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Severe hepatoxicity caused by aspirin overdose: a case report
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《医学前沿（英文）》 2015年 第9卷 第3期 页码 388-391 doi: 10.1007/s11684-015-0398-7
We report here the rare case of a 61-year-old man with multiple organ dysfunction caused by an aspirin overdose (4 g orally). The patient presented with a fever that reached 39.2 °C, a peptic ulcer, and massive upper gastrointestinal bleeding. His blood test results were as follows: white blood cell count, 1.8×109/L; absolute lymphocytes, 0.4×109/L; absolute neutrophils, 1.2×109/L; and electrolyte disturbances. A computed tomography (CT) scan showed evidence of bilateral inferior pulmonary infection and acute pancreatitis. Thick dark bile with visible floccule was drawn via a percutaneous transhepatic cholangiodrainage (PTCD). Klebsiella pneumoniae was detected in microbiological bile tests. Two years later, the patient died of chronic liver failure.
Acetyl salicylic acid attenuates cardiac hypertrophy through Wnt signaling
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《医学前沿（英文）》 2015年 第9卷 第4期 页码 444-456 doi: 10.1007/s11684-015-0421-z
Ventricular hypertrophy is a powerful and independent predictor of cardiovascular morbid events. The vascular properties of low-dose acetyl salicylic acid (aspirin) provide cardiovascular benefits through the irreversible inhibition of platelet cyclooxygenase 1; however, the possible anti-hypertrophic properties and potential mechanism of aspirin have not been investigated in detail. In this study, healthy wild-type male mice were randomly divided into three groups and subjected to transverse aortic constriction (TAC) or sham operation. The TAC-operated mice were treated with the human equivalent of low-dose aspirin (10 mg·kg−1·d−1); the remaining mice received an equal amount of phosphate buffered saline with 0.65% ethanol, which was used as a vehicle. A cardiomyocyte hypertrophy model induced by angiotensin II (10 nmol·L−1) was treated with the human equivalent of low (10 or 100 µmol·L−1) and high (1000 µmol·L−1) aspirin concentrations in plasma. Changes in the cardiac structure and function were assessed through echocardiography and transmission electron microscopy. Gene expression was determined through RT-PCR and western blot analysis. Results indicated that aspirin treatment abrogated the increased thickness of the left ventricular anterior and posterior walls, the swelling of mitochondria, and the increased surface area in in vivo and in vitro hypertrophy models. Aspirin also normalized the upregulated hypertrophic biomarkers, β-myosin heavy chain (β-MHC), atrial natriuretic peptide (ANP), and b-type natriuretic peptide (BNP). Aspirin efficiently reversed the upregulation of β-catenin and P-Akt expression and the TAC- or ANG II-induced downregulation of GSK-3β. Therefore, low-dose aspirin possesses significant anti-hypertrophic properties at clinically relevant concentrations for anti-thrombotic therapy. The downregulation of β-catenin and Akt may be the underlying signaling mechanism of the effects of aspirin.
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