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The management of antiphospholipid syndrome is hindered by heterogeneous clinical presentations. Whole-blood transcriptomics have the potential to identify previously unknown disease endotypes, which could inform new treatment strategies. However, such hypothesis-generating data must still account for the results of randomized clinical trials, such as those focused on direct oral anticoagulants in APS.
A pilot study suggests that the bispecific T cell engager blinatumomab may provide a new therapy for patients with refractory rheumatoid arthritis; larger studies and deep phenotyping will be crucial to thoroughly evaluate and optimize this approach.
In this Review, Knight and Erkan consider how the 2023 ACR–EULAR classification criteria for antiphospholipid syndrome (APS) can guide future research to subphenotype APS by understanding its pathophysiology, paving the way for the personalized and proactive management of individuals with APS.
Understanding the molecular endotypes that influence clinical phenotypes is a critical step for the stratification of patients with osteoarthritis (OA) into therapeutic subtypes that can help the development of targeted disease-modifying OA drugs (DMOADs) to provide genuine, long-term clinical benefit.
The management of antiphospholipid syndrome is hindered by heterogeneous clinical presentations. Whole-blood transcriptomics have the potential to identify previously unknown disease endotypes, which could inform new treatment strategies. However, such hypothesis-generating data must still account for the results of randomized clinical trials, such as those focused on direct oral anticoagulants in APS.
A pilot study suggests that the bispecific T cell engager blinatumomab may provide a new therapy for patients with refractory rheumatoid arthritis; larger studies and deep phenotyping will be crucial to thoroughly evaluate and optimize this approach.
The peptide hormone adropin, which is downregulated in dermal fibroblasts in patients with systemic sclerosis (SSc), inhibits TGFβ-mediated fibrosis in in vitro and ex vivo models of human skin, and has potential for the treatment of SSc.
Medication adherence in gout is low, and discontinuation of urate-lowering therapy puts patients at risk of flares and cardiovascular events. A strategy to regularly monitor serum urate levels and the dissolution of urate deposits (particularly if visualized by patients) might encourage adherence in the long term.