Correlations of Acute Cerebral Hemorrhage Complicated with Stress Ulcer Bleeding with Acute Physiology and Chronic Health Evaluation (APACHE) II Score, Endothelin (ET), Tumor Necrosis Factor-alpha (TNF-α), and Blood Lipids

Abstract

BackgroundThis study investigated the correlations between acute cerebral hemorrhage complicated with stress ulcer bleeding and corresponding indexes, including the Acute Physiology and Chronic Health Evaluation (APACHE) II score, vascular endothelin-1 (ET-1), tumor necrosis factor-alpha (TNF-α), and blood lipid factors.Material/MethodsA total of 53 patients with acute cerebral hemorrhage complicated with stress ulcer bleeding were selected as the observation group and 50 patients with simple acute cerebral hemorrhage were selected as the control group. The APACHE II score and the levels of ET-1, TNF-α, and blood lipid factors, including total cholesterol (TC), triglyceride (TG), high-density lipoprotein-cholesterol (HDL-C), low-density lipoprotein-cholesterol (LDL-C), and malondialdehyde (MDA), were detected and the correlations of were analyzed between the 2 groups of patients.ResultsThe blood lipid index TG, APACHE II score, ET-1, TNF-α, renal function indexes [blood urea nitrogen (BUN) and creatinine (Cr)], mortality rate, hemoglobin, and MDA in the observation group were significantly higher than those in the control group, while HDL-C in the observation group was obviously lower than in the control group (p<0.05). The APACHEII score had positive correlations with TG and TNF-α (r=0.8960, r=0.8563, respectively), while it was negatively correlated with TC, HDL-C, LDL-C, and ET-1 (r=−0.909, r=−0.9292, r=−0.8543, and r=−0.8899, respectively) (p<0.001 in all comparisons). APACHEII score, BUN, and Cr were all risk factors.ConclusionsStress ulcer in patients with acute cerebral hemorrhage is associated with blood lipid changes and inflammation, which provides clues for the diagnosis and treatment of acute cerebral hemorrhage.

Changes in biomarkers of endothelial function in the blood after intracerebral hemorrhage in rats with type 2 diabetes mellitus

“…Hypertriglyceridemia can also be identified as a risk factor for cerebral hemorrhage. In addition, it is known that the HDL levels in patients with intracerebral hemorrhage are much lower, and the degree of HDL reduction is associated with the severity of hemorrhage (Wang et al, 2018). Due to some inconsistencies in the available literature, which are associated with the reduction of total cholesterol in the blood in different pathological conditions, the advantage of using TC as a marker of atherogenesis becomes somewhat questionable, and the data obtained in the present study are the subject of further research.…”

“…The vasoconstrictive effect of ET-1 may be enhanced by its inhibitory effect on NO production (Kalani et al, 2008). A correlation between ET-1 levels and ICH development has also been identified (Wang et al, 2018).…”

Mechanism Study of the Protective Effects of Sodium Tanshinone IIA Sulfonate Against Atorvastatin-Induced Cerebral Hemorrhage in Zebrafish: Transcriptome Analysis

“…The hemoglobin and ferric ion released from blood cells caused secondary brain injury by activation of inflammation and oxidative stress in cerebral hemorrhage ( Wang et al, 2018 ; Macdonald and Katan, 2019 ). Free ferric irons also trigged ferroptosis, which is a novel form of cell death, and caused advanced neuron death ( Zhang et al, 2018 ).…”

Protective Effect of Ocotillol, the Derivate of Ocotillol-Type Saponins in Panax Genus, against Acetic Acid-Induced Gastric Ulcer in Rats Based on Untargeted Metabolomics

“…ET-1, an important pro-inflammatory cytokine for the contraction of blood vessels, plays a vital role in GU formation. The increasing secretion of ET-1 results in the reduced blood supply of gastric tissue and the occurrence of hypoxia, acidosis and ulcers [35]. A reduced ET-1 level is commonly associated with an increased NO level, because NO is a type of endogenous vasodilator that could inhibit the secretion of ET-1 and regulate the secretion of gastric acid.…”