With the advent of antibiotics one after another, the treatment of infectious diseases has gradually entered a new era. Antibiotics have only an antibacterial effect, but not the ability to remove endotoxin. Endotoxin can directly cause damage to target organs and target cells and can act on target cells to induce the release of inflammatory cytokines and oxygen-free radicals. In clinical studies, it has been found that the lysis of bacteria produced after antibiotic treatment can lead to the release of endotoxin, which further has a deleterious effect on hemodynamics. The level of endotoxin in the patient's blood is positively correlated with the change in hemodynamic parameters, thereby inducing a certain mortality rate. In addition, some patients do tend to increase endotoxin levels after antibiotic treatment. However, after some antibiotic treatment, the bacterial load suddenly decreased, but the endotoxin content in the body fluid increased significantly, causing significant side effects and causing harm to the body. Studies have concluded that antibiotics may significantly induce the release of endotoxin.
Figure 1. Antibiotic drugs.
The researchers revealed that endotoxin can stimulate the body to produce inflammatory factors, such as tumor necrosis factor and interleukin-1, and these pre-inflammatory factors can then initiate the release of a large number of inflammatory factors, resulting in systemic inflammatory response syndrome, leading to tissue cell damage and multiple organ failure, an important cause of death from Gram-negative bacillary sepsis. As early as the early stage of antibiotic application, it was discovered that antibiotics dissolve bacteria and suddenly release a large amount of endotoxin, which can cause shock in patients with Gram-negative bacillary sepsis, but there has been a lack of attention and systematic control research on its clinical significance. In recent years, clinical research has focused more on the difference and qualitative research on the release of endotoxin-induced by antibiotics, but there is still a lack of systematic and in-depth research on the impact of this phenomenon on the pathological changes, disease progression, curative effect and prognosis of patients.
Antibiotic-induced endotoxin release is clinically important. Some studies have found that after antibiotic treatment, blood endotoxin rises accompanied by blood pressure drop, lactic acid rise, and glucose drop, indicating aggravated tissue damage. In clinical research, it was found that in some patients with Gram-negative bacillary sepsis, blood endotoxin was significantly increased after antibiotic treatment, suggesting that endotoxin is closely related to antibiotics. In addition, the clinical significance of antibiotic-induced endotoxin release in the CSF of patients with meningitis has been demonstrated.
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