GlycA: Evaluation of a New Biomarker of Acute Pancreatitis.

GlycA: Evaluation of a New Biomarker of Acute Pancreatitis.
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DOI:
10.3390/biom13101530
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发表时间:
2023-10-16
期刊:
影响因子:
5.5
通讯作者:
--
中科院分区:
生物学2区
文献类型:
--
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背景资料:急性胰腺炎(AP)是胃肠道住院的主要原因,中重度AP患者的死亡率高达40%。糖蛋白乙酰化(GlycA)作为炎症期间释放的糖基化急性期蛋白的翻译后修饰的核磁共振信号(NMR)进行测量。我们的目的是研究GlycA作为AP炎症生物标志物的作用。方法:我们前瞻性纳入20例AP患者和22例健康对照者,并在入院和出院时采集EDTA血浆样本。使用400 MHz Vantera®临床分析仪从这些样品获得NMR光谱,并计算GlycA浓度(正常值= 400 μmol/L)。NMR光谱中2.00 ± 0.01 ppm处的GlycA NMR信号源自循环糖蛋白(如α1-酸性糖蛋白、触珠蛋白、α1-抗胰蛋白酶、α 1-抗胰凝乳蛋白酶和转铁蛋白)碳水化合物侧链内的N-乙酰基甲基质子。然后根据病因和严重程度,比较AP患者和对照组之间以及AP组内的GlycA水平。结果:人口统计学比较相似,除了AP患者的BMI高于健康对照组(29.9 vs 24.8 kg/m2; p < 0.001)。AP轻度10例,中度7例,重度3例。AP患者入院时GlycA水平高于健康对照组(578 vs. 376 μmol/L,p < 0.001),出院时GlycA水平高于健康对照组(655 vs. 376 μmol/L,p < 0.001)。出院时,中重度AP患者的GlycA水平显著高于轻度AP患者(533 vs. 757 μmol/L,p = 0.023),但入院时并非如此。校正BMI后,多变量回归表明GlycA水平> 400 μmol/L的患者发生任何严重程度AP(OR = 6.88; 95%CI,2.07-32.2; p = 0.004)和轻度AP(OR = 6.12; 95%CI,1.48-42.0; p = 0.025)的几率显著高于对照组。结论:我们的初步研究强调了GlycA作为AP患者炎症诊断的新生物标志物的用途。我们的研究表明,住院AP患者的GlycA水平显著高于健康对照组。与轻度AP患者相比,中度至重度AP患者在出院时的GlycA水平较高,表明重度疾病患者存在持续炎症。
Background: Acute pancreatitis (AP) is a leading cause of gastrointestinal hospital admissions, with up to 40% mortality in patients with moderate–severe AP. Glycoprotein acetylation (GlycA) is measured as a nuclear magnetic resonance signal (NMR) of the post-translational modification of glycosylated acute-phase proteins released during inflammation. We aimed to investigate the role of GlycA as an inflammatory biomarker of AP. Methods: We prospectively enrolled 20 AP patients and 22 healthy controls and collected EDTA plasma samples at admission and discharge. NMR spectra were acquired from these samples using a 400 MHz Vantera® Clinical Analyzer, and GlycA concentrations were calculated (normal = 400 μmol/L). The GlycA NMR signal, at 2.00 ± 0.01 ppm in the NMR spectrum, is derived from the N-acetyl methyl group protons within the carbohydrate side chains of circulating glycoproteins such as α1-acid glycoprotein, haptoglobin, α1-antitrypsin, α1-antichymotrypsin, and transferrin. GlycA levels were then compared between AP patients and controls, as well as within the AP group, based on etiology and severity. Results: Demographic comparisons were similar, except for a higher BMI in AP patients compared to healthy controls (29.9 vs. 24.8 kg/m2; p < 0.001). AP was mild in 10 patients, moderate in 7, and severe in 3. GlycA levels were higher in AP patients than healthy controls on admission (578 vs. 376 μmol/L, p < 0.001) and at discharge (655 vs. 376 μmol/L, p < 0.001). GlycA levels were significantly higher in patients with moderate–severe AP than in those with mild AP at discharge (533 vs. 757 μmol/L, p = 0.023) but not at admission. After adjusting for BMI, multivariable regression indicated that patients with GlycA levels > 400 μmol/L had significantly higher odds of having AP of any severity (OR = 6.88; 95% CI, 2.07–32.2; p = 0.004) and mild AP (OR = 6.12; 95% CI, 1.48–42.0; p = 0.025) than controls. Conclusion: Our pilot study highlights the use of GlycA as a novel diagnostic biomarker of inflammation in patients with AP. Our study shows that GlycA levels were significantly higher in hospitalized AP patients compared to healthy controls. Patients with moderate-to-severe AP had higher GlycA levels compared to patients with mild AP at the time of their hospital discharge, suggesting persistent inflammation in patients with severe disease.
DOI: 10.1177/0961203315617842
发表时间: 2016-03
期刊: Lupus
影响因子: 2.6
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