Higher lactate and purine metabolite levels in erythrocyte-rich fresh venous thrombus: Potential markers for early deep vein thrombosis

Maekawa, Kazunari; Sugita, Chihiro; Yamashita, Atsushi; Moriguchi-Goto, Sayaka; Furukoji, Eiji; Sakae, Tatefumi; Gi, Toshihiro; Hirai, Toshinori; Asada, Yujiro

doi:10.1016/j.thromres.2019.03.011

Cited by 29 publications

(40 citation statements)

References 39 publications

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“…The results of metabolome profiling in animals demonstrated that levels of several molecules involved in energy metabolism may be used as discriminatory factors between DVT and control animals [ 5 ]. Maekawa et al [ 34 ] studied metabolic alterations in venous blood and venous thrombus of rabbits with the use of capillary electrophoresis-time of flight mass spectrometry (CE-TOFMS). Their study demonstrated that lactic acid, glycine, glutamate, cysteine glutathione disulphide, glutamine, and lysine, in descending order were the most abundant metabolites in venous thrombus, and their concentrations were at least 5-fold higher compared to the venous blood.…”

Section: Deep Venous Thrombosis and Pulmonary Embolismmentioning

confidence: 99%

“…Their study demonstrated that lactic acid, glycine, glutamate, cysteine glutathione disulphide, glutamine, and lysine, in descending order were the most abundant metabolites in venous thrombus, and their concentrations were at least 5-fold higher compared to the venous blood. In turn, the concentrations of citric acid, glucose 6-phosphate, nicotinamide adenine dinucleotide phosphate+ (NADP+), tryptophan, and fructose 6-phosphate were considerably decreased in the venous thrombus compared to the venous blood [ 34 ]. Fresh venous thrombus of studied rabbits contained different levels of metabolites related to glycolysis, purine and tryptophan metabolism as well as redox reactions compared to venous blood.…”

Section: Deep Venous Thrombosis and Pulmonary Embolismmentioning

confidence: 99%

“…The competition between deoxyhemoglobin and glycolytic enzymes for the cytoplasmic domain of band 3 results in erythrocyte metabolic modulation under hypoxia [ 37 ]. In turn, the rise in the concentration of lactate levels and the reduction of glycolytic metabolite levels were suggested to be associated with boosted glycolysis in intra-thrombus erythrocytes [ 34 ]. Maekawa et al [ 34 ] found that platelets were the most abundant cellular component of venous thrombus.…”

Section: Deep Venous Thrombosis and Pulmonary Embolismmentioning

confidence: 99%

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Metabolomic Profile in Venous Thromboembolism (VTE)

et al. 2021

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Venous thromboembolism (VTE) is a condition comprising deep venous thrombosis (DVT) and pulmonary embolism (PE). The prevalence of this disease is constantly increasing and it is also a chief reason for morbidity. Therefore, the primary prevention of VTE remains a highly important public health issue. At present, its diagnosis generally relies on subjective clinical examination and ultrasound imaging. D-dimer is also used as a biomarker, but it is considered to be poorly specific and only moderately sensitive. There are also no reliable methods that could accurately guide the type of treatment and potentially identify patients who may benefit from more aggressive therapies without the risk of bleeding. The application of metabolomics profiling in the area of vascular diseases may become a turning point in early diagnosis and patient management. Among the most described metabolites possibly related to VTE are carnitine species, glucose, phenylalanine, 3-hydroxybutarate, lactic acid, tryptophan and some monounsaturated and polyunsaturated fatty acids. The cell response to acute PE was suggested to involve the uncoupling between glycolysis and oxidative phosphorylation. Despite technological advancement in the identification of metabolites and their alteration in thrombosis, we still do not understand the mechanisms and pathways responsible for the occurrence of observed alterations.

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Section: Deep Venous Thrombosis and Pulmonary Embolismmentioning

confidence: 99%

Section: Deep Venous Thrombosis and Pulmonary Embolismmentioning

confidence: 99%

Section: Deep Venous Thrombosis and Pulmonary Embolismmentioning

confidence: 99%

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Metabolomic Profile in Venous Thromboembolism (VTE)

et al. 2021

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“…Metabolomic analysis was conducted with the Basic Scan package of HMT using CE-TOFMS based on methods described previously 16) . Briefly, CE-TOFMS analysis was conducted using an Agilent CE capillary electrophoresis system equipped with an Agilent 6210 time-of-flight mass spectrometer, Agilent 1100 isocratic HPLC pump, Agilent G1603A CE-MS adapter kit, and Agilent G1607A CE-ESI-MS sprayer kit (Agilent Technologies, Waldbronn, Germany).…”

Section: Metabolomic Profiling Of Aortic Tissue Using Capillary Electmentioning

confidence: 99%

Upregulated Kynurenine Pathway Enzymes in Aortic Atherosclerotic Aneurysm: Macrophage Kynureninase Downregulates Inflammation

Nishimura

Yamashita

Matsuura

et al. 2021

JAT

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Aims: Inflammation and hypertension contribute to the progression of atherosclerotic aneurysm in the aorta. Vascular cell metabolism is regarded to modulate atherogenesis, but the metabolic alterations that occur in atherosclerotic aneurysm remain unknown. The present study aimed to identify metabolic pathways and metabolites in aneurysmal walls and examine their roles in atherogenesis. Methods: Gene expression using microarray and metabolite levels in the early atherosclerotic lesions and aneurysmal walls obtained from 42 patients undergoing aortic surgery were investigated (early lesion n =11, aneurysm n =35) and capillary electrophoresis–time-of-flight mass spectrometry (early lesion n =14, aneurysm n =38). Using immunohistochemistry, the protein expression and localization of the identified factors were examined (early lesion n =11, non-aneurysmal advanced lesion n =8, aneurysm n =11). The roles of the factors in atherogenesis were analyzed in macrophages derived from human peripheral blood mononuclear cells. Results: Enrichment analysis using 35 significantly upregulated genes (log2 ratio, ＞3) revealed the alteration of the kynurenine pathway. Metabolite levels of tryptophan, kynurenine, and quinolinic acid and the kynurenine-to-tryptophan ratio were increased in the aneurysmal walls. Gene and protein expression of kynureninase and kynurenine 3-monooxygenase were upregulated and localized in macrophages in the aneurysmal walls. The silencing of kynureninase in the cultured macrophages enhanced the expression of interleukin-6 and indoleamine 2,3-dioxygenase 1. Conclusion: Our study suggests the upregulation of the kynurenine pathway in macrophages in aortic atherosclerotic aneurysm. Kynureninase may negatively regulate inflammation via the kynurenine pathway itself in macrophages.

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“…A patient exhibited with chest pain for >30 minute with ST-segment elevated >2 mm in at least 2 contiguous pericardial electrocardiography (ECG) leads or a new left bundle branch block and arrived in our hospital within 12 hours or 24 hours with persistent chest pain were screening for enrollment. Exclusion criteria were as follows: (I) severe anaerobic condition including cardiopulmonary resuscitation, and any other forms of shock but not cardiopulmonary shock and thrombus (19)(20)(21); (II) lack of pre-procedural arterial lactate results before primary PCI; (III) end-stage renal disease and undergoing dialysis. All procedures performed in this study involving human participants were in accordance with the Declaration of Helsinki (as revised in 2013).…”

Section: Study Design and Populationmentioning

confidence: 99%

The relationship between pre-procedural elevated arterial lactate and contrast-induced nephropathy following primary percutaneous coronary intervention

Yang¹,

Guo²,

Ran³

et al. 2021

J Thorac Dis

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Background: Risk stratification has been one of the main steps in preventing contrast-induced nephropathy (CIN), which is a common complication after percutaneous coronary intervention (PCI). Elevated arterial lactate is a biomarker indicating severe disease condition and post-intervention complications. The relationship between lactate and CIN has not been established. This study is performed to investigate the relationship between elevated arterial lactate level and contrast-induced nephropathy (CIN). Methods:Patients diagnosed with ST-segment elevated myocardial infarction (STEMI) were prospectively enrolled, with lactate measured within 0.5-1 hours before primary percutaneous coronary intervention (PCI).Patients with cardiopulmonary resuscitation, any forms of severe anaerobic condition, or end-stage renal disease undergoing dialysis were excluded. CIN was defined as an increase in serum creatinine ≥0.5 mg/dL or 25% within 72 hours after PCI. The Mehran Risk Score (MRS) is widely regarded as a classic risk model for CIN and the risk factors of MRS were applied in our multivariate regression analysis. Results: Of the 227 enrolled patients, 47 (20.7%) developed CIN according to the definition. The mean lactate level was higher in the CIN group than in the non-CIN group (2.68±2.27 vs. 1.74±1.94, P<0.001).The arterial lactate level ≥2.0 mmol/L had 57.5% sensitivity and 75.6% specificity in predicting CIN.The performance of the lactate level in discriminating CIN was similar to that of the MRS (AUC lac =0.707 vs.

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Higher lactate and purine metabolite levels in erythrocyte-rich fresh venous thrombus: Potential markers for early deep vein thrombosis

Cited by 29 publications

References 39 publications

Metabolomic Profile in Venous Thromboembolism (VTE)

Metabolomic Profile in Venous Thromboembolism (VTE)

Upregulated Kynurenine Pathway Enzymes in Aortic Atherosclerotic Aneurysm: Macrophage Kynureninase Downregulates Inflammation

The relationship between pre-procedural elevated arterial lactate and contrast-induced nephropathy following primary percutaneous coronary intervention

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