The AST/ALT (De-Ritis) ratio: A novel marker for critical limb ischemia in peripheral arterial occlusive disease patients.

The AST/ALT (De-Ritis) ratio: A novel marker for critical limb ischemia in peripheral arterial occlusive disease patients.
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DOI:
10.1097/md.0000000000003843
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发表时间:
2016-06
期刊:
影响因子:
1.6
通讯作者:
Gary T
Gary T
中科院分区:
医学4区
文献类型:
--
作者:
Rief P;Pichler M;Raggam R;Hafner F;Gerger A;Eller P;Brodmann M;Gary T

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丙氨酸氨基转移酶(AST)/丙氨酸氨基转移酶(ALT)(De-Ritis)比值(AAR)是一种易于应用的血液检测。一方面,AAR升高与非酒精性脂肪性肝病(NAFLD)的增加有关。另一方面,NAFLD与心血管疾病、全因死亡率和糖尿病的增加有关。由于AAR在肌肉损伤的情况下也会升高,我们研究了外周动脉闭塞性疾病(PAOD)患者的AAR及其与严重肢体缺血(CLI)的相关性。在我们的横断面研究中,我们纳入了2005年至2010年在我们机构接受治疗的1782例PAOD患者。排除了长期饮酒(>20 g/天)的患者。计算AAR,并根据AAR将队列分为三分位数。通过应用受试者工作曲线分析来区分CLI和非CLI,计算连续AAR的最佳截止值。在我们的队列中,CLI的发生率随着AAR的升高而显著增加。AAR为1.67(敏感性34.1%,特异性81.0%)作为最佳临界值。分为两组,第一组包含1385名患者(AAR <1.67),第二组包含397名患者(AAR> 1.67)。    CLI在AAR> 1.67的患者(166 [41.9%])中比AAR <1.67的患者(329 [23.8%])更常见(P <0.001),既往心肌梗死也是如此(28 [7.1%] vs 54 [3.9%],P = 0.01)。      关于炎症参数,两个患者组的C反应蛋白(中位数8.1 mg/L [2.9-28.23] vs中位数4.3 mg/L [2.0-11.5])和纤维蛋白原(中位数427.5 mg/dL [344.25-530.0] vs 388.0 mg/dL [327.0-493.0])也存在显著差异(均P <0.001)。      最后,AAR> 1.67与CLI的比值比(OR)为2.0(95%置信区间[CI] 1.7-2.3)相关,即使在调整了其他明确的血管风险因素后。  AAR增加与CLI和其他心血管终点高风险患者显著相关。AAR是一种广泛可用且廉价的标记物,可能有助于突出血管终点高风险患者。
The aspartat aminotransferase (AST)/alanin aminotransferase (ALT) (De-Ritis) ratio (AAR) is an easily applicable blood test. An elevated AAR on the one hand has been associated with an increase in nonalcoholic fatty liver disease (NAFLD). NAFLD on the other hand is associated with an increase in cardiovascular disease, all-cause mortality, and diabetes. As the AAR is also elevated in case of muscular damage, we investigated AAR and its association with critical limb ischemia (CLI) in peripheral arterial occlusive disease (PAOD) patients. In our cross-sectional study, we included 1782 PAOD patients treated at our institution from 2005 to 2010. Patients with chronic alcohol consumption (>20 g/day) were excluded. AAR was calculated and the cohort was categorized into tertiles according to the AAR. An optimal cut-off value for the continuous AAR was calculated by applying a receiver operating curve analysis to discriminate between CLI and non-CLI. In our cohort, occurrence of CLI significantly increased with an elevation in AAR. As an optimal cut-off value, an AAR of 1.67 (sensitivity 34.1%, specificity 81.0%) was identified. Two groups were categorized, 1st group containing 1385 patients (AAR < 1.67) and a 2nd group with 397 patients (AAR > 1.67). CLI was more frequent in AAR > 1.67 patients (166 [41.9%]) compared to AAR < 1.67 patients (329 [23.8%]) (P < 0.001), as was prior myocardial infarction (28 [7.1%] vs 54 [3.9%], P = 0.01). Regarding inflammatory parameters, C-reactive protein (median 8.1 mg/L [2.9–28.23] vs median 4.3 mg/L [2.0–11.5]) and fibrinogen (median 427.5 mg/dL [344.25–530.0] vs 388.0 mg/dL [327.0–493.0]) also significantly differed in the 2 patient groups (both P < 0.001). Finally, an AAR > 1.67 was associated with an odds ratio (OR) of 2.0 (95% confidence interval [CI] 1.7–2.3) for CLI even after adjustment for other well-established vascular risk factors. An increased AAR is significantly associated with patients at high risk for CLI and other cardiovascular endpoints. The AAR is a broadly available and cheap marker, which might be useful to highlight patients at high risk for vascular endpoints.