bring this case up, just the importance of getting a vitamin A in every patient that comes with a concern or a possibility of autoimmune retinopathy because that's an easy fix and it's a lot better than getting immunosuppressed. So this guy ended up having vitamin A deficiency, got repleted and was just fine. And the Crohn's disease was a little bit of the clue because he probably has malabsorption and that's why he had vitamin A deficiency. So I tell my residents and my fellows that you need to prove to me it's not something else when you tell me a patient has autoimmune retinopathy. This is the list of everything I absolutely get on patients who come to me to rule out this diagnosis. So I get genetic testing on every single one. And this is the problem, the one disease, the inherited retinal degenerations that we often still have issues with because as I mentioned, the genetic testing is really helpful if it's positive. You've confirmed the diagnosis, they don't need to get any immunosuppression and they might eventually be eligible for gene therapy studies. But if it's negative, it's really not as helpful because the patient can still have an IRD of an as yet unknown genetic mutation. We do look at some clinical clues as delineated in the table there. ARS tends to be more sudden onset. Typically they don't have any family history of retinal generation. It's a little more asymmetric and they typically don't get bone pigment deposition like bone spectacles in the periphery and inherited retinal generation is the flip side of that. But none of these distinguishing factors really are 100%. And so that's why the genetic testing really helps us, especially if it ends up being positive. And I'm gonna show you a case to illustrate the point about genetic testing. So this is a 40 year old woman. So nine years before she came to see me, she noticed a dark circle, what we think is the scatoma in her left upper visual field. She was examined, everything looked fine. She was sent off. Four years she came back. Now she has these scatomas in both eyes. She's 2020 that exam is reported as completely normal. And she's diagnosed with an ocular migraine. She goes a couple more years, come along. She still has these symptoms. And now they're able to document temporal visual field defects and on a formal visual field testing. And she's diagnosed with ABC. So acute idiopathic blind spot enlargement. But she continues to complain bitterly and she's referred for possible autoimmune retinopathy. She has no family history of retinal degeneration and she's, as I said, 40. Visions great centrally anterior segment exam, totally normal. Here is her normal fundus exam. And on a quick look, yeah, looks pretty normal. If you look closely, there may be some RPE changes, but I think on a quick exam, many of us would call this normal. Here, she has some RPE changes probably around the arcades that are somewhat subtle and could easily be overlooked. The auto fluorescence, however, really shows it nicely. And auto fluorescence is another test that I mentioned in the list that is very useful. So you see this hyper auto fluorescent ring around the bovia. You see these stippled hypo auto fluorescent lesions in the temporal macula and nasal to the nerve. And in the left eye, they're even more prominent. Here, she has outer retinal loss and really only the fovea has preservation of the outer retinal layers on both sides of the fovea. She's lost the outer retina and that's highlighted here. She has peri central scatomas in both eyes. They correlate somewhat nicely with the auto fluorescence findings. And her ERGs are down there. It's not terribly down. You can see the normal range on the right. So she's mildly depressed in some parameters. It's actually normal. So she has ERG abnormalities. Did I, sorry, I skipped too much. So she had antiretinal antibodies. Her vitamin A was normal. We've ruled that out. And she had immunohistochemical staining of the photoreceptors. So she had an ERG abnormality. She has antiretinal antibodies. No other cause so far for visual function abnormality, not evidence of inflammation. So is this autoimmune retinopathy? Well, she wanted to have autoimmune retinopathy because the alternative was she had a genetic problem. So we sent the genetic testing and she in fact had two heterozygous variants for H2A. And this was what our inherited retinal degeneration specialist was the mildest case of H2A they'd ever seen. Remember, she's 40 years old, no family history. Her ERG, some of the parameters are still normal. And yet she has bona fide inherited retinal degeneration. And she didn't wanna have this because she knows there's no treatment for this. Whereas for autoimmune retinopathy, even though our treatments are not always great, at least we can offer them something. So she was very disappointed to find this out. But here is where genetic testing really makes a difference. And you might say, this 40 year old with mild ERG, how can she have an inherited retinal degeneration? And the genetic testing really is key for this. So she had a pericentral-like pattern of RP. So I hope that's sort of been a clear way to think about these patients and how to approach them and all the things that you really need to rule out before you give them that diagnosis. And once you make the diagnosis, the important thing to remember is that you have to rule out the occult malignancy. Half of the patients who have car will have their visual symptoms prior to getting their malignancy diagnosed. So we've been the ones to send them and have their CAT scan of the chest and where they first find out that they have a mass in their lung. Car has also been documented up to 10 years after diagnosis of cancer, so it can go either way. Small cell lung cancer is the most common one, although many other cancers have been reported to be associated with car. And if there's no known cancer in the patient, it's very important to talk to the primary care.  I send them to their dermatologist to get a full evaluation, make sure there's no melanoma anywhere, and make sure all their other cancer screenings are up to date, mammogram, colonoscopy, PSA, applicable, and then go from there. So those are the challenges in diagnosis and how to approach these patients. And then I'm gonna end up by talking a little bit about the challenges in treatment. One challenge is to find out, figure out how we can tell if the patient's treatment is actually working for them. Because a lot of these patients will present with advanced photoreceptor loss, and it's hard to know if we're doing anything with the treatments that we're doing. Their retinal cells are dead, they're not gonna come back most of the time we know that, and are we really affecting any change by treating them? Another question, when I was in fellowship and residency, my mentors would tell me they would follow antiretinal antibody titers. I've already told you that some people don't even bother to check them for diagnosis, but some people were following them serially over time as a marker of treatment effects. So if the antiretinal antibody titers went down or the number of antiretinal antibodies decreased, that would indicate to them that there was some positive response. So I'll talk a little bit about that. And then the issue that I alluded to, which is if we impair a patient who has non-pure neoplastic air with immunosuppressive therapy, and they have an underlying malignancy that their immune system is controlling, are we gonna impair their immune system from controlling their cancer and potentially unmask their cancer? And so we'll talk about these things. So here's a list of all the immunosuppressants local and systemic that have been tried with some reports in the literature of success with treatment. I will focus on rituximab and intravenous immunoglobulin because those are the ones that we've found to be the most effective. But all of these have some potential role in the treatment of these patients. I'll say that plasma phoresis acutely can help in some patients, but in my experience, it hasn't been very effective because the damage is already done. And if you remove the antibodies, the body's just recreating them immediately. And so I have never found that to be particularly helpful in my patients. So rituximab is typically the drug that I use first line. There's a rationale. Rituximab is an anti-CD20. So it knocks out B cells. This is thought to be at least in some cases antibody mediated. And so there's good rationale. So we reviewed the results of our patients treated with rituximab. Seven of them had cancer associated retinopathy, nine were non-perineoplastic and we had followed them for about 17 months. 13 of them had had some prior immunosuppression and three were treatment naive. And we tried to be very selective in calling something success. So for their visual acuity to be better, they had to improve two SNEL in lines and for their ERG to be better, they had to improve 40%, which is a high bar. So what we found, and what I used to counsel my patients when I'm talking about this treatment to them is that 14% of eyes had improvement in vision. And 63% of eyes had stable vision. So I tell my patients, the most likely thing is that we're just gonna be able to stabilize you. There's a small chance we'll make you better. And then in a quarter of the time, we're not gonna, you're actually gonna get worse despite our treatment. And ERG outcomes really didn't show much improvement with the rituximab. 25% of eyes had extinguished ERGs at baseline. So we had nowhere to go and we excluded them. But the remainder of eyes really had stable ERG parameters over the period of treatment.  Similarly, the OCTs did not get better when we looked at total macular volume or subfield macular thickness, they stayed the same. But I thought I'd highlight a couple of patients who improved because these are the patients who give me hope that sometimes we're doing something with what we suggest as a treatment to these patients. So this is a 69-year-old woman. She has non-perinatal plastic air. We gave her steroids and she really didn't improve very much with steroids. And then we gave her a rituximab weekly over four weeks. And you can see that her vision improved dramatically. She used to not be able to drive to my visits. She used to have to have someone drive her and she went from 2200 to 2025 in the right eye and to 2040 in the left eye. You can see her ERGs didn't change very much. They weren't severely suppressed. They were only moderately suppressed but they didn't change very much. But it made a big difference for her central visual acuity. And I'll show you another patient that also had that kind of result with a different treatment. This is my second patient with rituximab that improved. She was a young 23-year-old woman and we had treated her with milder things first. So mycophenolate. And you can see this graph of her vision at presentation. She's getting worse. We start her on cell sept and she continues to get worse. And then we start rituximab and then her visual acuity improves. So these are the minority of patients. I don't emphasize this with my patients. These are the exception but these are the patients that give me some hope that we're doing something. The other treatment we've been using quite a bit is intravenous immunoglobulin. So this is when we infuse pooled immunoglobulin into patients. It's used for many different autoimmune diseases. But we've reviewed our patients with this. This is a rare disease. So we had nine patients treated with IVIG with long-term outcomes. And what we tried to do in this study is actually compared them to natural history because some people, there's not a lot about natural history about autoimmune retinopathy. And sometimes you don't know if they were gonna stabilize anyway. That's the natural history of disease. They get worse initially and then they just stabilize. Or if your stabilization is actually due to the treatment that you're giving them. And so we took patients that either refused treatment or were followed. The neurofemologists at our institution used to follow these patients many years ago and they didn't used to treat them. So we took their data and compared them to the patients we treated with IVIG. So if you looked at the IVIG patients, a good percentage had visual improvement and the rest were stable. But if you looked at the natural history cohort, none of them had vision improvement. A third had stability, but two thirds had significant vision decline. And when we looked at ERG parameters over the long-term, the IVIG patients were less likely to decline compared to the natural history controls. And so typically now what we do is we start rituximab and we repeat rituximab on an every six month basis typically and in between we give intravenous immunoglobulin to this patient. So that's typically our first line treatment now. Almost always in conjunction, I can think of, if I think hard, probably I can think of a patient who didn't want to get rituximab for whatever reason and we've done IVIG alone. Or we only gave them maybe one dose of rituximab and they didn't tolerate it and then we just continued with IVIG. But typically I'd like to give the rituximab. So back to our radiologist. So we gave him IV steroids, prednisone taper, rituximab and then monthly IVIG. And seven months post diagnosis, his symptoms had improved, his vision was stable at 2020. Remember, this is a radiologist, 40 year old radiologist. So this is career ending for him if we can't preserve his visual acuity. And you can see that the area of the outer retinal disorganization is still there but it hasn't progressed towards the center of his vision and his symptoms are stable and he's able to work. And so that is the outcome for him which we're quite pleased with. So the other thing I alluded to was monitoring response to treatment is sometimes tough. We typically follow visual acuity, visual field, OCT and ERG. I showed this patient, I had a patient with cancer associated retinopathy who I treated with intervitral triumcinolone. And he would come, you can see that his vision would drop to hand motions and we would lose the outer retinal bands completely. And then I would give him an intervitral triumcinolone and I know those outer retinal bands don't look great but they show up after the intervitral triumcinolone at least in some degree and his vision would improve to 32. So intervitral or local steroids are also an option in these patients and avoid some of the issues with systemic immunosuppression that you might be worried about in patients with cancer. But this is an example of why OCT can be a good way to follow patients. But I'll say that antiretinal antibodies do not appear to be a good marker of disease and I don't follow them. I still get them at baseline. I think it's a force of habit. They rarely change what I do but I don't repeat them over time. And we looked back at our patients with air. There was five with car, one with mar and the rest non-perineoplastic. And we tried to correlate the number of bands of antiretinal antibodies to their visual acuity, their OCT and their ERG and there was no correlation. And so I don't really think the antiretinal antibodies are great for diagnosis and I think they're not useful for following patients either. So the take home points are that air is the diagnosis of exclusion. You have to prove it's not something else first. And in particularly you need to avoid over reliance on antiretinal antibodies when making the diagnosis. Just cause antibodies are positive doesn't mean they have the disease. You have to go through the exercise of ruling out everything else. We have, I've seen non-retinal specialists order antiretinal antibodies and send patients to me and they haven't gone through the, they haven't gone in an FA, they haven't ruled out vitamin A deficiency. So really antiretinal antibodies are a problematic test. And you shouldn't hang your hat on them. Always investigate alternative causes and in particular now with genetic testing being so available, always get genetic testing. Sometimes you'll be surprised in someone who you didn't think there's any chance they have an inherited retinal generation. They actually do have one. The malignancy workup always has to happen if you make this diagnosis and treatment can require trialing several agents, local or systemic steroids. And then in most, for us at least we're using Rituximab and IVIG most consistently cause they have the most efficacy in our experience. So I wanna acknowledge all my research fellows. Also our IRD service and the Arcalyr Genomics Institute which shares a lot. They both share patients with me and help me get genetic testing and help me rule out inherited retinal generations. And I'm happy to take any questions you might have. Is a very, oh, that for a residence is a very, very sensitive sign. I would say it's 80 to 90% of my patients that ever come in and say they have to have a flashlight around their house. Actually I have vitamin A deficiency. So that's the first thing you should think of. Then in terms of the question you showed for your inherited retina disease patient of the one with us to A, the auto fluorescence. Do you routinely get auto fluorescence? Is that helpful at least in diagnosing either excluding or in diagnosing autoimmune? I get auto fluorescence on everyone but it is not that helpful. So the perifovial hyper auto fluorescence ring you can see that in both diseases very commonly. It's actually the most common auto fluorescence finding in autoimmune retinopathy. And the stippling auto fluorescence changes also are not that helpful. If they're very symmetric that's the only time where I think maybe it pushes you a little bit. But even then honestly I've seen air patients look very symmetric as well on auto fluorescence. Thanks. Great. So welcome to Snowy Salt Lake. All I understand you've had some snow back in Boston here. We're familiar with snow, yes. Yeah. So if you think about the fact that these retinal antibodies are really quite common and that cancer is quite common and yet air is very uncommon. Has anybody looked to see what may be different about these patients that they're susceptible to when obviously the conditions that create it aren't that uncommon and yet actually having the condition is very uncommon. Yeah, I'm not aware of anybody who's been able to look at that. I think it would be interesting. It's rare the patient that presents and we can't find the cancer and later we find the cancer and it would be interesting to look more carefully at those patients and see if there were any clues early on about that. But I have to say, I mean I've have several patients with non-perineoplastic autoimmune retinopathy I followed for seven to 10 years now maybe even a little longer and they haven't developed cancer yet. So even those patients are rare and the ones that later develop cancer. I have more patients. Melanoma is a terrible disease as you all know and I have patients who develop more and sometimes I think that when they have immune reactions not just the more but also sometimes rental vasculitis or UVitis they actually have a better prognosis. Their immune systems revved up so much it's causing problems in their eyes but it's keeping their melanoma away and I've seen patients when I first met them where I was like, oh gosh, this is terrible this person's not gonna last and now I'm eight years later I'm still seeing them and they're doing great their eyes we controlled the eye inflammation somewhat but they're still controlling their cancer and it's really remarkable to me. The immune system interplay with cancer is mysterious. So I still do a retoxin and IVIG and most of them you would think you I always talk to the oncologist of course the oncologists are always like, sure why not? Because some of these agents are high doses used to treat cancer retoxin map obviously IVIG has no implications if a patient's really worried for whatever reason like they have a family history of cancer they really are worried. I tell them IVIG is not an immunosuppressant and it's safe for you to try and those are the patients that might avoid retoxin map the oncologists have never pushed back on me. I've seen a couple of these patients and what I tell my when I counsel my patients I have a similar discussion to those who have immunotherapy adverse events that we've seen anecdotally that patients who do have this robust immune reaction actually have a great response to their cancer. I have seen one patient who had a occult car with just very early symptoms that was accelerated by initiation of immunotherapy and it was such a robust and profound response over three days that we did plasma phoracis with very heavy immunosuppression with great success and found that they had durability of their just two infusions. So I like to use that as an example to kind of reassure other oncologists and the patients that they might still be having some effect on their cancers even if we're immunosuppressing them. Yeah, that's great. I mean, that's a great example of where plasma phoracis helps for us it's so hard to get plasma phoracis. And so by the time we arrange everything it's been weeks to months but there where you have a patient where you have the whole team on board and you can get things going quickly. I think that's a great scenario to try plasma phoracis on. Yes, yes. So how do you ask about Nectalopia? I've seen a few of our elderly VA patients who complain of a harder time seeing at night who have had ERGs for possible car. These patients can still get around in dim lighting and but have a harder time driving and reading. I mean, I don't have anything special about the typical question for IRDs is of course, can you see the stars at night? I don't necessarily think the Nectalopia is always so dense in these patients to ask for that. It's not a perfect symptom. Like I said, the symptoms in air are sometimes vague. So I just ask, do you have difficulty seeing at night but I'm not sure. As you said in some elderly patients, there are many reasons why they would have decreased night vision and it may not be that specific of a symptom. Did your radiologist have any other autoimmune conditions? None at all. Even though the antiretinal antibody testing may not be useful for diagnosis, they can be useful in convincing reticent insurance carriers they should pay for expensive treatments. Definitely possibly. I have, I can't remember anyone who has denied something because I didn't get, I mean, I always get antiretinal antibodies. So I guess I've never had this scenario but I often find that the reviewers for insurance companies have no idea about the diseases that we treat. They can't pronounce the word UVitis, for example, when I talk to them for the peer-to-peer review. So, but it's, but I'm sure that I think it could definitely happen that it is an important part for insurance coverage. Do you think there's still any relevance to the old term autoimmune related retinopathy and optic neuropathy? Specifically, do these patients have both an optic neuropathy and a retinopathy, I think? Do you think there's still a spectrum of disease involving both sites? Yes, I rarely have seen, Aeron is the acronym for this disease. I definitely have seen patients that have both retinal degeneration and pale optic nerves that are probably not just a secondary effect from retinal degeneration. They're pretty rare and often it's really hard to distinguish, to convince yourself that the optic neuropathy is there. Sometimes the MRI will show that their optic nerves are attenuated and then you have the ERG showing the retinopathy so then you feel like they have both things. So I think it's possible, but most of my patients with AR, their optic nerves and all their optic nerve function is fine. Yep. Yeah. Yeah, I, you know, I not always in my experience, I also had a patient who had MAR directly after their first checkpoint inhibitor infusion. So the next day, total night blindness. In my experience, the thing they noticed the most is just sudden night blindness and just peripheral vision feel loss. So for me, the symptoms, I don't really make, you know, I don't, I hear the vague symptoms, but I don't hang my head on any particular symptom. So I've redone it and I can think of a couple of patients when like six or seven years have passed and I know the panel has gotten significantly better and the patient I'm thinking of, it didn't show anything else. Six to seven years later. But yes, but I mean, within a couple of years, the panel is not gonna be that much better. So it's probably not worth it. So I do, so I do the induction infusions, usually two weeks apart and then six months later and then another one, six months after that. And then I try to extend out nine months and then a year. And if everything's really stable, I think about stopping it. And then after that, I stopped the IVIG. Yes. Yeah. So those patients who that's, so that dosing is typically for lymphoma. So the dosing of two weeks, two infusions, two weeks apart is the typical dose for autoimmune diseases like ankylvesculitis, et cetera. I, those, I had talked to a couple of people about that dosing and around that time that I was treating those patients. And so that I gave them more intensive treatment. I don't know if that's what made the big difference for them. I mean, the truth is after one retoxin infusion, your B cells are gone. I'm not really sure, four made a big difference and it's hard to get insurance, insurance companies to pay for four infusions. So going forward, I've only done two. So it was really, cause I think at that point I was like, what is the most I can give these patients to see if this really works. And I haven't really done, besides those two patients, I haven't really done many other patients with that dosing regimen. Yeah. Sure. I don't, only if they have new symptoms. I mean, they continue their normal age related, cancer screenings, but only if they have new symptoms. And I mean, I have a very clear discussion with them. You could have a, this could be a side that your body is controlling a cancer and you have any new symptoms, let us know. Thank you, thank you for your questions.


Hi everyone, Joe for jasmiescasebrakes.com coming at you with finally 2022 Panini Select Baseball 12 box pick your team number 10 It has indeed arrived. I know this break was supposed to be on Sunday No, let me turn on my camera. It's my first break of the day forgot to do that. There you go There we go. It's supposed to be on Sunday But the case was not available So we had to order a case right quick and our distributor sent it pretty quickly to us here on Tuesday So thanks for everyone's patience. Now, I don't think a single person requested a refund So I appreciate that so thanks everybody for your patience and hanging tight on this break right here Now if you saw that little rooftop next to your name That means you won that spot in that filler that we did on Sunday So if you want to see the results of that you can go back to our Sunday videos. There it is 2022 Select Baseball Let's pop this open fresh sealed case and let's see what we got in here six boxes back there six boxes right over here and We're looking for all sorts of fun parallels Including that ultra rare color wheel. I don't think it falls exactly one per case But hopefully we'll see one in this case among other nice hits looking for two autographs two memory billiards per box on Average good angle here. So thanks everyone for making this happen appreciate it The way we go for now to tease junior on the on the front of all these Not a not a good year for for Nana to tease junior breaking his wrist riding motorcycles and then getting pop for PED's Padres pulling the plug on a to tease junior bobblehead giveaway Not a good year for him go to what we got here. We're gonna lead off with Cedric Mullins with Maryfield and our first relic is Josiah great Okay, overall. I think he's had a pretty decent year for the Nationals Gregory with that one We got a Mike Yostremsky 57 out of 99 for the Giants Concourse edition there's a few different levels all card ship in this too just because of all the different levels What not and we got a Andre Jackson Jersey and autograph For my Dodgers actually don't know How he's been doing this year Let me just double check. I feel like it could be due for a Could be due for a September call-up maybe sort of a down year for him this year Five one six era over 17 starts 59 innings 64 strikeouts You like walks has been an issue for him Yeah, he's he's given up 50 walks and 59 innings You've got to get those walk numbers down It's just under a walking inning or something like that That's been the issue, but he can definitely he definitely has some swing and miss stuff. There's Ichiro Mariners edition 13 out of 50 That'll be for David M. And Seattle But Andre Jackson Dodgers that was David M. By the way, a lot of still has a lot of upside though Water Franco rookie relic for the Rays That's gonna be for the X-Line Jake Berger We got a Edmundo Sosa 123 out of 199 We got Eli Morgan Jersey rookie Jersey and Otto for the Guardians Cleveland. This is for you That's David Doreen With a spot that he won in the filler It's a rookie Jersey and autograph 58 56 out of 299 You go on the board and the Sosa goes to the Cardinals LV for the X-Line. All right good start first to box Down another box to go. This is kind of a longer break each box is probably I don't know five minutes or so maybe a little bit less if I kind of get into a good rhythm here, but Break by the time all that and done does take about an hour We'll put this break away. Then we got another break lined up Now nothing else was sold after the next break And we are trying to get that promo done tonight So I would encourage everybody if you're not especially if you're not in this break We've got a long ways to go in this break to visit jasky's case breaks calm Check out the latest promo giving away $5,000 of break credit We just got two high-end breaks to go and then we'll get there one of them's not too far away Handful of spots in some random number blocks Couple filler boxes for the random number blocks and then we are in breaksville on that National Treasures football then we'll work on that dual case break If we get that done tonight and give away a ton of money deadline is end of show tonight. All right. No little gold peeking out there Let's see what that's all about Got Drew Ellis For the diamond bags that'll be for Andy in Arizona 111 out of 250 we got a line green 68 out of 99 a keel of a dude for Steve and the Tigers Got a brand-in-march rookie relic for the halos. That's gonna be for Sean Healy Paul Goldschmidt Chris sale or Chris sale just bad luck from 002 out of 149 red socks Richard Serrano, and there's vado Matic little color match red parallel for the red legs Sean Barnes And we've got another Eli Morgan rookie Jersey and Otto so Dave you're starting your Your Eli Morgan PC whether you intended to or not This one is 129 out of 199 The other one was Out of 299 different parallel and then behind Matt Manning is Connor Wong Jersey and autograph for Serrano and the red socks 222 out of 299 that gold is Ronald Acuna junior three out of ten premier level gold nice That's that's Dave and the Braves got randomized the Braves in that filler. That's pretty sweet. Hey, there's Rick. You're welcome, Rick First of many I hope What else is going on here that Pirates Castro banned for one game? Remember he's the guy that a Where he's siding into third I think in a cell phone His mobile popped out of his back pocket or something like that. So Whoo Mets to call up touted third base prospect thing baby Brett baby, maybe Yeah, Brett baby One of the top prospects in baseball to help stem the tide of injuries in their infield baby 22 Years old is expected to fly to Atlanta where the Mets will play the second game of a four-game series Tuesday night. That's tonight He placed infielder Louisa Guilherme on the injured list Monday with a growing strain that I'll sideline him for more than a month Eduardo Escobar could join him on the injured list with a strained oblique He's a 37th best prospect in all of baseball according to ESPN's Kylie McDaniel Left-handed Hitting slugger went 12th overall in the 2019 draft some dinged him for being an older high school player, but but hey Between double a and a week towards the game to triple a he's he's slashing 315 410 and 533 with 19 homers and 60 RBI's Wow, I don't think when do the Mets Braves are? Are in about in about 30 minutes or so that game will First pitch in that game. I wonder if he's starting. I Would imagine so No, Brett baby is not starting. They might ease him into a pinch hitting situation or something like that There's Thai France 58 out of 199 for Seattle that'll be for David M And we got Labor Day Labor Torres 39 out of 149 for the Yankees That'll be for James and there's Jaren Duran Duran That'll be for Rick and the Red Sox We got a John Heasley hazely he's Lee Rookie relic for the Royals That's Nicholas Schuster with Kansas City with a spot that he won in the filler and behind Anthony Rizzo is a moonshot autograph That's Mike Zuninho Moonshots auto for the Tampa Bay Rays. That's the X line to the moon 24 out of 81 on that one We've got a Jackson Coar Jersey and autograph for Nicholas and the Royals 008 at a 199 and we got a Connor Siebold nine out of 35 for Rick and the Red Sox Be bold see bold. All right. What else is going on in? The ESPN comm MLB headlines here Carlos Carrasco a bleak strain may miss three to four weeks Red Sox getting all getting Kike Hernandez back from the IL nice One other prospect call-up the A's release Stephen Piscotti To call up member a Shea Lang Lears. I feel like we've pulled a lot of his stuff in recent times Cleared the way for top prospect Shea Lang Gears a Lang Lears to gain experience Down the stretch for the last place team in the AL West. He's a 24 year old catcher and left fielder selected ninth overall in that 2019 draft out of Baylor Hit 283 19 home runs 56 RBI is in 92 games for triple a Vegas Last Vegas after being acquired from Atlanta. That's right in that March trade that sent Matt Olson to the Braves So looks like that 2019 class because Brett Beatty was in that 2019 class It's like we're starting to see some of those 2019 Players start working their way up the ranks.  That's my guy max Muncie 24 out of 99 Taking it to the max to the moon That'll be for David M and the Dodgers picked up the Dodgers straight up Max Muncie think still lingering effects from that elbow surgery is now starting to Now starting to heat up a little bit. I want to say Let's see. Let's see how max Muncie's doing in the last In his last 15 games He's hitting 340 five home runs 13 RBI's seven walks 15 strike and stolen base in the last seven games over 24 of bats Three of those home runs of three of the five home runs in the last 15 games have come in the last seven games actually seven RBI's four walks six strikeouts pitting four 17 500 obp 958 slugging so he's starting to turn the season around probably at the at the perfect time leading into The last month or so month or two of the season month and a half Use the force Luke Luke Williams jersey and autograph 127 out of 199 Billy during this time with the Phillies So Billy on the board. I think this is the Castro kid that had his cell phone that Popped out of his pocket. He's suspended for a game That'll be for Pittsburgh. That's going to go to Jorge Who got the pirates last last bot mojo? Let's see if we can find some hits for that last bot mojo spot So you're on alvarez to 35 For the strokes that'll be for nicholas There's a rookie o'neill cruise For Jorge and the pirates One of the more exciting youngsters Here in the league. That's a premier level Bryce harper to 199 And we've got vedelle brujan Piece of his jersey going to the x-line and the rays the Bryce harper will go to billy and the Phillies Next box two other stories are here Nick plumber designated for assignment a's shut down paul blackburn for the rest of the season Yeah, I don't know if we talked about this, but ranger is firing manager chris, uh, woodward former Dodgers bench coach Orioles promoting dl hall Tariq scoogle visiting a uh Oh, that's not good visiting Specialist with an elbow issue expected to miss the remainder of the season Michael brantley underwent a Season ending shoulder injury Poor danie duffy is suffering a setback unlikely to pitch for the Dodgers in 2022 All right next box. Good luck We got a joziah gray piece of his jersey for greg and the nationals We've got a dance v swanson for the braves to 199 And we got an out of 10 Spencer strider three color patch That looks really sharp. That's going to go to david and the braves Three out of 10 It's really cool. Got tyler mailie 28 out of 99 for since natty And it'll be for shan barnes Got a christian javier jersey and autograph for the stroves nicolas With the astros Jersey and autograph 007 Out of 199 And uh and another astro Chas macormick for nicolas shuster 29 out of 199 and there's 38 out of 149 brandon woodruff For the brew crew That's for rick serrano box six of 12 After this will be halfway through This uh full case break. All right, no finals right? Yeah, I think all all games I've not even started a couple games have started Padres are in miami at the end of the first marlins zero padres zero I think I read a stats or I heard a stat somewhere that the marlins have scored three or fewer runs in like the last Two weeks or something like that, which is a Which is a record kind of crazy Um at the end at the top of the second Phillies and reds have a hit of peace No runs cubs are in dc We got steel and a disappointing season for patch of corbin four and 16 With a 702 ura. That's rough Red socks are in pittsburgh pavetta and keller rays are in the Bronx springs and cortez Orioles it's a bird-on-bird match of Orioles blue jays dean kramer and alec manoa There there's a wander franco rookie card And here's another john heasley for um For kansas city that'll be for nicholas 42 out of 250 The wander franco rookie card going to the x-line It's premier level and we'll do it. We'll do a recap a hit recap at the end of this too. So if you're Just joining us Kyle Tucker for nicholas and the straws to 199 and we have a jaren duran duran No, I won't cry for yesterday. There's an ordinary world From how I've got to cry uh rick with the red socks Colton welker And a ryan mount castle 25 out of 50 Steve mozer with the o's And we've got a hosé devours 44 out of 99 I think there is a relation right at cousins devours cousin rafael devours So some some pedergy there richard yahanson With that auto And we got a sparks signatures read detmer 70 out of 199 Uh had a no-hitter early this season if I remember correctly. Let's go to the halos Sean h And chris bassett 004 to 149 ryan steward with the a's We had a remember last season 2021 seemed like they had a we had a record number of no hitters And this season how many have we had? Could we count them all on one hand? Maybe see what other other games are happening here tigers are in cleveland Cleveland quietly having a great season. They're top the al central We got hill and police act On the mount although police acts have been struggling this year two and ten four three two you're a Mets are in atlanta taiwan walker charlie morton Royals are in minnesota zack ranky sunny gray Rockies in st. louis freeland and cantana a's are in In texas playing the rangers Astros white sauce burlander dylan the seas that's a good pitching match up there Burlanders 15 and 3 with a 185 e r a Dillon's east is 12 and 5 with a 196 e r a My dodgers playing in about an hour. They're in milwaukee ryan pepio the Dodgers prospect Facing brandon woodruff. We just saw one of his parallels a bit earlier mariners are in uh In anaheim robbie ray And then josez suarez. I think josez suarez on the mount. It's cal ripkin zebra print for steve and the orioles and the late game Will be a diamond backs at giants maryl kelly and unis Face off against each other's matt brash 222 out of 250 a little bit of a little peeling there on the back coating There but that goes to david m in seattle Saw him throw some heat the other night against the angels two nights ago last night two nights Against the Yankees, I think actually He's got some some electric stuff There's drew ellis 94 out of 99 Sparks autograph that is for andy in arizona And we got tyler mcgill 113 out of 2 99 Bit of that metz pinstripe in there and his autograph I feel like he started the season off hot and tailed off a little bit That's still goes to the metz james with the metz won the metz in that filler Got a madison bum garner to 199 for arizona And I love these in select 20 out of 20 yusaka kuchi for seattle tie dye One of the tie dye parallels in select this will go to david m And seattle Another chasm cormac piece of his jersey this time for nicholas Excuse me And riz huskens 3 out of 99 riz huskens goes to billy and the fillies And madison bum garner going to andy in arizona all right Another box old news rex. I already I already announced that Pretty much at the beginning of this break Try to keep up rex Rex just rex announcing that bread baby's about to get the call up We already talked about it rex. All right next box There's joe ryan for the twins A piece of his jersey Been there done that I'm exactly in that generational wheelhouse. There's cabrion haze 26 out of 50 That is for picksburg. That's for uh, Jorge Otto lopez 165 out of 299 and auto auto jersey and autograph We got jake meyer 68 out of 99 jersey and auto the oh, sorry the auto auto by the way goes to toronto mike Who won the blue jays in that filler? Gets that one and Houston, I feel like it's been getting some nice stuff. Nicholas with his straws Elvis and rex announcing elvis just died elvis presley just passed away That's on brand for rex Ramon loriano ryan steward with the a's Another asteroch has mccormick piece of his jersey going to nicholas There's a wander franco in fuego refractor It's a nice one for tampa bay the x-line I think those were the refractors do do make a difference In a secondary mark val the show. Hey, othani 99 out of 199 Red parallel color match for sean heli randy ars irania With a homerot a three run jack off of nester cortez Yankees fans panicking now uh speaking of the The bret baby call-up. We were just talking about that draft class That 2019 draft class We're starting to see a lot of those players getting the call-up adley rushman Is playing with the orioles right now with the big club? He was the number one overall pig bobbywood jr. Is with the royals, of course. I think andrew von Playing with the whitesot. I guess we haven't seen j is jj bladé been called up That with the marlins Maybe he's still working on things in the miners riley green. Maybe Cj a berns was just involved in that trade nick ladolo. Have we seen any of them? I feel like josh young's been playing right shei lang lears Is going to get called up by the a's And I don't think we've seen hunter bishop alakmanoa, of course all-star alakmanoa For the blue jc starting tonight, then bret baby was the 12th pick Have we seen kilny kivakko for the twins that I don't remember I feel like bryce and stott started the season with the fillies, but maybe he's been up and down Don't know about will wilson Some people are high on corbin carroll the 16th overall pick for the diamond bags I don't think we've seen any of the other Names here right corbin carroll jackson rutledge. These are all the first-rounders quinn priesters ak thompson's george kerb Maybe we've seen a little george kirby bradon shoemake greg jones michael toga daniel isfino. I feel like we've seen cody hosie for the dodgers has not made an appearance yet Blake wallson ryan jensen eith and small logan davidson anthony vulpe michael bush quarry lee But we're starting to see those 2019 guys Yeah, rex might have some uh bret baby bowman first refractors Somewhere around there dust them off. There's liam hendrix 37 out of 37 out of 99 another wander franco and a nicky lopez 52 out of 105 For kansas city Right wrong wrong auto rex. You're thinking a glenn auto for the rangers Jay-z. Yeah, I hope we get to all of your breaks and everyone else's too nicky lopez for the royals nicolas with nicky another wander franco for tampa bay And a redemption Remember marin play to the whistle We are not close to being done with this break just yet Another elie morgan this time just a piece of his jersey for cleveland going to dave Cleveland, this is for you We've got a yoan mancada 13 out of 50 There is a jaga de grond firestorm insert. I feel like I don't see these too often. This might be a short print It's james with the mets jacob de grond has been On fire And his last couple starts after the il. There's cal rolly for seattle david m with the m's yoan mancada goes to dante and the white socks And we got a louise castillo reds edition 31 out of 199 Rex has got a guess for the redemption either a franco or a soto That's rex's guess It is Boom wander franco. You got it rex Nice rookie jersey autographs cracked ice wander franco tampa bay rays That's the x-line picking up the rays straight up scared money. Don't make money The future is bright for wander franco cracked ice maybe numbered to 99 or something like that All right three boxes to go 12 hits to go two autos and two relics per box All right next one pretty thick card right there from the final three boxes Good luck There is luke williams 155 out of 250 Use the force luke that's for billy doring and the fighting fills Nice little philly pinstripe right there as well We got it in fuego jacob de graham for the mets it's for james and jacob alex verdugo To 199 for the red socks Nick that that that line will apply at any time It's always good to remind people about that. There's han's kraus For billy and the fillies billy filly Not numbered And we got a gene sagura 9 out of 10 diamond level. I think that's the shortest print Nice gene sagura for billy and the fillies billies fillies And we got a six-dose sanchez 23 out of 60 jersey and autograph. That's richard j With miami and another thick card coming up And that is shane boss 9 out of 10 two color patch and autograph For the tampa bay rays That's the x-line with the rays Nice rookie patch and autograph great low number Big ceiling high ceiling for that guy 147 out of 149 Hyunjin Roo for toronto Brian haze and freddy freeman Hyunjin Roo goes to mike and toronto. All right two boxes to go We never do nick was All right two boxes go Another thick card here that might be another out of 10 Maybe even lower. All right. Good luck. We got a kyle muller Rookie relic for david and the braves Another wander franco got a tristan mackenzie for cleveland to 199 What a shot by flat jr. It's out of 25 It's bended mckay Select swatches Two colors one out of 25 brennan mckay What's his status lately? I feel like he's just had a lot of setbacks Yeah, he's been he's been rehabbing something, but I think he had shifted to a single a About a couple weeks ago starting up a rehab assignment shoulder issue, but I think he was Originally touted as a possible two-way player. I wonder if they're just gonna have him be a just convert him just to Pitching only or something Although if those shoulder issues persist then maybe Be converted to a hitter. I don't know. We'll see Let's see a wait and see for that guy. Here's a mike trout To 35 he's been seeing some uh live batting practice Slowly making his way back and there's alex manoa toronto blue j And nick nappy their adjacent is ready for you on instagram for your personal box We don't rip those unless you're in that instagram chat So jason needs you in there 22 out of 199 Uh blue jays once again mike g who won that team in the filler angels. Sean. Healy gets that mike trout And behind jake of the grom is a mat mani 93 out of 199 jersey and autograph That is for steve m cat team mojo big cat mojo 93 out of 199 Joey vato 4 out of 99 and there's bren crofford in fuego insert All right Final box fingers crossed Good luck everybody. Thanks for getting in. I appreciate it Thanks for your patience too on this break. We finally got it done. I think no not a single person Requested a refund. So I thank you for that It's just a couple days. We didn't have to wait too long. So that was nice The distributor is getting nick ordering it quickly and our distributor is getting out to us pretty quickly too. So thanks To everybody and apologize for that inconvenience. So we finally got made it We made it I'll do a quick little recap after this as well. All right. Good luck everybody There's riley adams 190 out of 250 jersey rookie jersey for uh gregory and the gnats Mookie bets and fuego silver for the Dodgers that's going to go to david m Got an austin riley diamond level refractor And you darvish red to 199 for the friars That austin riley goes to david and the braves. I think he just got a Nice little contract extension recently Uh-oh martin retracting messages. I didn't I didn't even see it You're lucky I didn't see it martin brandon marsh to 25 cracked ice I think billy and david must have taken all of your all of your mojo martin So got some hits left though brandon marsh goes to shan and the angels We've got a henry davis 175 out of 299 youth explosion autograph That's the uh former number one overall pick whorehay with the pirates last spot mojo 70 percent of the time Hits 100 percent of the time And that is 175 out of 299 nice We've got a out of 75 cal raleigh 18 out of 75 jersey and autograph for seattle david m with the mariners I think that might be why I think we might have one more relic and we've got some I've got a willy stargill 48 out of 99 for whorehay lime green And then we got a hans cross for billy during And the fillies hans cross rally Oh, I hope so too. That's got that's coming up right after this Got brice harperer John's in india And a moonshot shohay otani and that my friends is that now just as A small token of appreciation for everyone's patience on this break um I'm going to give away 20 dollars of break credit to somebody here Just says a little thank you three into six nine times name on top after nine 20 dollars of break credit one two three four five six seven eight and ninth and final time after nine Nicholas there you go 20 dollars of break credit going your way thanks for your patience on this break Nicholas and everybody here's the recap From the last box to the first box pretty solid break. We did not see the color wheel Which is not guaranteed one per case. It might even be slightly more shorter printed than that, but If we get another case of this select nice wander franco right here If we get another case of that select, maybe we'll We'll go color wheel searching again In fact, I think uh, we do have some loose boxes on the personal break side So if you want to buy a personal box of select baseball there, maybe You might want to continue your your hunt there if you'd like Plenty of baseball and the group breaks out of things to jaspyscasebreaks.com Thanks everybody. I'm joe for jaspyscasebreaks.com. That was picker team at 10 2022 panini select baseball I'm joe and i'll see you next time for the next baseball break. Bye