Points to Consider in D2M/Treatment Refractory axSpA
Despite an increasing number of highly effective therapies for axial spondyloarthritis (axSpA), a proportion of patients continue to experience difficult-to-manage (D2M) disease.
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To Pulse or Not to Pulse in ANCA Associated Vasculitis?
Randomized trials typically get top billing at ACR Convergence, but the past three years have seen “target trial emulations” land coveted plenary sessions and oral abstracts. These are not actually trials; instead, they are a new-ish approach to generating causal inferences from observational datasets. One particularly interesting oral presentation from ACR used this idea to investigate a critical question in ANCA associated vasculitis: should we be giving pulse dose steroids?
Two Prescriptions, One Patient
Obesity, in particular in psoriatic arthritis (PsA) was widely covered at #ACR26. This is from the recognition of the size of the problem.
ACR 2026 Day 4 Report
The last day of ACR 2026 was a half-day but a busy day, with several exciting reports, especially coming from the late-breaking abstracts.
TRBV9+ a novel treatment approach for AxSpA?
HLA-B27 is the strongest genetic risk factor for AxSpA positive in 90% of rAxSpA and 30-40% of PsA patients. B27 is an MHC class1 molecule which presents peptide to CD8 T cells. Current therapies treat inflammation but do not eliminate the cellular drivers of disease and only 40-60% of AxSpA patients achieve adequate disease control. Further, only 45% of PsA patients achieve minimal disease activity.
Check the genetics in your patients with ILD
Genetics seems to be playing an increasingly huge role in autoimmune diseases, and certainly in ILD, and we are only now starting to recognize it.
T-Cell Engagers in Autoimmunity: CRS From 12% to 67% Across Six Reports
Six ACR 2026 reports put BCMA, CD19, CD20 and gamma-delta engagers side by side in autoimmune disease. The efficacy signal is consistent. The safety signal depends almost entirely on how the molecule was built.
Cardiovascular Risk in Axial Spondyloarthritis
When a patient with axial spondyloarthritis patient sits in your clinic, their joint inflammation is only half the story. To truly achieve disease control, one should ask: “Am I consistently and aggressively screening them all for cardiovascular risk?"
CAR T Gets the Spotlight. Are We Missing the B Cells That Matter?
CAR T is having its moment in rheumatology. But William Robinson’s presentation at ACR Convergence 2026 raised a question I find even more compelling: are we failing to eliminate the right B cells with therapies we already have?
Falls Hide in Plain Sight in Rheumatic Disease
Katherine Wysham, MD, in the session “Rheumatology for Every Age” at ACR 2026 noted that falls are common in people with arthritis and underreported. A fall tends to start a cycle: lost confidence, less going out, reduced social participation, deconditioning, and then more falls and fractures. As patients age, rheumatologists will see this cycle more often, and about 25% of hip fracture patients die within a year.
Is It Still Inflammation?
A 34 year old female has axSpA. Her CRP is 3, her MRI is quiet, and her BASDAI is 7. She has tried two biologics and is asking about a third. Before we write that prescription, #ACR26 challenges us to ask a different question: is it still inflammation?
Pre-RA: Antibodies Sort the Risk, Ultrasound Erosions Flag Severity
Three ACR 2026 abstracts from the Leeds CCP cohort tested how to triage anti-CCP positive individuals with musculoskeletal symptoms. Serology and a few clinical items carried the prediction, while ultrasound erosions spoke to severity after arthritis began.
Efgartigimod: A New Mechanism for Myositis?
Abstracts come and go, but new trials and new mechanisms stay with us for the long haul. One of the more interesting new mechanisms is the FcRn drugs, and at ACR Convergence 2026 we got to see positive results from the Phase 3 ALKIVIA trial for efgartigimod.
“Age old” biomarkers in ILD and pulmonary fibrosis
At #ACR26, there was a poster on senescence being increased in SARD-ILD, including progressive pulmonary fibrosis, showing epithelial remodeling from DNA damage. This led me to look at the biomarkers of NISP (nonspecific interstitial pneumonia) that will transition to fibrosis, as the latter is considered irreversible and the former is potentially reversible.