QD clinics on ILD - lessons from the Clinic Save

Hello, everyone. I'm Richard Conway from Dublin, Ireland, and this is QD Clinics for RheumNow. The title of today's QD Clinic is Stick or Twist. So this is the case of a 65 year old lady. She has seropositive rheumatoid arthritis, strongly positive for both rheumatoid factor and CCP.

And she's been attending my clinic for the last twenty five years with her rheumatoid. She's currently on methotrexate twenty milligrams weekly and adalimumab forty milligrams every two weeks. And she's been on these medications for ten years or more. And for that time, since she started adalimumab, her disease has been under good control. She comes in, she has no complaints ever, no problems with the medication, no flares of the rheumatoid.

Her C. Generally runs around zero or one. So she's happy out. And she's had a CT scan done. It's a CT, thorax, abdomen, and pelvis, and it's been done somewhere else for the investigation of a little bit of weight loss.

Maybe a scan that didn't need to be done at all, but it has been done. It has come back largely normal. But the physician who's ordered a scan for her has contacted me in a panic because the scan has been reported as showing interstitial lung disease. So the question here is, what do we do with this? We've got a lady who is well, she's asymptomatic.

Her rheumatoid is under very good control on her existing medications of methotrexate and adalimumab, but she has this finding of interstitial lung disease. And we all know that rheumatoid arthritis interstitial lung disease, at least traditionally, has a very, very poor prognosis associated with high mortality. So it is something that makes us sit up and pay attention. But maybe now that we're doing more scans on asymptomatic people, we could be identifying interstitial lung disease that is not associated with such a severe prognosis. So the first thing here we should do, again, double check the lady has no symptoms.

She doesn't. Have a listen to her chest. She has a few little crackles in the bases of her lungs, but nothing too dramatic. Then have a look at this CT scan that's been done. So this CT, it does have interstitial lung disease.

It has basal subpleural predominant fibrotic change consistent with UIP or consistent with rheumatoid arthritis interstitial lung disease. But it's not very much. It's only a little bit that's there. It's not extending throughout the lower lobes or throughout the whole lung field. It's only a little bit of the basis.

So then we look back, see if this lady has had any scans previously that we could compare it to. She hasn't. She hasn't done any pulmonary function tests. So yes, some of those done to assess how her pulmonary function is. Her FVC comes in at 105%.

Her DLCO is 65%, so a little bit reduced. But it's always important to look at other reasons this might be. So we asked this lady, Did you ever smoke? And she did. She used to smoke quite a lot.

She the next smoker, stopped twenty years ago, but was smoking a pack of cigarettes a day before that. So then the question becomes, we have a lady who is essentially asymptomatic. She possibly has normal pulmonary function given her background history of smoking, or we have another explanation for that. And should we change anything? Should we change methotrexate?

Should we change adalimumab to some other agents? So, the methotrexate, for me, is the one that always comes up. Our pulmonologists get very excited by methotrexate and its effect on the lungs. We know that methotrexate can cause an acute pneumonitis. It very rarely causes this.

It's about zero point three percent of people on methotrexate. But it does happen. That's not what this is. This isn't a pneumonitis. This is interstitial lung disease with a fibrotic pattern.

So that's not what we're dealing with here. And we know the best evidence available to us from the ERAS and ERAS studies, from other studies like Philip Dewitt has done, has shown us that methotrexate is not associated with an increased risk of rheumatoid arthritis interstitial lung disease. And if anything, it seems to be protective, both for the development and the progression of this condition. So I'm very comfortable saying we should definitely stay on methotrexate in this case. And the adalimumab then.

So adalimumab and TNF inhibitors have been associated with a suggestion that they might be more associated with the progression and development of rheumatoid interstitial lung disease compared to some of our other agents. The evidence base for that is relatively weak. And it's hard to know if there is an association there, why it happens. And the important thing is that there is one thing that we do know quite convincingly seems to be associated with RAILD development and progression, and that's disease activity. And we have this lady who has absolute pristine disease activity control for ten years or more.

And to me, there seems to be no justification to switch her biologic to an agent that there may be some very weak evidence might be better for interstitial lung disease than the TNF inhibitor, when we have somebody under good disease control and we're gonna risk worsening her disease control, to switch to an agent that there might be a small benefit for. And the other thing we don't know in this case is we don't know what way this is going. We have no past data there. So I would say that it's very, very reasonable to leave this NAD on recurrent treatment, do another set of pulmonary function tests whenever you think is appropriate, three months, six months, a year. I probably leave it a year in a case like this.

But something around that on a scale and see how things are progressing. We have time here. We don't need to overreact to this incidental finding on a CT scan. So that's today's case from QD Clinics. It is when you shouldn't change treatment in RA ILD.

So tune into the room now for more from QD Clinics.

Hello. Welcome to ILD QD Clinics. I'm Doctor. Elena Jerns from Rochester, Minnesota. Today's case is entitled Patient with Interstitial Lung Disease, Positive SSA and a Rash.

So I had a 65 year old lady who came to see me. She had developed symptoms of dyspnea and cough for the past year, and then developed this itchy, scaly rash, particularly on her elbows over the past six months. She came to pulmonology first, who diagnosed her with ILD. She showed NSIP pattern, or non specific interstitial pneumonia pattern. They checked her serologies, which showed positive SSA 52.

ANA titer was actually low, but had cytoplasmic pattern, and she also had high inflammatory markers. She was started on mycophenolate and prednisone. They were concerned for an autoimmune disease in her, so they sent her to me. They asked specifically, Is this dermatomyositis ILD, given the positive SSA 52 and the rash on the elbows? So when I saw her, her rash improved a lot with prednisone, She had no stigmata of dermatomyositis or another autoimmune disease such as scleroderma.

Her elbows actually looked like psoriasis to me. In addition, I looked at her scan and she had a lot of fibrosis. With her only having symptoms for a year, that just did not seem like dermatomyositis ILD to me. If this was dermatomyositis, I would have expected it to look more inflammatory, like cellular nonspecific interstitial pneumonia or organizing pneumonia are more commonly seen in dermatomyositis ILD, especially kind of early on. She was still feeling awful on the mycophenolate and the prednisone and was quite dyspneic.

I asked dermatology about those elbows. They thought the rash did look like psoriasis on the elbows, but the biopsy that they were able to perform was inconclusive. So you have a woman with ILD with fibrotic NSIP pattern, some positive serologies, namely cytoplasmic DNA and SSA fifty two, and a rash, which I guess could be dermatomyositis or psoriasis or something else entirely. What would you do? You're not really sure what to call her.

Is this psoriasis or ILD? Is this interstitial pneumonia without immune features, IPAF, and some sort of rash? Is this myositis ILD? What do you do next? Do you have enough data to give her rituximab?

What if it's psoriasis and you make psoriasis worse? What other options do you have? She has no scleroderma, she has no arthritis, it's tough to argue for tocilizumab. Would you do Adathioprine, IVIG, JAK inhibitors, calcineurin inhibitors, cyclophosphamide? Would you just keep her on mycophenolate and prednisone?

Would you add an anti fibrotic or change her to an anti fibrotic? Ultimately, I decided to treat her as psoriasis IOD, but also cover my basis for dermatomyositis. I felt she really warranted immunosuppression due to steroid responsive, NSIP, high inflammatory markers, rash that was responsive to steroids, and also, of course, positive serologies. She was feeling pretty bad on mycophenolate, and also the mycophenolate side effects were actually precluding us from starting an anti fibrotic such as nantetinib. I decided against rituximab in her case because based on case reports, it can exacerbate preexisting psoriasis, so I was a little bit nervous about that, and also I wasn't sure if rituximab would be as helpful if this was psoriasis ILD.

So for psoriasis, what other options do we have? We have abatacept, we have cyclosporine JAK inhibitors. They all also help in interstitial lung disease, but abatacept is not really used in dermatomyositis ILD, and what if I was wrong? So I started her on a JAK inhibitor. At follow-up six months later, she weaned off prednisone, her PFTs improved, and she felt symptomatically much better, and her rash was minimal.

Then she was able to start vantetinib for additional anti fibrotic action. So while ILD in psoriasis was historically considered to be rare and many meds such as TNF inhibitors and methotrexate have been blamed for it historically, this case for me emphasized the prevalence of ILD in psoriasis. I read a lot about it. I'm still not entirely sure whether it was psoriasis, but dermatologists thought so, and this kind of looked more like that to me as well. There was a recent Japanese study that found ten percent ILD prevalence in one hundred and seventeen patients with psoriasis upon diagnosis prior to exposure to any meds.

Anecdotally, I also not infrequently see patients like this. And most importantly, this case emphasizes therapeutic potential of a JAK inhibitor, particularly in less clear cases. JAK inhibitors may be helpful in a variety of autoimmune ILDs. They have clear utility in myositis ILD, they have emerging evidence in RA ILD, and there is some indirect evidence in scleroderma. Additionally, there was a recent trial proposed to study JAK inhibitors in Sjogren's ILD as well.

And due to their approval in psoriasis, they may be a very viable option in those afflicted by psoriasis ILD. That's all I have today. Thank you so much for your attention. See you next time.

Hello, everyone. This is Jeff Sparks, rheumatologist at Brigham Women's Hospital and Harvard Medical School in Boston. And I am here with QD Clinic as part of the ILD campaign for the month of September 2025 with RheumNow. And we are going to talk about bronchiectasis and rheumatology. And I'm going to talk to you about a patient that I had seen and some of the difficulties that can come from this.

And this patient is a patient with rheumatoid arthritis and bronchiectasis. This is a 68 year old woman with seropositive RA, strongly seropositive CCP and rheumatoid factor. She's had RA for about ten years. Joints overall doing pretty well, but she's been on a couple biologics. She's on tocilizumab and methotrexate and a little bit of prednisone.

And she's a bit on the frail side, underweight, and she saw me saying, Yeah, my joints are feeling okay. I can't come off of prednisone. I'm stuck on three milligrams, but I've had this nagging cough and I'm sometimes coughing up sputum. She doesn't do much around the house. She doesn't have stairs.

She's pretty sedentary, doesn't work out, hasn't lost any abrupt weight. She's always been a bit on the thin side. And so I was confronted with, you know here's someone who has a cough and sputum and certainly the differential is quite wide there. And she didn't really complain too much of shortness of breath. So the first thing to do besides the history is do auscultation.

She basically had some rales, did not feel like she had crackles, but sounded a bit junky. The next thing that I would do is get imaging and PFTs. She had bronchiectasis. It looked to be kind of moderate in severity, diffuse across both lungs, and PFTs also showed some obstruction- she's a non smoker by the way- and she's someone that's been immune suppressed. She's stuck on a little bit of steroids.

She's on both methotrexate and tocilizumab, and so you certainly worry about infection. These are the patients I think kind of keep you up in the middle of the night because she's someone that kind of has a poor baseline and a pneumonia can really push her over the edge. She could get admitted or even worse. And is she brewing in ammonia? Is this like a viral infection that's persistent?

Is she colonized? So you know this is a patient where you might even think about Z Pak, azithromycin. Minocycline is actually- has some efficacy in rheumatoid arthritis and certainly might help out with infections as well. It's a rare patient, but maybe a patient with bronchiectasis and infection might be someone where you even think about something like that. So as far as what happened with this patient, we got the CT scan and PFTs that I mentioned.

This continued to linger. I'll mention she did not need oxygen, she did not de sat when walking, but it basically continued to linger and you started to worry about mycobacterial infection, maybe cancer, maybe other things. So I did send her to pulmonary who decided to do a bronchoalveolar lavage which really did not show a chronic infection. There is this Lady Windermere syndrome of chronic MAC and you've probably heard or even seen patients that have bronchiectasis and MAC and RA and you get into this chicken and egg debate about whether the MAC caused the bronchiectasis or the bronchiectasis caused the MAC and it's really hard to disentangle these patients. And I will say that this is not an uncommon scenario.

Our data show that around ten to fifteen percent of patients have some bronchiectasis, even isolated without ILD, and we really don't know what to do with these patients. Certainly they are at risk for infection. They have mucus buildup in there and floppy airways so they can get pneumonias, viral infections, bacterial infections, so certainly making sure they're vaccinated. But reversing this is really not possible at least at this moment. There are some medications being trialed for bronchiectasis, in particular DPP1 inhibitors that had a positive phase three trial.

However, immune suppression was an exclusion criteria from those trials, so it's not clear how that would help out apply to patients with RA that are on immunosuppression. So really for these patients unfortunately you're trying to be vigilant about vaccination, trying to treat infections that happen, certainly thinking about inhalers, respiratory referring them to pulmonary, following to make sure that things don't progress, making sure that they don't have ILD, and you know if you can trying to offload the immunosuppression in order to decrease that infection risk. We recently had a paper that showed that bronchiectasis really increases the risk of serious infection, and otherwise it's really reassurance that you know a lot of these patients while they have quality of life impact often it does not get much worse and again trying to keep the RA disease at bay while minimizing immunosuppression. So hopefully you can see here that bronchiectasis is a tough problem. We need a lot of solutions.

This is probably something you've encountered with before. The thing we worry about is infection. We really need more treatment options. So this was RA and bronchiectasis in the QD clinic with RheumNow and thanks for your attention.