Rheumatology
Clinical discussions on autoimmune diseases, biologic therapies, vasculitis, and musculoskeletal conditions.
Recent Discussions
How would you approach the evaluation and management of a patient with rheumatoid arthritis receiving leflunomide who presents with progressive peripheral pulmonary cavitary nodules, with biopsy revealing necrotizing granulomatous inflammation?
Given the association between leflunomide and nodules with necrosis and giant cells (though quite rare), I would consider stopping leflunomide and moving to another agent. I would, of course, make sure that cultures are negative on those nodules, given it could be mycobacterial, fungal, or even GPA.
How do you manage patients with scleroderma who present with finger ulcerations without other signs of soft tissue infection and MRI demonstrates potential concern for osteomyelitis?
I think this is a tricky situation. Sometimes there is bone damage from acro-osteolysis from the ischemic injury of the scleroderma itself, which can sometimes be difficult to distinguish from osteomyelitis. I would consider watching closely for other signs of deeper infection. You could also consid...
What additional workup and steroid-sparing option would you choose in a patient with potential medium-vessel vasculitis (petechial rash, sensorimotor neuropathy, renal infarcts, renal artery micro-aneurysms and ischemic/ulcerative duodenitis), hypocomplementemia, ASO 1525, negative blood cultures and normal echo?
This is a challenging case. Generally, PAN should be confirmed histologically, particularly if there are atypical features. In this case, hypocomplementemia is atypical, as non-HBV-associated PAN is generally normocomplementemic. Further, PAN more commonly causes ulcers/nodules/reticular lesions tha...
In what clinical situations would you favor IM methylprednisolone over a short oral prednisone taper for managing an RA flare?
I am not an RA expert; however, I am well-versed in the use of IM steroids for flares.After Dr. Petri's FLOAT study in SLE (Danowski et al., PMID 16395750), we have utilized IM steroids instead of daily PO prednisone as our "go-to" treatment of choice as much as we can over Medrol dose packs and QD ...
How do you manage patients with severe hand OA (no synovitis on exam, negative serologies) who fail to respond to NSAIDs but respond very well to oral steroids?
I have used Hydroxychloroquine with some success and offer that to patients for a trial for 4 months if they are willing.
Is a history of Zoster ophthalmicus a contraindication to starting upadacitinib?
A history of HZO (herpes zoster ophthalmicus) or herpes zoster in any dermatome is a relative contraindication to the use of upadacitinib or any JAK inhibitor. HZO is often a very unpleasant disease with pain, ocular discomfort, and vision loss, so the chance of reactivation should be minimized. The...
Would you add romosozumab to denosumab for a year or switch to romosozumab for a year in a patient who fractures on long term denosumab therapy?
My preference, if insurance were not an obstacle, would be to add romosozumab (Romo) rather than switch. The data are limited, and certainly this is "off-label," but the rationale is reasonable. Denosumab (Dmab) treatment leads to increased sclerostin levels which would be targeted by the addition ...
How would you approach management of a patient with seropositive RA and UIP-ILD, with concern for active lung disease?
There is a potential benefit of adding additional immunosuppression for an RA patient with a UIP pattern on HRCT. My go-to-drugs are either abatacept or rituximab. While MMF is a standard first-line medication for many forms of ARD-ILD, it was tried for RA joint disease many years ago and the study ...
Does significant eosinophilia (8-44%) in a patient with suspected granulomatosis with polyangiitis (GPA) based on sinusitis, pulmonary nodules and positive PR3 change your management approach?
This is an important question because at times the distinction between GPA and EGPA can be difficult to make. In general, I would rely on clinical symptoms as a key distinguisher. For example, sinusitis in GPA differs from that of EGPA, with the former often causing crusting, erosions/necrosis on EN...
Would you initiate antifibrotic therapy in a patient with CTD-ILD experiencing worsening symptoms and declining lung function, despite no clear evidence of fibrosis on CT scans?
If the predominant findings on CT were ground glass opacities and/or nodules without any evidence of fibrosis on CT, I would not start with an antifibrotic and, instead, would start with immunosuppression as a first-line agent. Based on the American College of Rheumatology (ACR) and American Thoraci...