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Background: Multiple takayasu arteritis (TA) is a chronic nonspecific large to medium vasculitis disease that mainly accumulates the aorta and its branches. Pulmonary vascular disease is often seen as stenosis and occlusion, and patients may show no moderate to severe pulmonary hypertension (PH). This study aims to summarize the clinical characteristics and analysis of prognostic factors in patients with PH caused by TA., Methods: Patients diagnosed with aortitis involving the pulmonary artery by pulmonary arteriography or pulmonary artery and total aortic computed tomography arteriography (CTA). All patients underwent detailed clinical assessment, laboratory data collection, and analysis of imaging data. Patients were followed up and factors affecting the prognosis of the pulmonary arteries were analyzed., Results: Most of the patients' complaints were chest tightness, shortness of breath, decreased activity tolerance, hemoptysis and chest pain. 56.90% of the patients were in at the time of admission. Echocardiographic estimation of pulmonary artery systolic pressure was 90.39 ± 22.87 mm Hg. In terms of laboratory tests, 39.66%% of the patients had elevated C-reactive protein and erythrocyte sedimentation rate, and amino-terminal natriuretic peptide precursor on admission. In terms of imaging, all patients had pulmonary artery involvement, which was combined with aortic involvement in 31.03%. Nuclide lung perfusion/ventilation imaging of the patients revealed multiple perfusion defects/absences in the segmental and subsegmental distribution of the lungs. Univariate Cox regression model analysis suggested that patients' WHO functional class at admission, age ≧ 51 years at the time of consultation, and amino-terminal natriuretic peptide precursor ≧ 3500 pg/mL were factors affecting the prognosis. Further multifactorial Cox regression model analysis suggested amino-terminal natriuretic peptide precursor ≧ 3500 pg/mL was an independent predictor of poor prognosis with a hazard ratio (HR) value of 5.248., Conclusion: Electrocardiogram and echocardiogram may suggest an increased right heart load; some patients have elevated serum inflammatory indexes. Characteristic imaging manifestations include widening of the main pulmonary artery, multiple pulmonary segmental and subsegmental stenoses., Competing Interests: The authors have no conflicts of interest to disclose., (Copyright © 2024 the Author(s). Published by Wolters Kluwer Health, Inc.)

Objective To investigate the potential mechanism of follicular regulatory T (Tfr) cells in the pathogenesis of rheumatoid arthritis (RA). Methods The percentage of CD4 + CXCR5 + FOXP3 + ICOS + Tfr cells in the peripheral blood of 20 patients with RA and 20 healthy subjects were detected by flow cytometry, and the correlation between the proportion of Tfr cells and the clinical laboratory index of RA was analyzed. The serum levels of interleukin-10 (IL-10), IL-12, IL-2, transforming growth factor-β (TGF-β) and C-X-C motif chemokine ligand 13 (CXCL13) were measured by ELISA. The mRNA expression of Bcl6 and B lymphocyte induced mature protein 1 (Blimp-1) in peripheral blood mononuclear cells (PBMCs) was detected by real-time quantitative PCR. Immunohistochemistry was used to detect the expression of Bcl6 and CXCL13 in synovium of RA patients. Results The percentage of Tfr cells in the RA patients significantly decreased compared with the healthy controls, which was negatively related to the C reactive protein (CRP), rheumatoid factor (RF), erythrocyte sedimentation rate (ESR), disease activity score in 28 joints (DAS28). The serum levels of IL-12 and CXCL13 in the patients with RA went up obviously, while the levels of IL-2, IL-10 and TGF-β went down remarkably. The Bcl6 mRNA level in PBMCs of the RA patients was significantly raised, while the expression of Blimp-1 mRNA was significantly reduced. Bcl6 and CXCL13 were highly expressed in the synovium of the RA patients. Conclusion The decrease of the proportion of Tfr cells in the peripheral blood may be related to the occurrence and development of RA.