Ischaemic Markers in Acute Hepatic Injury

Panda, Suchismita; Jena, Sushanta Kumar; Nanda, Rachita; Mangaraj, Manaswini; Nayak, Parsuram

doi:10.7860/jcdr/2016/16699.7680

Cited by 4 publications

(3 citation statements)

References 18 publications

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“…We, therefore, hypothesize that serum ALT/LDH ratio reflects the hypoxia-induced liver damage, which can be clinically used for the evaluation of intrahepatic hypoxia. Indeed, several studies have reported serum ALT/LDH ratio reflects a hypoxic marker in the prognosis of ALI patients ( 16 , 17 ), but little has been reported on intrahepatic hypoxia classified serum ALT/LDH ratio histologically.…”

Section: Introductionmentioning

confidence: 99%

Microcirculatory disturbance in acute liver injury

et al. 2021

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Microcirculatory disturbance is thought to be involved in the pathogenesis of acute liver injury (ALI). The current study examined the pathophysiologic role of hepatic microcirculatory disturbance in patients with ALI and in mouse models of ALI. Using serum aminotransferase (ALT)/lactate dehydrogenase (LDH) ratio as a hypoxic marker, 279 patients with ALI were classified into the low ALT/LDH ratio (ALT/LDH ≤1.5) and high ALT/LDH ratio group (ALT/LDH >1.5). In the low ALT/LDH ratio group, serum ALT, LDH, fibrinogen degradation products and prothrombin time-international normalized ratio were increased relative to the high ALT/LDH ratio group. Histologically, hepatic expression of tissue factor (TF) and hypoxia-related proteins was enhanced in the low ALT/LDH ratio group, and this was accompanied by sinusoidal fibrin deposition. Sinusoidal hypercoagulation and intrahepatic hypoxia was also analyzed in two different mouse models of ALI; Concanavalin A (ConA) mice and Galactosamine/tumor necrosis factor (TNF)-α (G/T) mice. Serum ALT/LDH ratio in ConA mice was significantly lower compared with G/T mice. Pimonidazole staining revealed the upregulation of hypoxia-related proteins in ConA mice. Recombinant human soluble thrombomodulin improved liver damage in ConA mice in association with reduced sinusoidal hypercoagulation and intrahepatic hypoxia. The present study provides evidence that serum ALT/LDH ratio aids in the identification of patients with ALI and intrahepatic hypoxia as a result of microcirculatory disturbance. The results facilitate the improved understanding of the pathogenesis of ALI, thereby offering a novel therapeutic strategy against ALI, which arises from sinusoidal hypercoagulation.

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Section: Introductionmentioning

confidence: 99%

Microcirculatory disturbance in acute liver injury

et al. 2021

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“…Some serum enzymes, such as alkaline phosphatase (ALP), lactate dehydrogenase (LDH), alanine aminotransferase (ALT), aspartate aminotransferase (AST) and gamma glutamine transferase (GGT), are commonly used to assess liver dysfunction [1] [2]. However, these enzymes have been studied as potential predictors of all-cause and speci c-cause mortality in the general population [3][4] [5][6] [7].…”

Section: Introductionmentioning

confidence: 99%

Serum Enzymes in Myocardial Infarction Patients: a Study of Survival Time After Recovering

Chien,

Nie,

Thuan

et al. 2023

Preprint

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The present study analyzes the long-term relationship between levels of serum enzymes (lactate dehydrogenase, alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, gamma glutamine transferase) and mortality of all causes, cardiovascular disease, and coronary heart disease in patients who survived an incident of myocardial infarction. A total of 1496 patients (1064 men and 432 women) aged 35–69 were enrolled in the study and followed for 14–22 years. Lactate dehydrogenase was inversely associated with mortality from all causes, cardiovascular disease, and coronary heart disease. In contrast, alanine aminotransferase was positively associated with cardiovascular disease and all-cause mortality, aspartate aminotransferase was positively associated with all-cause mortality, and no significant association was found between gamma glutamine transferase and alkaline phosphatase and any of the mortality outcomes. The observed associations were independent of the potential confounding effects of age, sex, blood pressure, serum glucose and cholesterol, BMI, smoking, and alcohol use.

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“…Acute liver injury (ALI) refers to a destructive hepatic inflammatory disease, which can be caused by virus infection, hepatotoxic drugs, alcohol abuse, and so forth [1,2]. Severe and persistent ALI can eventually lead to liver failure, liver cirrho-sis, and tumorigenesis [3]. To date, the pathological mechanism of ALI is not completely clear.…”

Section: Introductionmentioning

confidence: 99%

The Role of Serotonin in Concanavalin A-Induced Liver Injury in Mice

Pang

Jin

et al. 2020

Oxidative Medicine and Cellular Longevity

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Serotonin is involved in the pathological processes of several liver diseases via the regulation of inflammatory response and oxidative stress. We aimed to investigate the role of serotonin in Concanavalin A- (Con A-) induced acute liver injury (ALI). ALI was induced in C57B/6 wild-type (WT) mice and tryptophan hydroxylase 1 (TPH1) knockout mice through tail vein injection of Con A (15 mg/kg body weight). Another group of TPH1 knockout ALI mice was supplied with 5-hydroxytryptophan (5-HTP) in advance to recover serotonin. The blood and liver tissues of mice were collected in all groups. Markedly increased serum levels of serotonin were identified after the injection of Con A. Increased serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and stronger hepatic tissue pathology were detected, suggesting that serotonin could mediate Con A-induced liver damage. Serotonin significantly facilitated the release of serum and intrahepatic inflammatory cytokines, including interleukin-2 (IL-2), interleukin-6 (IL-6), interleukin-17A (IL-17A), interferon-gamma (IFN-γ), and tumor necrosis-alpha (TNF-α), after the administration of Con A. In addition, serotonin significantly increased the intrahepatic levels of oxidative stress markers malonaldehyde (MDA), myeloperoxidase (MPO), and nitric oxide (NO) and decreased antioxidant stress indicator glutathione (GSH) in Con A-treated mice. Additionally, serotonin promoted hepatocyte apoptosis and autophagy based on B-cell lymphoma-2 (Bcl-2), Bcl-2-asociated X protein (Bax), and Beclin-1 levels and TUNEL staining. More importantly, serotonin activated nuclear factor kappa B (NF-κB) and upregulated the hepatic expressions of high mobility group protein B1 (HMGB1), toll-like receptor-4 (TLR4), and downstream molecules in Con A-mediated liver injury. Serotonin 2A receptor was upregulated in liver tissue after Con A injection, and serotonin 2A receptor antagonist Ketanserin protected against Con A-induced hepatitis. These results indicated that serotonin has the potential to aggravate Con A-induced ALI via the promotion of inflammatory response, oxidative stress injury, and hepatocyte apoptosis and the activation of hepatic HMGB1-TLR signaling pathway and serotonin 2A receptor.

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Ischaemic Markers in Acute Hepatic Injury

Cited by 4 publications

References 18 publications

Microcirculatory disturbance in acute liver injury

Microcirculatory disturbance in acute liver injury

Serum Enzymes in Myocardial Infarction Patients: a Study of Survival Time After Recovering

The Role of Serotonin in Concanavalin A-Induced Liver Injury in Mice

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