MCAS Overcoming Testing And Treatment Challenges

Lawrence Afrin, MD

Well, it’s kind of a long story. But to make the proverbial long story short, I came across a patient a number of years ago who was represented to me as having a particular diagnosis, which when I saw her really didn’t add up and began looking for what was the correct diagnosis. And to make a very long story short, I eventually determined that she had what at the time I could only call as an atypical mastocytosis. And upon giving her appropriate treatment, she got much better for the first time in many years. And I then from all that I had learned through the process of trying to figure out what was going on in her and getting her better, I began to recognize that this condition, which soon became known as mast cell activation syndrome was actually present in a lot of other patients who were chronically, mysteriously, multisystemically ill. And the more I began looking for it in patients who had no clear diagnosis to explain their many troubles, the more I found it. I mean it certainly is not the explanation for every mysteriously ill patient, but I began learning fairly quickly that it’s actually not the rare disease that mastocytosis is. It’s a very common disease, but one has to learn how to recognize it. It’s a complex and highly variable disease from one patient to the next. So coming to understand, I mean like every disease, there are patterns to it. 

But it’s challenging to learn how to see those patterns when the superficial symptoms are so different from one patient to the next. But once you learn how to recognize it, you can diagnose it because there are tests that can be run. And once it’s diagnosed, good news, that there are many treatments that have been found helpful in various patients. And even though we don’t have any reliable way yet to predict which of these treatments will best help the individual patient, nevertheless, if the doctor and the patient, both of them are sufficiently patient and persistent, and methodical in stepping through the trials of these deep different treatments one at a time. In my experience, most of these patients, no matter how many years or decades, they’ve been mysteriously unwell. Most of them actually can eventually identify some cocktail of mast cell targeted treatments, which gets them significantly better. And as I began to see how many of these mysteriously ill patients actually could be legitimately diagnosed with this and treated and actually improve with mast cell targeted treatment, things just kind of naturally fell into place. And that it was a good way for me to focus my career at that point so.

Beth O’Hara, FN

And-

Lawrence Afrin, MD

That’s a short version.

Beth O’Hara, FN

Well, you’ve brought so much hope both of my own life dealing with mast cell activation syndrome and I know the lives of hundreds of thousands of people who go from specialists to specialists. And seems like people can take up to 10 years or longer to figure out what’s going on, if they’re lucky enough to get a good diagnosis. What are some of the… I know you’ve done a good amount of research on the types of symptom presentations that can show up And that’s what makes this so challenging at times, because there are these variable presentations. One person looks completely different than another person. What are some of the symptoms that people can be looking for and how does this present?

Lawrence Afrin, MD

Probably better than focusing on specific symptoms is to look at the categories of symptoms that mast cell activation syndrome patients present with. The symptoms are direct consequence, the symptoms of this disease are direct consequences of the natural effects of the various mediators that are naturally produced and released by mast cells, which in truth are present everywhere in the body. Though dominantly at the environmental interfaces and in the walls of vessels and neurons. But the biologists have now documented that the mast cell produces more than a thousand mediators, each of which has a huge range of effects all throughout the body. And it would take forever to go through the details of what each mediator can do. But if you’re looking at the broad themes of what this, of what the majority of the mast cell mediators do, the first theme, this is the universal constant of mast cell activation syndrome, is chronic multisystem inflammation. Obviously, the specifics of how inflammation can manifest are gonna be different specific symptoms in different organs, different systems, different tissues in the body. For example, inflammation in the respiratory tract. Maybe congestion, and coughing, and shortness of breath. 

Inflammation in the GI tract could be abdominal pain, nausea, diarrhea, and so on and so forth. It’s the specific symptoms are just quite different from one organ system to the next. But inflammation, chronic multisystem inflammation, is the universal constant. The second broad theme to the clinical presentation of this disease are allergic-like phenomena. And I put a plus/minus in front of that. So, chronic multisystem inflammation plus/minus allergic type phenomena. And the reason I say plus/minus is there actually are plenty of MCAS patients who don’t have a spec of allergy to them. And then at the opposite end of that spectrum, there are the relatively few, thank goodness, poor souls who, if you can even imagine such misery, they are literally suffering 24/7 anaphylaxis. And then, everybody else with MCAS is somewhere in between those polar opposite ends of the allergy spectrum. There’s one more broad theme we very commonly see with this disease, but this is the hardest of all to recognize because these manifestations emerge the slowest of all. Inflammatory phenomena, allergic type phenomena tend to blossom and flare up fairly quickly. But it turns out that many of the mast cell mediators are also integrally involved in guiding growth and development in all tissues in the body. So when you have chronic, inappropriate production and release of various and sundry of the growth guiding mediators, I think it’s easy to then understand how you can get any of a huge variety of abnormalities in growth and development in potentially any tissue or organ in the body. 

So for example, sometimes it’s insufficient growth, like slow, or delayed, or poor healing from a wound. Sometimes it’s overgrowth, excessive growth. And some of the most common types of overgrowths we see are cysts. And not that I’m saying that every cyst and every person is a consequence of mast cell disease. I’m just saying that cysts in various organs in the body are a very common type of growth abnormality in these patients. So we see cysts. We see abnormal scarring and excessive fibrosis and scarring. We see, for example, uterine fibroids developed. We see a whole range of abnormal, excessive, vascular growths. And fortunately, the vast majority of these abnormal growths are benign. But on occasion, they can be malignant. And sometimes such a malignancy obviously can come fairly quickly to dominate the clinical picture and really overshadow all the rest of the stuff that’s going on with the mast cell activation. It can make it even more difficult to recognize or actually is a problem with mast cell activation in that patient. 

So, chronic multisystem inflammation plus/minus assorted allergic type phenomena, plus/minus abnormalities in growth and development or what we call diastrophisms. This is the general clinical picture of this disease. I know it’s a nebulous picture, but it kind of hard to rationally expect a more tightly focused picture when the disease is the consequence of a zillion different patterns of inappropriate production and release of so many different, of these very potent mediators that are produced and released by the mast cell.

Beth O’Hara, FN

And if we even just think about the number of possible permutations between the locations of these mast cells that are being triggered, there are over 1,000 mediators that can be released in these various combinations and then the over 200 receptors that can be triggered.

Lawrence Afrin, MD

One of the lessons that was hammered home to me very early in my coming to understand the behavior of this disease with regard to just how differently different mast cell patients can present with respect to any particular biologic parameter. The very first patient in whom I came to recognize that what was really at the root of her troubles was a mast cell activation syndrome, I mean she had a great many different problems. But the dominant problem that had led her to being referred to me, a hematologist oncologist, was a diagnosis of something we call polycythemia vera, which is a malignancy in the bone marrow in which there’s gross over production of red blood cells. But the very next patient, I mean literally the next patient whom I came to to recognize it what was underlying her vast spectrum of illness, she had actually been referred to me for completely the opposite hematologic problem. And I’m not saying that every mast cell patient has hematologic problems. Again, it’s highly variable. But I’m a hematologist oncologist. 

So before I started focusing in mast cell disease, patients were referred to me for hematologic and general hematologic and oncologic problems. But the second patient had a condition that five other hematologists before me had absolutely proven was something called pure red cell aplasia, in which the bone marrow completely gives up making red blood cells. It’s exactly the opposite. And yet both of those patients turned out to have a mass cell activation syndrome at the root of their problems. And with appropriate mast cell targeted therapy, they both got better pretty quickly. And I soon came to realize that this possibility of seeing polar opposites in any particular biologic parameter, this can easily be seen with mast cell disease. It just depends on the particular pattern in which the patient’s dysfunctional mast cells are producing and releasing these various mediators. Many of the mediators the mast cell has will push a particular parameter in the body in one direction. And the mast cell also produces other mediators, which will push that parameter in exactly the opposite direction. And the net effect you see on that parameter in any given mast cell patient depends on what the balance is of the pushes that are coming. 

The pushes on that parameter that are coming from the different mediators that are being put out by the mast cell. Bone growth is a great example. Many people are familiar with the condition of weakening of the bones called osteopenia or it’s more severe form osteoporosis. And actually, I mean there can be many causes of osteopenia and osteoporosis, but mast cell disease, MCAS, is absolutely can drive osteopenia and osteoporosis. But at the same time, there also are ways by which mast cells or I should say improperly behaving mast cells can produce the opposite condition of an excess of thickening of the bones that we call osteosclerosis. And so, not only can you see some mast cell patients present with osteoporosis and other mast cell patients present with osteosclerosis, but you also can see the same mast cell patient present with osteoporosis at one point in his or her life and osteosclerosis at a different point in that patient’s life. Because the particular pattern of inappropriate mast cell mediator production at one point in a mast cell patient’s life can be a good bit different than the pattern you see at another point in life. 

And in fact, there even are occasional patients who, mast cell patients who will present with both osteoporosis and osteosclerosis at exactly the same point in time, just in different bones in their bodies. And this comes about because the dysfunctional mast cells in one part of the body are misbehaving with a different pattern than the dysfunctional mast cells in another part of the patient’s body. Many times, both patients and doctors assume that the pattern of improper mast cell mediator production and release that you see in any given mast cell patient, that it’s a single pattern. There’s a single manner in which all of the dysfunctional mast cells in the patient’s body are misbehaving, but actually that’s too simplistic a view of the reality of the matter. We know from the research that mast cells in different parts of the body, both normal mast cells and abnormal mast cells in different parts of the body, quite often behave in considerably different fashions. So, this just adds to the variability of the disease from one patient to the next. As you said, the permutations are almost incalculable.

Beth O’Hara, FN

And it, we have to remember too that the mast cells in one part of the body don’t have the same concentration of particular receptors as in another. So, this is a very simple example of the amount of H2 receptors in the GI tract on the mast cells versus in other tissues. This is gonna lead to what you’re describing as well, which has made this mystifying for the vast number of practitioners who are trying to find their way through and even patients trying to figure out what’s happening for them. They’re going specialist, to specialist, to specialist, but somebody has to zoom out and look at how are all of these symptoms connected and is there mast cell involvement. So, I know you look a lot the symptomology and I’ve worked with several of your patients and senior, incredible reports that you send with them. And I know you do a good bit of testing as well. And there’s a lot of debate about the testing and whether, first of all, which testing to use, and second of all, what happens when all the testing is negative, which isn’t uncommon. Can we talk about the types of testing that you’re finding most valuable in your practice?

Lawrence Afrin, MD

It’s a good bit different from one patient to the next. Again, it’s a very heterogeneous disease. The mast cell puts out more than a thousand mediators, but the fact is that the great majority of them are not presently testable in any clinical laboratories anywhere. They’re testable in research laboratories. That’s how we know they exist. But most of them are not testable in the clinical laboratories. Of the minority that we can test for in the clinical laboratory, the majority of those are not particularly specific for the mast cells. So as an example, we can test for the level in blood or urine of a mediator called interleukin-6, IL-6. It’s a very potent inflammatory mediator. And when we find an elevated level of IL-6 in the blood of the urine, we know there’s a strong inflammatory state going on in that patient’s body. And the mast cell does make a good bit of IL-6, but so do a number of other types of cells. 

And so if we find an elevated level of IL-6 in the blood or the urine, it doesn’t necessarily mean that the mast cells are at the root of the problem there. So in the end, even though these cells are putting out more than a thousand different mediators, there really are only about 10 or so that we can measure in at least some clinical laboratories and which are fairly specific to the mast cell. But if you think about it, if you’re only measuring 10 out of more than a thousand, the odds are overwhelming. That the symptoms at any given patient is having is coming, the symptoms are coming about from inappropriate expression of mediators other than what we’re measuring. Clearly, what we’re measuring in these patients is a terribly poor surrogate for the totality of the signaling chaos that’s going on in this disease between the mast cells and all the other cells in the body. But at the moment, these 10 or so, this is the best we can do for detecting, for fairly specifically detecting, activation of the mast cells. 

And so, this is what we do. But it is challenging testing. Many of these tests are available only at a very few specialized reference laboratories scattered around the world. Many of these mediators actually have very short lifespans in the blood or the urine at room temperature, let alone at body temperature. And so for many of these mediators, one has to pay good attention to keeping the specimens continuously chilled. And that’s not just at the time of collection in the collecting laboratory, but at every point they’re on. ‘Cause again, most of these tests are specialized tests. It can only be performed in a few laboratories. So, many of the specimens have to be packed up and shipped out to these reference laboratories. And one has to take care to pack the specimens in a way that they will stay continuously chilled. I’ll be the first to acknowledge it. It’s not easy. But once you learn all the nuances of this, I will say, and if you have the opportunity to have a chat with the laboratory personnel who are involved in collecting and processing the samples, I mean, it’s a matter of education. Just like doctors need to be educated about this, so do the laboratory personnel and pharmacists, and insurance companies and so forth. It’s all a matter of education. 

But once you can kind of get the pipeline in place and have everybody up to speed, then I would describe it as a straightforward process. Not easy, but straightforward. But it does take some effort up front in learning these nuances and then making sure everybody else in the chain of handling is aware of these nuances as well. I mean, again, it’s not easy. So, I’m aware there are many doctors who are for one reason or another, not able to surmount these challenges. And so, they’re coming to make a diagnosis of the disease purely on a clinical basis, basically just best clinical guess. And you know, I can’t say there’s anything, absolutely wrong about doing that. If the patient or the doctor are facing limitations in what they can do in the diagnostic process, then you do the best you can with the resources you’ve got available. But I find that given that most doctors don’t yet have any awareness of the disease. And therefore, the patients are likely going to have to be convincing their local doctors who have never heard of this disease before that this really is what’s at the root of their troubles. It’s really the laboratory evidence that’s gonna be speaking loudest by far on the patient’s behalf in convincing their local doctors. Not only now, but for the rest of their lives. 

That they really do have this disease. So I think if it’s possible to access the testing, it’s probably to the patient’s long-term benefit to acquire the laboratory evidence that bolsters everybody’s confidence in the correctness of the diagnosis. At present, there are two different camps of thought about what testing is appropriate and reasonable to pursue in looking for the laboratory evidence of this disease. There’s one group that focuses largely on a marker of mast cell disease called tryptase. And that’s largely the only marker they look at. There’s another group that feels that based on the available data that tryptase is a good marker for the rare mast cell disease, the mast cell cancer that’s called mastocytosis. But it’s not so good a marker for the much more common, the much more prevalent mast cell activation syndrome. So even though we still do check tryptase in patients with suspected MCAS, we also check, like I said, these other nine or 10 other mediators that we feel also can give a fairly specific indication of activation of the mast cells. So, there is that difference of opinion among different groups of doctors at present.

I imagine that in time as more research gets done, the… I mean, this is the way science works is that you do more research, more studies, and bit by bit, you get closer and closer to the real truth of the matter. And then, our diagnostic processes at that point probably will be much more precise. I mean it has to be kept in mind that even though this in truth is not a new disease, it is a newly recognized disease. It’s only been about 15 years since the first case reports of this were published. So, there really hasn’t been that much time for research to be done in this area. And in truth, not much research has been done. And I think it’s only fair to characterize all of the research that has been done so far as preliminary. So, everybody has to keep those caveats in mind and in setting their expectations as to how much about this area of medicine and biology we can reasonably be expected to know for sure. We’re very early-

Beth O’Hara, FN

That’s-

Lawrence Afrin, MD

With this.

Beth O’Hara, FN

And I think about it in terms of how long there’s been diagnostic criteria for things like type II diabetes or Alzheimer’s disease versus I believe the ICD-10 code for mass activation syndrome came into existence around 2016. That’s quite new. but we know we have some markers around histamine, heparin, prostaglandin D2. One of the other things I often wonder… And we have a urinary marker for histamine. But I often wonder, well, what if it’s not the vascular mast cells that are involved? Are we going to see any elevation in these blood markers at this point.

Lawrence Afrin, MD

Well, in my experience in most mast cell patients we did, keep in mind that there are very few mast cells actually circulating in the blood at any given point. And actually, most of those mast cells are immature mast cells. Mast cells don’t actually mature and really blossom in their activity until they exit the bloodstream and penetrate into various tissues all throughout the body. But if we, again, if we attend with due diligence to the nuances of testing these sensitive mediators, usually, we’re able to find a reasonable amount of laboratory evidence to support the diagnosis in a patient whose symptoms are consistent with chronic inappropriate activation of the mast cells and by symptoms that are consistent with chronic activation. Again, I’m talking about this general picture of chronic multisystem inflammation plus/minus allergic phenomena, plus/minus diastrophism. And not just the chronic picture, but of course, many mast cell patients, say the large majority of mast cell patients, in addition to their chronic symptoms, they also have from time to time these acute flares of various symptoms. It’s not absolutely necessary, not every mast cell patient has such flares, but most do. The ultimate acute flare, of course, is life threatening anaphylaxis. But the preliminary published research to date suggests that only about 7% of MCAS patients have anaphylaxis or anaphylactoid behaviors. So obviously, the large majority of mast cell patients don’t have that. They fortunately do not have that pretty scary event in their history. They may well have acute flares of other symptoms, but.

Beth O’Hara, FN

But fortunately not the, anaphylactic necessarily

Lawrence Afrin, MD

Not necessarily anaphalyctics.

Beth O’Hara, FN

Yeah. So we have this multisystemic, meaning it has to be an at least two or more systems so people can have, they may have skin symptoms and GI symptoms, or they may have, for example, heart palpitation. They may have some various nervous system type symptoms. They may have the what seems to be quite ubiquitous, the postnasal drip and the throat clearing and these kinds of areas, but we’re not gonna have just basic allergies. We’re gonna have a few different things going on for this person. Then, there’s testing available that hopefully if the samples can be handled correctly, which is tricky and requires being chilled through the entire process, hopefully of these about 10 different types of testing mediators, we can get an increase. Although, we’re not sure about the odds of 10 within a thousand possibilities. And then, we have the third part, which is that there’s gonna be a positive response at some point to a mast cell stabilizing medication or an antihistamine, some kind of agent, but the possibilities there are quite vary.

Lawrence Afrin, MD

Yeah. And this brings us to the another difference between these two camps of thought about diagnosing the disease. That at the first camp that focuses largely on tryptase testing. They actually have a requirement in their diagnostic criteria, their proposal for diagnostic criteria for this disease. That you have to demonstrate a response in at least some of the symptoms to some mast cell targeted treatment. Whereas the other group that looks at a larger range of mediators, it doesn’t take quite such a strict approach and says that yes, a response to treatment may contribute toward a diagnosis, but it’s not necessary. And that kind of looseness was consciously put in those criteria because it was recognized that the disease is so variable in its behavior from one patient to the next that it’s quite likely that at least some mast cell patients are just not going to respond to the first one or two, or maybe even three or four treatments that are almost randomly selected to be tried in the patient. And keep in mind, we do have a lot of treatments that have been found helpful in various mast cell patients, but no ways yet, no methods yet for reliably predicting which treatments are gonna help any particular symptoms in any particular mast cell patient. 

And so, I think we can imagine this scenario where if mast cell disease is suspected in a given patient and the doctor then goes to empirically try to treat that patient. And then applies one treatment, sees no benefit. Tries a second treatment, sees no benefit. I mean how many of those doctors would then be willing to continue suspecting that it’s likely mast cell disease going on here and move on to trying a third or a fourth drug, even if they really can’t think of any other diagnoses that better account for what’s going on with the patient. So, that’s why this second group says that yeah, a response to therapy can be helpful. But just because a patient has not responded to the first few treatments you’ve empirically tried, it doesn’t even begin to say that it’s definite, that the patient does not have MCAS. A highly, highly variable disease in it’s behavior from patient to patient, to patient. Not just in terms of which symptoms you’re gonna see, but also in terms of which treatments are gonna be helpful in any given patient.

Beth O’Hara, FN

And I think that’s why it’s so important that we keep coming back to these, all these possible permutations between the mast cell locations, the over 200 receptors, the over a thousand mediators. Because each of these, there’s no one mast cell medication that’s gonna hit all of the receptors, address all of the mediators. So we’ve got antihistamines, we’ve got some inhibitors, these types of things.

Lawrence Afrin, MD

It comes back to the importance of the research. I’ll give you another example of the variability. I long ago lost count to the number of mast cell patients where when I applied drug X to them, I see one sort of response. But then there’s another large number of patients and whom I apply drug X at the same dose. And even if they superficially appear to have the same symptoms, drug X actually does nothing in those other patients. Now, there obviously has to be some biological reason why there’s the difference between those groups. But unfortunately, the state of the science, the state of the research in this area at this point is so immature that we are nowhere close to understanding why there are these differences. I’m actually fairly confident and optimistic that as the decades roll on, and yeah, we’re talking about decades, not years. But as the decades roll on, yes, we will make scientific progress. 

We will come to much better understand why a given drug has such and such an effect in one patient and different effects in another patient. And as we come to better understand those mechanisms, then we will get to a point where we can start reliably predicting which drugs ought to work in a given type of mast cell disease and a given type of mast cell patient. And that’ll allow us to transition away from the current kind of trial and error, and much more smartly predict which drugs ought to be helpful in the individual patient based on a better understanding of the science and more sophisticated testing that will inevitably follow from a better understanding of the science. So we’ll get better with this, but it’s going to take decades. And in the meantime, don’t despair because I mean, think of where we stand today. Just 15 years from when this was first recognized, at least we know that it exists, which is a whole lot better situation than we were in before we knew it existed. I mean it’s not that these patients didn’t exist before we knew about the diagnosis. They were always there. It’s just they went from virtually cradle to grave, never being properly diagnosed, ’cause we didn’t even know the disease existed. 

And if you can’t make the right diagnosis, the odds of finding effective treatment are pretty slim. So, these patients were just chronically ill their entire life. But now, even though the state of the science is very immature, we know the disease exists. We already know that there are a lot of different treatments that have helped various mast cell patients. We also know that most mast cell patients, again, if they and their doctors are sufficiently patient and persistent and methodical in stepping through the trials of these different treatments, most of these patients actually will get to the goal of feeling significantly better than the pre-treatment baseline the majority of the time. And another fortunate thing is that as best as anybody’s been able to tell so far from, again, the very preliminary research, most of these patients seem to have a relatively normal lifespan, which means they’re going to live, they’re likely going to have the time that’s going to be needed by them and their doctors to explore these different treatment options, to find the particular cocktail of mast cell targeted treatments that’s actually gonna be optimal for the individual patient. It usually is a pretty unique cocktail for the individual patient that optimally serves that patient.

Beth O’Hara, FN

And sometimes, that might be a combination of H1, H2 antihistamines, sodium. Maybe ketotifen. We’ve got Singulair. What are some of the other agents that you use most frequently?

Lawrence Afrin, MD

Oh, it’s all over the map. Nonsteroidal, anti-inflammatory drugs. Even just plain old, simple aspirin can be very helpful in some mast cell patients. We need to be a little bit careful with the nonsteroidal anti-inflammatory drugs, the NSAIDs, because in some mast cell patients, those drugs actually turn out to be triggers for flaring up their mast cell activation. But NSAIDs can be helpful. Low doses of benzodiazepines can be helpful. Various other anti-inflammatories like ketotifen, flavonoids, like quercetin and luteolin, cannabidiol, CBD. And an analog called polyetherimide sometimes could be helpful. Low dose-

Beth O’Hara, FN

Just EA. Most people know that as EA.

Lawrence Afrin, MD

Well, low dose naltrexone, LDN, sometimes can be helpful. I actually was seeing a patient in follow up just yesterday, who was reporting into me after her first, a few weeks on LDN. And it was remarkable how much improvement. She was gaining variety of symptoms, including just energy. I mean chronic fatigue is one of the most common symptoms with this disease. And I’m not saying that LDN is what fixes chronic fatigue in the majority of mast cell patients. We know it isn’t. But we don’t have any particular drug that is a fix for chronic fatigue in the majority of patients. It’s different in different patients. But still in her, in this particular patient, it was remarkable how much low doses of naltrexone were helping her. So, sometimes we wind up applying cromolyn not to just one place in the body. We apply it to multiple places in the body. And sometimes, we wind up using drugs from a class called the tyrosine kinase inhibitors. Unfortunately in the US at present, they typically are very expensive drugs. But in many other places around the world, they’re relatively inexpensive. And sometimes, some of those drugs, certainly not all of them, some of them can be helpful. Honestly, we could spend days talking about all of the treatments that have been found helpful in this disease.

Beth O’Hara, FN

Well, one, I know you have an incredibly busy schedule and I wanna thank you so much for taking time out to talk with us both personally but for the people watching your summit. I wanna express a gratitude for what you’ve done and how you’ve brought so much awareness, so much hope and possibilities for people. I wanna tell people about your book, “Never Bet Against Occam,” which is a game changer. And it has really changed the face of what we know about this. And this is one of my first introductions and made a huge difference in my own life and my practice. And do you still take patients? I know I send people your way. You’re one of the maverick diagnosticians in this area. And for people who maybe have more than mast cell activation syndrome, I always encouraged that they get a full diagnostic workup with you if they can get in.

Lawrence Afrin, MD

Well, I don’t know that I’d agree with the word maverick. That kind of means off the reservation. I actually try to be fairly rigorous in my diagnostic approach.

Beth O’Hara, FN

Rigorous is a good word.

Lawrence Afrin, MD

I try to adhere very strictly to the peer reviewed published diagnostic criteria for this disease. But yes, I am still taking new patients. The wait time, it’s a few months, but it’s not ridiculous. I also see patients by, at least here in the US, I see them by telemedicine. I actually see patients abroad by telemedicine too, but those patients do need to actually come see me in person for the initial consultation. But if anybody wants to consider formally consulting with me, they just need to contact my office to inquire about their policies and appointment availability and that sort of stuff.

Beth O’Hara, FN

And I believe your website is aimcenterpm.com?

Lawrence Afrin, MD

aimcenterpm.com, the Aim Center for Personalized Medicine. I practice in Purchase, New York.

Beth O’Hara, FN

Thank you again so much. Appreciate your time and all of your wisdom and your research.

Lawrence Afrin, MD

Great. My pleasure.