髓过氧化物酶(MPO)和高敏c反应蛋白(hsCRP)作为超重高血压患者内皮细胞和白细胞活化的炎症生物标志物

Pub Date : 2021-03-15 DOI:10.5603/AH.A2021.0003
Dunja Buljubašić, I. Drenjančević, Aleksandar Kibel, L. Zibar, Vedrana Vizjak, S. Mandić, T. Bačun
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引用次数: 1

摘要

目的:轻度炎症介导超重与心血管疾病发生的关系。该研究旨在研究超重高血压患者的髓过氧化物酶(MPO)和hsCRP(高敏c反应蛋白)是否可以作为内皮细胞和白细胞活化的生物标志物。方法:纳入75名受试者;原发性动脉高血压(AH) 38例,正常对照组(NC) 37例,分为超重组(OW;BMI≥25kgm -2)和正常体重组(NW;BMI<25kgm-2)。评估身体质量指数(BMI)、炎症标志物浓度、MPO和hsCRP与AH和/或超重的关系。结果:AH患者MPO较高(中位数为132.5pmol/L, IQR为53.8-691.9)(P<0.001),而hsCRP与正常对照组(NC)相比无显著差异。NW- ah患者MPO高于正常NW患者(P=0.02)。正常血压的OW和NW患者MPO相似,而OW患者hsCRP浓度显著高于NW(中位1.85 mg/L, IQR 0.47-7.19)(P=0.01)。与正常的NW和OW患者相比,OW- ah患者的MPO(中位数为137.4pmol/L, IQR为53.80-703.4)(P=0.002)显著高于正常的NW和OW患者(P<0.001),可能反映了高血压的中性粒细胞活化。此外,OW-AH患者的hsCRP(中位1.71mg/L, IQR 0.22-14)显著高于正常血压的NW患者(P=0.005)。在AH组(ρ=0.41, P= 0.009)和NC组(ρ=0.38, P=0.01)中,hsCRP与BMI呈显著正相关,而MPO不相关,支持OW炎症,特别是OW与AH。结论:综上所述,结果提示炎症可能介导AH和OW的相互关联,提示MPO可作为AH和hsCRP的炎症生物标志物。
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Myeloperoxidase (MPO) and high sensitivity C-reactive protein (hsCRP) as inflammatory biomarkers of endothelial and leukocyte activation in overweight hypertensive patients
Aims: Low-grade inflammation mediates the relation between overweight and the development of cardiovascular diseases. The study aimed to examine if myeloperoxidase (MPO) and hsCRP (high-sensitivity C-reactive protein) in overweight hypertensive patients can be used as biomarkers of endothelial and leukocyte activation. Methods : Seventy-five subjects were included in the study; 38 had essential arterial hypertension (AH) and 37 were normotensive controls (NC), subsequently divided into overweight (OW;BMI≥25kgm 2) and normal weight subgroups (NW;BMI<25kgm-2). Body mass index (BMI), inflammatory markers concentrations, association of MPO and hsCRP with AH and/or overweight were assessed. Results : AH patients had higher MPO (median 132.5pmol/L, IQR 53.8–691.9)(P<0.001), while hsCRP did not significantly differ compared to normotensive controls (NC). NW-AH patients had higher MPO (P=0.02) than normotensive NW patients. MPO was similar between normotensive patients OW and NW, while hsCRP concentration was significantly higher in the OW (median 1.85 mg/L, IQR 0.47–7.19)(P=0.01) compared to NW. OW-AH patients had significantly higher MPO (median 137.4pmol/L, IQR 53.80-703.4) (P=0.002) compared to normotensive NW and OW (P<0.001) patients, likely reflecting neutrophilic activation in hypertension. Additionaly, OW-AH patients had significantly higher hsCRP (median 1.71mg/L, IQR 0.22-14) (P=0.005) than normotensive NW patients. hsCRP significantly positively correlated with BMI in both AH (ρ=0.41, P=0,009) and NC groups (ρ=0.38, P=0.01), while MPO did not correlate, supporting inflammation in OW, particularly in OW with AH. Conclusions: All together, the results suggest that inflammation may mediate mutual association of AH and OW, suggesting MPO as inflammatory biomarker for AH and hsCRP for overweight.
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