 All right, before I get started, I just wanted to take the time to introduce one of our new international guests. This is Dr. Badr Dean. She's actually from Mongolia, so if everybody could say hi, that would be really nice. All right, so I'll get started with my presentation. The title is, Which Would You Pick? All right, so we'll start out with the case presentation. We had a 38-year-old female. She comes in complaining of a blurry spot in their center of vision in the ride-eye since the morning. She had poor vision in her left eye for the past 10 years due to a choreo-retinal scar of unknown etiology. She denied any phutopsias, floaters, headaches, or any eye pain associated with this. Her pastoral history was significant for diabetes type 2 asthma, high blood pressure, fibromyalgia, depression. She also had a history of valley fever, but no history of autoimmune diseases. The rest of her history was non-contributory. So on exam, her visual acuity with correction was 2050 in the ride-eye and then 2200 in the left eye. Her pressures were normal. She had an ather and pupillary defect in the left eye. On confrontational visual field, she had this central scatoma mainly in her left eye. On slit-lamp exam, her external exam was completely unremarkable, as well as her anterior segment exam. Most notably, her anterior chamber had no cellar flare, basically no inflammation in that area. She also had no vitreous inflammation either. However, on dilated fundus exam, she had these yellowish-white lesions in the macula, as well as multiple punched-out scars out in the mid-periphery. This was in the ride-eye. In the left eye, she had some evidence of sub-retinal fibrosis in the center of her macula, as well as multiple punched-out lesions in the mid-periphery as well. On fundus autofluorescence, corresponding to lesions, you see these areas of hypo-autofluorescence and this surrounding halo of hyper-autofluorescence. You can see something similar in the left eye, but a little bit more extensive. On fluorescine angiogram, many of those lesions exhibited early hyperfluorescence with late staining and leakage in the ride-eye. On left eye, it was staining due to the sub-retinal fibrosis and scarring. On OCT, through one of the lesions in the ride-eye, what you see is the sub-RP accumulation of material, oftentimes extending into the inner retina. This was in the ride-eye through another one of those lesions. On left eye, exhibited sub-retinal fibrosis atrophy and some cysts overlying that area. So our differential diagnosis at this point includes many of the white dots and drums, such as multifocal corditis and panubiatis, PIC, bird shot, like Reese was talking about, diffuse sub-retinal fibrosis, mutes, should always think about sarcoidosis as well, or an infectious etiology, something that's bacterial, fungal, or even viral. Pancerology and imaging testing was done, which came back all negative, including the chest x-ray. At this point, she was given a diagnosis of punctate interchloridopathy with an associated chloride on the obascular membrane in the ride-eye. She was given an avast injection in the ride-eye. We decided to start her on methotrexate with an oral steroid taper because she had a monocular status. Also, the lesions were very proximate to herphobia. The instituted INT therapy. Two months later, her visual acuity improved to 2020 in the ride-eye. She had a quiescent exam. Over the next year, she had recurrent activity of the lesion nasal to the phobia, despite continued injections of osoridex and avastin. And that's why we escalated care to switching her from methotrexate to cellsept, and she obtained a successful quiescence. In the subsequent year, she had new active lesions in the phobia of the ride-eye. Therefore, cyclosporin was added, along with continued avastin and osoridex injections. So, what exactly is punctate interchoreography? It's considered an idiopathic inflammatory disorder, where it was first described by Walski and colleagues back in 1984. They described 10 patients who were myopic and Caucasian that complained of utopias, blurred vision, as well as scatomas in the center of their vision. What they characterized were the small, discrete yellowish-white lesions at the level of the interchoreoid and the RPE, and it was mostly localized to the posterior pole. Most importantly, there was no associated anterior chamber inflammation or any vitreous inflammation as well. Now, who gets PIC? Well, a global case series showed that 97% of their patient population who had PIC were women, 90% were Caucasian, 85% were myopic, and they had a median age of 30 years old, and there was no associated systemic disorders. On presentation, they'll complain of metamorphopsia, paracentral scatoma, photopsias, and asymmetric loss of central acuity. Fundus findings, as we discussed, there's this yellowish-white choreoretinal lesions. They can typically range between the size of 50 to 200 microns. They rarely extend to the mid-peripherate, and over time they progress to form these atrophic scars with associated pigmentation. Sometimes you can see serous retinal detachment over confluent active PIC lesions, and most importantly, by definition, there's an absence of vitritus or AC inflammation, anterior chamber inflammation. On fluorescein angiogram, you typically see early hyper fluorescence of lesions with late staining. On ICG, you see these mid-phase hypo fluorescence of lesions, oftentimes more numerous than you would see on clinical exam or even FA. And on OCT, you see the sub-RPE accumulation of material, oftentimes extending into the inner retina. The most vision-threatening complications associated with PIC include carotoneobasperate, carotoneobasperin membrane formation, and subretinal fibrosis. And the treatment choices really depends on the clinical presentation, so you would typically observe there are no visual manifestations. You can institute periocular and systemic cortical steroids if there's poor initial visual acuity or the acute PIC lesions are very proximate to the phobia, as it was in our case. And IMT, or immunomodulatory therapy, is reserved for persistent or recurrent PIC. Anti-vegeth laser and PDT, which is photodynamic therapy, is administered for carotoneobascularization that's associated sometimes with this. So at this point in my talk, I want to segue into the discussion section of the two prevailing theories regarding PIC. Some experts believe that PIC and multifocal coriditis are part of the same disease spectrum. The reason why they think this is because there's a lot of overlap in the clinical presentation between these two diseases. Also, there was a genome-wide association study done in the United Kingdom showing that patients with multifocal coriditis and PIC shared the same haplotype for interleukin-10. The other prevailing theory is that PIC and multifocal coriditis and panubiitis are completely separate disease entities, and this is mostly because of the way they've been described historically. Now what are some of these differences? The main one is that in PIC, the lesions are typically smaller. They're localized mainly to the posterior pole, and they very rarely extend out to mid periphery. Also in PIC, there's no associated anterior chamber inflammation and detritus as I've been hammering. Also, there's no structural complications due to recurrent inflammation as occurs in multifocal coriditis. Some of those include cystoid macular edema, epiretinal membrane formation, as well as cataract formation. Now it's this recurrent inflammatory, chronic nature of multifocal coriditis that distinguishing these two diseases clinically sometimes is important because studies have shown that early IMT, or Immunomodulatory Therapy for patients with multifocal coriditis, can decrease the risk of complications associated with recurrent inflammation. Actually, one study done by Thorne and colleagues down at Johns Hopkins showed that if you actually institute early IMT therapy in patients with multifocal coriditis, there's an 83% decreased risk of getting posterior pole complications due to recurrent inflammation. So since the advancement of imaging technology, distinguishing these two diseases has become much easier. So on fluorescein angiogram and multifocal coriditis, the active PIC lesions typically show up in the early phase as hypo fluorescent lesions, and in the later phase they become hyper fluorescent. And PIC, as I already stated before, there's early hyper fluorescence and then late staining or late hyper fluorescence. And then you'll see some leakage as well, as you can see in the center, in the center of the macula there with associated carotidoneovascular membranes. On ICG, you'll see in the mid phase that the lesions typically show a hypo fluorescence. Oftentimes, many times it's more numerous than you see on a clinical exam, and that's very similar to what you see in PIC as well, but the lesions are typically smaller, as we said in PIC. Fundus autofluorescence is where things get really interesting because FAF has been used to delineate subclinical lesions. So if you see here in panel A, there's no... You don't see any lesions along that branch of the... I don't want this vascular, this branch of the vascular, okay, right here. So you don't see lesions there in the red free photograph or on clinical exam. However, on the fundus autofluorescence, you see these hypo autofluorescent lesions. Three years later, these lesions actually show up on clinical exam as well as on the red free photograph, and the lesions on fundus autofluorescence actually are larger than they were three years ago. And PIC, fundus autofluorescence, is also very interesting. What happens is that it's used to mark areas or identify areas that has uncontrolled inflammation and are prone to reactivation, and they typically show up as this hyper-autofluorescent halo. So you see this patient here with an active PIC lesion in panel A, and you have this surrounding hyper-autofluorescent halo. However, after instituting cell cell for a month later, this hyper-autofluorescent halo has actually decreased in size as well as in intensity. Contrast that to the two panels below where you see a patient with persistent PIC. And what you see is this hyper-autofluorescent halo, and this patient didn't respond to therapy, and over time, that hyper-autofluorescent halo has actually increased in size and intensity as well as consistent with the progression of the disease, as you can see in the area of the hypo-autofluorescent lesion. On OZT, multifocal coriditis, you can see the lesions that typically have a disruption of the ISOS or outer rental layers. Also, they can exhibit this sub-RP accumulation of material, overlying vitreous, indicated by the blue arrows there, and this hyper-reflective band in the coroidal layer. On PIC, inactive lesions show a sub-RP accumulation of material as well as loss of the ISOS or outer rental layers. OZT can also be used to track response to treatment. Here in the above image in panel C, you see the sub-RP accumulation of material after prompt treatment and good response to treatment. You actually see that that area has actually decreased in size. So what are the take-home points? First one, imaging utility. Multimodal imaging can help distinguish between these two disease entities, and this is really important because you want to identify multifocal coriditis because instituting early immunomodulatory therapy can help prevent a lot of the posterior pole complications that are associated with this chronic recurrent nature of this disease. Some other take-away points. PIC should always be considered and all the white dots in the differential diagnosis. Coroidal neovascularization and sub-retinal fibrosis are the most vision of threatening complications of PIC. And IMT or immunomodulatory therapy should be instituted. You should consider this in patients with PIC that's persistent and recurring, as was in our case. And lastly, but not least, PIC and multifocal coriditis should be considered, may be considered as part of the same disease, but further studies need to be completed in order to test this hypothesis. On that note, I'd like to thank Dr. Vitale for giving me the opportunity to present this case as I've learned a lot from this. Thank you. Really. I have a question. This is on one of your early slides. You said that the incidence is 110 cases per year in the U.S. Yeah, in the U.S., from one study. That sounds incredibly low. I mean, I've seen a couple cases. That would imply that there would be one new case a year in each of them. Yeah, so there is a bias for that in the earlier studies because a lot of times these diagnoses have been diagnosed improperly as pose, presumed ocular histoplasmosis syndrome, or even other white dot syndrome. So when they finally get to the UBIBIS center, it's possible that a lot of the other ones that have been misdiagnosed haven't actually been diagnosed as pigs. So it was a study that was done in the 80s or so. Yeah, I think that's definitely wrong. It's much more common. Yeah, that would be an incredible disease. You know, it's actually a very interesting disease. I think that part of the kind of controversy in terms of are they the same disease or not and stuff that it has to do with who's seeing them and who's reporting them. So, I mean, multi-fogal corditis comes to the UBIBIS people, so more advanced diseases with inflammation and various, I think in a retina practice, you might be more optimistic to see a pig. So I think that people are thinking, well, we are seeing different things. Patients with multi-fogal corditis, as Renee pointed out, present with many more structural complications than patients with a pig. So cataracted at the rebel membrane, macular demon, as opposed to a pig. The most common presentation is with curly vascular membrane, really, and decreased vision. You might pick up multi-fogal corditis in a patient that has macular demon or inflammation in the eye. And the importance of this and why I put these two together, we're starting out with birch. That really requires systemic therapy. You pretty soon have to be on set. With multi-fogal corditis and panugasin pick, you might, if a patient came in with character secretions of pick, they're inactive, there's no inflammation, you might be through a bad patient. And one about any menopause, patient with multi-fogal corditis and panugasin, you might treat them with periac or steroids, but you have a lower threshold to treat them with immunomotor. And the other thing is that I think that the distinction in terms of treating the patient, sometimes it's artificial because if we had a patient, this patient of pick had really advanced disease, they're already behind the curve with a very poor outcome in one eye, and in the fellow eye, they've got a lesion that's threatening their phobia. So we are presuming that this entity is an inflammatory cause and that placing the patient on an anti-inflammatory course, in addition to treating it according to the master membrane seems to make sense. Historically, patients, people were treated with periac or steroids for inflammatory part of the master membranes. And the membranes, as Paul, as you know, are different in pick than they are in AMD, so these are type two type of membranes that are usually above the red pigment epithelium, are more classic in nature and respond pretty well to any veggie therapy. Okay, so... Thank you.