Rheumatology
Clinical discussions on autoimmune diseases, biologic therapies, vasculitis, and musculoskeletal conditions.
Recent Discussions
How would you approach potentially tapering maintenance mycophenolate mofetil in a patient with a history of class IV LN that has been in remission for >5 years?
I would tell her, absolutely, and I'm sorry I did not consider this 2 years ago after being in remission for 3 years. ;-) I then proceed to explain the options and make a shared decision-making process. CHOICE 1 (my recommendation): A significant enough lupus nephritis patients are not in true patho...
What is your approach to further workup, monitoring, and treatment of Sjogren's syndrome patients with positive cryoglobulins but no clear signs of vasculitis?
Sjogren's disease patients who have cryoglobulinemia should have a thorough examination including a neuro examination to evaluate for vasculitis. Laboratory evaluation should include urinalysis, creatinine, and urine protein to creatinine ratio to evaluate for renal involvement. Serum and urine immu...
When would you consider using G-CSF in patients with rheumatic disease who have received cyclophosphamide?
Our primary concern would be our patients with systemic lupus erythematosus. There are reports of severe flares in SLE patients treated with G-CSF (vasculitis and nephritis; Vasiliu et al, PMID 16832843) and even reports of cardiac arrest (Ragsdale & Hall Zimmerman, PMID 34748466).Of course, this ne...
Do you recommend uric acid lowering therapies for asymptomatic hyperuricemia in chronic kidney disease?
There is conflicting literature about what to do with elevated uric acid levels in CKD patients. In my practice, I do usually treat high uric acid level over 10 even if asymptomatic. I definitely give allopurinol earlier if elevated uric acid levels and history of kidney stones, even if they are not...
How do you approach hypocomplementemia in Sjogren’s without features of lymphoma?
Low C3 and/or C4 support immune activity. Therefore, I look at all domains that SjD can potentially affect for further clues. Low complements in SjD are associated with systemic disease activity (Ramos-Casals et al., PMID 24162151). Low C4 may suggest a more severe disease (Pavlakis et al., PMID 223...
How would you approach medication de-escalation in a patient with a history of rapidly progressive CTD-ILD who responded to and is currently on mycophenolate 3 grams daily and IVIG 2mg/kg monthly infusions and has been stable for two years?
This is an excellent question with the very little data to go by. We spend most of our time studying escalation of therapy and very little time discussing de-escalation. It has been my experience as a rheumatologist for almost 37 years that many autoimmune diseases initially can be quite immunologic...
How do you approach management of a patient with idiopathic PAH and +ANA, but no other current symptoms/signs of active rheumatologic disease?
(1) Of note, abnormal nail fold capillaroscopy is associated with PAH in several systemic immune diseases: This is famously true for systemic sclerosis, but there are also publications reporting this association for other diseases, notably those in the “lupus family“ like SLE and dermatomyositis. As...
How would you approach the management of a new SLE patient presenting with lupus podocytopathy with FSGS and severe proteinuria (Pr/Cr 18) without immune complex deposition?
Hopefully one of the nephrologists will chime in on this one. However, this reminds me very much of a similar SLE patient I started to take care of about 6 years ago (BX = podocytopathy and FSGS; had marked proteinuria and renal dysfunction). I treated her with high-dose steroids, hydroxychloroquine...
Do you consider the use of antifibrotics at presentation in patients with a radiographic UIP pattern of pulmonary fibrosis in the presence of positive serologies without any symptoms of CTD who have not yet demonstrated evidence of a progressive phenotype?
I really like this question, because it succinctly encapsulates several areas of clinical uncertainty that we are routinely forced to address in our ILD clinics! Let’s unravel some of the subtleties here. For starters, if the radiographic pattern is convincingly that of UIP, our patient will technic...
How would you approach a young patient with bilateral lower extremity muscle weakness and positive anti-Smith, dsDNA, RNP, Raynaud’s, and pericardial effusion but normal muscle enzymes?
The timeline of weakness may be helpful, but another possible cause of weakness in the setting of normal CK would be an inflammatory demyelinating polyneuropathy (can be acute or chronic). EMG and NCS would be helpful in evaluating this.