Background Lactate is considered a prognostic indicator in critically ill patients; however, studies on linezolid-induced lactic acidosis (LILA) are limited, and data from patients older than 85 are even more scarce, therefore we evaluated the risk factors for LILA in patients older than 85 years and established a risk prediction model. Methods In a retrospective cohort study, patients older than 85 years who were monitored for blood gas analysis and arterial lactate levels during the use of teicoplanin or linezolid were enrolled. After using propensity score-matched analyses we compared the incidence of lactic acidosis between teicoplanin or linezolid therapy and identified the risk factors of LILA. Results After propensity score-matched analyses, the incidence of lactic acidosis with teicoplanin therapy was significantly lower than that with linezolid therapy (0% vs 35.7%; p<0.0001). Duration of linezolid therapy ≥9 days (OR,3.541;95%CI,1.161-10.793; p=0.026), arterial blood glucose level ≥8 mmol/L (OR, 4.548; 95% CI, 1.507-13.725; p=0.007) and high sequential organ failure assessment (SOFA) score (OR, 1.429; 95% CI, 1.213-1.685; p<0.0001) were risk factors for LILA. A risk model is predictive of LILA (area under the curve, 0.849; specificity, 65.1%; sensitivity, 91.4%, with a negative predictive value of 93.2% and a positive predictive value of 59.3%) with high stability. Conclusions LILA can occur in patients older than 85 years with a relatively shorter duration of linezolid; hence, the close monitoring of blood gas and arterial lactate levels during the use of linezolid in the super-elderly population is necessary.

In the era of precision medicine, with the deepening of the research on malignant tumor driving genes, clinical oncology has fully entered the era of targeted therapy. For non-small-cell lung cancer (NSCLC), the development of targeted drugs targeting driver genes, such as epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK), has successfully opened up a new model of targeted therapy. At present, proto-oncogene rearranged during transfection (RET) fusion gene is an important novel oncogenic driving target, and specific receptor tyrosine kinase inhibitors (TKIs) targeting RET fusion have been approved. This article will review the latest research about the molecular characteristics, pathogenesis, detection, and clinical treatment strategies of RET rearrangements especially in China.