All Conditions & Treatments

SLE in the Age of COVID-19 (New Thoughts)

A Presentation in Honor of National Lupus Awareness Month 2020

This May 27, 2020, presentation for healthcare professionals was hosted by LANtern® (Lupus Asian Network) at Hospital for Special Surgery in partnership with the Chinese American Medical Society (CAMS).

Joining Dr. Lockshin were Eliza Ngan-Dittgen, LANtern Program Supervisor, and Ning Lin, MD, neurosurgeon at Weill Cornell Medicine, and Treasurer of CAMS (2020-2022).

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Highlights from this presentation

Dr. Lockshin started by touching on the health issues that Asian lupus patients face due to their unique cultural values and beliefs. He then shared what he learned so far on the link between COVID-19, lupus and experimental treatments. Dr. Lockshin also discussed incomplete SLE (in which patients present with signs of systemic autoimmunity and clinical manifestations of SLE but do not fulfill all the American College of Rheumatology ACR classification criteria for SLE) – why is it important to call for more clinical studies. The presentation ended with a Q&A session.

Complete transcript

OK, good evening. Hope everybody can hear us. My name is Ning Lin. On behalf of Chinese American Medical Society, welcome to our annual lupus talk. I'd like to thank everybody for coming. I'm going to wait for a couple more minutes. We're about to start.

OK, we'll get started. Again, good work, good evening, and thanks for everyone to come. Thank you, Eliza for being here, Dr. Lockshin to be here. And thanks for LANtern (Lupus Asian Network), and Hospital for Special Surgery, for sponsoring today's event. Just a few housekeeping things to remind everybody, and Eliza will introduce Dr. Lockshin.

So all attendees should submit questions through the Q&A box. You should be able to see a Q&A box at the bottom of your screen. And we'll ask all the questions to be answered at the end of the talk, after Dr. Lockshin has finished his lecture. So, without further ado, I will turn over to Eliza to introduce our honored guest speaker.

Thank you, Dr. Lin. Thank you. Can everyone hear me? Give me a thumbs up. You can hear me, right? OK.

So good evening, everyone. This is Eliza. I'm with LANtern (Lupus Asian Network), at HSS, Hospital for Special Surgery. Our program is a lupus patient support and education program catered for Asian-Americans. In honor of National Lupus Awareness Month, which is this month, we are delighted to present this seminar, "SLE in the Age of COVID-19," and are so pleased that you can join us tonight. A special shout-out to Jamie Love, Dr. Ning Lin, our moderator, and CAMS for this collaboration opportunity. Thanks so much.

It's my absolute pleasure to introduce our speaker tonight, Dr. Michael D. Lockshin. Dr. Lockshin graduated from Harvard College and Harvard Medical School. He did his rheumatology fellowship at Columbia Presbyterian Hospital. He became extramural director and acting director of the NIH National Institute of Arthritis and Musculoskeletal and Skin Diseases in 1989. Dr. Lockshin is currently the director of Barbara Volcker Center for Women and Rheumatic Disease at HSS, and Professor of Medicine and OBGYN at Weill-Cornell Medical College.

He is an innovator in integrating personal health care issues that arise for patients with chronic illnesses into their medical care. His most renowned research is on autoimmune diseases, particularly those that affect women, such as SLE, APS, and pregnancy-related problems. Dr. Lockshin is the author of hundreds of research papers, book chapters, and books, and was editor-in-chief of Arthritis and Rheumatism, the premiere journal of the American College of Rheumatology, from 2005 to 2010. Now, let's welcome Dr. Michael Lockshin.

OK, well, thank you, Eliza, and thank you all for joining in this somewhat strange time that we live in. The audience, I understand, has quite varied training and experience, so I'm going to give a general kind of talk on lupus. But all of us have had our lives turned over in the last few months with COVID-19, and we've had a lot of rethinking about what we do.

I am informal. I don't mind questions. If you want to talk about something else, please ask that. But the plan will be that I'm just going to give you a general introduction and then go on to some of the things that we've learned since COVID-19 hit the United States. Next slide, please. Can you change? OK.

Well, the topics that I'll cover are first about Asians and the disease lupus because there's a number of things that have been written about it. I'll go from there to standards of care for 2020 and some experimental treatments that are being done right now. Then I'm going to go on for a little bit more to talk about a particular problem that's been of interest to us, which is, incomplete lupus. And then we'll talk about what the interactions with all of this is to the COVID-19 pandemic, and we'll talk a little bit about what I think the future will bring. Next, please.

So the question comes up all the time about, do Asians differ from other patients? There are many studies that show different things. For instance, listed here in some epidemiological studies, the prevalence of lupus is two or three times higher in non-whites – that's for Asians, as opposed to whites – and I'll give you some more details about this in a minute. Some people feel Asians have more active disease. Some people feel they have a higher prevalence of nephritis as opposed to other manifestations. And this is where our LANtern group is particularly important.

There are issues of anxiety and depression and cultural influences that make caring for patients of Asian backgrounds different from, say, African-Americans, and different from Hispanics, and different from Caucasians and that specifically reflect stigma and discrimination issues, as well. And there are a number of different educational interventions. Again, I would point out the LANtern group as being a leader in this, to enhance the communication among all ethnic groups. Next, please.

I hope this is visible to you – in the epidemiology I'm going to show you, I want you to pay attention to the top of the slide because studies of different populations come up with different answers. This is a study based on large data from the entire United States, and it talks about the prevalence and the sex ratios of lupus in various racial groups. What I've highlighted there is that, in this particular study, the prevalence was about 85 per 100,000 persons. That was equivalent to that of whites, well below that of Blacks, and very much below that of Native Americans and Arctic populations. Next slide, please.

This is from metropolitan New York, and specifically, Manhattan. And one of the reasons I want to point this out is that in almost every study, Asian includes Pacific Islanders, and makes no distinctions between Japanese, and Koreans, and Malaysians, and oftentimes South Asians are included in this group, as well. And I think what's going to happen is that the differences that you see are reflecting more which culture dominates in the area that is studied than anything else.

Here you see, on the top, the incidence, and I put little stars over Asian. It generally is higher than white, particularly in the younger, and it is much lower than African-Americans And when you look at prevalence, obviously, that's looking at survivors, you see the same sorts of patterns. Generally, Asians have somewhat more disease, possibly somewhat more severe than whites, but less frequent and less severe than in African-Americans. Next, please.

This is from San Francisco, and it looks at the types of organ abnormalities that are seen in lupus patients by racial groups. I've just highlighted on the arrows, there, if they're visible to you. There are only two circumstances in which there may be a bit of a difference.

The top arrow is for nephritis, and this group, which is listed as Asian and Pacific Islanders, has about 70% more nephritis than do whites. It gives the risk ratio of 1.68. The other arrow points to hematological abnormalities. That's just slightly – it's 7% more frequent than in Caucasians, not terribly important, but the nephritis may be, again, in the San Francisco population. Next, please.

And this is also the same San Francisco population. And this is not survival. It's time to occurrence of nephritis. And the arrow points to the bottom line, which is the Asians, Pacific Islanders, in that group, at least on the West Coast. Again, I'm emphasizing that the mixtures of populations are not just Chinese, but all sorts of other ethnic groups.

There's where the nephritis shows up, and it's about half of the patients have nephritis by about 10 years. Now, it's also important to look at this saying, it's 10 years to get to that point. It's not an immediate point, and you're out at 20 and 30 years before the absolute majority of patients have nephritis. Next, please.

Bottom line, and this is sort of a summary – and then this is national data again – of mortality. And here, despite the nephritis, this is kind of interesting because the mortality rate – Asians are at the top – is only 4.36 per 1 million per year. North American whites are just slightly better at 4.11. And then if you look at the bottom, the mortality rate for high-risk urban African-American patients is up to 16.14 deaths So, again, mortality on the low side on a national scale, and approaching that of whites, much less than African-Americans. And this depends on where you live and whether it's urban or rural. Next, please.

Summary of those facts – this is trying to put the different populations that have been studied together. Asians have a higher incidence than Europeans, but less than other groups, and it varies with place and ancestry in terms of the prevalence. Nephritis may be somewhat higher than in other groups. Mortality may be somewhat lower than in other groups.

And there are no real explanations that have been offered for the differences, though things like socioeconomic and genetic explanations have been offered. One of the reasons that I bring this up is that almost no clinical trials, when you talk about treatment, looks at different groups differently, except there's some that look at African-Americans separately from other groups. But it would be very hard to sort out on clinical trials what is specific for a given group. Next slide, please.

Very briefly I'm going to go over what is the standard of care for lupus today. And it's important to think of this as lupus is a very complex disease. It goes over long periods of time. It involves multiple organ systems. So I can't give you, just, if you have lupus, do this or that. On the next slide, you'll see a little of this complexity. Next, please.

I've already said the first parts of this slide. In terms of the treatments, the treatments are generally based on organ systems, and on severity, and on duration. That is, you treat a brand-new patient differently than one who's been treated for 5 or 10 years, and, obviously, sicker patients are treated more aggressively. There are many patients that in any given clinic, it may be up to half at one time, who are doing so well that they don't need any treatment at all, and you'll just monitor.

Most commonly used drugs, obviously, are corticosteroids, usually low-dose prednisone, but it can be given parenterally, intravenously, very high-dose steroid can be given, and for people with rashes but not for other indications, topical corticosteroids. Hydroxychloroquine I'm going to come back to, again, because it's been very much in the news, but it's now recommended for essentially all lupus patients, unless there's a contraindication.

When it comes to kidney disease, and for patients who can't get on lower dose prednisone, various immunosuppressive drugs are used. And there are reasons for choosing one or another. Arthritis patients are often treated with methotrexate. Kidney patients are treated with mycophenolate, certain types of kidney disease with tacrolimus, and azathioprine is also widely used. The biologics like belimumab and rituximab are increasingly in use in more severe circumstances. And cyclophosphamide is sort of our last ditch thing for very, very seriously ill patients.

Many patients require other types of therapy, particularly if they have antiphospholipid syndrome or clotting. They may be on warfarin or heparin. Obviously, hypertension control and a variety of other medications are used as necessary.

One of the things that's important to think about when you're talking about a lupus patient, is when you think of a decision, this is not a pneumonia, and it is not appendicitis. The decision you make today may play out in 10 years or 20 years. So if you choose to use high-dose corticosteroids, for instance, for something, you have to understand the risks of osteoporosis and of osteonecrosis. If you use a drug like cyclophosphamide, you have to consider the effect on infertility. You have to think both in the short term and the long term with virtually every patient with lupus. Next, please.

All right. So this is just sort of a summary of things. You'll have recording of this, so I'm not going to spend a lot of time on this kind of complicated slide.

I did put the HCQ, for hydroxychloroquine, highlighted for mild and severe disease in almost every instance. The only two places where I didn't indicate hydroxychloroquine is that patient who is doing so well that you think she, and it's almost always a she, doesn't need any treatment at all. You don't have to offer that drug. And in a severe neurologic disease, it's not so clear that hydroxychloroquine works. As I mentioned, the other drugs are used based on both severity and on duration, like the good of your having to continue it for long periods of time, and your fear of long-term complications. Next slide, please.

So what kinds of treatments are being considered today? Well, you don't just say, lupus, treat. You end up having to think of it in terms of the organ systems or the disease process. And most research right now in lupus is based on disease process more than anything else. So next slide, please.

This is here just to frighten you. I'm not going to go into the detail But it's the type of diagrams – you can see, it's from Nature Rheumatology – the types of diagrams they love show a huge amount of abnormal immunological interactions that occur in lupus patients in various circumstances. And all those little red rectangles that you see are drug interventions that are targeted to one or another immunological cell phenomenon.

Most lupus trials right now are not just saying, let me see all your nephritis patients, or let me see all your arthritis patients. They'll look at the biology of the patient and then say, let's target that pathway. And, at this moment, all of those pathways are under examination. There is no consensus target that says, if we get this one, now we'll take care of the disease. None of these medications that are listed here has risen to the top and looks like it's going to be the new cure.

So you're going to hear about a lot of medications over the next few years. Some will be hyped more than others, but we're still working to find something that really, really works, as opposed to just tuning down the disease. Next, please.

Bottom line for this, and I just welcome your questions. If you want to talk about standard medications, the corticosteroids, methotrexate, mycophenolate, rituximab, belimumab, tacrolimus and cyclophosphamide. Experimental therapies are mostly attacking B-cells, interferon pathways. "JAK" inhibitors are being tried. Interleukin inhibitors are being tried. There are even antiviral drugs that are being tried. And then there are some other things that are just out in the very weird category, and we are kind of hoping that one of these will show something really important. But at the moment, nothing as of today that I can tell you will be the breakthrough drug. Next, please.

I want to spend just a couple of minutes talking about Incomplete SLE. And one of the issues – well, next slide, please – is that in our current practices, about half of patients coming to our clinic for the diagnosis of lupus do not fit the criteria that you see that are well known, 4 out of 11 abnormalities that make a diagnosis of SLE.

And there are lots of reasons why this happens. For one, lupus is a chronic illness, not an acute illness. And sometimes it takes years to evolve. Two or three years from first symptoms to having enough findings to call it lupus is not all that uncommon. Sometimes someone will start looking like lupus and eventually over five years or 10 years look more like rheumatoid arthritis, what we call overlapping disease. And some just never change. They stay with these iffy kind of symptoms.

There are two big problems with this. No treatment trial looks at these patients. The trials, because of the way the FDA works, and because of the way people think, take criteria-positive lupus patients for their trials. And so you're not going to find much about the patients with incomplete lupus.

And the second big problem is if – for those of you in practice and have filled out forms – what happens if you don't say the patient has lupus, insurers often refuse treatment and payment for the test. You want to use a medication like belimumab that's approved for lupus only, you'll get turned down. And it ends up with a great deal of fighting between physicians, and patients, and insurers, and other payers to be able to treat these patients. The reason I bring it up is that our own institute is now very much interested in this topic, not just for the money point of view, but for the fact that there's no data on these patients, and we'd like to be able to define them because, as I said, they constitute about half of the patients that we see. Next, please.

OK. We've been looking at this for some while, but we've had, starting for the past year, a formal program registry of all these patients. We've got about 120 patients on whom we have preliminary data. And what we've found, for instance, is that some unusual genetic abnormalities in the complement pathways and in the interferon pathways, in particular, in a few of them. And they're not the same ones, but it's going to demonstrate that all those pathways that I showed on that very complicated slide earlier. We're thinking we're going to be able to pin this down a little bit.

Another thing that we're finding is that there are hints at triggers. That is, someone who might show up with joint pains and maybe a low white count, but not enough to call lupus, may go along for a while until there's a trigger – usually it's an infection, sometimes it's a medication – that suddenly changes the course of the illness. That's happened in a few times. That is, turns it from these incomplete phenomena to what we would formally call lupus. And the other is that sometimes it just takes time for findings to develop. And I'm happy to discuss this more if you have questions at the end. But I think this is one of the more interesting areas that we're going to be looking at. Next, please.

Let's talk about COVID-19. Obviously, we've all been inundated with more than we ever wanted to hear about COVID-19, but one of the more interesting things, and something that I think is going to take us very far in the future, is that there's a lot of COVID-19 that looks like lupus, and a lot of lupus that looks like COVID-19. So next slide, please.

First question that everyone asks because lupus patients are on immunosuppressive drugs and are chronically ill, and so on – are they more at risk for COVID-19? Next, please. Well, the first paper that came out a couple of months ago in the New England Journal looked at people on rheumatic disease treatment and asked whether they were at risk. And I don't need to go through all of these numbers, but listed on here are pretty much all the medications we use – methotrexate, TNF alpha inhibitors, the glucocorticoids, everything else, rituximab, and so on – and there didn't seem to be anything particularly unusual in patients receiving those drugs. This was done at NYU. Next slide, please.

The problem with that study, from my point of view, is for reasons that I don't understand – or, I actually think I know why – they didn't count lupus in this group of patients. The patients that they were looking at had rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, and the other sorts of things. The other thing is that – and this surprised me more – there was no mention of race or socioeconomic status in this paper. Next, please.

We've been doing our own studies. We haven't published it yet. And not only are we doing it at our own hospital, but there are both national and international collaborative groups right now that are gathering data, and I'm on the Zoom calls with these folks all the time. What it is appearing is that lupus patients, in fact, do not look much different from anyone else. They don't seem to have higher susceptibility to this. And one of the things that was of interest when the president was talking about hydroxychloroquine, hydroxychloroquine doesn't appear to be protecting anyone from Covid-19.

Lupus patients look pretty much like the rest of the world in terms of risk for COVID-19. So if you're 75 years old with diabetes, or renal failure, or respiratory disease, you have a tougher time of it. But if you're a 25-year-old and not all that ill, the situation will be pretty much the same, so far as we know. That's very preliminary. The data are being collected right now, and I don't have final answers. Next.

However, there are some really strange things happening in the COVID world. Next slide, please. This is from the newspaper just in the past few weeks, and it points out – I don't need to go to the individual stories – there are blood-clotting complications that are killing patients, strokes in very young patients. For those of you who know about Kawasaki disease, a pediatric disease which is basically a cytokine storm and extremely serious, there are patients with COVID that seem to have what effectively looks like Kawasaki disease and all sorts of things, mostly blood-clotting issues. So next slide, please.

These are some pictures that I've seen. The toes are from a picture in the New York Times. We don't have as good a one. The two on the right-hand side of your screen are patients from New York Presbyterian Hospital. These are the type of lesions that you see. The livedo in the arm – that's on the top on the right – the areas of skin necrosis on the bottom on the right, the, what are referred to as COVID toes, are microvascular disease that can end up in gangrene. And these have been seen in a lot of COVID patients. Next, please.

So there are now a number of reports of antiphospholipid antibody being present and possibly causing the dramatic manifestations of the COVID disease. The slide up here is we've just submitted is a study in which one of our fellows looked at all of the reports on lupus anticoagulant antiphospholipid antibody in COVID patients, asking the question, how carefully did they define the abnormalities? And the biggest problem is that, number one, almost no study looked at the details of how you do these tests and what the false positives might be, and no studies did all the studies that are necessary to define antiphospholipid antibody.

One of the reasons we're extremely curious is that there are a number of infections, syphilis, most obviously, but all sorts of other infections – leprosy is one. Lyme disease is another – where patients can develop transient antiphospholipid antibody that may or may not cause clotting. What you see here is that – and I don't need to go through all of it in detail – but just doing the lupus anticoagulant test, you generally can't do that if a patient has been given anticoagulants. But, in fact, many of the studies did not exclude patients who were on heparin already. The methodology of doing a lupus anticoagulant test is quite complicated and requires a lot of exclusions. Almost none of the studies provided that methodology, even though most of the patients that were reported had lupus anticoagulant.

For the anticardiolipin antibody, it depends which isotype it is, whether it's IgG, IgM, or IgA, what its titer is, and most studies didn't look at that in any degree. Antibody to beta-2 glycoprotein 1, which is another antiphospholipid antibody, also not reported. And finally, it's common to report all three types of tests, that is, lupus anticoagulant, anticardiolipin, and beta-2 glycoprotein 1, and refer to people as single, double, or triple positive, and almost none of the published studies did that. So what the bottom line for that is, is that I don't think we have an answer to whether the lupus anticoagulants being seen in COVID-19 patients is the same as the antibody that we know of in lupus patients. Next, please.

There are some other things that are different from the COVID patients, as opposed to the lupus and antiphospholipid patients. For instance, most patients with lupus and antiphospholipid antibody, if they are clotting have low platelets, most of the COVID-19 patients have had normal platelets. Prothrombin time is not affected by lupus anticoagulant and is usually normal in the lupus patients, but it's slightly high in the COVID patients, suggesting that fibrin split products are interfering. The activated partial thromboplastin time is usually extremely high in lupus patients, and it's generally been normal in the COVID patients. The other way of determining lupus anticoagulant with dilute Russell viper venom time is high in both circumstances.

There are specific tests that you can do after the screening test to confirm lupus anticoagulant. They've generally not been done in this population. And then the anticardiolipin antibodies have generally been, at most, moderately high, and more IgM, whereas in the lupus patients, they tend to be very high, and IgG more than IgM. And D-dimer is variable on the lupus patients. It's universally high in the COVID patients.

So my thinking on this is that we're probably looking at a different process. Whether the antibody is the same is unclear right now. Obviously, there are a number of different circumstances that can make that, but I'm skeptical that this is going to be a way of finding out how we develop antiphospholipid syndrome. Next slide, please.

However, when you look at the autopsies and the other pathology of COVID patients, there are some very strange things happening, as well. Is the vascular lesion that is seen, is it due to inflammation, thrombosis, endothelial damage, a combination of factors, or something else? And then what does that teach us? Next, please.

OK. I'll go over this quickly because we're going to be running out of time, but the answer is we've got all the mechanisms. This is from a study from our institution, which shows arterial thrombosis, capillary injury, little inflammatory response. It's complement mediated. This is skin and lung that you're seeing here. And in the bottom right, when you look also, the virus is present at the sites of the lesions by immunofluorescence. And next.

There's evidence for immune complex disease. And this comes from a very large and nice study from China looking at different types of nephritis. This could be what you see in inflammation and fibrin thrombi, you could see in lupus patients, as well. And immune deposits – I don't know if you can see, there are little arrows on the electron microscopic chart to show the immune complexes. A pathologist could look at this and say, yeah, this could be lupus, but in this case, they're saying, yeah, this could be COVID-19.

Next slide, please. OK. And the other thing is that in the kidneys – so this is the same study – there is evidence by immunofluorescence, by the nucleoprotein antibody, by electron microscopy, that the virus is present in these lesions. Next, please.

So the bottom line is that it's possible that all mechanisms apply, that it's not one thing or another, but it depends on the time after the infection is acquired. The virus gets into your body. It attaches. It probably injures endothelial cells, as some biology supports the idea that it actually has an unusual attraction for endothelial cells, as opposed to other cells.

Initially, there's acute inflammation of pneumonia, or anything else. Patient responds by making an antibody. It's possible that that antibody is an antiphospholipid antibody. It's possible that the antibody is cross-reacting with the virus, or with an endothelial cell marker like von Willebrand factor. And that antibody, down the line, two or three weeks after the illness, leads to the in situ thrombosis, and the immune complex nephritis. In other words, starts as a virus, then turns into a lupus-like illness. Next, please.

This basically summarizes the same sort of thing, just saying, early on, virus infection, patients are asymptomatic at that point. Symptoms appear. It's like a bacterial pneumonia at that point. They start deteriorating at about three weeks. That's due to an immunological overreaction that is very lupus-like. Next, please.

So the questions you have to ask in your COVID patients, where are you in the course of the illness? And what we're asking right now – and I don't have answers for you for this – is we think that the late phase of COVID-19 is an SLE-like illness. What we don't know is why it moves so fast, whereas lupus moves so slowly. And what we don't know is whether it's going to be transient and be gone in three months or six months or not. We are intending to follow up COVID-19 patients to see what happens to them.

On the other hand, if we learn how to turn COVID-19 around, will that give us some reason to think differently about treating lupus? If, for instance, remdesivir, or something like that, turns out to be very good, can we use that information to treat lupus? Next, please.

Couple of practical questions – I feel very strongly about this. I'll talk about it if you want. COVID-19 patients should not take hydroxychloroquine. There is no evidence to support it. It caused a major problem for our patients in their not being able to get their medications on which they depend. And later data are showing that it actually may be harmful in COVID-19. No hydroxychloroquine for COVID-19 patients.

Should COVID-19 patients be anticoagulated? And that's probably because of the thrombosis. Next, please. In fact, the American hematologists – next slide, please – the hematologists have put together a protocol where you should consider anticoagulation in COVID-19 patients. You'll have that on the recording, or you can look for it at the International Society of Thrombosis and Hemostasis web page to find that. Next, please.

So bottom line today, no increased or decreased susceptibility of lupus or other autoimmune disease patients to COVID-19. No unusual courses in those patients, but courses in COVID-19 that suggest lupus. Hydroxychloroquine doesn't help, and it should not be stopped in lupus patients who get COVID-19. There are trials in COVID-19 that are using medications that we use for lupus, like anakinra, tocilizumab, hydroxychloroquine you know about, JAK kinase inhibitors like baricitinib, and antivirals, and others. At this moment, rheumatic disease interventions, if effective at all, will be at the specific phase of the illness when the autoimmune phenomena appear to occur. Next, please.

What can we look forward to in 2020? Lupus is much more manageable today than in the past. We don't have a cure, or a magic bullet for it, but we have many more treatment options, and we're looking forward to being able to use those judiciously. Recognition of pre-disease will give us much better understanding of how people develop lupus. Lupus is teaching us important lessons about COVID-19, and COVID-19 will teach us important lessons about lupus. Next, please.

And I want to thank Eliza and the Lupus Asian Network. Contacts are available for you, as listed on this particular slide. It's been wonderful help for us in managing our patients. I encourage you to have your patients contact us. Next, please.

[Thank you IN CHINESE] Thank you for listening to this. You will be asked to evaluate this program. And I will answer your questions to the extent that I can read them and understand. Thank you.

Thank you, Dr. Lockshin. Thank you very much. For those of you who would like to have a free bilingual brochure sent out to your office, please connect with us by leaving a message in the chat box with your contact information. We're happy to follow up with you.

And for this evaluation, we value your feedback. If you could kindly take a moment before you leave the meeting today to complete the link, it will be posted in the chat box as we speak. The chatbox is located on the bottom of your screen on the toolbar. Thank you very much. And I would like to turn it over to Dr. Lin for Q&A.

Well, thank you very much, Michael. That was a wonderful lecture. I learned quite a lot from it. And thanks for sharing some of your current research projects. I know these are hot off the press, or may not even be in press yet, so thanks for sharing those.

All right.

We have a number of questions over here. One thing I personally have is a burning question to ask. Are we considering COVID-19 a chronic disease condition, or this is still something acute and after patients are cured, they are cured, or this is going to be a chronic process?

It's a critical question, and the answer is, I don't know. In terms of things like lung damage and kidney damage, that's clearly going to be chronic for those people who have them. The reason we have initiated this long-term follow-up study is to find out whether this is going to turn into some of our chronic rheumatic diseases or not.

I mentioned Kawasaki earlier. I don't know how much of the audience knows about Kawasaki. As you may have gathered from its name, it was first seen in Japan as an epidemic disease in children. It moved, then, to Malaysia, to Hawaii, to the west coast of the United States, to the east coast of the United States. It has to be an environmentally-induced disease. No one knows what the environmental agent – whether it's mycobacterial, or an environmental of any sort – is, but it appears to be something that triggers a specific reaction in certain people.

I think COVID-19 is going to be doing that, as well. But this time we actually know what the virus is, so we have a much better chance of figuring out how it does it, which particular people, and whether that's going to be genetic, diet, any environmental sort of thing, or just bad luck. We don't know. But the point of following these patients is to see if we can figure that out.

Right. So we have a few questions from the audience over here. So any comments on patients who have lupus, but also develop COVID? Should they continue the hydroxychloroquine treatment? Should they stop it? You mentioned that patients who have lupus, maybe they have the same susceptibility as everybody else. But if they have lupus, and has COVID, are they more or less likely to have a bad outcome from it?

The official answer is neither better nor worse. There are actually some hints that they may be doing better. And partly it's because of the immunosuppressive drugs that they're on are also ones that are not tamping down the inflammation in the COVID-19 patients.

I have a couple of rules for patients, and I've said this repeatedly, almost daily, for the last two months. Please do not stop your medicines without talking to your physician. A patient in lupus flare is much worse than a patient who is not in lupus flare. These medications keep the disease quiet.

And the second is, should you get COVID and be hospitalized, please keep with you information about your illness, your doctor's contact, and have your doctors work with the physicians. I'm not dealing with ICUs right now. I'm actually retired from practice, so I've not had to deal with this, but having worked in ICUs before, what I'm used to seeing is that ICUs tend not to focus on the underlying illness, and sometimes they make some bad mistakes. So if the physician who knows you well is available to talk to the physicians there, you can avoid getting into trouble because someone just wasn't thinking about the lupus part.

I see. A number of questions concern hydroxychloroquine which is a hot topic in the press, obviously. The question is, you mentioned that you would not suggest COVID patients to take hydroxychloroquine. But if a lupus patient is taking the medication, and have a COVID, would you change their medication dosage?


You change anything?

No, I would continue it throughout at the same dosage.

I see. And there are some thoughts on the reason hydroxychloroquine may not be effective for COVID is people take that too late. When they came to the hospital, already have a serious disease. Do you think taking the medication early would help?

The quick answer to that is no, I don't think it would help. A couple of things are that hydroxychloroquine wasn't just picked out of a hat. There were some theoretical reasons to think that it might work in interfering with virus binding to cells. That's point number one.

But point number two is when you use it to treat lupus or rheumatoid arthritis, you have to give it for about three months before it starts having an effect. Although blood levels are reasonable within a few days of taking the drug, it apparently has to be taken up in body tissues to be effective.

Now, lupus moves much more slowly, and it's not so clear that the same mechanisms apply, but my own experience with hydroxychloroquine is that you don't see anything happening. And, in fact, you end up having to tell patients, don't tell me in a week that you feel the same because it's too early. We'll talk about this in three months.

And so I think if it were to do something in COVID, you'd probably have to be on it long before you ever got exposed to the drug. I don't know that for a fact, but that's just what the experience with lupus suggests would happen.

I see. I see. I guess the same theory goes that it probably does not have a prophylactic effect on COVID, unless you are taking that for a long time before you were exposed.

Yeah. And that's why I say we're kind of curious. There's an international study right now that has about 25,000 patients and we're interrogating that database to see if the frequency of COVID is less than, equal to, or greater than the frequency in the areas from which it comes. Now, obviously, New York is contributing a large part of that, but it's coming from virtually all over the world. And our impression right now is that lupus patients are actually not getting it as much as we'd expect.

There's a question specifically about patients who are on other immunosuppressant medication and their risk of COVID. Specifically, if patients are on rituximab effusion, are they having higher risk of having COVID?

We think not and our advice has generally been not to get too nervous about rituximab and belimumab, in particular, but some patients have been spacing out the doses. And the general rule – I don't know if rule is too strong a word that it is not too dangerous, if reducing doses, to double the time between doses So if they're getting belimumab monthly, maybe you can go to two months, rituximab every six months, maybe go to nine months, or 12. But keep in mind that these drugs are doing something to keep the disease under control, and you're safer if your disease is under control.

OK. I think we are about to be on time. And then I think that's about the questions we have. Well, thank you so much for joining us, Michael. That was a wonderful lecture. Thank you very much, Eliza, for sponsoring the event.

You're very welcome. Thank you for the opportunity. And please, may I remind once again, go to the chatbox, fill out the evaluation through the Gizmo link. We will greatly appreciate that. And thank you so much for your time.

Thank you, Eliza, for doing this, and thank you for teaching me 'xie xie' (thank you)


Michael D. Lockshin, MD.

Michael D. Lockshin, MD
Director Emeritus, Barbara Volcker Center for Women and Rheumatic Disease

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