Objectives: Giant cell arteritis (GCA) is a large/medium-vessel granulomatous vasculitis, and the PD-1/PD-L1 coinhibitory pathway seems to be implicated in its pathogenesis. CD4 T cells expressing high PD-1 levels, CD4+CXCR5-PD-1hi peripheral helper (Tph) and CD4+CXCR5+PD-1hi follicular helper T cells (Tfh), are key mediators of autoimmunity. Their frequencies are elevated in the peripheral blood of subjects with several autoimmune conditions but have not been investigated in GCA.
View Article and Find Full Text PDFObjectives: To estimate the incidence of clinical fragility fractures in postmenopausal women with rheumatoid arthritis (RA) and analyze risk factors for fracture.
Methods: Incidence of clinical fragility fractures in 330 postmenopausal women with RA was compared to that of a control population of 660 age-matched postmenopausal Spanish women. Clinical fractures during the previous five years were recorded.
Objectives: Analyse clinical and bone metabolism features in a case series of patients with multiple vertebral fractures after discontinuation of denosumab (DMab).
Methods: An observational descriptive study analysing data from ten patients with multiple vertebral fractures after DMab discontinuation that were admitted to our rheumatology department between 2015 and 2018.
Results: There were a total of 49 spontaneous fractures after an average of 6 DMab doses and 10.
Objectives: To assess the validity of Doppler ultrasound in the diagnosis of giant cell arteritis (GCA), using the American College of Rheumatology (ACR) criteria and biopsy and using as gold standard the patient's definitive clinical diagnosis.
Methods: An observational, descriptive and analytical study of 451 consecutive patients with suspected GCA was conducted, and the clinical history and ultrasound findings of the patients were reviewed. The validity of ACR criteria, temporal arteritis biopsy (TAB) and Doppler ultrasound in the diagnosis of GCA was calculated using the final diagnosis of the doctor in charge as the gold standard.
Introduction: Anti-TNF drugs have proven to be effective against spondyloarthritis (SpA), although 30% of patients fail to respond or experience adverse events leading to treatment discontinuation. In rheumatoid arthritis, the presence of anti-drug antibodies (ADA) against the first TNF inhibitor influences the outcome after switching. Our aim was to assess whether the response to a second anti-TNF drug is related to the previous development of ADA to the first anti-TNF drug SpA patients.
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