Association of antiphospholipid syndrome with infective endocarditis and sepsis induced by Staphylococcus aureus: A U.S. nationwide inpatient sample analysis

医学 优势比 败血症 感染性心内膜炎 内科学 心内膜炎 置信区间 耐甲氧西林金黄色葡萄球菌 逻辑回归 混淆 金黄色葡萄球菌 遗传学 生物 细菌
作者
Bahy Abofrekha,Jessica Schwartz,Chloé Lahoud,Ahmad Mustafa,Chapman Wei,Salman Khan,Mitchell Weinberg,Martin Miguel Inocencio Amor
出处
期刊:Lupus [SAGE Publishing]
卷期号:34 (11): 1158-1165
标识
DOI:10.1177/09612033251366391
摘要

Background Antiphospholipid syndrome (APS) predisposes patients to thrombosis and cardiac valve lesions such as Libman-Sacks endocarditis. These vegetations are sterile yet can provide a nidus for infection; the risk of infective endocarditis (IE) and other serious infections in APS patients remains poorly quantified in large populations, representing a knowledge gap. Objective To quantify the risk of the primary outcome, IE, and secondary outcomes of MRSA sepsis and MSSA sepsis, associated with APS using a large, nationally representative inpatient database. Methods We conducted a cross-sectional study using the National Inpatient Sample (NIS) database from 2016 to 2020. Hospitalized patients aged 18–75 with APS were compared to those without APS. Patients with major pre-existing risks for IE or significant confounders (e.g., prosthetic valves, specific congenital/rheumatic heart diseases, ESRD) were excluded. Multivariable logistic regression was used to calculate adjusted odds ratios (aORs) with 95% confidence intervals (CIs). Results 297,459 patients fitted our inclusion criteria. On multivariate analysis, APS was significantly associated with over double the odds of IE (aOR 2.03; 95% CI 1.22–3.37). Importantly, APS also conferred considerably increased risks of MRSA sepsis (aOR 1.75; 95% CI 1.18–2.58) and MSSA sepsis (aOR 1.86; 95% CI 1.28–2.70). Conclusion APS emerged as a significant independent risk factor for IE, Methicillin-resistant (MRSA), and Methicillin-sensitive Staphylococcus aureus (MSSA) sepsis. This suggests a broader vulnerability to infection, possibly linked to underlying endothelial dysfunction or immune dysregulation inherent in APS. These findings highlight the critical need for increased clinical suspicion, vigilant monitoring, and potentially tailored prophylactic or treatment approaches for severe infections in patients with APS.
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