Reye syndrome is characterized by an encephalopathy and fatty infiltration of the liver and other organs. Reye syndrome is usually associated with influenza B or varicella. Frequently these patients have been treated with aspirin-containing compounds. Other disorders may mimic the phenotypes of Reye syndrome, and these conditions include various intoxications and some inborn problems of metabolism. This is to report our experience in a case of Reye like syndrome combined with the aspirin medication after Kawasaki disease. We present this case with a brief review of related literatures.
Aspirin ; Chickenpox ; Humans ; Influenza, Human ; Liver ; Metabolism ; Mucocutaneous Lymph Node Syndrome* ; Phenotype ; Reye Syndrome*

To develop a more efficient antithrombotic way after coronary artery bypass grafting (CABG), the anticoagulant effects were compared of human tissue factor pathway inhibitor (TFPI) gene transfection and aspirin oral administration (traditional method) on vein grafts. An eukaryotic expression plasmid pCMV-(Kozak) TFPI was prepared. Animal model of carotid artery bypass grafting was constructed. In operation, endothelial cells of vein grafts in TFPI group and empty plasmid control group were transfected with pCMV-(Kozak) TFPI and empty plasmid pCMV respectively, while no transfection was conducted in aspirin control group. After operation, aspirin (2 mg.kg(-1).(-1)) was administered (i.g.) in aspirin control group. Three days later, grafts (n=10) were harvested for RT-PCR, Western blotting and immunohistochemical analyses of exogenous gene expression and for pathological, scanning electron microscopic observation of thrombus. Thirty days later, the patency rates of remnant grafts (n=10) were recorded by vessel Doppler ultrasonography. Human TFPI gene products were detected in gene transferred vein grafts. Three days later, thrombi were found in 7 animals of aspirin control group and in 8 animals of empty plasmid control group, but in only 1 of TFPI group (P<0.01). Thirty days later, 5 grafts were occluded in empty plasmid control group, but none of grafts was occluded in the other groups (P<0.05). The endothelial surfaces of grafts in both of the control groups were covered with aggregated erythrocytes and platelets, and it were not seen in TFPI group. It was suggested that the anticoagulant effects on vein grafts of human TFPI gene transfection are better than those of aspirin.
Administration, Oral ; Anticoagulants/*metabolism ; Aspirin/*administration & dosage ; Aspirin/metabolism ; Coronary Artery Bypass ; Disease Models, Animal ; Lipoproteins/*metabolism ; Plasmids/metabolism ; Tissue Transplantation/*methods ; Transfection ; Ultrasonography, Doppler/methods ; Veins/*transplantation ; Venous Thrombosis/metabolism

BACKGROUND AND OBJECTIVES: It is well known that anti-platlet agents decrease the rate of subacute thrombosis after intracoronary stenting significantly. The aim of this study is to assess the antithrombotic effect and safety of 2-month combined regimen of cilostazol and aspirin on intracoronary stenting. METHODS: The study population consisted of 78 lesions of 57 patients (age: 58.1+/-10.3, male 47, female 10) with ischemic heart disease who were underwent successful intracoronary stenting. They were received cilostazol(200mg/day) and aspirin(100mg/day) two days before intracoronary stenting and continued for 8 weeks, and then aspirin was medicated continuously during the study. The laboratory and clinical findings were evaluated before cilostazol administration, 4 weeks, 8 weeks and 6 months after intervention. The excercise treadmill test was done at 6 months after intervention. RESULTS: Subacute thrombosis occurred in 2 patients(3.5%). Target lesion revascularization(TLR) was done in 4 patients(7.3%). Clinical restenosis (symptomatic or positive stress test, subacute thrombosis and TLR) occurred in 15 patients(26.3%). There was no granulocytopenia, or severe liver dysfunction. HDL-cholesterol was increased significantly at 2 months(36.6+/-7.4 mg/dl versus 41.6+/-9.3 mg/dl. p<0.01) and 6 months(36.6+/-7.4 mg/dl versus 42.4+/-10.6 mg/dl. p<0.01) follow up. CONCLUSION: Two-month combined regimen of cilostazol and aspirin was effective and safe after intracoronary stenting. Subacute thrombosis and clinical restenosis rate were comparable with pervious reports. Further large randomized trials are needed for the evaluation of favorable effect of cilostazol on lipid metabolism.
Agranulocytosis ; Aspirin* ; Exercise Test ; Female ; Follow-Up Studies ; Humans ; Lipid Metabolism ; Liver Diseases ; Male ; Myocardial Ischemia ; Stents* ; Thrombosis

BACKGROUND AND OBJECTIVES: It is well known that anti-platlet agents decrease the rate of subacute thrombosis after intracoronary stenting significantly. The aim of this study is to assess the antithrombotic effect and safety of 2-month combined regimen of cilostazol and aspirin on intracoronary stenting. METHODS: The study population consisted of 78 lesions of 57 patients (age: 58.1+/-10.3, male 47, female 10) with ischemic heart disease who were underwent successful intracoronary stenting. They were received cilostazol(200mg/day) and aspirin(100mg/day) two days before intracoronary stenting and continued for 8 weeks, and then aspirin was medicated continuously during the study. The laboratory and clinical findings were evaluated before cilostazol administration, 4 weeks, 8 weeks and 6 months after intervention. The excercise treadmill test was done at 6 months after intervention. RESULTS: Subacute thrombosis occurred in 2 patients(3.5%). Target lesion revascularization(TLR) was done in 4 patients(7.3%). Clinical restenosis (symptomatic or positive stress test, subacute thrombosis and TLR) occurred in 15 patients(26.3%). There was no granulocytopenia, or severe liver dysfunction. HDL-cholesterol was increased significantly at 2 months(36.6+/-7.4 mg/dl versus 41.6+/-9.3 mg/dl. p<0.01) and 6 months(36.6+/-7.4 mg/dl versus 42.4+/-10.6 mg/dl. p<0.01) follow up. CONCLUSION: Two-month combined regimen of cilostazol and aspirin was effective and safe after intracoronary stenting. Subacute thrombosis and clinical restenosis rate were comparable with pervious reports. Further large randomized trials are needed for the evaluation of favorable effect of cilostazol on lipid metabolism.
Agranulocytosis ; Aspirin* ; Exercise Test ; Female ; Follow-Up Studies ; Humans ; Lipid Metabolism ; Liver Diseases ; Male ; Myocardial Ischemia ; Stents* ; Thrombosis

Many reports have been published that provide epidemiological evidence supporting the efficacy of aspirin and non-steroidal anti- inflammatory drugs (NSAIDs) in cancer prevention. The presumed mechanism of chemoprevention is inhibition of cyclooxygenase (COX)-2. Aspirin exhibits an anticancerous effect through several inter-related mechanisms: prostaglandin synthesis and catabolism in epithelial cells, inhibition of Wnt-β-catenin signaling, inactivation of platelets, and the host immune response. Several clinical studies have demonstrated that aspirin and NSAIDs exhibit chemopreventive effects in stomach cancer. However, well-designed clinical studies to answer critical clinical questions such as additional benefits of aspirin or NSAIDs after eradication of Helicobacter pylori, and the net benefit despite the adverse effects of long-term intake of aspirin or NSAIDs, are needed.
Anti-Inflammatory Agents, Non-Steroidal ; Aspirin* ; Chemoprevention* ; Epithelial Cells ; Helicobacter pylori ; Metabolism ; Prostaglandin-Endoperoxide Synthases ; Stomach Neoplasms*

This study explored the effects of Buyang Huanwu Decoction(BYHWD) on platelet activation and differential gene expression after acute myocardial infarction(AMI). SD rats were randomly divided into a sham-operated group, a model group, a positive drug(aspirin) group, and a BYHWD group. Pre-treatment was conducted for 14 days with a daily oral dose of 1.6 g·kg~(-1) BYHWD and 0.1 g·kg~(-1) aspirin. The AMI model was established using the high ligation of the left anterior descending coronary artery method. The detection indicators included myocardial infarct size, heart function, myocardial tissue pathology, peripheral blood flow perfusion, platelet aggregation rate, platelet membrane glycoprotein CD62p expression, platelet transcriptomics, and differential gene expression. The results showed that compared with the sham-operated group, the model group showed reduced ejection fraction and cardiac output, decreased peripheral blood flow, and increased platelet aggregation rate and CD62p expression, and activated platelets. At the same time, TXB_2 content increased and 6-keto-PGF1α content decreased in serum. Compared with the model group, BYHWD increased ejection fraction and cardiac output, improved blood circulation in the foot and tail regions and cardiomyocytes arrangement, reduced myocardial infarct size and inflammatory infiltration, down-regulated platelet aggregation rate and CD62p expression, reduced serum TXB_2 content, and increased 6-keto-PGF1α content. Platelet transcriptome sequencing results revealed that BYHWD regulated mTOR-autophagy pathway-related genes in platelets. The differential gene expression levels were detected using real-time quantitative PCR. BYHWD up-regulated mTOR, down-regulated autophagy-related FUNDC1 and PINK genes, and up-regulated p62 gene expression. The results demonstrated that BYHWD could regulate platelet activation, improve blood circulation, and protect ischemic myocardium in AMI rats, and its mechanism is related to the regulation of the mTOR-autophagy pathway in platelets.
Rats ; Animals ; Rats, Sprague-Dawley ; Drugs, Chinese Herbal/therapeutic use* ; Myocardial Infarction/genetics* ; Myocardium/metabolism* ; Aspirin/therapeutic use* ; TOR Serine-Threonine Kinases/metabolism* ; Membrane Proteins/metabolism* ; Mitochondrial Proteins

Aspirin intolerant asthma (AIA) is frequently characterized as an aspirin (ASA)-exacerbated respiratory disease (AERD). It is a clinical syndrome associated with chronic severe inflammation in the upper and lower airways resulting in chronic rhinitis, sinusitis, recurrent polyposis, and asthma. AERD generally develops secondary to abnormalities in inflammatory mediators and arachidonic acid biosynthesis expression. Upper and lower airway eosinophil infiltration is a key feature of AERD; however, the exact mechanisms of such chronic eosinophilic inflammation are not fully understood. Cysteinyl leukotriene over-production may be a key factor in the induction of eosinophilic activation. Genetic studies have suggested a role for variability of genes in disease susceptibility and response to medication. Potential genetic biomarkers contributing to the AERD phenotype include HLA-DPB1* 301, LTC4S, ALOX5, CYSLT, PGE2, TBXA2R, TBX21, MS4A2, IL10 -1082A > G, ACE -262A > T, and CRTH2 -466T > C; the four-locus SNP set was composed of B2ADR 46A > G, CCR3 -520T > G, CysLTR1 -634C > T, and FCER1B -109T > C. Management of AERD is an important issue. Aspirin ingestion may result in significant morbidity and mortality, and patients must be advised regarding aspirin risk. Leukotriene receptor antagonists (LTRA) that inhibit leukotriene pathways have an established role in long-term AERD management and rhinosinusitis. Aspirin desensitization may be required for the relief of upper and lower airway symptoms in AERD patients. Future research should focus on identification of biomarkers for a comprehensive diagnostic approach.
Animals ; Asthma, Aspirin-Induced/drug therapy/*genetics/*immunology ; Eosinophils/metabolism ; Genetic Predisposition to Disease/genetics ; Humans ; Leukotriene Antagonists/therapeutic use ; Leukotrienes/metabolism ; Models, Biological ; Polymorphism, Genetic/genetics/physiology

OBJECTIVETo study the activation of platelets in children with Kawasaki disease (KD) at molecular level.

METHODSThe expression of platelet surface glycoproteins CD(41), CD(42a), CD(61), CD(62p) and CD(63) in 20 KD patients was measured by flow cytometry before and at 1, 2, 3 week after treatment with aspirin and high-dose (1 approximately 2 g/kg) intravenous gamma-globulin (IVIG).

RESULTSThe expression of glycoprotein CD(41), CD(42a), CD(61), CD(62p) and CD(63) were higher in KD group than in control group. Aspirin and IVIG could not inhibit these high expression of glycoproteins. Higher expression of CD(62p) was observed in patients with coronary artery injury.

CONCLUSIONPlatelets were highly activated in KD patients which may be one of the most important pathophysiological step in KD. It provided a theoretical basis for treatment of KD with antagonist of glycoprotein of platelets. Obviously increase of CD(62p) can be taken as a criterion for predicting coronary artery injury in KD patients.

Aspirin ; pharmacology ; Blood Platelets ; drug effects ; metabolism ; Child ; Child, Preschool ; Coronary Artery Disease ; complications ; metabolism ; Female ; Humans ; Injections, Intravenous ; Male ; Mucocutaneous Lymph Node Syndrome ; metabolism ; pathology ; P-Selectin ; metabolism ; Platelet Activation ; physiology ; Platelet Membrane Glycoproteins ; metabolism ; gamma-Globulins ; pharmacology

OBJECTIVETo investigate the effects of puerarin with aspirin on the markers of damaged vascular endothelial cells, as von Willebrand factor (vWF), and thrombomodulin (TM) in patients with acute cerebral infarction (ACI).

METHODForty-five patients with ACI were included in this study and divided into basic treatment and puerarin groups, meanwhile 26 healthy persons selected as control group. The serum vWF and sTM concentrations were measured by enzyme-linked immunosorbant assay (ELISA) and national institute health stroke scale (NIHSS) score was evaluated at admission and 14 days later after treatment.

RESULTThe level of serum vWF significantly increased in patients with ACI compared to control and major stroke had higher vWF level than minor stroke (P < 0.01), but the serum level of sTM had no obviously differences respectively. Correlation analysis showed that there is a positive correlation between the level of vWF and NIHSS score (P < 0.05, r = 0.368), while the significant correlations between the level of vWF and sTM, sTM and NIHSS score were not observed. After 14 days treatment, the level of serum vWF and NIHSS score were obviously decreased in patients treated with puerarin and aspirin, not in basic treated patients. The level of sTM was increased in patients after 14 d, while puerarin treated patient has lower sTM level than patients with basic treatment (P < 0.05).

CONCLUSIONPatients with ACI cotreated with puerarin and aspirin improved the neurological function, decreased the levels of serum vWF and sTM, indicating puerarin with aspirin had the protective effects on the damaged vascular endothelial cells.

Acute Disease ; Aged ; Aspirin ; administration & dosage ; Cerebral Infarction ; drug therapy ; metabolism ; Endothelial Cells ; drug effects ; metabolism ; Female ; Humans ; Isoflavones ; adverse effects ; Male ; Middle Aged ; Thrombomodulin ; metabolism ; von Willebrand Factor ; metabolism

AIMTo study the effect of aspirin on chronic hypoxia and hypercapnic pulmonary hypertension.

METHODSSD rats were randomly divided into normal control group (A), hypoxic hypercapnic group (B), hypoxic hypercapnia + aspirin group (C). The concentration of TXB2 and 6-keto-PGF1alpha in plasma and in lung were detected by the technique of radioimmunology.

RESULTS(1) mPAP was significantly higher in B group than those of A and C group. Differences of mCAP were not significant in three groups. (2) Light microscopy showed that WA/TA (vessel wall area/total area) and PAMT (the thickness of medial smooth cell layer) were significantly higher in B group than those of A and C group. (3) The concentration of TXB2 and 6-keto-PGF1alpha in plasma and lung as well as the ratio of TXB2/6-keto-PGF1alpha were significantly higher in rats of B group than those of A and C group.

CONCLUSIONAspirin may inhibit hypoxic hypercapnia pulmonary hypertension and pulmonary vessel remodeling.

6-Ketoprostaglandin F1 alpha ; metabolism ; Animals ; Aspirin ; pharmacology ; Carotid Arteries ; pathology ; physiopathology ; Epoprostenol ; metabolism ; Hypercapnia ; physiopathology ; Hypertension, Pulmonary ; metabolism ; pathology ; physiopathology ; Hypoxia ; physiopathology ; Male ; Pulmonary Artery ; pathology ; physiopathology ; Rats ; Rats, Sprague-Dawley ; Thromboxane A2 ; metabolism