Rheumatology
Clinical discussions on autoimmune diseases, biologic therapies, vasculitis, and musculoskeletal conditions.
Recent Discussions
In an RA patient with positive RF and CCP abs who is stable on TNFi biologic, how would you approach incidentally found low titer positive DsDNA abs?
ANA and dsDNA antibodies can generally be overlooked in seropositive RA if one is planning to treat (or is treating) with TNF antagonists. There are rare instances of TNFi-induced lupus-like diseases but these are not predicted by pre-existing ANA or dsDNA antibodies.
Do you combine oral and topical NSAIDs for pain relief?
This is a challenging situation but a clinical scenario frequently faced by a practicing rheumatologist. Topical NSAIDs rarely achieve a measurable blood level, and frequently can provide good pain relief at the site of symptoms. It can be a useful way to reduce the milligram dose of an oral NSAID, ...
Would you be comfortable using a JAK inhibitor in a patient with baseline thrombocytosis?
Knowing the etiology of this patient's thrombocytosis is a critical piece of information required before determining whether a JAK- inhibitor drug could be safely prescribed. Mutations in JAK-2 are responsible for several myelodysplastic disorders, some of which present with thrombocytosis. Therefor...
How would you manage a patient with osteoporosis on denosumab who develops significant renal insufficiency where it is difficult to continue denosumab due to increased risk of hypocalcemia (i.e. eGFR in the low 20’s)?
This is an interesting question. Denosumab, unlike bisphosphonates, does not have a warning about use with renal insufficiency. However, denosumab does reduce osteoclast activity for a few weeks after the injection, and this can cause hypocalcemia in patients with renal insufficiency as these patien...
How do you approach diagnosis and treatment of HLH/MAS following CAR T-cell therapy?
I maintain that immune effector cell associated hyperinflammatory syndrome is NOT HLH. Most patients post CAR-T cell therapy fulfill the criteria for HLH even if they don’t have hyperinflammatory syndrome, so it makes diagnosis very challenging. Many patients with this “HLH-like” hyperinflammatory s...
In the setting of secondary HLH associated with initial diagnosis of lymphoma, would you adjust steroid dose and type to account for differences in HLH and lymphoma treatment protocols?
I don’t necessarily recommend changing the steroid dose, unless symptoms don’t resolve with chemotherapy. I do recommend using an etoposide-containing lymphoma therapy. Many patients will respond well to lymphoma therapy and have recurrent symptoms before the next cycle is due; in those patients, I ...
What would be your next step in treating a patient with osteoporosis who developed AFF on denosumab and who then completed one year of romosozumab?
There is no evidence-based answer for this question. First of all, the development of AFF while on osteoporosis doses of denosumab is very rare. It usually occurs in people who have previously been on bisphosphonates. I would most appropriately assess fracture risk after the romo and then determine ...
How do you approach dosing of anakinra in MAS?
We generally start with dosing per the rheumatology guidelines of 100 mg/day (1-2 mg/kg in children) subcutaneously. Based on case reports, if this is insufficient to control the hyperinflammation, can be increased (see Ajeganova et al., PMID 33281955).
What is your approach to using nintedanib in patients on baseline immunosuppression?
Typically I start antifibrotic therapy in a few situations: The most common reason is ILD progression despite adequate immune suppression, defined as no extra-pulmonary disease activity (usually joint disease, but can tailor according to the patient's disease/situation, such as by presence of rash, ...
How would you approach a patient who has well controlled SLE on HCQ but develops cotton wool spots on routine ophthalmologic screening?
Cotton-wool spots are estimated to occur in 10-15% of SLE patients. Etiology is either thrombotic pathology from associated APS, vasculitis or atherosclerosis. Treatment is targeted to the underlying etiology: eg anti-coagulation for APS, immunosuppression for vasculitis or minimization of atheroscl...