Anna Postolova, MD, MPH: Allergy and Immunology for the Rheumatologist

Rheumatology Network: Hi, Dr. Postolova. Thank you for joining me today.

Anna Postolova, MD, MPH: No problem. Nice to see you again.

RN: To begin, can you give me a generalized brief history and overview of intravenous immunoglobulin treatment?

AP: Sure. So I'm going to have my notes in front of me too. It's a lot to remember. So, in 1890, actually, is when a gentleman by the name of Bombaring showed that serum from rabbits immunized with tetanus was protective in naive rabbits. And then in 1910, human sera was first used to treat infectious diseases, allergies, as well as cancers. In the 1930s, and 1940s, a gentleman by the name of Cohn, Dr. Cohn, found antibodies in the globulin compartment of sera when he was actually trying to fractionate the use of albumin during the war. In the 1950s. Bruton used it for the first time in primary immunodeficiency. And then between the 60s and 80s, we refined IV IG product, it became standard therapy in the 1980s. And then in the 1990s, after being used in patients with immunodeficiency, it started to be used for anti-inflammatory uses. And then finally, in around 2006, we started using subcutaneous IG. So that's the history of it.

RN: So how does this treatment help patients with rheumatic diseases?

AP: Great question. So, you know, it's probably most used in myositis, polymyositis, and dermatomyositis. And we don't know exactly how it works, we think it's a combination of anti-inflammatory cytokines, chemokines, that are infused with the IV IG. There's also properties to the IV IG and the FC and then the FA B portion of it, that bind other antibodies that bind to receptors and help expel the auto antibodies that we think are causing disease, as well as just regulate an inflammatory cascade through binding sites and macrophages as well.

RN: Your presentation mentions data, what are the data concerning this treatment that you've discussed at the RWCS?

AP: So we talked about a lot of different data, it's kind of hard to say exactly, you know, we talked about the strongest data right now for our diseases being under myositis and myositis. It's used less for other diseases. But there is anecdotal and case reported data for some of the vasculitides as well as lupus. And then we talked briefly about engineering of IG. And its use later on of how we're trying to instead of just acquiring immunoglobulin from patients, engineering immunoglobulin to be more effective, more efficient, and lower concentrations.

RN: Moving on to your other presentation, which is Hot Topics in Allergy and Immunology for the Rheumatologist, what are some of the hot topics in allergy and immunology that you've discussed at the RWCS?

AP: This year, we focused on NSAID, or non-steroidal anti-inflammatory drug, hypersensitivity. So, this is hypersensitivity to any of the NSAIDs. So, aspirin, ibuprofen, diclofenac are some examples. And we talked about the five different types of reactions somebody could have to them, touched on some key points of triggering reactions, and then we also talked about what we know to date about COVID vaccine reactions.

RN: And what do you know, to date about COVID vaccine reactions?

AP: Complicated question. So, you know, we're really focused on this being a moving field/ moving target. The two main theories are potentially a hypersensitivity or allergic reaction to PEG or polyethylene glycol, one of the excipients in the vaccine, or this not being an allergy at all, and actually being activation of the complement cascade. And this is something that's undergoing a lot of research right now. You know, allergists are going back and forth about which one is responsible for it and whether we should be testing patients or not, how we manage them and really the risk of the vaccine. I do have a caveat is that it's actually very safe. So despite some of the press it's getting, you know, as a whole when you look at the numbers, reactions are still exceedingly rare. And getting COVID is not exceedingly rare. So although there are reactions, really, most people should be getting this vaccine.

RN: That's reassuring to hear. Why do rheumatologist need to be aware of allergy and immunology when treating patients with rheumatic diseases?

AP: Most rheumatologists are actually immunologists, right? Our training includes immunology, all of our drugs target cytokines really as well as other mechanisms of the immune system. So I think immunology is inherent to rheumatology. Allergy is important because it's, you know, you can think about it as kind of an extension of the spectrum of rheumatology, right. It's just a different hyperactivation over response of the immune system, focused in the TH 2 versus the TH 1 response. And our patients have allergies. We have a lot of overlap diseases like potentially EGPA is treated by both allergist and rheumatologist and knowing each other's field is always complimentary.

RN: Are there any trends that you're seeing with allergy or immunology in general or as it pertains to rheumatology?

AP: I am seeing the 2 probably work together more. I think that allergy immunology and rheumatology immunology again, both of those, you know providers are immunologists. So there's an overlap, you know, our patients tend to be immunocompromised. I think one of the you know, kind of the hotter topics of the overlap is patients with autoimmunity, who also have immunodeficiency, or vice versa. Our immunodeficient patients who develop autoimmunity. And this is something we talked about last year at RWCS. Patients with immunodeficiency are now being treated effectively with antibiotics. And they're not succumbing to the viruses and bacteria, they used to succumb to unfortunately. And so now we're seeing the next frontier of immune dysregulation, which is autoimmunity in these patients. And the question comes up, how do we treat this best, right? How do we safely immunosuppress them? And then another really cool topic that I think is evolving is genetic testing. And again, rheumatologic diseases we think, are multifactorial, they're really not monogenetic. There are many monogenetic immunodeficiencies. And we learn from those aberrations on what patients progress to experiencing them. And we also know we learned how to block, you know, some of the pathways leading to their autoimmunity. So I really think the 2 working together can aid patients in a very special way.

RN: Is there anything else that you'd like to add before we wrap up?

AP: No, I think you know, this was a great conference. Thanks for Artie and George for putting it on. And, you know, hopefully next year, we all feel safe to hopefully go to Hawaii.

RN: Well, Dr. Postolova, thank you very much for taking the time to speak with me today. I really appreciate it.