伴有或不伴有血友病的日本 HIV-1 感染者的冠状动脉狭窄。

IF 1.9 Q3 PUBLIC, ENVIRONMENTAL & OCCUPATIONAL HEALTH
Ran Nagai, Mikiko Ogata, Shuji Kubota, Masaya Yamamoto, Haruka Uemura, Junko Tanuma, Hiroyuki Gatanaga, Hisao Hara, Shinichi Oka, Yukio Hiroi
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引用次数: 0

摘要

在我们之前的研究中,无症状的日本血友病患者(HIV-1 携带者,JHLH)中中度至重度冠状动脉狭窄(CAS)的发病率极高(12.2%)。造成这一现象的原因仍然不明。我们对无血友病的 HIV-1 感染者(无血友病的 PLWH)进行了 CAS 筛查,以比较 JHLH 和无血友病的 PLWH 中 CAS 的患病率,并确定包括炎症标志物在内的风险因素。研究随机选取了在2021年6月至7月期间在本院门诊就诊的97名年龄匹配的男性无血友病 PLWH 患者,并使用冠状动脉计算机断层扫描血管造影术(CCTA)对69名知情同意的患者进行了 CAS 筛查。本研究中,JHLH 病例数为 62 例。与无血友病的 PLWH 相比,JHLH 中度(> 50%)至重度(> 75%)CAS 的发病率明显更高 [14/57 (24.6%) vs. 6/69 (8.7%),p = 0.015],需要紧急干预的 CAS 比例也明显更高 [7 (12.3%) vs. 1 (1.4%),p = 0.013]。在炎症指标中,JHLH 患者血清中细胞间粘附分子-1(p < 0.05)和白细胞介素-6(p < 0.05)的滴度明显高于无血友病的 PLWH 患者。虽然在年龄匹配研究中患者的一些人口统计学特征有所不同,但可以推测血管内炎症可能会促进JHLH中的CAS。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Coronary artery stenosis in Japanese people living with HIV-1 with or without haemophilia.

An extremely high prevalence (12.2%) of moderate-to-severe coronary artery stenosis (CAS) was documented in asymptomatic Japanese haemophiliacs living with HIV-1 (JHLH) in our previous study. The cause of this phenomenon remains unknown. We conducted the CAS screening in people living with HIV-1 without haemophilia (PLWH without haemophilia) to compare the prevalence of CAS in JHLH and PLWH without haemophilia and to identify the risk factors including inflammation markers. Ninety-seven age-matched male PLWH without haemophilia who consulted our outpatient clinic between June and July 2021 were randomly selected, and 69 patients who provided informed consent were screened for CAS using coronary computed tomography angiography (CCTA). The number of JHLH cases was 62 in this study. The prevalence of moderate (> 50%) to severe (> 75%) CAS was significantly higher in JHLH [14/57 (24.6%) vs. 6/69 (8.7%), p = 0.015], and the ratio of CAS requiring urgent interventions was significantly higher [7 (12.3%) vs. 1 (1.4%), p = 0.013] in JHLH than in PLWH without haemophilia. Among the inflammatory markers, serum titres of intercellular adhesion molecule-1 (p < 0.05) and interleukin-6 (p < 0.05) in JHLH were significantly higher than those in PLWH without haemophilia. Although some patient demographics were different in the age-matched study, it might be possible to speculate that intravascular inflammation might promote CAS in JHLH.

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