背景:探讨系统性红斑狼疮(SLE)患者发生肺动脉高压(PAH)的危险因素。
方法:通过中国知识基础设施(CNKI)计算机检索SLE患者发生PAH的危险因素相关文献,PubMed,和Embase,文献检索仅限于至2022年10月的图书馆建设期间。两名研究者独立进行文献筛选和文献信息提取,包括第一作者,发布时间,案件收集时间,样本量,并研究因素,并采用纽卡斯尔-渥太华量表(NOS)对文献质量进行评价。根据比值(OR值)及其95%CI评价SLE患者各项临床表现和实验室指标与PAH发生的关系。
结果:共纳入24种出版物,包括23项病例对照研究和1项NOS≥6的队列研究,文献总体质量较高.发生雷诺现象的SLE患者发生PAH的风险高于未发生的SLE患者[OR=2.39,95%CI(1.91,2.99),P<.05];抗RNP抗体阳性的SLE患者发生PAH的风险高于抗RNP抗体阴性的SLE患者[OR=1.77,95%CI(1.17,3.2.65),P<.05];合并间质性肺病变的SLE患者发生PAH的风险高于无合并间质性肺病变的SLE患者[OR=3.28,95%CI(2.37,4.53),P<.05];合并浆膜炎的SLE患者发生PAH的风险高于无浆膜炎的患者[OR=2.28,95%CI(1.83,2.84),P<0.05]。合并心包积液的SLE患者发生PAH的风险高于无心包积液的患者[OR=2.97,95%CI(2.37,3.72),P<.05];合并血管炎的SLE患者发生PAH的风险高于无血管炎的患者[OR=1.50,95%CI(1.08,2.07),P<0.05;类风湿因子阳性SLE患者发生PAH的风险高于类风湿因子阴性患者[OR=1.66,95%CI(1.24,2.24),P<0.05]。
结论:雷诺现象,血管炎,抗RNP抗体,浆膜炎,间质性肺损伤,类风湿因子,心包积液是SLE患者发生PAH的危险因素。
BACKGROUND: To investigate the risk factors for the development of pulmonary arterial hypertension (PAH) in patients with systemic lupus erythematosus (SLE).
METHODS: The literature related to risk factors for the development of PAH in SLE patients was searched by the computer on
China national knowledge infrastructure (CNKI), PubMed, and Embase, and the literature search was limited to the period of library construction to October 2022. Two researchers independently performed literature screening and literature information extracting, including first author, publication time, case collection time, sample size, and study factors, and used the Newcastle-Ottawa Scale (NOS) to evaluate the quality of the literature. The relationship between each clinical manifestation and laboratory index and the occurrence of PAH in SLE patients was evaluated based on the ratio (OR value) and its 95% CI.
RESULTS: A total of 24 publications were included, including 23 case-control studies and 1 cohort study with NOS ≥ 6, and the overall quality of the literature was high. The risk of PAH was higher in SLE patients who developed Raynaud phenomenon than in those who did not [OR = 2.39, 95% CI (1.91, 2.99), P < .05]; the risk of PAH was higher in SLE patients who were positive for anti-RNP antibodies than in those who were negative for anti-RNP antibodies [OR = 1.77, 95% CI (1.17, 3.2.65), P < .05]; the risk of PAH was higher in SLE patients with interstitial lung lesions than in those without combined interstitial lung lesions [OR = 3.28, 95% CI (2.37, 4.53), P < .05]; the risk of PAH was higher in SLE patients with combined serositis than in those without serositis [OR = 2.28, 95% CI (1.83, 2.84), P < .05]. The risk of PAH was higher in SLE patients with combined pericardial effusion than in those without pericardial effusion [OR = 2.97, 95% CI (2.37, 3.72), P < .05]; the risk of PAH was higher in SLE patients with combined vasculitis than in those without vasculitis [OR = 1.50, 95% CI (1.08, 2.07), P < .05]; rheumatoid factor-positive SLE patients had a higher risk of PAH than those with rheumatoid factor-negative [OR = 1.66, 95% CI (1.24, 2.24), P < .05].
CONCLUSIONS: Raynaud phenomenon, vasculitis, anti-RNP antibodies, serositis, interstitial lung lesions, rheumatoid factor, and pericardial effusion are risk factors for the development of PAH in patients with SLE.