Association between Serum Sialic Acid Levels and Nonalcoholic Fatty Liver Disease: A Cross-Sectional Study

He, Jian; Mao, Weilin; Zhang, Juanwen; Jin, Xi

doi:10.1159/000435839

Cited by 4 publications

(3 citation statements)

References 35 publications

(32 reference statements)

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“…Although the sialyation status of fibrinogen in patients with nonalcoholic fatty liver disease has to our knowledge never been assessed, it has been reported that free plasma sialic acid levels are increased in patients with diabetes 70 and patients with nonalcoholic fatty liver disease. 71 Interestingly, the permeability of plasma clots from patients with fatty liver disease-related cirrhosis was much lower compared with that of clots from patients with alcohol-induced cirrhosis of comparable severity. Part of this difference was explained by fibrinogen levels, which were much higher in patients with fatty liver disease-associated cirrhosis.…”

Section: The Special Case Of Nonalcoholic Fatty Liver Diseasementioning

confidence: 97%

Alterations in Fibrin Structure in Patients with Liver Diseases

Lisman

Ariëns

2016

Semin Thromb Hemost

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The hemostatic balance in patients with liver diseases is relatively well preserved due to concomitant alterations in pro- and antihemostatic pathways. Thrombin generation studies support the notion of hemostatic competence in liver diseases, but in such tests alterations in fibrinogen level and function are not taken into account. We have recently studied structural and functional properties of the fibrin clot in patients with liver diseases. Although we have confirmed previous findings that hypersialylation of the fibrinogen molecule in patients with liver diseases contributes to a defective fibrinogen-to-fibrin conversion, we have found that once the clot has been formed, it has a thrombogenic nature as assessed by permeability assays. These thrombogenic properties of the fibrin clot in cirrhosis relate to incompletely characterized intrinsic changes in the fibrinogen molecule, which may include oxidation and hypersialylation. In addition, in patients with nonalcoholic fatty liver disease thrombogenic properties of the fibrin clot are not only due to liver disease but also to obesity and the metabolic syndrome. During liver transplantation, the clot normalizes and becomes increasingly permeable, and the functional properties of the fibrin clot are markedly normalized by fibrinogen concentrate, when added to plasma samples in vitro. These new insights in the functional properties of the fibrin clot in patients with liver diseases facilitate a more rational approach to treatment and prevention of both bleeding and thrombotic complications.

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Section: The Special Case Of Nonalcoholic Fatty Liver Diseasementioning

confidence: 97%

Alterations in Fibrin Structure in Patients with Liver Diseases

Lisman

Ariëns

2016

Semin Thromb Hemost

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“…Sialic acids in glycolipids or glycoproteins have diverse functions, including formation of a protective cell surface barrier, involvement in interactions of white blood cells with endothelial lining of blood vessels, recognition by pathogens and toxins and facilitation of cell migration by some cancers [ 216 ]. Circulating sialic acid levels have been positively associated with metabolic syndrome and with NAFLD [ 217 , 218 ]. Fucosylated glycans are also involved in a variety of physiological and pathological procedures, including cell adhesion and migration, angiogenesis, malignancy, tumor metastasis as well as immune cell development and regulation [ 219 ].…”

Section: Glycomicsmentioning

confidence: 99%

The role of omics in the pathophysiology, diagnosis and treatment of non-alcoholic fatty liver disease

2020

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Non-alcoholic fatty liver disease (NAFLD) is a multifaceted metabolic disorder, whose spectrum covers clinical, histological and pathophysiological developments ranging from simple steatosis to non-alcoholic steatohepatitis (NASH) and liver fibrosis, potentially evolving into cirrhosis, hepatocellular carcinoma and liver failure. Liver biopsy remains the gold standard for diagnosing NAFLD, while there are no specific treatments. An ever-increasing number of high-throughput Omics investigations on the molecular pathobiology of NAFLD at the cellular, tissue and system levels produce comprehensive biochemical patient snapshots. In the clinical setting, these applications are considerably enhancing our efforts towards obtaining a holistic insight on NAFLD pathophysiology. Omics are also generating non-invasive diagnostic modalities for the distinct stages of NAFLD, that remain though to be validated in multiple, large, heterogenous and independent cohorts, both cross-sectionally as well as prospectively. Finally, they aid in developing novel therapies. By tracing the flow of information from genomics to epigenomics, transcriptomics, proteomics, metabolomics, lipidomics and glycomics, the chief contributions of these techniques in understanding, diagnosing and treating NAFLD are summarized herein.

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“…Serum SA levels have been reported to be elevated in patients with coronary artery disease (CAD), type 1 and type 2 diabetes mellitus (DM), obesity, nonalcoholic fatty liver disease, and chronic renal failure, including patients on dialysis . Moreover, serum SA concentrations have been found to correlate with atherosclerotic risk factors, including blood levels of LDL‐C, triglycerides (TG), HDL‐C, fibrinogen, lipoprotein (a) (Lp(a)), and uric acid, as well as with albuminuria and carotid intima media thickness (CIMT) .…”

Section: Introductionmentioning

confidence: 99%