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PO:03:070 Risk factors for pulmonary artery hypertension in systemic lupus erythematosus

lupusscimed · 2026-03-01 · canonical JSON source

10 visible annotations · policy: published · automated confidence ≥ 75.00%

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Objectives Pulmonary artery hypertension (PAH) represents one of the most severe cardiopulmonary complications of systemic lupus erythematosus (SLE), contributing substantially to morbidity and mortality. Although advances in immunomodulatory and vasodilatory treatments have improved outcomes, early recognition of patients at risk remains challenging. A better understanding of risk factors could enable earlier diagnosis, individualized monitoring, and targeted therapeutic strategies.Methods A narrative literature review was performed following a comprehensive search of PubMed, Web of Science, Scopus, and the Cochrane Library databases up to April 2025. Search terms included ‘systemic lupus erythematosus’, ‘pulmonary hypertension’, ‘risk factors’, ‘autoantibodies’, and ‘vascular remodeling’. Original clinical studies, observational cohorts, and reviews addressing SLE-associated PAH were included. Relevant data were extracted and qualitatively synthesized to identify consistent clinical, serological, and demographic predictors.Results The available evidence supports a multifactorial pathogenesis of SLE-associated PAH involving autoimmune-mediated endothelial injury, chronic inflammation, and microvascular thrombosis ( figure 1). Reported independent risk factors include longer disease duration, Raynaud’s phenomenon, high disease activity (SLEDAI > 10), positivity for anti-U1-RNP, anticardiolipin, oranti-beta2-glycoprotein I antibodies, and female sex. Additionally, reduced diffusing capacity for carbon monoxide (DLCO), elevated NT-proBNP, and early echocardiographic changes (elevated tricuspid regurgitant velocity, right atrial enlargement) show potential as early indicators. Heterogeneity in study design and sample size limits definitive risk stratification, highlighting the need for harmonized prospective registries.Abstract PO:03:070 Figure 1Conclusions SLE-associated PAH results from the interplay of autoimmune, vascular, and thrombotic mechanisms. Recognition of specific serological and clinical predictors may allow earlier identification of high-risk patients and improved outcomes through timely screening and therapy. Future multicenter prospective studies are warranted to validate predictive biomarkers and establish standardized diagnostic algorithms.