Rheumatology
Clinical discussions on autoimmune diseases, biologic therapies, vasculitis, and musculoskeletal conditions.
Recent Discussions
How do you approach incidental NXP-2 antibody positivity in patients without current clinical evidence of myositis or systemic autoimmune disease?
A positive anti-NXP2 antibody in an asymptomatic patient may indicate either a false positive or a subclinical form of dermatomyositis. The initial step is to review the testing method (e.g., ELISA, immunoblot). If possible, confirm the result with a different assay, ideally immunoprecipitation, tho...
Before re-challenging a patient with ICI after grade 1-2 pneumonitis, do you re-image to confirm resolution of pneumonitis?
Grade 1 pneumonitis is defined as confined to one lobe of the lung or <25% of the total lung parenchyma, while grade 2 pneumonitis is defined as involving more than one lobe of the lung or 25-50% of the lung parenchyma. Grade 1 pneumonitis is typically an incidental finding on CT in an asymptomatic ...
How do you decide on the next therapy for post-ICI triple M syndrome (myositis/myocarditis/myasthenia) after steroids, PLEX, and IVIG?
The short answer is that there is no standard of care, and no way to reliably predict which of the third-line treatments will work best for each individual. As an introduction, 3M syndrome is a horrible combination of 3 immune-related adverse events (iRAEs) after ICI exposure for cancer, including m...
Should the use of avacopan be limited to those patients at increased risk of steroid toxicity given the anticipated high cost of this medication?
Once Avacopan is available for clinical use in the treatment of patients with AAV, providers will need to carefully weigh risks and benefits of the medication while considering other factors including cost.The ADVOCATE trial used a novel glucocorticoid toxicity index that captures common GC-related ...
Do you always pursue biopsy confirmation before diagnosing IgA vasculitis?
Technically, yes (by definition), but practically, not necessarily: Biopsy for direct immunofluorescence (DIF) testing would be required to confirm the status of IgA in cutaneous vasculitis. However, the presence of lesional IgA correlates positively with the clinical presentation (e.g., Henoch Schö...
Is there a period of time after which you would not resume ICI after a patient has had an irAE and required a prolonged steroid taper?
Typically if a patient has required treatment with steroids for four to six months, it was because their irAE was significant (grade 2-4) and refractory to initial treatment. If the patient received combination immunotherapy, such as anti-CTLA-4 and anti-PD-1 agents, one could consider resuming the ...
How long would you recommend that a patient continues guselkumab prior to deciding that the therapy is not effective?
Many trials have a placebo-controlled period of 12-24 weeks. Thereafter, all patients receive active treatment. Even if the original treatment allocation remains unknown to the patient and doctor, they know that from that moment on, everyone receives active treatment. This will have an influence on ...
How do you interpret treatment response in the DISCOVER-2 Trial when patients were allowed to remain on up to 10mg of prednisone equivalent for disease control while on guselkumab?
The dependence on the use of systemic glucocorticoids may indeed be a good reason to change treatment. Especially in patients with psoriatic arthritis. So, if patients are unable to stop systemic glucocorticoids and there are still treatment options for the patient, this could be tried. It is diffic...
For a pediatric patient with Takayasu arteritis with persistent enhancement and mild progression on imaging after recent transition to tocilizumab (2 months), would you continue tocilizumab therapy, increase to q2 week dosing, or transition to cyclophosphamide?
Would add to the methotrexate and steroids, shortened interval of the tocilizumab, followed by moving to Cytoxan. There is less experience with B-cell-targeted treatment, such as Rituxan or obinutuzumab, for cluster of differentiation 19 (CD19) or CD20.
Is there any role for immunosuppressive therapy in patients with primary Sjogren's disease with severe pulmonary artery hypertension without ILD findings?
PAH (WHO Class I PH) in/and SJD is not a common relation, and as such would Rx as we Rx regarding PAH in PSS? The pathophysiology of PSS is, at least in part, a vasculopathy that SJD may not share. The question is, however, specific regarding Primary SJD and the assumption then is that this is not a...