RESUMEN
Objective: This study was designed to analyze the clinical characteristics, etiological characteristics, drug resistance, and empirical use of antibiotics for community-acquired pyogenic liver abscess (PLA) to provide a basis for rational and effective empirical treatment of PLA in the local area. Methods: The clinical data, etiological characteristics, drug resistance, and empirical anti-infective therapy schemes of 606 patients with PLA were collected and analyzed retrospectively. Results: The included patients were mainly males, with a male-to-female ratio of 1.3:1. The average age of the patients was 60.3 ± 14.1 years. The underlying diseases were diabetes and biliary tract disease, accounting for 38.7% and 22.3%, respectively. The main clinical manifestations were fever (92.9%), abdominal pain (44.7%), and nausea (33.3%). Imaging findings: the proportion of patients with a single lesion was 74.7%, and 67% of the patients had involvement in the right lobe of the liver. The main pathogen was Klebsiella pneumoniae accounted for 74.9% in blood culture and 84.1% in pus culture, mainly extended-spectrum ß-lactamase. In 272 strains negative for extended-spectrum ß-lactamase (ESBLs), 100% were resistant to ampicillin and less than 50% were sensitive to nitrofurantoin. Only 36 ESBL-positive strains had higher than 80% sensitivity to carbapenems, ß-lactamase inhibitor compound, and amikacin. Patients treated with different treatment methods showed significantly different average length of hospital stay (14 [9-21] vs 13 [8-18]). Empirical anti-infective therapy: Beta-lactamase complex, carbapenems, cephalosporins, and quinolones were used in 280 (37.6%), 180 (29.7%), 180 (29.7%), and 147 (24.3%) patients, respectively. Conclusion: Patients with community-acquired PLA in this area are mainly males, and the underlying diseases are mainly diabetes and hepatobiliary system disease. The main clinical manifestation is fever, so patients with fever of unknown cause should pay attention to possible liver abscesses. Based on drug sensitivity tests, the empirical use of antibiotics is somewhat unreasonable.
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Alcoholic liver disease is one of the diseases with the highest fatality rate worldwide. The cellular process of autophagy which recycles damaged organelles to maintain protein and organelle homeostasis is found to positively influence survival during hepatic insufficiency, although the mechanism is poorly understood. Palmatine (PLT) has a variety of biological functions, such as broad-spectrum antibacterial action, neuroprotective, antioxidant stress, and antiviral and anti-inflammatory activities. However, it is not known whether PLT has a protective effect against alcoholic liver injury. Here, we investigated the protective effect of PLT in a cellular model of alcohol-induced acute liver injury and further explored its mechanism of action. In this study, we show for the first time that PLT attenuates alcohol-induced hepatocyte injury by promoting autophagy to play an essential protective role. As PLT treatment induced a brief increase in LC3-II conversion and p62 degradation, it also upregulated the expression of ATG5 and ATG7. The expression levels of the proapoptotic proteins Bax, Caspase 3, and Caspase 9 significantly decreased, while the antiapoptotic protein levels of Bcl-2 upregulated after treatment with PLT. However, in presence of the autophagy inhibitor, 3-methyladenine, the effect of PLT in inhibiting ethanol-induced hepatocyte injury reversed significantly. Mechanistically, the protective effects of PLT may be mediated by promoting the activation of the AMP-activated protein kinase/mammalian target of rapamycin signaling pathway. Therefore, we believe that the development of alcoholic liver injuries may be controlled by PLT by inhibiting hepatocyte apoptosis through the autophagy pathway. The study lays a solid theoretical and practical basis for future animal models and clinical studies of PLT.
Asunto(s)
Proteínas Quinasas Activadas por AMP , Hepatopatías Alcohólicas , Animales , Proteínas Quinasas Activadas por AMP/metabolismo , Autofagia , Serina-Treonina Quinasas TOR/metabolismo , Hepatocitos/metabolismo , Hepatopatías Alcohólicas/tratamiento farmacológico , Hepatopatías Alcohólicas/metabolismo , Etanol , Mamíferos/metabolismoRESUMEN
Background: Infective endocarditis (IE) can be caused by a variety of pathogens. Endocarditis due to the Coxiella burnetii (C. burnetii) infection is common in patients with negative blood culture results and usually occurs in patients with previous valvular heart disease, impaired immune function, and during pregnancy. The diagnosis is difficult based on the conventional diagnostic method, and serious adverse outcomes may occur in the case of delayed diagnosis. Case Report: In the present study, a case of a 43-year-old male patient with previous valvular heart disease was reported. The patient was admitted with a diagnosis of IE, but the etiology was unclear. Accurate diagnosis and treatment were achieved by combining metagenomic next-generation sequencing (mNGS) with Q fever serological antibody assay. Conclusion: Metagenomic next-generation sequencing has been increasingly applied in clinical practice in recent years to detect the DNA or RNA in samples, and this could play a decisive role in the etiological diagnosis of some infectious diseases.