Gary T, Pichler M, Belaj K, Eller P, Hafner F, Gerger A, Brodmann M
Division of Vascular Medicine, Department of Internal Medicine, Medical University of Graz, Graz, Austria.
Int J Clin Pract. 2014 Dec;68(12):1483-7. doi: 10.1111/ijcp.12495. Epub 2014 Oct 31.
The lymphocyte-to-monocyte ratio (LMR) is easily determined from the white blood cell count. Lymphocytes were previously investigated as a part of the neutrophil-to-lymphocyte ratio (NLR) in patients with atherosclerotic disease and an elevated NLR was negatively associated with cardiovascular endpoints. As monocytes play a leading role in the progression of atherosclerosis, especially in peripheral arterial occlusive disease (PAOD), we investigated LMR and its association with critical limb ischemia and other vascular endpoints in PAOD patients.
We evaluated 2121 PAOD patients treated at our institution from 2005 to 2010. LMR was calculated and the cohort was divided into tertiles according to the LMR. An optimal cut-off value for the continuous LMR was calculated by applying a receiver operating curve analysis to discriminate between CLI and non-CLI. In our cohort occurrence of CLI decreased significantly with an increase in LMR. An LMR of 3.1 was identified as an optimal cut-off. Two groups were categorized, one with 1021 patients (LMR < 3.1) and a second one with 1100 patients (LMR ≥ 3.1). CLI was more frequent in LMR < 3.1 patients [426 (41.7%)] than in LMR ≥ 3.1 patients [254 (23.1%)] (p < 0.001), as was also the case with prior myocardial infarction [60 (9.5%) vs. 35 (3.2%), p = 0.003] and congestive heart failure [136 (13.3%) vs. 66 (6.0%), p < 0.001). As to inflammatory parameters, C-reactive protein [median 9.0 mg/l (4.0-30.0) vs. median 4.0 mg/l (2.0-8.0)] and fibrinogen (median 438 mg/dl (350-563) vs. 372 mg/dl (316-459.5)] also differed significantly in the two patient groups (both p < 0.001). A LMR < 3.1 was associated with an odds ratio (OR) of 2.0 (95% CI 1.8-2.2, p < 0.001) for CLI, even after adjustment for other vascular risk factors.
A decreased LMR is significantly associated with a high risk for CLI and other vascular endpoints. The LMR is an easily determinable, broadly available and inexpensive marker that could be used to identify patients at high risk for vascular endpoints.
淋巴细胞与单核细胞比值（LMR）可通过白细胞计数轻松得出。既往在动脉粥样硬化疾病患者中，淋巴细胞作为中性粒细胞与淋巴细胞比值（NLR）的一部分进行研究，NLR升高与心血管终点呈负相关。由于单核细胞在动脉粥样硬化进展中起主导作用，尤其是在外周动脉闭塞性疾病（PAOD）中，我们研究了PAOD患者的LMR及其与严重肢体缺血和其他血管终点的关联。
我们评估了2005年至2010年在我院接受治疗的2121例PAOD患者。计算LMR，并根据LMR将队列分为三分位数。通过应用受试者工作特征曲线分析来计算连续LMR的最佳截断值，以区分严重肢体缺血（CLI）和非CLI。在我们的队列中，CLI的发生率随LMR的增加而显著降低。确定LMR为3.1为最佳截断值。将患者分为两组，一组1021例（LMR < 3.1），另一组1100例（LMR≥3.1）。LMR < 3.1的患者中CLI更常见[426例（41.7%）]，高于LMR≥3.1的患者[254例（23.1%）]（p < 0.001），既往心肌梗死的情况也是如此[60例（9.5%）对35例（3.2%），p = 0.003]以及充血性心力衰竭[136例（13.3%）对66例（6.0%），p < 0.001]。关于炎症参数，两组患者的C反应蛋白[中位数9.0 mg/l（4.0 - 30.0）对中位数4.0 mg/l（2.0 - 8.0）]和纤维蛋白原（中位数438 mg/dl（350 - 563）对372 mg/dl（316 - 459.5）]也有显著差异（均p < 0.001）。即使在调整其他血管危险因素后，LMR < 3.1与CLI的比值比（OR）为2.0（95%CI 1.8 - 2.2，p < 0.001）相关。
LMR降低与CLI和其他血管终点的高风险显著相关。LMR是一种易于测定、广泛可用且廉价的标志物，可用于识别有血管终点高风险的患者。
