Schwartzman, MD: The second patient is a 48-year-old gentleman who classically presents with stiffness in the morning. This person does not have any significant any significant medical problems. He is treated initially with ibuprofen by his primary care doctor. The rheumatologist does confirm that the patient has synovitis and notes a nodule on his left elbow, which is interesting to me. If I try to look at the numbers of patients that I have with nodular disease in this day and age, compared to what this was 30 years ago when I was a fellow, it’s amazing to me how few patients I have who have nodular RA (rheumatoid arthritis). I’m not sure I completely understand that. I think the easy answer is that we’re treating them earlier, and we’re treating them better because we have better therapies. That might be the answer, but I’m wondering if the phenotype of rheumatoid arthritis is independently changing for reasons that we don’t understand.
I could say the same thing for other extraarticular manifestations. I have an interest in autoimmune eye disease, for example. If I look at my patient population who have RA and ask what percentage of them were not referred to me because they have/had scleritis, it’s tiny. I do have a number of patients who have scleritis, but that’s that’s the reason that they were referred to me.
So extraarticular manifestations, I think, are uncommon in RA—pericarditis, for example. Pulmonary hemorrhage, which had a mortality of 50% when we saw it in the past, and was probably due to rheumatoid vasculitis, are things that I don’t see that much anymore in this patient population.
The patient did have a high CRP (C-reactive protein) and sedimentation rate.Rheumatoid factors and CCP (cyclic citrullinated peptide) were likewise elevated. This patient, as opposed to our first one, did not have erosive disease yet. This patient was not treated as aggressively. Remember, the other one was in 25 mg of parenteral methotrexate within a month. This one was the creep-up approach.
As opposed to the first patient, I don’t think it’s as urgent to use a biologic as it was in the first scenario because that patient had already lost function and had erosive disease. This patient has not lost function and doesn’t technically have erosive disease yet, so it’s not an unreasonable choice. My view, given the recent guidelines by the ACR (American College of Radiology) and NPF (National Psoriasis Foundation) for psoriatic arthritis, is that we are beginning to move to using these more aggressive therapies earlier, meaning that the role of methotrexate over the next 3 decades isn’t going to go away. It’s going to be less frequently used.
I didn’t know this ahead of time when we picked this, and the reason that we chose an anti-IL6 receptor monoclonal antibody was because they did have one study that was interesting, which is on the add-on effect of tocilizumab to background methotrexate. The major issue that would make an anti-IL6 potentially attractive is in people who have high CRP and sedimentation rates, in people who have some of the systemic features. We’ve talked a little bit about COVID (coronavirus 2019), the effectiveness of COVID treatment with tocilizumab in patients who have the cytokine storm. You have to be very careful how you word that. I think if you read through the ACR guidelines on the management of COVID, anti-IL6 therapy does have a unique spot because it has been fairly successful to use to treat that component of cytokine storm.
Transcript Edited for Clarity