Rheumatology
Clinical discussions on autoimmune diseases, biologic therapies, vasculitis, and musculoskeletal conditions.
Recent Discussions
What findings on routine monitoring PFTs prompt you to pursue HRCT in your patients with SARDs?
That’s an excellent question, and the strategy might vary somewhat by the specific SARD, but in general, in any SARD patient undergoing annual PFTs, the presence of any of these should prompt an HRCT to evaluate for the development of ILD. FVC drop ≥ 10% DLCO drop ≥ 15% Moderate decline in FVC (5-9...
In patients with isolated anti-centromere antibody positivity and Raynaud's phenomenon without other features of systemic sclerosis, what is your approach to screening for pulmonary complications?
In patients with isolated anti-centromere antibody (ACA) positivity and Raynaud's phenomenon, even without overt systemic sclerosis, the primary concern is pulmonary arterial hypertension (PAH), which can develop at any point, including decades after initial presentation. Notably, ACA-positive patie...
How do you approach patients with fibromyalgia who are reluctant to consider a psychiatric component to their illness but present with clear mood or anxiety symptoms?
Since patients with fibromyalgia (FM) are often stigmatized and worried that clinicians think “it is all in my head,” it is important to discuss FM treatment and mental health referral from a biopsychosocial perspective. This might include introducing concepts such as the pain/depression dyad, centr...
What specific criteria or patient conditions would make you hesitant to use fluoroquinolones early in the treatment course for managing MSSA joint infections with oral antibiotics?
For MSSA joint infections, I have moved away from using FQ to using high-dose cephalosporins as a step-down therapy, particularly cefadroxil 1 g twice daily, given less frequent dosing/increased adherence. Considering the risk-benefit analysis, I prefer using FQ as an oral option in polymicrobial an...
What is your approach to a patient with RF+/CCP+ rheumatoid arthritis that was previously on TNFi now with high-titer ANA and dsDNA (crithida 1:2560), +chromatin, +histone?
This scenario reads like TNF inhibitor drug-induced serological lupus. The first clinical issue is: are there accompanying symptoms or signs of systemic lupus erythematosus (SLE) beyond the underlying inflammatory arthritis, which would be better attributed to the seropositive rheumatoid arthritis (...
Do the results of FIBRONEER-ILD change your approach to antifibrotic treatment in patients with sarcoidosis related PPF?
According to the FIBRONEER-PPF data, no sarcoidosis-specific outcomes have been reported, and one can only infer that the sarcoidosis-related PPF subpopulation has tracked similarly to the other ILD subtypes, which is a big assumption. It is important to remember that in the INBUILD study, which exa...
In routine clinical practice, how do you operationally define ‘progression despite therapy’ in PPF to justify escalation to combination treatment?
ILD patients undergo regular monitoring with intervals based on concern for progression. In addition to symptom review, objective testing includes PFTs with spirometry and DLCO, 6-minute walk testing that provides information on distance walked, symptoms experienced, and whether or not the patient d...
Should TNF inhibitors be held in patients undergoing radiation therapy?
We do not hold TNF inhibitors when needed for patients undergoing radiation therapy.
In a patient with biopsy proven statin associated immune-mediated necrotizing myopathy who previously responded well to methotrexate but now presents with recurrent proximal leg weakness and rising CK/aldolase levels after several years of stability, what would be your preferred next-line treatment strategy?
That's an excellent question. I would approach this as a probable disease flare, after excluding potential triggers such as statin re-exposure, including over-the-counter supplements (e.g., "natural" cholesterol-lowering mushroom products that may contain statin-like compounds). In that setting, I w...
In a patient with statin induced immune-mediated necrotizing myopathy (+ anti-HMGCR antibodies), would you consider brepocitinib in the treatment algorithm?
Unlike dermatomyositis, anti-HMGCR IMNM generally lacks a strong interferon signature. Therefore, the biologic rationale for JAK inhibition is less compelling, and I would not routinely consider brepocitinib in this setting.