Ahmet Karakoyun, Yasemin Akkubak, Mevlüt Hakan Göktepe, Pınar Diydem Yılmaz, Cengiz Kadıyoran, Mustafa Oğul, Adem Kucuk
{"title":"AS患者PCSK9升高与cIMT相关:强直性脊柱炎患者亚临床动脉粥样硬化的有用标志物","authors":"Ahmet Karakoyun, Yasemin Akkubak, Mevlüt Hakan Göktepe, Pınar Diydem Yılmaz, Cengiz Kadıyoran, Mustafa Oğul, Adem Kucuk","doi":"10.46497/ArchRheumatol.2024.10625","DOIUrl":null,"url":null,"abstract":"<p><strong>Objectives: </strong>This study aims to investigate the relationship between proprotein convertase subtilisin/ kexin type 9 (PCSK9) levels and subclinical atherosclerosis (SA) in patients with ankylosing spondylitis (AS).</p><p><strong>Patients and methods: </strong>Between January 2022 and March 2022, a total of 56 patients (33 males, 23 females; mean age: 37.8±9.3 years; range, 20 to 60 years) who were under regular follow-up in our clinic and fulfilled the criteria of the Modified New York Diagnostic Criteria for AS and American College of Rheumatology (ACR) for AS were included. Age- and sex-matched 56 healthy volunteers (25 males, 31 females; mean age: 38.4±8.2 years; range, 20 to 60 years) were also recruited as the control group. Demographic, clinical, and laboratory data were recorded. The PCSK9 level and carotid intima-media thickness (cIMT) were evaluated using appropriate methods.</p><p><strong>Results: </strong>The mean serum PCSK9 levels in AS patients (609.3±149.9 <i>vs.</i> 136.3±120.8 ng/mL, p<0.001) and the mean cIMT values (0.51±0.19 <i>vs.</i> 0.43±0.08 mm, p=0.003) were higher than healthy controls. In the multivariate stepwise regression analysis, there was an independent relationship between SA and PCSK9 (β=0.324, p=0.001). Additionally, there was an independent relationship between carotid plaque and PCSK9 (β=0.265, p=0.006). Based on the receiver operating characteristic curve analysis, the optimal PCSK9 cut-off value for plaque was 472.0 ng/mL, sensitivity 90.9%, specificity 65.0% (area under the curve [AUC]=0.759; 95% CI: 0.660-0.857, p=0.005). The optimal PCSK9 cut-off value for SA was 459.5 ng/mL, sensitivity 63.2%, specificity 63.0% (AUC=0.625; 95% CI: 0.512-0.739, p=0.031).</p><p><strong>Conclusion: </strong>Our study showed that serum PCSK9 levels in patients with AS were higher than that in healthy individuals and were associated with SA and arterial plaque formation. In the light of these findings, PCSK9 may accelerate SA and carotid plaque formation in patients with AS, regardless of the LDL cholesterol level. There may be no relationship between PCSK9 levels and disease activity in patients with AS.</p>","PeriodicalId":93884,"journal":{"name":"Archives of rheumatology","volume":"39 4","pages":"652-661"},"PeriodicalIF":1.1000,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11883255/pdf/","citationCount":"0","resultStr":"{\"title\":\"Increased PCSK9 associated with cIMT in AS: A useful marker for subclinical atherosclerosis in patients with ankylosing spondylitis.\",\"authors\":\"Ahmet Karakoyun, Yasemin Akkubak, Mevlüt Hakan Göktepe, Pınar Diydem Yılmaz, Cengiz Kadıyoran, Mustafa Oğul, Adem Kucuk\",\"doi\":\"10.46497/ArchRheumatol.2024.10625\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objectives: </strong>This study aims to investigate the relationship between proprotein convertase subtilisin/ kexin type 9 (PCSK9) levels and subclinical atherosclerosis (SA) in patients with ankylosing spondylitis (AS).</p><p><strong>Patients and methods: </strong>Between January 2022 and March 2022, a total of 56 patients (33 males, 23 females; mean age: 37.8±9.3 years; range, 20 to 60 years) who were under regular follow-up in our clinic and fulfilled the criteria of the Modified New York Diagnostic Criteria for AS and American College of Rheumatology (ACR) for AS were included. Age- and sex-matched 56 healthy volunteers (25 males, 31 females; mean age: 38.4±8.2 years; range, 20 to 60 years) were also recruited as the control group. Demographic, clinical, and laboratory data were recorded. The PCSK9 level and carotid intima-media thickness (cIMT) were evaluated using appropriate methods.</p><p><strong>Results: </strong>The mean serum PCSK9 levels in AS patients (609.3±149.9 <i>vs.</i> 136.3±120.8 ng/mL, p<0.001) and the mean cIMT values (0.51±0.19 <i>vs.</i> 0.43±0.08 mm, p=0.003) were higher than healthy controls. In the multivariate stepwise regression analysis, there was an independent relationship between SA and PCSK9 (β=0.324, p=0.001). Additionally, there was an independent relationship between carotid plaque and PCSK9 (β=0.265, p=0.006). Based on the receiver operating characteristic curve analysis, the optimal PCSK9 cut-off value for plaque was 472.0 ng/mL, sensitivity 90.9%, specificity 65.0% (area under the curve [AUC]=0.759; 95% CI: 0.660-0.857, p=0.005). The optimal PCSK9 cut-off value for SA was 459.5 ng/mL, sensitivity 63.2%, specificity 63.0% (AUC=0.625; 95% CI: 0.512-0.739, p=0.031).</p><p><strong>Conclusion: </strong>Our study showed that serum PCSK9 levels in patients with AS were higher than that in healthy individuals and were associated with SA and arterial plaque formation. In the light of these findings, PCSK9 may accelerate SA and carotid plaque formation in patients with AS, regardless of the LDL cholesterol level. There may be no relationship between PCSK9 levels and disease activity in patients with AS.</p>\",\"PeriodicalId\":93884,\"journal\":{\"name\":\"Archives of rheumatology\",\"volume\":\"39 4\",\"pages\":\"652-661\"},\"PeriodicalIF\":1.1000,\"publicationDate\":\"2024-12-12\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11883255/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Archives of rheumatology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.46497/ArchRheumatol.2024.10625\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/12/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q4\",\"JCRName\":\"RHEUMATOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Archives of rheumatology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.46497/ArchRheumatol.2024.10625","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/12/1 0:00:00","PubModel":"eCollection","JCR":"Q4","JCRName":"RHEUMATOLOGY","Score":null,"Total":0}
引用次数: 0
摘要
目的:探讨强直性脊柱炎(AS)患者亚临床动脉粥样硬化(SA)与蛋白转化酶枯草素/酮素9型(PCSK9)水平的关系。患者与方法:2022年1月~ 2022年3月,共56例患者,其中男性33例,女性23例;平均年龄:37.8±9.3岁;年龄在20岁至60岁之间),在我们的诊所接受定期随访,符合《修改的纽约AS诊断标准》和美国风湿病学会(ACR)的AS诊断标准。年龄和性别匹配的56名健康志愿者(25名男性,31名女性;平均年龄:38.4±8.2岁;年龄从20岁到60岁不等)作为对照组。记录人口统计学、临床和实验室数据。采用适当的方法评估PCSK9水平和颈动脉内膜-中膜厚度(cIMT)。结果:AS患者血清PCSK9平均水平(609.3±149.9 vs. 136.3±120.8 ng/mL);(0.43±0.08 mm, p=0.003)高于健康对照组。在多元逐步回归分析中,SA与PCSK9存在独立关系(β=0.324, p=0.001)。此外,颈动脉斑块与PCSK9之间存在独立关系(β=0.265, p=0.006)。根据受试者工作特征曲线分析,斑块的PCSK9最佳临界值为472.0 ng/mL,灵敏度90.9%,特异性65.0%(曲线下面积[AUC]=0.759;95% CI: 0.66 -0.857, p=0.005)。PCSK9检测SA的最佳临界值为459.5 ng/mL,灵敏度63.2%,特异性63.0% (AUC=0.625;95% CI: 0.512-0.739, p=0.031)。结论:我们的研究表明,AS患者血清PCSK9水平高于健康人,并与SA和动脉斑块形成有关。根据这些发现,PCSK9可能加速AS患者的SA和颈动脉斑块的形成,无论LDL胆固醇水平如何。AS患者的PCSK9水平与疾病活动性之间可能没有关系。
Increased PCSK9 associated with cIMT in AS: A useful marker for subclinical atherosclerosis in patients with ankylosing spondylitis.
Objectives: This study aims to investigate the relationship between proprotein convertase subtilisin/ kexin type 9 (PCSK9) levels and subclinical atherosclerosis (SA) in patients with ankylosing spondylitis (AS).
Patients and methods: Between January 2022 and March 2022, a total of 56 patients (33 males, 23 females; mean age: 37.8±9.3 years; range, 20 to 60 years) who were under regular follow-up in our clinic and fulfilled the criteria of the Modified New York Diagnostic Criteria for AS and American College of Rheumatology (ACR) for AS were included. Age- and sex-matched 56 healthy volunteers (25 males, 31 females; mean age: 38.4±8.2 years; range, 20 to 60 years) were also recruited as the control group. Demographic, clinical, and laboratory data were recorded. The PCSK9 level and carotid intima-media thickness (cIMT) were evaluated using appropriate methods.
Results: The mean serum PCSK9 levels in AS patients (609.3±149.9 vs. 136.3±120.8 ng/mL, p<0.001) and the mean cIMT values (0.51±0.19 vs. 0.43±0.08 mm, p=0.003) were higher than healthy controls. In the multivariate stepwise regression analysis, there was an independent relationship between SA and PCSK9 (β=0.324, p=0.001). Additionally, there was an independent relationship between carotid plaque and PCSK9 (β=0.265, p=0.006). Based on the receiver operating characteristic curve analysis, the optimal PCSK9 cut-off value for plaque was 472.0 ng/mL, sensitivity 90.9%, specificity 65.0% (area under the curve [AUC]=0.759; 95% CI: 0.660-0.857, p=0.005). The optimal PCSK9 cut-off value for SA was 459.5 ng/mL, sensitivity 63.2%, specificity 63.0% (AUC=0.625; 95% CI: 0.512-0.739, p=0.031).
Conclusion: Our study showed that serum PCSK9 levels in patients with AS were higher than that in healthy individuals and were associated with SA and arterial plaque formation. In the light of these findings, PCSK9 may accelerate SA and carotid plaque formation in patients with AS, regardless of the LDL cholesterol level. There may be no relationship between PCSK9 levels and disease activity in patients with AS.