Component-resolve diagnostics (CRD) enables precise risk stratification in peanut allergy by distinguishing true peanut allergy from cross-reactive sensitization. Storage proteins (Ara h 1, 2, 3, 6) are species-specific, heat-stable, and strongly associated with systemic reactions, making them high-risk markers. In contrast, profilin (Bet v 2) and PR10 (Ara h 8) are pan-allergens that cause cross-reactivity with other plant species and typically result in mild oral allergy syndrome rather than severe systemic reactions. This molecular approach helps clinicians differentiate between patients who will have life-threatening reactions versus those who may safely undergo food challenges, enabling personalized management and avoiding unnecessary dietary restrictions.
CRD Webinar Series 2.0 | Session 3: Peanut allergies and CRDAñadido:
final webinar and for what promises to be a clinically rich and scientifically rigorous session. So before we begin let us have a few important housekeeping notes. Uh this webinar is organized by thermophicia scientific in partnership with ISAS the initiative for sleep a sciences. The content presented tonight is intended purely for medical and scientific education of healthcare professionals. This session is being recorded. By continuing to attend you provide your consent to be part of this recorded session. The recording will be used for internal educational purposes.
The views and opinions expressed by the speakers are their own and are based on their clinical experience and interpretation of available evidence.
They do not necessarily represent the position of thermopic scientific. No promotional claims are being made during this session. Any reference to diagnostic tools or technologies is purely in the context of clinical and scientific discussion. If you have any objections to being part of the recorded session, we request you to please disconnect at this time. Thank you. We are glad you are staying with us. Let us get started. So tonight as we close our three-part series with a topic of enormous clinical and public health relevance advanced molecular allergy diagnostics that is ped allergy and cross reactivity in Indian patients. So ped allergy is one of the most fear diagnosis in allergy practice and for good reason. It is amongst the most common causes of severe anaphylaxis and unlike many food allergies it is rarely res rarely resolving with the age. But here is what makes it genuinely complex.
Not all penis sensite patient patients are equally at risk. Some will have mild localized reaction. Others may be life-threatening allergic reactions. So the clinical challenge and tonight's core question is this. How do we differentiate this allergic condition.
So this is precisely what what our expert faculty will help us address tonight through the lens of CRD and allergy diagnostics. So we have an outstanding faculty with us evening. We will have a panel discussion a series summary and as always please drop your questions in the chat as we go. So before we session before the session begins we are honored to have with us Dr. Nirj Gupta senior pediatric allergy specialist from sir Gangaram hospital Delhi founder ISAS and allergy school who will set the context for today's session for the evening. Over to you Dr. Nish Gupta.
>> Thank you Alka. Thank you so much. First of all, I would like to thank and simultaneously congratulate Thermofficial Scientific. Uh your uh singlelex component IMOAP is gold standard but more so this particular series is more than the gold standard. I would say it has set the bar so high that uh in the last two webinars the viewership has crossed more than 1,000 views in just only 10 days time. So that speaks the volume that speaks the quality of the content which is there.
That also speaks about the need. That also speaks that where the people where the doctors are facing difficulties and where they actually want to learn more and more about their components and they want to learn more and more about and turn their practice towards precision medicine. When we have already covered the important components of dustmite, milk, egg and wheat and now another important component which is peanut an integral part which needs to be covered and then there is always a question about cross reactivity, pan allergens and then pollins. So all these questions we will be covering up today and ultimately at the end how to actually use all this knowledge into providing the care to the patient like precision medicine which is the ultimate goal. So my best wishes to the webinar and once again I am thankful to your team and simultaneously to Scott and all the run faculty for joining us tonight. Thank you.
>> Uh thank you so much Dr. N. So to open tonight's session and lay the scientific foundation our first speaker will take us through peanut components and risk stratification. Scott uh the senior clinical educator from thermophicia scientific brings deep expertise in the molecular imunology of food allergens and ext extensive experience translating complex science into clinical practice.
So this is the scient scientific map that he will be navigating for the rest of the evening. So over to you Scott. A warm welcome to you. The floor floor is yours yours now.
>> Great. Thank you. Just a moment. Let me find my presentation.
Can you hear me?
Uh, yes, Scott.
>> Okay, I'm pulling up my presentation.
Just give me one second.
>> Yes, >> thank you for being patient.
All right, you should be able to see it.
>> All right, thank you all for having me today. I I certainly do appreciate it to be part of a panel with with such esteemed colleagues from the from our Indian physicians and thank you for having me. And I'm going to just cover the first part today where uh we'll talk about some food allergy of course and and and has already been said the the risk stratification for the peanut allergy. So to jump right into it and to be respectful of your time, she's already introduced me. I uh my background is in ENT as well as in allergy. And the point of all of this, let me just level set that part. The point is that you know we know that patients have over reporting of food allergies whether they've diagnosed themselves or someone has diagnosed them and we don't want to be adding to that by by misdiagnosing patients who are truly not having food allergies and this is where the whole allergen as well as those components come into play and they come into play because the uh you know I'll give you the bottom line up front and that is that the the um when we're talking about risk stratification we know that the components actually dramatically increase that specificity for our patients for the risk of peanut allergy. So keeping that in mind, this is how we usually do it, right? This is how most folks practice the med practice allergy medicine. And we do that great clinical history first and after that clinical history, we then have a pre-est probability, get the whole allergen. And once that whole allergen, in this case it'd be peanut. Once that whole allergen is ordered and if it's positive for the whole allergen, you could reflex over or order it separately all of those components. And what that's going to do for us is ask about uh making that the decision if we should have an oral food challenge for that patient or if we should put take them off that food with a diagnosis of uh of peanut allergy. And that's real the personalization of management for those patients. So I I want to use a different analogy just to level set for everybody who are not real familiar with components. I just want to level set to say that um another disease state like cholesterol. If you do a history in a physical on a patient who is at risk at risk for cardiovascular disease, you can do a total cholesterol and it will give you some information.
But if you take that total cholesterol and break it up into its components, the HDL, the LDL, the triglycerides, the apoloprotein B's, you get better decisions. And it's the same way when it comes to components. You can get good information from the whole allergen peanut. You can get some information, but if you break it up into its individual components, you get better information. And these are the components that are peanut components that are available in India, the ones up here on the right. And then you also have the birch pollen, the betu, which is the proofline over here. And we'll talk about each of these in context of how they are used. So the buzzword we always use for peanut is cross reactivity because we know with cross reactivity that uh some of those components are not necessarily species specific to the peanut and they are more cross-reactive to other plant species because there's those components that are in other plants such as the birch and other ones too that we'll see with the profilin. So when you take that whole allergen peanut, break it up, it gives you great improved decision- making. And the way to really show that again, but before we jump into it is if you can see these circles here each represent that whole allergen. You can see over here the birch pollen and the gray is one whole allergen and in the middle the peanut ho allergen for peanut and then over here in the peach is the ho allergen. You can see that they share they share certain components. And how we look at that is that this dark blue component will cause both the peanut and the peach to be positive on the whole allergen. And this light blue one here, the PR10 would cause the whole allergen birch as well as the peanut to be positive. So keeping that in mind that when we get our ho allergens back and we get that positivity back, it could be species specific to the peanut like the red ones here or it could be something that's just cross-reactive and as a shared protein. Now is cross reactivity common? Absolutely. Is very common and we know that there's lots of studies out there. This one was published in the journal of allergy and clinical immunology. And what they did was they just screened a bunch of patients and the numbers that came up was pretty high where patients who were screened were positive to IG to that actual peanut.
But when you actually did food challenges on them or detailed history and they have been eating peanuts without any problems, it turns out that 3/4 of those patients who have whole allergen peanut positivity, whether or not that skin prick test or or the blood test either one are going to have a higher number. And in this study, 77% 3/4 of those patients were not allergic to anything. So keeping keeping that in mind, not allergic to the peanut at least. So keeping that in mind. So these are the available components as I showed you on your a moment ago and these are the ones we'll cover real quick. And the best way to cover these is using what we call a risk ramp. This risk ramp here as you can see lists out all of the components for peanut. So the peanut if the whole allergen is positive it should reflex over to these up here. And we'll start over here on the far right on the storage proteins. As you can see on these storage proteins, if any one of these four come back positive and the higher the number, the more likely to be a problem or more likely to cause a systemic reaction. You can see that all of these components are storage proteins. They're species specific to just the peanut. They're stable to heat and digestion and they are associated with systemic reactions. So, we consider those to be the highest risk ones and those are RH1, 2, 3, and six. And we'll talk more about that in just a moment.
And as we go to the left, you can see the lipid transfer protein, which is also a peanut component. This one is stable to heat and digestion, and it's associated more with just some itching around the mouth and some pollen, food, allergy symptoms, but a real high number can can and in some cases can cause a more systemic reaction. And it kind of sits in the middle between the high-risisk ones and the very low risk ones. But rarely will you get it back completely by itself. Usually if you get a RH9 back, you'll get something from one of these categories over here or something from one of these over here.
But really, you have to rely upon your history and how that RH9 would fit in to that diagnosis. And as we go to the left, you can see the RH8. Well, that one's very labeled at heat and digestion. this RAH8 another component the one that we consider to be um more associated with birch pollen and pollen activity for cross reactivity is the RH8. So if a patient has this positivity to this one but is absent one of these over here and the storage proteins then you can you can have a high index of confidence that that patient perhaps could pass a food challenge and would not necessarily be truly allergic. And the last one we'll talk about is the prolin. The prophylin is way over here and prophylin is in many many um many plant species and because of that we know it's in lots of plant species and you can have a uh uh that bit2 the profilin you can have that positivity and in reality it is nothing but just just some cross reactivity from some other plant species that is out there.
So, how does this look when it when you actually plot this out? When you plot this out on a a raw curve, you can see where the sensitivity and specificity is actually um uh plotted out for us here.
You can see that when you plot out that sensitivity and specificity that RH2 is way up here. So, it is the strongest predictor of clinical activity. RH2 is well known, wellstudied, and well accepted um as as uh something that is going to most likely and I say likely because we're talking about allergy and everything's a likelihood and a probability, but I will say that it's very very likely. Same thing with one and three. You can see it's up here in the left side of that rock curve. And then you can see on the same time that RH9 and 10 are not are predictive of not having clinical reactivity. And then over here we have the RH6 on this other rock curve of the RH2. So this is all just to show that the confidence that we have in those storage proteins, the 1 2 3 and six is pretty high that is going to have some clinical reactivity if it comes up positive. I'm going to put this into a case real quick and then I'll I'll turn it back over to the next speaker. In this case, we have a four-year-old male and he has a history of some eczema and acute reaction to tree nuts. not the peanut, just to the tree at H2. But then we did some whole allergen testing on our patient and it came up positive for walnut, pecan, and peanut. Now, we have in this case, we have a history of having a problem with tree nuts. So, we can fit that in for the walnut and pecan, but we have no history of any problem with peanuts. We don't know is this um positivity, is this something that we can fit into and make a diagnosis. So we have unclear history for our pre-est probability. So because of that we'll first get a whole allergen peanut. Whole allergen peanut came out positive is 10.3. So we know his history. We know he doesn't have a pre-est probability for peanut. But we have a 10.3 kilo of allergen per liter for the whole allergen peanut.
Fortunately we can put some components to help us determine is this something that could be concerning or not. Well, fortunately what or or what I should say is I'm going to give you three different sets of components just for the teaching purposes and for the seminar. The first set of components uh would let's say his components came back like this. You can see his PO components came back positive to RH1 2 and three not to six. And what's important to note is it does not need to be all four of them. It can just be one of them or two of them or or all four. It doesn't matter. But in this case, it came back positive on his reflex that for RAH1, 2 and three, which we know are the storage proteins and which we know those are very high risk for having a systemic reaction. So if this was his result, he would not be a candidate for a food challenge because he would likely fail that food challenge. Now let's take the same history physical and whole allergen and this time what if his components came back like this. If they came back like this with a PR10 proteins is just 5.2 for the PR10 the RH8 but he's absent anything in this category over here. If this was his result he could be a candidate for a food challenge because he does the likelihood is it's just birch pollen. The birch pollen is the cross-reactive p pollen. It's probably just birch. And he is not truly going to have a high risk of having a systemic reaction because he has none of the storage proteins positivity.
And the last hypothetical set of components was this. Let's say it's the same history and physical and his whole allergen was 10.3. Everything else was negative and it was all this profilin right here. Same thing. The risk is very low as depicted on our risk r. And you can see that it's way down here. And we can say, you know what, this profflin it's probably just some cross reactivity from some other plant. And we can blame that whole allergen 10.3 all on that proffin. So hopefully what I've been able to show you is that that these components right here, these components that are available as well as the proofline, the the the BETV V2, these components can really help stratify for your patients which ones are more at risk for having a true reaction or systemic reaction and which ones are less at risk. And the ones that we key in on, as I said, was the RH1, 2, 3, and six. But any one of these components can cause that whole to be positive. And with that, I don't think we're taking questions now. So, I think we'll just go on to the next speaker.
>> I think you're on mute.
Am I audible now?
>> Now, now we can hear you. Okay.
>> Okay. Uh thank you so much Scott. Uh that was an exceptional overview and understanding which peanut component drive true systemic reaction uh risk versus cross reactive sensitization is exactly the clarity that CRD brings to uh the diagnosis that can otherwise feel dangerously uncertain. So building on that molecular foundation our next speaker will take us deeper into the clinical reality specifically the fascinating and most often un misunderstood world of cross reactivity and panel allergens. Uh Dr. Tipti Pujari she joins us as our clinical expert on cross reactive sensitization a phenomenon that is far more common in Indian patients. Uh she is an experienced pediatrician and allergies based in Pune with over 20 plus 25 plus years of experience. She specializes in pediatrics, allergy and clinical imunology offering services as dinar at Mangeshra Hospital Pune and her own clinic in Pune. Uh her talk will help us understand why a patient is sensitized to one allergent source may react to several other others and how molecular diagnostics can unravel than clinical puzzle with precision. So over to you Dr. Deepti. A warm welcome. Please go ahead with the session ma'am.
>> Thank you Alka for this nice introduction and I thank you Dr. Deni Gupta and the ISAS team for giving me this opportunity. I hope I'm clearly audible and my screen is visible. Okay.
>> Yes ma'am.
>> Sure. So uh I would request everyone to please stay with me. This is a huge huge topic. Pan allergens mean I'm going to take you through all the allergens and tell you try and explain what is the cross reactivity between all of them. So it's a huge topic. I hope I do justice to it. So what is pan allergen? When we say uh panel allergen, what are we talking about? So uh panel allergens are structurally similar proteins shared across unlimit unrelated plants and foods. They cause IG mediated cross reactivity. So here I've shown you this diagram. As you can see bet V1 it's a birch polar. Okay. And down through AV1 is cherry. Now cherries are fruits and birch are pollen from the trees. The body gets confused. The IG gets confused because looking at them closely they almost look the same. Even our eyes cannot differentiate. So even the IG's cannot and the IG's get confused. If a person is allergic to birch polands and sometimes he or she they eat cherry fruit the body is confused the IGS get confused and we react to cherry fruit also this is called colon food allergy syndrome or cross reactivity so now coming to pan allergens there are so many p allergens uh plant pan allergens are prophylins PR10s polins non-specific with lipid transfer proteins and then animal pan allergens there are tropomyins lipocans parvelments serum elbumments and the newer ones on the block are cyclopilins let me quickly go through it and I'll only try and emphasize the most important points that are clinically relevant to all of us okay so profilin can be considered as the archetypical pan allergen why because it is present in almost everywhere as Scott was saying it's present in almost all ukareotic cells so it is archetypal pan allergen fel2 okay is highly cross-reactive profilain of phylm pretense now phylm preins is a grass timothy grass and it is represented as felp 12 and felp 12 is a pan allergen from the profilins group okay as a rule now Remember this point very important point as a rule profilin sensitization follows sensitization to primary major allergenic colon source. Up to 50% of colon allergent patients are sensitized to profilin. What does this mean? So it is very rare that you will find someone only allergic to felp12.
Mostly there is a primary sensitizer.
And what could that primary sensitizer be? It could be felp1. It could be cyanodactylon one. It could be you know any major allergen sensitization is primary then follows your fel12.
Okay. So it mostly follows primary major allergenic source and these are all your profilins. So can you see timothy grass felp phylm pretitins felp 12 is the prime uh pan allergen of this group but uh pet v2 birch then hazel there are so many of these uh your uh weeds grasses wall pelletary your trees so many pan allergens are present and then they can crossreact with so many of the fruits your apple maldi P4, pro P4, peach, pear, pelon, kiwi, celery, carrot, or orange, you name it. And they are crossreacting. Why? Because they are minor allergens. They are present everywhere. So they tend to create not much of a havoc. Okay? They will mostly create minor symptoms. So cross reactivity between profilins from different. So the point what I want to tell you is so uh this is your timothy grass uh felp 12 but the tomato can also react with peach it can react with melon melon can react with peach melon can react with your hazelnuts it can react with celery celery can react with this with peach with tomato with grass grass can react with tree can react with it is so difficult so you are not supposed to Learn once you come to know that your profilins are present you will try and find out what is the major allergen primary sensitizer and you know they can easily crossreact with each other they are minor allergens so the reaction won't be too great okay so what is the clinical relevance as plant food allerg 50% sensitized may have food allergies oral allergy syndrome in most cases raw tomato melon watermelon so mostly They cause reaction when they are eaten raw.
Processing the food, it de denatures this profilin protein and it is no more allergenic. So patients tend to tolerate processed foods. Profillin cosensitization to lipid transfer protein or seed storage protein decreases the severity of reaction due to lipid transfer proteins and seed storage protein. So profilen dampens their reactivity. Okay. Okay. Now very important profilin and um latex allergy.
So NRL contains natural rubber latex.
Profillain that is have B8 heavier breances is the latex that scores often positive with multiple poland sensitization. Why is it important?
Because we as a doctors especially whoever is staying in the hospital, doctors, nurses who are coming in contact with lot of latex gloves or instruments or a CP patient who is having lots of tubes or spinobipida patient where latex exposure is lot then we tend to see this. It is called latex fruit syndrome. So if you are allergic to one of these latest products that are seen on the left side, there are 35% chances that you will react to one of these profilins. Okay? Either your kiwi, peach or chestnut, banana, avocado, papaya, tomato, raw potatoes, and your figs. And if you're allergic to one of these fruits that are mentioned on the right side, there are 11% chances that you could react to latex also. So 35 versus 11. There is lot of cross reactivity between uh heavy B8 and your profilins.
So immunoap specific IG thermopisher has these uh profilins in their um current currently available that is felp12 bet4 that is your birch pro4 that is your peach and heavy B8. Now Alex has some more 4d2 that is date palm and enlel mercury and melon. So this is your Indian nettle. Okay.
Uh now that we know that profilins are very minor allergens and even Scott had said the first one was profilin hardly any reaction to peanuts. Moving to the next stage your PR10 like allergens.
Okay. So there the primary one was felp 12. Here the major birch colon allergen is bet. This is your birch pollen. Now PR10 is really freaking me out friends.
I'll tell you why. As we move in the uh slides, I'll tell you why it's really I know quite annoying group uh because the primary sensitizer itself is bet v1 perch tree hardly seen in India only in the Himalayan belt. So I don't know all those slides that I'll be presenting are they relevant to our scenarios. Okay. So now bet1 is the archetype of all um PR10 allergens and is the primary sensitizer in birch pole and endemic regions which it's not our case. So testing for bet one is spec enough for IG sensitivity and other allergens other faggels are beaches, chestnuts, oak and so on. None of them are you know so relevant to our country. Now they crossreact with rosacei fruits and birch related or oral allergy syndrome is very common. When I say this what I mean? So these are all the Poland allergens of feals uh family here. Can you see Between one then that there is elder hazel hornbeam beach oak saw to oak holly oak Mongolian oak. So that's why I feel this group is really really not suitable for our country. We don't see all of these other than in the Himalayan regions. So these are all the crossreacting plant colons. They can if you are allergic to birch you might well react to hazel colon also. And then these react to your uh fruits. And again most of these fruits you know like green kiwi, golden kiwi, raspberries, pears, peaches, cherries, apricots, these are not our Indian fruits. But as Scott was saying see peanut era H8 it's a mild allergen. PR10 are mild allergen. So if Rih8 is positive, you don't know whether it's just the sensitization. You would want to give a challenge to this patient. Okay. So these are all the cross-reacting fruits. So your birch is the primary allergen and so many crossreacting fruits and foods are present in this PR10.
And why there is so much of cross reactivity? Because can you see this mild one? This is your apple. This is fry a one, apricot, peach. They all look so alike. Your soya, your um peanuts, they almost looking the same. So your body is confused. IG is confused. It keeps crossreacting to one another.
Okay. And this is I've taken I saw to it that copyright issues were not there.
And I've taken this from Google and look at it. It is present in clinical and transitional allergy. Profillin is a huge group and so is your bet 1 PR10 so much of cross reactivity going on so it sometimes can be really really confusing it is also called mirage of allergens and cross reactivity you are confused you don't know what is the primary sensitizer which is the secondary is it true allergy cross reacting and that's where your you know if you are having profilain positive in your component resolve diagnosis you know most likely it's a minor allergen cross reactive not a primary allergen if your PR10 is positive you know it's a mineral minor allergen cross reacting and mostly not primary so this is the beauty of your uh component result diagnosis so this is what I'm saying this group is really freaking me out in fact we are uh thinking of collecting our own data I would like to speak to alcohol also regarding this I have already made excel sheet look India is screen There is nothing except for this small Himalayan belt. There is nothing. Look at here again. Betw we homologous plants. It's we are absolutely clean and we keep saying cross sensitivity primary sensitizer. We need to have our own data. So I've already made Excel sheet.
I've started collecting. I'm going to do it pan India. One person presenting a data doesn't make any sense. We have to come together. We all Indians who are doing this. We need to come together, pull our data, see what are our pan allergens, what are our primary sensitizers, what are our major allergens and we need to go ahead from there. We are in the process.
So potential symptoms as we know of cross reactivity, let's skip this slide quickly. It could be just mild itching of the oral mucosa, nasal irritation or it could be some sneezing, throat irritation, swelling. Sometimes it can go even down and it can cause breathlessness or whole body might react and it can lead to anaphylaxis also very rare. Okay. So this was your oral allergy syndrome. Mostly it is local oral because by the time the allergens reach the stomach the acid denatures it and they become non-allergenic.
Okay. So conclusion on clinical relevance sensitization to PR10 like allergen bet 1 and its homologous proteins in Poland's from faggels tree species occurs worldwide except in South Africa and tropics can you see tropics comes here even forget tropics in you know all those Nordic countries your bet is so high and your PR10 is all positive you come down slowly little down in Spain and Italy your bet one is gone. It all all your felp 12, Felp 7 and CND. So mostly only in your Nordic countries up there northern Europe you get PR tests and tropics of course we don't have it.
We need our own data for sure and we are in that process. Whether imunotherapy with tree polar it's the golden million dollar question whether imunotherapy with tree pollen extract has beneficial influence on associated plant food allergies. Nobody can give you one right answer. Nothing uh there are so many studies and research papers I was scanning. Some studies say if you treat the primary sensitizer there is definitely some benefit in the uh crossreacting allergens. Some studies says no there is no not much benefit. So it's all up to the individual. So again let me put one thing very clear. There is no right or wrong answer when we are dealing with pan allergens cross sensitivity in general allergy as such you know it is more individualized practice. It is onetoone practice. How comfortable is your patient? How comfortable are you? But if there is major colonel eleation and it is causing lot of allergy and there are major cross reacting allergens to it then yes imunotherapy to primary allergen may help in reducing the allergenicity of the crossreacting allergens. Okay. But not all the studies have said this. They say no it doesn't work.
Okay. Now coming to some very very important non-specific lipid transfer protein. This is stronger allergen than prophylins and PR10. It's plant food allergen in southern Europe. Now we are moving slightly down from northern Europe to southern Europe. So uh the clinical reactions can be systemic and severe. Okay. For prophylins and PR10 it was mostly oral. Here it could be systemic and severe. Pro P3 is the major allergen of peach. Okay. And plays a precursoral role in the sensitization of other NSLTPs.
So peach is considered the major allergen and it is very heat stable. Now mind you this is again from southern Europe more of Italian and you know Spanish countries are seeing this. In our countries, I have seen my patients having NSLTP positive without peach sensitization. Okay. So again, this doesn't hold absolutely true for our country.
So these are the you know big list as I said prunus pera c3 is the major sensitizer in our country. I feel maldi3 you know malas domestica the apple is more relevant. Then can you see your peanut your aracus hypogia era H9 is the uh cross-reacting food. So yes as Scott was saying H9 can sometimes have oral allergy syndrome or it can sometimes give severe anaphylactic reaction also because NSLTPS are stronger allergens compared to your PR10s. And here again you see latex he have B12 and there are so many again here there is reweed mugward volator olive again name itself oolia Europia we don't see olives olive again is a sensitizer in nsltp not relevant to our countries so this is all the peach is the primary sensitizer and there are so many crossreacting uh allergens even latex plays an important role here.
Now some very important facts about LTP clinical reactivity. I said it could be mild to severe analysis. Okay. Now co-sensitization with PR trend and profilins decreases the allergenicity of NSLTP meaning what if you are allergic to suppose RH9 is positive but in that same patient if some PR10 bet 1 is positive there are chances that this RH9 reaction would be less severe okay so co-sensitization with profilence and PR10 reduces the allergenicity of LTP P and one very interesting point in NSLTP co-actors.
So there is a possibility you are eating peanuts with RH9 positive and you are fine but suddenly you have high temperature viral infections you are stressed you have taken some uh you know your non-steroidal anti-inflammatory group of drugs you might suddenly react to your peanuts. Okay. So, co-founding factors like your uh you non-steridal anti-inflammatory, stress, exercise. So, you eat you are eating your peaches and your apricots and you're fine. But suddenly you eat your peach and you exercise, you might throw up a huge reaction. So, this is very important.
Fever, alcohol, stress, NSAIDs, all these can trigger the reaction to NSLTP.
Okay. Nuts and cereals. Now oral allergy syndrome to s severe systemic reactions in LTP sensitized patient. And what are these nut groups? Walnut, hazelnut and peanut. Wheat, maze and rice can also cause this. Okay. So some cereals, some nuts are also cross-reacted.
At present there are nine different NSLTP available in iminoap and some 15 inx2.
Okay. And the respiratory allergens that are present with thermopisher are your par 1 o 7 art that is your artisia and pla that is wall pelatory and ks that is your cannabis.
Now I'm warning to all the doctors who are listening this alternative sensitization route marijuana inhalation that is your ks3 can cause severe nsltp.
So please if anyone who's taking maruana stop it you can throw up a severe NSLTP reaction because this is now also being considered as an alternative sensitizer in our country specifically down south Europe and towards the tropics African countries where um peach is not the main sensitizer. Okay. In areas of heavy pollen again olive pollen is not um very much in our country. Ole A7 is also considered as a primary sensor. So we have peach, we have marijuana and we have olive olive. Okay, these three are considered primary sensitizers. Peach is no more a single primary sensitizer. LTP are present in all vegetable tissues and can always be ideological proteins in vegetable mediated allergies. The situation now again an important point the situation for each single food should be evaluated before its exclusion. Now you cannot just because some NSLTP is present you cannot exclude all these foods. So if patient you see so many positive wheat is positive maze lettuce and peanut are positive you cannot stop all of them. You have to see individually give challenges and decide what you are going to avoid. Okay. So that is a must pan blanket statement should never be done. It could just be sensitization. To prove allergy you have to do challenges.
Okay we'll quickly go through this in 1 minute. P calcins they are marker for polyensitization extensive IG cross reactivity um colon p calcins and felp 7 G a 3 that is your chinopodium elbum and bet 4 are the primary sensitizers minor allergens in grass trees bushes weeds not present in plant food and they are extensively present simultaneous sensitization to poor calcins and profilins okay there could be longer duration of symptoms and more severe respiratory. So if pole calcins come with profilence then your reactivity can increase. Okay.
And these are all the cross- selecting polins from your polisonson family. And these are all the allergenic pole calcins. We'll quickly go through it.
Coming to very important group which is very relevant to us that is uh uh tropomy.
Now tropomyins are theostable proteins.
Okay. Because they are theostable their allergenicity is very high. Considered an inter uh invertebrate pan allergen.
High degree of cross reactivity.
Seafood allergy is also a sign because of them. Mite and esceris. Now ascarus is so common in our country. It also has tropomy. So look at the big list of tropomy. And can you see here derpy 10, durf 10, bluy 10, uh, blah gi 7. These are all our housees, cockroaches and then your giant tiger prawns, pen m1, pen a1, shrimps, all these are cross-reacting allergens. And when I say crossreacting, this is the whole group.
And the ones that are in the inner circle, the gray ones, derpy 10 and all bloated and these are all your tropomycins. So your house dust mite crossreacting with your cockroaches crossreacting with your tiger prawns. It could be all due to tropomycin your derpy10 and derf 10 and bloat 10 blumatropicalis.
Okay this is what I meant. So these are all have tropomyins and they keep cross-reacting with each other when there is uh uh this um the cross reactivity between you know the nondashed arrows is very high and the dashed ones have minor cross reactivity okay so why do they crossreact because I have shown the molecular models of tropomycin they are so so similar so definitely IG is again confused and it doesn't know what it is reacting to and so our body reacts to everything.
Coming to another group serum elbumins highly consumed sequence of high amino acid sequence identity identities maintained minor respiratory allergen of animal gender food allergen of milk and meat and allergen implicated in poor cat or bird egg syndrome again poor cat is not very relevant to us because we Indians don't eat pork a lot but boss D6 wine serum elbumin is the marker allergen and it is denatured by heat. The good point is it is denatured. So boss D6 causes respiratory allergen. It's a minor allergen in animal denders. So whenever there is in dender, it will be respiratory allergen and whenever it is in food like milk and meat, it will cause food allergy syndrome. Okay. So it has to be uncooked meat, uncooked milk because it is heat sensitive, heat labile protein. So chicken serum albamin gel5 which is present in egg yolk also is an inhalent and food allergen implicated in bird egg syndrome or egg bird syndrome depending upon the primary exposure. So these are again cross-reacting serum elbowins. We'll quickly go ahead and last but not the least seed storage proteins. Now these are considered to have severe reactions because they are very heat stable proteins and these are present in almost all the possible seeds. So there are three categories 2S elbomins, 7S globulins and 11S globulins. They are marker allergens for a clinically relevant sensitization to legumes, tree nuts and seeds. Okay. sensitization to them cause severe reactions because they are very heat stable. Now again you cannot learn all this but once you get the report as Scott was saying can you see Rh2 6 7 RH1 RH3 all your seed storage proteins they can throw a very severe reaction and can you see the cross reactivity huge the list is big okay so clinical relevance of 2s albumin can you see these dark um arrows so there is these are major allergens Peanut uh peanut tree nuts they can all cross react with one another. Walnut with peacon nut your cashew nut with pistachio and your hazelnut with walnut.
So these can all cross react with one another. RH2 RH6 your walnut jug R1 and your sesame ses 1 and two are the major allergens. So also your 7s globulins all the legumes including your soy pea lentils they all cross react and your ar1 is there. So again sealance globulin strong cross reactivity severe reactions because heat stable okay and all your peanuts can cross reacted with lupines peas sesame everything then your 11s globulins again seed storage pro present in high amount in hazelnuts and almonds and again a h3 corin from hazelnut and glyam from soya bean they all crossreact with one another So some facts IG cross reactivity can occur between the members of same protein family like 2s albumin amongst itself but it can also occur between different families of seed storage protein like albamine cross reacting with globuline 11s cross reacting with 7S globulin. Okay. All allergic uh symptoms which are elicited by IG binding to these allergens can reach to mild oral itching to lifethreatening conditions like anaphylaxis because they are severe proteins heat stable proteins. Last I thought I'll quickly put a word about cyclopilins. They are new proteins pan allergens on the card. They are phoggenetically conserved ubiquitous intracellular enzymes that function as cross-reactive panel allergens share high amino acid sequence homology across distant species.
They are present in fungi and molds like your Malaysia Mala S6, your asperulus SP F11 also present in colon like your bet 7, plain tree, reweed, foods like carrots and RH18 peanuts. Now clinical significance autoimmunity is seen because cyclopilins are highly conserved. Fungal or environmental cyclopilins can exhibit structural similarities to human cyclopilins in severe conditions like chronic aminotopic dermatitis. These proteins can act as autoallergens and perpetuating inflammation even without exogenous exposure. So this is very typical for these cyclopilins. They can cause autoallergies and you need not even need any other exposure of outside allergen. Polyensitization is there because they are broad and they are almost pan. For example, a patient sensitized to fungal cyclopines might may experience cross reactivity when exposed to unrelated polons. Okay.
Including at least one cyclopin in multiplex test is deemed necessary for comprehensive assessment. So my take-home message is pan allergens are responsible for wide algae cross reactivity between related and unrelated allergenic sources include reactions between various pollen sources, pollen and plant derived fruits, invertebrate derived or inhaled food. Sensitization to pan allergen can lead to multiple sensitization and may worsen the prognosis of allergy. Clinical manifestation of panel allergen sensitization are often linked to geographical exposure and exposure very very important geographical there's no point thinking of olive sensitization when we know there is no olive no birch here okay so very important you clinically correlate just sensitization is not enough because pan allergens will be positive in many cases palerent can cause false positive that's exactly what I was saying false positive reactions in both vivo and Vitro food allergies associated with pan allergen generally follow respiratory sensitization involve lower allergen doses and rarely pose life-threatening because they are mild. So primary sensitizer is mostly respiratory allergen colons component resolve diagnosis can help in distinguishing cross reactivity from primary sensitization and these are my references I have not put in all the pages I have collectively kept them.
Thank you so much for this patient hearing and giving me this opportunity and and thank you so much ma'am. Uh thank you so much Dr. Deepti. A genuinely eyeopening talk and the concept of pan allergens and how they explain so many of puzzling uh sensitization patterns that we see in the patients is something every practicing allergist and iminologist needs in their diagnostic toolkit. So now we move on to the final presentation of our series and perhaps the most clinically actionable segment of the evening CRD in precision allergy management. Dr. Vikram Patra, senior pediatrician and allergy practitioner from Mumbai and co-founder of ISAS is here to bring it all together. Uh showing us how everything we have discussed tonight and across this entire series translates into real clinical decisions. who needs an oral full challenge and who should carry on auto injectors and how we counel families with precision instead of uncertainty.
So Dr. Vikram the floor is yours now sir over to you Dr. Vikram.
>> Thank you Alka for the nice introduction. Uh thank you Isas and official for this for bringing out the CR2 after last year's success. The CR2 is also getting hit. And um let me start and go to my slides.
I hope my slides are visible.
>> Yes.
>> Yes sir. Yes.
>> Yeah. So till now we have been uh for the last three sessions and today also when Dr. Dipy mentioned about various cross reactivity we learned about various pan allergens which are present in various pollen groups various food and pollen groups. So we are bound to have false positive results when we entirely depend on the aquis whole extract uh testings like skin brick test and and the serum serum IG what we do um on serum specific IG we do invitro test so that there comes the role of CRD now my job is to highlight and um concise everything what we learned how it can help in our management ment.
Now precision medicine, we talk about precision medicine in every field. Now precision is no longer optional.
As we know now crude extracts blur the clinical picture despite our strong clinical history. We may get confused with uh crude extract reports leading to misdiagnosis and not only misdiagnosis unnecessary dietary restrictions and failed allergen imunotherapy. We'll talk about that.
Why? How we fail? So the extract illusion because India is a diverse arrow allergy and high endemic exposure is there creating IG cross reactivity.
Now when we are testing whole extract our IG is reacting to the whole allergen as such but we know the allergen itself is composed of major allergens, minor allergens, pan allergens and to increase our trouble we have CCDs.
So component result diagnosis provide the essential molecular clarity required to confidentially stratify risk and select the definitive therapy for every patient and it helps in isolating genuine specific marker allergens to dictate precise allergen imunotherapy as well as in case of food allergies proper dietary advice and management.
So the paradigm shift from diagnostic noise to molecular clergy. So when we are testing crude extract we can see here these allergens may have primary sensitizers. These primary sensitizers are high-risk allergens. Then we have spec specific minor allergensions. These minor allergens remember these are not the panelions. These are specific to the same allergens but not represented in the majority of the patients but they are also clinically relevant and significant. And then we have this cross reactive panel allergens which we detail which was discussed in detail. Now what why this happens because we have this molecular lexicon this primary markers.
Now we have primary markers for each and every be it be a food allergen be it be a pollen allergen be it be dust mites be it be cockroach every allergen is going to have some primary marker if that marker is positive that is suggestive of true allergy then we have this PR10ilins which are responsible for cross reactivity uh cross reactivity among various pollins and cross reactivity of between pollen and the food leading to the pas that is the pollen food allergies syndrome then the storage proteins and SLTPin and aluins all were discussed the three clinical pillars of molecular diagnostic is to differentiate this cross reactivity now here CD is going to help us and not only differentiating stratifying severity risk from the Dr. Scott's lecture we heard about various components of peanuts we once we know our request the whole extract test is going to say just peanut sensitization but when we do the components we will be able to say whether the patient will go into anaphylaxis or will have just oral allergy syndrome and then we can predict allergen imunotherapy efficacy are the days like previously what we used to say we used to say In 70 to 80% of the patient they respond to imunotherapy but and then how we used to conclude after one year of continuous imunotherapy if the patient used to response we used to continue otherwise we used to stop. Now whether we can predict beforehand yes predictability can be determined by knowing whether the major allergens are present marker allergens are present or no and by choosing the right imunotherapy allergy.
Now go through these two reports. Uh you can see um though it's a busy thing but you can see different pollins when this imunotherapy was ordered. You can see the imunotherapy while it it is mixed with this dashmite 1 ml uh amaranth.5 ml cannabis sativa 1 cyanodon dactyl in.5 reinous communist.5 then so so I'm not considering the mixing I'm not talking about the mixing whether they are suiting they are suitable mix or no but I'm just talking how this polymixing of the allergen is going to help. So, so you can see weeds are there, grasses are there, trees are there, all these are mixed the just because the skin prick test came positive for all these allergens and just imagine taking.5 ml of cyanodon in a 5 ml while vial of a sublingual imunotherapy how much it is going to help. So what we are doing we are diluting. So the this is the most common cause of therapeutic failure because unnecessary allergens into the vial it cause the dilution the maximum therapeutic dose is not delivered to the patient. So here comes the C's role where you can choose and do monotherapy.
So we always discourage polytherapy monotherapy should be done and CR is going to help in case of polyensitization.
Now dissecting the hierarchy formulating the aid. Now just skin prick test is showing various wheel sizes. Now here also this is a patient where sensorization was found to grass weed and house mites also the first report what I showed. So what when when we did the CRD the values the higher the values the more is the likelihood of having sensitization or clinical relevance. So while selecting we can have the mixture in this proportion only. So this is how we can prepare and deliver a proper AIT while V to a patient. Now why this confusion is there? Because in our subcontinent India is a large country where we have different climatic areas though we call oursel as a subtropical country but our Himalayan belt and northeast states it's like a temperate area. So there the flora and fauna are different and the coastal area is different and the decle is different and this all leads to various cross reactivity and confusion what to do and which one to be selected in our imunotherapy.
Now there are regional variations also northern India will have different polands central eastern and southern India will have different polins. Now common to have it in a nutshell this is a table which tells us common allergic plants of different seasons in India.
Now we have not only the geographical distribution we have um the seasonal distributions also and then we can see there is overlap between grass weeds and trees in a particular season. Now here is the main confusion. If we depend only on the clinical history and the whole extract test, we may get confused because everything will get come positive in that particular season because we say if grossly we say if the symptoms are more during uh say January to April May we consider around pre-allergens and monsoon post monsoon we think about grass and wheats but there will be confusion if there are they there are there there is cross reactivity among them. So what we are going to do we are going to mix unnecessarily the grass weeds and trees allergen in the same while V.
So the diagnostic mirage of this polyensitized patient. So the our clinical dilemma is are we seeing genuine severe multi-specy sensitization or a clinically irrelevant cross activity. This is the decision what we need to make before prescribing imunotherapy.
So why this no noise is there? because already Dr. We mentioned about this cross reactive agents. These are profilins, CCDs, PR10, polalins and then gibbereline regulated proteins driving severe food pollen syndromes. This is one group which is less top down. Now here the component resolve diagnosis is going to filter out this pan allergen noise. Why we get false positive? You can see the profilins they are present in the grasses the poetic group. The estasia weeds like mugwart, ragweed, parthnium in our country. Then desert weeds like amaranthsia.
Uh then faggal trees like birch oak all all of these are having this profilence.
Poly calcins are present in grasses and weeds and PR10 is present in particularly in the birch tree and PR10 is present in weeds now and food items also and CCD is present everywhere. Now when we are talking about birch Dr. very well mentioned that the bush we are not exposed to burst tree but is it only the birch which is giving us PR10 we don't know we need to have our data but it is seen that PR10 is present even in this estia weeds parthnium holoptellia group from the trees they also contain PR10 we may get sensit because we generally we all will agree that in our reports we are getting PR10 sensitization and we are not exposed to if you ask the patient He will say he has never visited Himalayan belt. Still PR 10 is posture. So maybe these other allergen allergen sources are responsible for sensitization.
Now how should be our approach? So if we are getting poly sensitization to pollen of trees, weeds and grass the next step is to check for if we get a the CRD multiplex is considered in such conditions where you get polyensitization.
Now serial IG to allergen specific to primary sensitizer. If we are getting primary sensitizer in our CR report or we are getting specific IG to pan allergen. This is going to tell us whether we should go for AIT or no. If it is specific, yes, AIT is going to help. If it is positive to polyalcine or profil it is explaining the reason for polyensitization and it is not going to get modified with the AIT. Now if profylins as well as the marker is present marker or the major allergen of a particular pollen is present then you choose the pollen. This profilin the sensitivity is just because of the profil component or the policy. Now the major tree allergens what we have is faggels elder beach birch hazelnut oak.
These are present in our Himalayan bells. Then we have um this fees group the acesia posis these are desert plants which are present in our Indian plains also then we have olesia group though we don't have olive but I'll show you we have olive cross reactivity the markers the sensitizers are different for olive olive one uh then when we talk about this group the bur group the PR10 is the major allergy and this is responsible for various oral allergy syndrome when it comes to cups group the cup A1 reactivity is the specific marker olive pollen allergy is caused by O E1 sensitation in about 70% of the cases and it has got cross reactivity to various other problems I'll show you that table then we have platinia group PLA A1 and PLA A2 may serve as a marker for primary sensation to plane plain tree poland now we don't get the typical bulisa bed but we have this bula utilis bhpatra it is called as in hindi it's there in our himalayan belt then cup these trees are seen in the himalayan belt this belong to the order penels now group PR 10 elder the beta vicosa then the hazel all these they crossreact to this PR10 then coming to tropical countries. Now as Dr. Let me mention whether those are interesting to us but these are interesting to us. Proves Julifura Flora and Aacia bubble tree this group they are present in our country. Do we have representation in our CR? No we don't have but pro Julie flora if you go through it's and eacia you can see the markers the major allergens proj and echa F1 they are only E1 like protein family members. So that's why in our patients though they are not exposed to olive tree are only E1 comes positive because we are exposed to procase. So if you are getting sensitization for proopius on your skin praches the chances of having this component in your C is more.
Then this plant platinia this group is PLA A1 is not there but sometimes in the C it may come positive because this LTP is also there A3 it is again NSLTP group from PH. Now algorithm for suspected tree pollen allergy when it comes monor reactivity to any tree directly go for deunotherapy but poly reactivity is seen to profiline or poly calcin of any of the pollins then no ait is suggested and if you get poly reactivity to plant or olive tree you go for a if lt is positive like ply a3 and e7 then no aid is suggested for sensitizations Now coming to glass polizations these are again temperate glass flippy 1 2 and flippy 12 may compost you because of the profiling but what we get in our country is sin D1 that the bermuda grass and most of these grasses they react with each other because of the profilene component but if sin D1 is present it's a true sensitization to this and we should go for we should go for allergen imunotherapy against is now the sign D1 is present in our multiplex as well as single plex.
Now this is the diagnostic algorithm for suspected grass pollen allergy. Uh if now previously we used to have if we are importing some allergens we get grass mix. So that contains me this flippy the flappy one is present or grasp and aid we should go for if this flippy 2 5 11 are present then you should not go for a if flippy 12 is present it is suggestive of cross reactivity.
Now coming to weed pollen allergens. Now weeds are very common ragweed ambrosia is not present in our country but we are the parthnium and ragweed they cross they have structural homology to each other we have mboard artisia russen thistle and English plantin are important in summary but in our country what we are more important for us parthnium is the most common around 40% of our population is sensitized to parthnium and mward artsia group now when we are talking about um the Cross activity you can see this ragwid ragwid sunflower mugwart and the parthnium all these belong to estratia group whereas this wall pelatory and the this is the artigasia group now articia group remember this paria the p j two it is there in the component but in India we don't get wall pin for decoration purpose Some places may have but it is not the name for our country.
What is new to our country from this group is holoptalia. We are getting holia sensitization very much common in our country and then you don't have any component for whole I but the if you are getting par2 that is that has got structural homology for the holoptalia then we have amaranthia group where zopodium amaranthus and Russian thel they are present now Russian thel again is a desert not native to our country but again if if our patient is sensitized to amar and thus group or synopedium group in the C multiplex you can have the sal positivity.
Now very interesting this artisia and parthnium they cross with with each other and when it comes to selecting the imunotherapy if RB1 is present then we should go for artisia we should not go for parthnium.
Now you can see ambrosia a that is the ragwid it is the mainly pactate lias it has got cross reactivity with artamesia 6 and sunflower when we talk about artisia group it has got sensitivity with parthnium and ambrosia so your skin page when you are testing your artsia will also come positive and parthnium will also come positive but on ctv1 is present and RH1 is not present you should go for only monotherapy with artificia we need not mix both this in our imunotherapy and LTP we have artimesia v3 now artimia is a we which is commonly present in our country now when it comes to nsltp we don't have peach it is a meditarian area now as Dr. Dr. was mentioning we have to search which is the primary sensitizer sorry primary sensitizer for LTP in our country. So is it food or is it is uh the pollen source for LTP. If it is the pollen source now your CRD will show RV3 positive and RV1 also positive along with positivity for your legumes. then you can think of and obviously you will look at the titles also the values also but if RTV RV1 is positive and RV3 is positive then you know the sensitizer here is a pollen but if your legume LTP is present and RV3 is positive but RV1 is negative then there is always a debate food allergens can also be a source of uh LTP so the legumes itself can be a source of LTP uh sensitive ation.
Then only one as I already mentioned this only one is crossed with a centisel protopius and aca group.
This is a flowchart diagnostic algorithm for suspected weed pollen allergy. IG regid the patient with say respiratory allergy having skin page positive with mugwart as well as parthnium or ragwid then you go for serial specific IG. If both are present you look for the specific component or the major allergen. If RV1 is present then you go for primary mugwward imunotherapy. If MB is ambrosia is present then you go for ambrosia. In our country if we go for par we will go for paranom and if both are present then co-sensitization true cosensitation is there then you can mix.
So uh the C decision framework for colon AIT step one multiple positive extracts then only gets it gets confused and then you have to look for the panel allergens and artifacts like CCDs. Then step three is to isolate primary spec specific markers RV1 sodium D1 PH in parthnium and BV1 etc. and then check for the homology as I was mentioning about the homology structural homology for our country aspect and then formulate highly targeted highdose single or at the most dual spaces ait never go for polyther therapy. So to conclude the pillars of precision allergy, it differentiates genuine versus artifacts.
It prevents AIT dilution. My main purpose of this talk was to prevent AIT dilution and that gives bad name to imunotherapy.
Then it simplifies the prescription. You are not confused to which one you should select. And when it comes to food or legumes, you talk about the systemic risk. LTP, GRPs hiding uh behind respiratory uh symptoms and then it ensures allocated imunotherapy is developed only when true primary sensitization is confirmed maximizing clinical success. So the paradigming shift is we should understand extract shows what might be happening but component resolve diagnostics explains why it is happening. So in a in an ecologically diverse environment like our country with overlapping flora and high invertebrate exposure shared is not an academic luxury. It is necessary for precise risk stratification. So our transitioning from guesswork to precision imunology is the key. Thank you.
>> Uh thank you so much Dr. program uh truly comprehensive and uh clinically grounded close to our presentation segment this evening. Uh now we move on to the part of the evening that is very I personally look forward to the most that is the panel discussion. So tonight's discussion will be moderated by Dr. Kashapi Nagaraju a prominent consultant allergy specialist and Eert surgeon based in Chennai known for her expertise in diagnosing and treating complex allergy conditions who brings both clinical depth and sharp instinct for the questions that matter most to the practitioner on practitioners on the ground. So to our audience please drop your questions in the chat uh we we are watching and we will route them to the panel. Dr. Dr. Kashapi over to you ma'am.
Yeah. Am I audible and my slides are visible? I hope.
>> Yes ma'am. Yes ma'am.
>> Excellent. Okay. Um good evening at the outset. Thank you so much Dhama Fisher and Tis uh for this wonderful initiative and uh I would not say need of the hour it's it's need of the next decade I would actually say for that matter. Uh so let's move on. Let's not waste any time. I'm sure uh everyone of you must have uh uh paid utmost attention to whatever was discussed today. Let us try and apply the same to a couple of case scenarios. Uh I have our esteemed expert panelists who are also our uh uh you know speakers today Mr. Scar, Dr. Dipti and Dr. Vikram Patra. So the first case uh is a 8-year-old boy Rishi who returns from UK where he was diagnosed with a peanut allergy after anaphilaxis. So he did have hives, wheezing, vomiting after consuming a a peanut butter sandwich.
The parents are now in Chennai. They've moved back and they want a clarity before they get him back to the school uh and get him enrolled. So the previous allergist has advised strict peanut avoidance and also to carry an epipen.
Uh the skin prick test uh to a peanut extract was found to be 8 mm wheel and the total IG levels were 420. Now the parents also report that Rishi reacts to chickpeas and lentils as well and so they are asking if he's allergic to all sorts of legumes and the the component result diagnosis uh picture of this patient is as follows. So RH2 that is to alamin is 18.5 Rh1 is 6.2 RH8 and 9 are relatively low and bet one is negative.
The first question would be to Mr. Scott. So given that the RH2 is quite strongly positive, do you consider uh this uh already a confirmed diagnosis or is there any role for a oral food challenge in this scenario?
>> Oh, thank you for the question. Uh can you all hear me? Can you hear me? Okay.
>> Yes.
>> Okay. Yeah. Thank you for the question.
you know, um, if we were to see this patient here in the United States, if this patient presented to us based on the fact that he has a strong pretest probability, he ended up in the emergency room, had some rescue drugs pushed, all those things, as well as the whole allergen and now with that strong RH2, I think that he is uh, very well diagnosed as having a true peanut allergy and would not be a candidate for a oral food challenge. I think that would be a a poor choice to present him for a po food challenge because he would likely fail based upon all the information.
>> All right. Okay. Uh Dr. Vikram Patra, so in India where chickpea and lentil are our staple foods, how aggressively do you think uh such a patient should be uh restricted or even a challenge has to be performed in such cases.
>> Mute.
>> Sir, you're on mute sir.
Yeah. Uh thank you Dr. Kashi for bringing out this practical uh question.
Now if you don't read the report thoroughly then we may get confused and unnecessary we ask the patient to stop many things. Now when it comes to chickpea and lentil you mentioned that the parents have started saying that they the patient react but we don't know what kind of reaction is it something severe or it's a mild reaction. So here now though peanut belongs botnically belongs to a legume group but the structural homologue to the other lentils and chickpea is rare to the extent of 5 to 10% only. So in such conditions if we are not getting strong storage protein for other peas and all this thing in the multiplex we should go for challenge rather than restricting.
>> Okay. All right. Thank you sir. Uh Dr. Deepti uh would you consider a peanut oral imunotherapy in this child especially given the high levels of RH2 in this patient?
>> Yes. So a very good question and a relevant question. Thank you Dr. Kashipe. So now I want to make one thing very clear oral imunotherapy when we give it is only to decrease the chances of analysis.
This one point I want to make very clear. We'll not go into the nitty-g gritties of oral imunotherapy. It gives you sustained desensitization.
So you yes I would give uh peanut oral imunotherapy because there are two three reasons. First this child is reacting very badly having anaphylaxis. Secondly he has come to India and now he'll be going to school. Our Indian culture is such that we share our tiffens. The children share their tiffens in the school. There are midday meal programs in the school. Teachers, the chefs in the school are not so aware like in the US and the UK. So here they'll say no, we have not put peanut. But even if you're some person who is very allergic especially Rah2 even touching the spoon or using the same oil or the same pan can go give rise to severe anaphylactic reaction.
Okay. So for this very reason because this child has come to the new environment would be going to the school I would re really consider oral imunotherapy in this child depending whether I have the facilities if I don't have facility I'll send it to someone who is doing it. It has to be done in a controlled fashion following proper protocols. And here when I say oral imunotherapy it doesn't mean he can just take as much peanut as he wants. We bring it to a particular stage where he needs to continue taking that much of peanut every day and this is only for preventing severe reactions, preventing deaths, preventing anaphylaxis in an accidental exposure to peanuts.
>> Excellent. Excellent. Thank you Dr. Deepti. Uh Mr. Scott. So uh we don't really see uh a very high load of uh uh you know peanut allergies in India at least not yet. Uh it is definitely increased over the past decade but still so do you do you suggest any additional strategy strategies that have to be uh followed by the child to manage at a school level?
>> At a school level yes thank you again for the question. So um you know uh if you're not seeing very many of them in in uh in India uh it's just like Dr. Diffy was just saying, you know, the the the likelihood this patient is going to be exposed to peanut is probably pretty high with the shared utensils and all the the cafeteria, all the all the things they have. So, a you know, education for this patient is going to be paramount for the family and for the patient. They're going to need to be educated on not only what they can can do to avoid if they can avoid things, but what they do when something happens.
when something happens, how to recognize his own symptoms, what are his symptoms when he when he is exposed and what should he do at that point um and and he should have a rescue uh some some epi rescue. I'm sure you have that there in India where you have the rescue and uh shown how to use it and also shown and have some confidence for the family members as well as the patient confidence in being able to use that that uh rescue and then if the rescue if the EpiPen does not work uh then they need to know what's the next step and the teachers and maybe the administration would know the next step is to get him to the emergency department.
>> Got it. Thank you. uh just to summarize this uh I would ask the uh esteemed panel if the summarization is okay. So now that we have uh the tests and the interpretation the RAH2 confirms the peanut allergy. So there is a definite risk of anphilaxis. The RH1 confirms a severe allergy again true pinet storage protein. RH8 it is a non-pollen related protein. RH9 is it is definitely not LTP driven. So it is uh you know confined to peanut as well and there's no bud pen sensitization. Uh let's move on to the next case. Uh here we have a 28-year-old female which presents with tingling and itching in the mouth and throat every time she eats raw peanuts.
Especially we use uh peanuts as ground nuts here in uh in making chutneys and uh you know uh dips and all. So she notices similar symptoms uh when she has apple, peach and rock carrots at at time two but she has never uh ever given a symptom of systemic reaction as such. So she has also never reacted to a roasted peanut either a roasted uh delicacy that we eat here called shiki or even to a ground nut oil. And she is actually a gardener and she does have chronic rhinitis symptoms which go worse during the season of spring. Uh so the uh skinflick test was P for peanut was found to be 6 mm whereas both the pollen and the rest of the food that she said she was sensitive to was negative in skin test. That's the reason we have done a multiplex testing in this patient. And here are the results. Rah8 is 9.4 which is strongly positive. H1 and H2 are quite negligible. Between 12.7 and maldi 1 is 8.1. The first question is to you Mr. squat. So this patient has a positive uh peanut uh skin brick test but rah2 is negative. So how do you prevent overdiagnosis in peanut allergies in such patients?
>> Could you go back to the last slide? I I didn't show up at first. Okay, thank you. Uh negligible RH2 is negative. The eight is positive and the 10 and Okay.
Yeah. So um because she does not have the uh the storage proteins because it is not there then the likelihood is that this patient could be a candidate and because she hasn't had a significant uh um systemic reaction is all based on the oral allergy syndromes the palm food allergy syndromes in the itching in the mouth if she is willing to go through she may be a candidate for a food challenge for this patient.
>> Excellent. Thank you. Uh uh Dr. Deept, so how relevant is birch sensitization?
I'm sure you've covered this in your uh presentation as well, but just recapsulate.
>> Okay. So, can you please go to the uh previous? No, the first one >> um the previous >> the first case.
>> Yes. No, no, no. This this this case only. Yes.
>> So, let's not even go to the component resolve diagnosis. Okay. Let's see because not everyone 100% of the time you're not supposed to do CRD. Let's think clinically. Let's put a clinical you know acumen. She is reacting to raw peanuts. Definitely when she's roasting it in the form of chicky the allergenicity is going. So we know it is a mild crossreacting allergen. It is nothing or seed storage. So we are fine. Now she also notices similar symptoms with apple, peaches and raw carrots. So it's very clearly written raw carrots, apples, peaches. They are all eaten raw.
Again when something is eaten raw we know it is mostly oral allergy syndrome because once they are cooked they lose their allergenicity. Again it shows that it is something profilence or PR10. Now we know with peanuts it's PR10 with apple, peaches and carrots it's PR10.
What is the relevance of here you have written she does react to Poland she has chronic rhinitis worse in the spring so definitely there is some Poland sensitization in this case maybe she's leaving uh living in a you know imin belt or the northeast part there is allergic reaction she's showing chronic rhyitis can you please go to the next slide >> yes >> yeah and here you have mentioned that BetV1 is positive. So yes, the bet V1 which is the primary sensitizer for um PR10 is positive. How relevant it is?
Again, it is the primary sensitizer.
The reactions are mild. Uh so I would not and here mildy one again it could be considered as a primary sensitizer for PR10. PR10 are cross reacting allergens.
They are mild. So I would just leave it at that and tell her maybe educate her regarding her Poland and cross sensitization.
Of course avoiding all PR tense is absolutely a big no and she should be fine with this. No allergen imunotherapy is required in this case according to thank you. Uh again that was my next question. Thank you for answering that as well. So the my next question was will she require a pollen sensitization imunotherapy? Uh so uh uh this question is again to Scott. So should such patients carry adrenaline auto injectors? What do you suggest? Do you come across such cases and do you think that they should carry uh auto injectors at all times with them?
>> Uh and this particular patient I would say does not necessarily need an auto injector. I think this particular like Dr. Dipy was saying, you know, she may not need even to have the food challenge just based on the symptoms alone and the explanation of those symptoms alone. She could just keep that food in her diet and with the understanding and the education that uh the oral allergy syndrome that she's getting, the pollen food allergy syndrome is just because of those cross react or those those PR10s.
Uh but definitely I I would not necessarily since she has no systemic reaction history there's no need to send this patient for a to prescribe an auto injector.
>> Thank you. Thank you so much. This was extensive. Uh just a last question to uh Dr. Vikram. So uh do you see a lot of birch pollen sensitization in your practice? Uh and and how do you approach them in general especially when they're primary sensitized to birch pollen?
Generally if we are getting primary sensation only to VB1 and not to any other then definitely we take go and ask history over about the travel to the Himalayan belt. I come to the point where you are asking whether pollen uh imunotherapy will be required for this patient because now the patient is having chronic rhinitis and typically uh during the spring uh now during the spring now the the patient is a gardener she's exposed to various weeds also various flowering trees also and geographically if she has never visited him belt and she is in our south India or the dean tube Then I would like to consider that this Br10 again may be cross reactivity. This B 10 because of the structural homology is showing. If I go in detail I may think of giving imunotherapy to something like already you have mentioned the SPT as has come negative for this patient. For other polins, we may consider retesting retesting with standardized allergens if available and imunotherapy may help in management of the chronic rhinitis part.
But whether it will help in oral food, pollen food allergy part, we are not sure. There is always a controversy for that.
>> Okay. Thank you, sir. Uh next, let's go to the case number three. Here we have a 40 42 year old male uh who is a fitness enthusiast who presented with two episodes of anaphilaxis when he came uh to the uh outpatient department. So the first episode he does remember what he ate. He had a meal of uh wheat-based roti the tomato curry fruit salad and the second episode when he had he doesn't remember exactly what he ate but he did does remember that he did uh do a workout right after eating the meal.
Though other than this he does tolerate small amounts but gets mild symptoms of bloating and uh uh you know uh stomach pain or urgency to uh uh you know uh pass tools but he also informs that whenever he consumes walnuts he has similar symptoms as well and otherwise he doesn't have no allergic rhinitis symptoms and he lives pretty much in the interior part of Tamil Nadu southern part of India away from the major pollen sources as such. So the skin prick test uh revealed a peach uh peel a 9 mm wheel whereas wheat was 7 mm and tomato was 5 mm. So again complent result diagnosis was done for this patient which shows propy 3 peach as 22.6 which is strongly positive tray 14 11.4 cor 8 for hazelnut 4.3 and rah9 3.2 two for uh peanut whereas birch was found to be negative. So the first question to Dr. Vikram here with multiple LTP positivities that we saw in this patient how do you define the primary sens sensitizer over here?
>> Now as I mentioned in my talk also there is always a debate about the primary sensitizer when it comes to LTB whether it is pollen or whether it is food. So now in Mediterranean country peach is considered to be the primary sensitizer but in our country if we are talking about food as a primary sensitizer then definitely apple and then legumes are considered to be the uh primary sensitizers and if other respiratory symptoms are there but in in his condition there is there are no respiratory symptoms. So purely he has got anaphylaxis and non-respiratory symptoms. So and when we are looking up the titers for the LTP present in the peanut, the hazelnut, birch, legume and peach here definitely the peach is the titer for the peach is high as well as on your skin prick test also peach peel was 9 mm. So here strongly the peach is should be considered as the primary sensitizer.
>> All right thank you sir Dr. Deepti. So now in such a scenario do you classify this patient as a LTP syndrome or do you classify this as a weed dependent excise indexis variant or is it both?
>> So if you can go to the previous slide please. Yes. So looking at this if you see it is a strong case of LTP syndrome.
Okay. And the worst part worst part is his bet V1 PR10 is negative. What does this mean? If PR10 is negative, then his LTP might show severe reaction.
Co-sensitization with PR10 decreases the reactions of LTP. So here try A14.
Why most likely it is LTP syndrome?
Because as I was telling in my lecture non-specific lipid transfer proteins they might show very severe reaction in a confounding factor like exercise. When he was exercising he was showing reaction. Okay. Otherwise he was fine.
So exercise was the trigger for his try A14 V LTP which otherwise shows Baker's um amma and group P3 it was sky high. So peel and that was also peel uh uh peach because peels are considered 220 times more severe than the pulp of peach and he specifically had peel of the peach which again goes for LTP. Core A8 again goes for hazelnut LTP. Era H9 again LTP.
So yes, this is LTP syndrome less likely uh food uh your food dependent exercise inducer omega 5 gliden. Now let's be very truthful to ourselves. We are discussing this case clinically and we have got uh CRD multiplex in our country. When we do this your try A19 automatically is there in the result. So we need to just see whether our omega 5 glidein is positive or not. In either way, in either way, doesn't matter whether it's omega 5 gin positive that is try 19 or try 14. We have to tell him that 2 hours before and 3 hours after taking the wheat and wheat like products, he has to stop exercising because he's reacting to taking his meals and then exercising. So when we are doing multiplex, we'll definitely come to know here it looks like LTP syndrome.
>> Thank you ma'am. Uh Mr. Scott uh do you have uh any dietary restrictions in such patients uh given that uh they are allergic to uh you know a pan LTP uh scenario.
>> So yeah thank you for the question and and and and Dr. Dipy I did not know that you could get omega 5 in India you know we can get omega 5 here >> have ls >> yeah that's great yeah if you have the omega 5 and now you have to explain something to me is roti roti is that wheat is that a wheat based okay so if if he had some wheat and he had the exercise and it had the symptoms and the omega-5 was the was omega 5 the try 19 was positive well then any wheat product would be would be concerning on that.
Um, but I I would probably take it the way um Dr. Dipy was just saying where we have to give the counseling about the exercise more than just the food because sometimes in the foods you don't know everything that you're eating in the food and you may not have the exposure completely unless you know it's the wheat which you and you know in this case or if it's the peach but but I would say a good good advice for this patient would be uh you know refrain from eating and exercising before or after and that'd be the safest way to do it.
>> All right. Thank you. Uh Dr. Vikram, Ju just a last question regarding this case again. Uh uh is there a role for imunotherapy or desensitization in LTP syndrome? Currently in India we definitely don't but do you have any experience from your colleagues overseas? to actually LTP syndrome there is not yet any defined standardized protocol for LTP imunotherapy but there are few studies with the peach sublingual imunotherapy where they have shown to have less reactivity because of LTP exposure so they are under experiment and trial basis few studies from Europe are published uh >> Mr. Scott, do you do you want to add something to this? Especially regarding desensitization for LTP or do you have any experience with that?
>> No, I don't have any experience with that. I agree with Dr. Vicram. It's it's probably the same, you know, more research needs to be uh more more data and more research needs to go into that.
Yeah.
>> Right. Thank you. Let's move on >> Dr. Kash. Shall I add something over here? Now this this this patient clinically we look it will be clearly look like um say V dependent exercise induced asthma anaphylaxis sorry um so so now when we talk about co-actors we always think of try A19 the omega 5 >> but we should remember that LTP also depends on co-actor and also the GRPs also they also depend on the co-actors where they can present like NFlexis now in when it comes to try We are sure that we can restrict the patient after we will say that after taking wheat products you should not do exercise for next 4 hours or 6 hours. But when it comes to LTP even post legume I have two cases where after legume where LTP was positive they develop analysis after doing exercise after consumption of legume where they had not consumed wheat. So not only wheat here we need to understand LTP containing food items which are showing strong positivity they should not do excess after having these food items.
>> Thank you sir. Thank you for the wonderful >> Can I add one thing also before you go to case 4. Could you back up one slide >> because I think you had the wheat was a 7 millimeter on the whole allergen. Uh yeah, just a second.
>> So what I wanted to point out was that that the um the the um the components of wheat the GL, you know, the the the um the try 19, try 14 or the try 19 is under represented in that. So even if you got back a normal, you know, got back much lower, you still the high index of suspicion for the wheat dependent exercise induced anaphilaxis, you would still get that component because it's not going to show up in that or the whole allergen.
>> Thank you. Thanks a lot.
Okay, let's move on to the next case. Uh again, this this is a typical scenario that we come across in our uh country especially. I'm sure Dr. Deepti and Vikram would agree with this. uh she's a 29year-old uh homemaker with complaints of recurrent episodes of atricaria and episodic androidma and occasional episodes of rhinitis. The symptoms are almost always after a food intake. So this was her presentation and she's visited multiple clinics and she has been told that she's you know typically allergic to everything every every food possible. No, now her reactions are quite mild though. She only has oral itching and uh very mild uh nasal symptoms but she never had any life-threatening symptom as such. And the skin prick test was pos to be positive to raw banana, kiwi, melon, orange, tomato, celery, raw potato, peanut uh you know pretty much uh uh almost all the uh you know antigens which are mentioned here. Now retrospectively we did go and ask she does tolerate the cook forms of all of these vegetables actually. So now again the component testing was done for this patient which looks pretty much like this. The birch profilain is 14.6 the timoth grass felp 12 is 12.1 art mag is 7.2 which is uh quite positive rah5 6.8 8 is again positive and RH2 is negative.
So I'm I'm am I okay with the slide? Can I move to the questions?
>> Yeah.
>> Yeah. All right. So the first question is how do you assess uh the predominant multiple food related but vague symptoms? So how do you assess this such a patient Dr. Vikram?
>> So basically from the history if we go back to the uh case summary slide.
>> Yeah.
>> Yeah. So he you can very well clearly see that the reactions are mild.
>> Yeah.
>> Articaria with episodic enjoyma and mild reaction to oral itching nasal symptoms.
But vaguely she's saying she's allergic to everything.
>> And to scare her we have this positive report of SPD which has come which has been shown to positive or sensitized to everything.
>> Now now she tolerates cooked. So that means whatever she is allergic they are heat lab by.
>> Yeah. So, so having so much of washed representation we are dealing with profilin or pan allergen syndrome rather than having true allergy because here from this table you can see RH2 the peanut whistling the storage protein is negative whereas profilin from various groups like from peanut and weed grass as well as tree everything profiline has composted and this is why this uh this is a classical feature of what we can call it as pollen food allergy syndrome.
All right. Thank you sir. Dr. Deepti, the next question is how commonly do you see a misdiagnosis due to a extractbased skin prick test in your practice? I'm sure all of us must be facing this over here in this uh country right now.
>> So I would say I would go one step ahead and tell you that it is just not misdiagnosis on extract based SPT. It is misdiagnosis on component resort diagnosis itself. When we see a big huge report, so many positives, dark reds, I have seen patients coming with reports and saying we have stopped eating everything. Now what should we do? We have lost 4 kgs weight. So it is very very important that today's lecture we now know that there are pan allergens, there are cross reactive allergens, they are profilins, they are mild.
One step one slide back Dr. Kashi.
>> Yeah. So here we see there is birch timatigras all are profilins.
>> Yeah.
>> Yeah. I would have been happy if you would have shown me the reaction for felp one or art one because mostly profilence they are there is some primary sensitizer mostly so mostly when we see pan allergens there is some primary sensitizer which I don't see here. So here there is definitely with crude extract lot of misdiagnosis but with now this report we should be very clear that these are all mild oral allergy syndromes reacting to the polins >> all right you again you've answered my next question if proffillain is positive how do we rule out uh true allergy versus cross reactivity uh Mr. Scott, do you think there's a role of challenge testing in such uh uhh cases?
>> No, I I I don't think there's a role for challenge uh any kind of oral food challenge. I I just want to point out one thing also that I really agree with what Dr. Vickrim said that, you know, that's going to scare her. The skin prick testing is going to scare her a little bit. She's going to see that and she's going to get frightened by that a little bit. So, education and reassurance and and explaining what it is and what it's not and what it tells us. Really taking the time to really explain all that is really going to to to make a big headway with this patient that um she you know what she can and can't avoid in cooking the food and all the other things and that this is not something that's extremely concerning for a systemic reaction.
>> Understood. Thank you. Uh >> can I add something over here?
>> Yeah, please. Please go. So here here when we are sure now from this thing that we are dealing with some profil.
>> Yeah.
>> Now now we should go for challenge in such condition not to prove >> but to disprove that the and to say that to the patient that these food items are safe for so we should go for oral food challenge and once we do that in front of us parents or the patient will feel confident in eating those food items.
>> All right. Thank you. Thank you so much.
>> I was an option. Yes. All right. So do you consider uh allergen imunotherapy for any underlying pollen allergy to improve the patient symptoms as well?
>> So basically if if a major allergen is positive like Dr. Dipy mentioned some primary sensitizer has to be there.
>> Yeah.
>> Yes. Uh definitely it will help in respiratory uh symptoms but not for these weak symptoms it will not help.
>> Understood. Okay. Thank you sir. All right. So now we have a 34 I'm sorry.
Okay, moving on. 34 year old uh hospital worker presence with history of atricaria and throat tightness after eating a banana and an avocado uh which we are starting to get over here. She also had a reaction during a dental procedure while using latest gloves. Uh no clear pollen allergy, allergic rhinitis or any other respiratory symptoms as such. And uh the skin prick test to banana was around 7 mm to latex was 9 mm and avocado was 8 mm and kiwi was 6 mm. Uh the component panel looks pretty much like this. Uh H heb6 that is latex LTP is around 14.2 musa 4 banana LTP is 9.4. RH2 peanut is 8.7. Uh so moving on to the questions here. Do you consider this as a primary latex allergy Dr. Deep?
>> So you know what Dr. Kashuki this FB6 it is pro heavens this is a primary sensitizer for latex. Okay it's a strong sensitizer for latex. So if that is positive and the typicality of this HVB is it is very much common in healthare workers and if I'm not wrong your history suggested that this per person was some hospital worker healthare worker so these healthare workers doctors nurses who are exposed to latex tubings and all these things a lot they do get sensitized to latex and then this shows a lot of cross reactivity to banana bananas, avocados and uh you know all that fruit latex syndrome. So yes uh sorry what was your question?
>> Uh my question was uh do do you consider this as a primary latex?
>> Yes, it is a primary latex allergy because B6 is a primary sensitizer for latex.
>> All right >> includ B6 is also a strong primary sensitizer of latex.
>> All right. uh Dr. Vikram uh with a negative bet we won in this patient uh can we uh completely exclude you know pollen food allergy syndrome in this patient >> yes here we need to understand the concept of latex food syndrome and the polen food allergy syndrome so when we think of pollen food allergy syndrome yes we are expect we expect PR 10 to be positive now here also the reaction to banana is also there avocado is there and that is because of this TLP tp is like protein which is like a pathogenous PR it's it belongs to PR5 rather than PR 10 it belongs to PR group only but PR5 so there so this is latex fruit allergy rather than pollen food allergy now this case is not only this latex fruit syndrome but also a H2 is positive so this patient is having multiple food allergy syndrome we can call it as so true sensitization to even to his posture. So this patient may go into severe reaction on exposure to peanut.
>> This was my another question as well. Do you classify this patient as latex fruit allergy syndrome or a multiple primary food allergies?
>> Yeah.
>> All right. Thank you sir. So uh let's move on to our last case uh today. uh I'm sure pretty much was covered but uh here we have 48 47 year old homemaker from Delhi living in northern part of India had two episodes of anaxaxis once while grinding fresh mustard which is significantly used here for the chutney and once after a celery based soup at a wedding so she has chronic rhinitis especially worse during the months of August through October. She also has reacts to fennel seeds and coriander powder. Again, very widely used uh uh over here. And she's a strict vegetarian and eats no peanuts or tree nuts as such. And skin prick test suggestive of mustard 10 mm, celery 8 mm, and mag pollen as 9 mm. The blood workup showed RTV 1 to be 24.3 which is strongly positive, RV3 as 11.2, 2 Sina 1 which is mustered uh to S albaman as 8.4 APG1 salary as 6.7 and RTV4 mugwward as 4.1.
So now the questions here are how do you classify this patient? Is it a PA you know pollen food allergy syndrome variant or a true food allergy syndrome?
Uh Dr. Vikram or Dr. Deepti anyone?
So look here see uh here RV1 is present positive. Okay this is a major polen sensitizer. So this is a major allergen.
Okay but when you see she was reacting strongly to the mustard seeds. She was just grinding and she threw a reaction.
That is your uh 2S elbumin. These are seed storage protein. They are totally different from your RV1 which is the primary sensitizer. So here we cannot call it food colon syndrome. Okay. This is a separate protein altogether. Then your RV3 mug word it is again a separate thing. It is lipid transfer protein.
RTV3 is from another group. Your celery is PR10. So these are all coming from different sets of groups. So definitely we cannot say they are crossreacting. I would tell them say that she's allergic to uh mustard seeds. She's allergic to celery. This is not just food allergen cross reactivity. She even threw anaphylaxis to her celery soup. So these are all causing food allergies to her separately and RTV1 mugward is a major colon sensitizer here.
>> Thank you ma'am.
>> I would like to add over here something.
uh we have the concept called as mugwart mustard salary syndrome so which is primarily driven by the atmosia artisia pollen only the RV1 but there we don't expect to have enough alexis because of mustard here Dr. We mentioned here the mustard is albamine the storage protein.
>> So along with that now epg one that PR is also pos. So along with and LTP is also there. So it is not only true there are what do you say the PR the pol food allergy syndrome is also there. LTP is also there. True food allergy to mustard is also there in this case.
>> Exactly. Sir again uh the next question is for you. So now with so much coexistence of LTP and storage protein sensitizations, so do you think that there is a higher severity rate in this patient, do you think that the patient may react to a broader uh spectrum of foods or more unpredictable reactions?
Yes. Yes. For all these three actually if LTP and storage protein they have co-sensitization uh unlike co-sensitization with profilin they are going to have severe reaction and broader food reactivity to because LTP are present in other legumes and peanut also. So definitely and unpredictable many of times because we say LTP will be depend on co-actor but storage protein will make it unpredictable.
>> Uh Dr. Deep do you think the patient will benefit from magnotherapy in this scenario?
>> Let me go back please to the first slide >> first.
>> Yeah.
>> Okay. She has chronic arinitis which gets worse in August and October. So definitely clinical problems are there.
Uh to the next slide please.
Plus with all this mugward word being the major plus there is cross reactivity with prolins. So we don't know she could be reacting to many other uh foods also.
So in such cases where the primary sensitizer is strong then it is worth trying a allergen imunotherapy there is definitely a benefit. If your RTV 1 was negative and only RV3 and RTV 4 were positive then I would have said no but RTV 1 is the primary sensitizer for mugwward. So yes allergen imunotherapy benefits in such patients.
>> All right thank you. Uh so let's before closing we have uh two questions especially to uh Indian context. Uh so the both the questions are to both Dr. Deepri and Dr. Vikram. So while dealing with patients with a IG mediated reaction but a non-anaphilaxis uh uh reaction as such. So which component resolve diagnostic molecules are to be sent for testing? Do do you have any particular panel or do you have any particular single plex molecules that you want to include?
Oh single plex uh is always based on the history always. You cannot predict or you cannot you know think out of nowhere. So good history and then single plex is the best way. Multiplex can lead you to lot of confusion. If you're not sure which is the primary sensitization, which is crossreacting and if you're not taking the history, if you're just going by the result of multiplex, then you are done. The patient is in big trouble because of you. So ideal you correctly said single plex is the uh word today depending upon the history. So here with CRD molecule we'll take the history we'll see what the child is telling and accordingly we'll ask for the test Dr. Vikram do you have to add any?
>> Yeah. So now we have this top to bottom approach and we have bottom to uh top approach. Now when clinical history is clear your skin prick test is not is also clear here we are going to send single plex before starting imunotherapy to predict the efficacy. So here single plex is very very very useful and we have started doing for most of our patients when we are asking but when if there is a poly sensitization seen and you are confused even if it is non-flexis then sometimes we may go for multiplex to rule out the pan allergens in such conditions >> all right thank you sir we should only be guided by the history that's the bottom line only guided by the history otherwise CRD will not make any sense.
>> It will cause more confusion.
>> I I'll keep this as the last question.
I'm sure Dr. Vikram has already covered this pretty much but uh we do have indigenous pollen uh sensitization that is like parthenium holopilia to specifically only to India. So how do we apply the knowledge of CRD to the patients who are sensitive to these Dr. Vikram and followed by Dr. Deepi as well. So as I already mentioned a tree alertion where we don't have the marker in the multiplex as well as in the single plex we should look for the the old pelary group that that has got structural homology and parthnium again is not represented only the extract is there uh there again the parthnium has got cross reactivity with artimesia group so art has got structural homologus with parthnium.
And when we are dealing with proopies, um we have the olig group.
>> All right. Thank you sir. Dr. Deepti, anything that you >> Same thing we have to extrapolate. So we need to know our local allergens. We need to know our trees, our weeds, our grasses and we need to see which group they are falling into. That much we need to have. We can make a chart keep it on our desk and we can quickly refer okay this is positive. So what it could be correlating to our scenario okay there's no point saying o 7 is positive we know it is crossreacting to our chrosupus so we would extrapolate it to that okay so basically we need to see our allergence we can just see what is correlating and then interpret accordingly >> all right uh thank you thank you so much before before we conclude uh I would actually like to take the opportunity to uh bring out blast from the past. So we we were always told uh that blood test is actually you know a supportive diagnosis history history history is always the key when it comes to any allergic diagnostics but uh with with single plex I think all these uh especially all these training especially the CRD module that's come up the first and the second I think that has uh pretty much made all the practicing allergists very confident of writing single plex rather than just sending across all the panel uh based testing and just getting confused more and more and more and more and it makes also makes the uh physician the allergist pretty strong at what they actually want to order only if you know the uh signs of CRD that is when you will actually uh you know go ahead and order a single plex as as rightly told. So uh thank you so much for Dharma Fisher and also uh team Isis for bringing out such a wonderful program and strengthening the knowledge of allergy especially using the right texts at the right time at the right moment. Thank you so much uh Mr. Scott, thank you Dr. Vikram and Dr. Deepti and over to you.
>> Thank you >> uh thank you Dr. Kashipi and uh it was really a wonderful panel discussion.
Thank you to all the panelists. uh we will now hear closing remarks and a summary of the full CRD webinar series 2.2 from Dr. Vikram Patra who will draw together threads from all the three versions all the three webinars that we had into a final set of take messages for clinical practice over to you Dr. Vikram >> thank you Dr. Alka and thank you Dr. Kashi for bringing out such an important and practical panel discussion which which must have solved various queries regarding the practical problems when we are dealing with CR. Now thank you ISAS and thermopishicure for bringing out this webinar series very much needed when this is actually CR is a double-edged sword. If not rightly used we it is going to lead to confusion. Now over the first three webinars we have traveled from the foundations of molecular allergology diagnostics to its real world application in respiratory allergy, pediatric food allergy and finally advanced precision based allergy management. So this series highlights one important transition uh in allergy practice from what is the patient allergic to which specific allergic molecules are driving disease severity persistence and risk. So we are in an position to answer all these questions. Now from the webinar one where it was dealt with house dust m allergy which is the commonest allergen in our allergy practice understanding molecular allerg allergy diagnostic and clinical application. The first webinar laid the scientific foundation for the CR series.
The key learning points were the difference between extract based testing and molecular diagnosis. their role where we should order understanding genuine sensitization versus cross reactivity in house mites and the practical importance of having the knowledge about the major allergen components like derp1 df1 derpy 2 derp 23 and derp 111. Now risk of molecular profiling in allergic rhinitis asthma risk assessment attopic dermatitis selective appropriate candidate for imunotherapy was extensively discussed over there. So important clinical message given in that in the first session was patient with the same dashmite positive report may actually have very different molecular sensitization patterns which directly influence disease severity and frequent response. So beforehand also before starting imunotherapy we are now in a position to predict the outcome from the webinar to very important it dealt with the food allergy periodic food allergy.
So there it was discussed about the risk prediction and management using C because in our country we have seen because of these uh multi or poly positivity reports in with the whole extracts unnecessary diet restrictions leading to under nutrition malnutrition in the pediatric age group. So it focused the second webinar focused on one of the most clinically impactful uses of molecular diagnosis the pediatric food allergy. The key learning points were the molecular basis of food allergy. Uh understanding stable versus label produce was discussed in the detail. Then which components were helpful in predicting the severity, persistence and risk of systemic reaction and particular milk components, egg components and wheat allergens were discussed in detail.
So the clinical applications was highlighted for avoiding over diagnosis, reducing unnecessary dietary restrictions, better counseling of parents, guiding oral food challenge decision and long-term prognosis prediction were discussed. Then important clinical message given was not every sensitized child is clinically allergic and not every allergy carries the same risk. So here comes the role of C which helps move towards individualized management instead of blanket avoidance advice. The webinar 3 today we discussed about the peanut allergy by Dr. Scott and the cross reactivity. So peanut component based risk stratification was discussed distinguishing primary peanut allergy versus the cross reactive sensitation.
We discussed about the different pan allergens and their cross reactivity and their significance in having a poly sensitized patient. We discussed about PR10, profilins, polycins, lipid transfer proteins and their molecular interpretation in the Indian context. So clinical relevance of today's talk was to improve diagnostic confidence, risk assessment, patient counseling, dietary recommendation and precision in allergen imunotherapy prescription. So important clinical message given today was a positive peanut IG alone does not uh define clinical risk whereas molecular components help identify which patients are truly at risk for severe reaction.
So major take-home themes across the webinar series first point I would like to highlight allergy diagnosis is becoming more precise. We are moving extract positivity towards molecular level understanding of disease. CR help differentiate genuine allergy, cross reactivity, clinically relevant sensitization, low risk sensitization.
This reduces confusion and improves decision making. Precision diagnostic leads to precision management. CRD can guide imunotherapy decisions, food challenge planning, risk prediction, dietary counseling and prognosis assessment. So we must understand molecular allergysis diagnosis must always be clinically correlated without clinical history without clinical knowledge without knowledge of molecular algorithology just need to understand laboratory result alone is never the diagnosis we must treat the patient and not the report clinical history remains central to interpretation Indian data and Indian phenotypes matter sensitization pattern in Indian patients may differ from western population due to climate wide geographical distribution, dietary habits, environmental exposure and the regional allergen profiles. So building Indian molecular allergy experience is therefore extremely important. My final closing message will be a molecular diagnosis remember is not going to replace our clinical medicines. It is not going to replace our standard gold standard diagnosis by skin prick test but it is going to strengthen it. When used appropriately, C allows us to improve diagnostic accur accuracy, predict clinical risk better, avoid unnecessary restriction, personalized management is the need of the R and ultimately improve patient outcomes. The future of allergy practice is increasingly moving towards precision allergy medicine and CR is becoming one of its most important tool. Thank you all the faculty members, organizers, panelists and participants for making the academic series meaningful and impactful. I thank Tamu Vishar for bringing out this series.
>> Thank you so much Dr. Vikram and uh it was exceptional. I mean it is a perfect note to close an exceptional series on and on behalf of Tamopic Scientific and ISUS uh I would like to extend my deepest gratitude to all the faculty who made this series possible and to our audience thank you three webinars in and your engagement your questions your commitment to advancing allergy diagnostic practice in India is what makes this series truly worthwhile. Uh recording of all the sessions will be uh shared with everyone all the registered participants. So good night, stay curious and thank you for being part of this wonderful journey. Thank you so much everyone.
We are closing uh the session. We can leave.
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