Background: Socioeconomic status (SES) is a strong determinant in the development of various diseases. We evaluated the relationship between SES and the incidence of chronic obstructive pulmonary disease (COPD) by using a community-based cohort data. Patients and Methods: Four-year follow-up data of 6341 adults (aged ≥ 40 years), who underwent serial pulmonary function test were analyzed. Incidence of COPD in the participants was defined as the absence of airflow obstruction compatible with COPD (pre-bronchodilator forced expiratory volume in 1 second/forced vital capacity ratio of < 0.7) at baseline but documentation of airflow obstruction in serial testing. SES of patients was divided into quartiles according to household income and educational level. Multivariate logistic regression analyses were performed to estimate the association between SES and COPD incidence. Results: A total of 280 (4.4%) patients developed COPD during the follow-up. The proportion of subjects with lowest education (elementary school) and lowest household income levels (1st quartile) was significantly higher in the COPD group than in the non-COPD group (37.9% vs 29.5%, p< 0.011 and 48.4% vs 30.8%, p< 0.001, respectively). Logistic regression analysis revealed that education level of elementary school was independently associated with COPD incidence after adjustment for sex, age, body mass index, white blood cell count, residence area, and occupation (odds ratio 1.879, 95% confidence interval 1.124– 3.141, p=0.016). Conclusion: In the general population, educational level of elementary school was an independent risk factor for COPD among the components comprising SES. Our results indicate that the implementation of preventive strategies for COPD in those with low educational status could be beneficial.

Phosphate concentrations change continuously throughout hospitalization; however, it is unclear which available phosphate measures are most clinically important for predicting hospital mortality. Therefore, we investigated phosphate concentrations in association with hospital mortality following admission to the intensive care unit. We retrospectively enrolled all adult patients receiving mechanical ventilation. Phosphate concentrations were divided into three categories: initially measured phosphate (iP); maximum–minimum phosphate values (ΔP); and phosphate arithmetic average (Pmean). In total, 175 patients were enrolled. The hospital mortality rate was 32.6%, and the most common primary diagnosis was respiratory failure. In multivariable logistic regression analyses, the odds ratios for hospital mortality in association with ΔP and Pmean values were 1.56 and 2.13, respectively (p < 0.0001). According to the obtained receiver operating characteristic curve, ΔP (0.75) and Pmean (0.72) each showed a fair predictive power for hospital mortality. In evaluating relative risks, we found that higher concentrations of Pmean and ΔP were each associated with a higher hospital mortality. ΔP and Pmean values were significantly associated with hospital mortality in critically ill patients, compared to iP. These findings showed that throughout hospitalization, it is important to reduce phosphate level fluctuations and maintain appropriate phosphate concentrations through consistent monitoring and corrections.

Tyrosine kinase inhibitors (TKIs) have transformed the treatment of epidermal growth factor receptor (EGFR)-mutant non-small cell lung cancer. However, treatment resistance remains a major challenge in clinical practice. The tumor microenvironment (TME) is a complex system composed of tumor cells, immune and non-immune cells, and non-cellular components. Evidence indicates that dynamic changes in TME during TKI treatment are associated with the development of resistance. Research has focused on identifying how each component of the TME interacts with tumors and TKIs to understand therapeutic targets that could address TKI resistance. In this review, we describe how TME components, such as immune cells, fibroblasts, blood vessels, immune checkpoint proteins, and cytokines, interact with EGFR-mutant tumors and how they can promote resistance to TKIs. Furthermore, we discuss potential strategies targeting TME as a novel therapeutic approach.

Kim BK, et al. Yonsei Med J. 2021 May;62(5):417-423. https://doi.org/10.3349/ymj.2021.62.5.417

Background: Currently, lung transplantation (LTX) is considered to be a curative treatment option in patients with end-stage lung disease. Although pulmonary hypertension (PH), confirmed by cardiac catheterization, is a prognostic factor in patients undergoing LTX, the prognostic value of PH in Asian lung transplant recipients remains uncertain. In this study, we aimed to determine whether PH before LTX may serve as a prognostic factor for survival in Asian patients. Methods: The medical records of 50 patients [male, 27; female, 23; mean age, 51.0 (41.0–60.0) years], who received preoperative right heart catheterization (RHC) and echocardiography before single or double LTX at Severance Hospital between January 2010 and December 2014, were reviewed. The relationship between 1-year survival after LTX and PH [mean pulmonary arterial pressure (mPAP) ≥25 mmHg at rest] was evaluated. Results: The mean right ventricular systolic pressure and mPAP were 48.5 (22.8) and 30.0 (24.0–40.0) mmHg. Of the 50 patients, 17 (34.0%) died within a year after LTX. The 1-year survival rate among patients with mPAP ≥25 mmHg (58.8%) was lower than the survival rate among patients with mPAP <25 mmHg (87.5%). Pre-transplantation mPAP of ≥25 mmHg was associated with post-transplantation survival [hazard ratio (HR), 4.832; 95% confidence interval (CI), 1.080–21.608, P=0.039]. The presence of preoperative PH was also associated with an increased risk of postoperative complications. Conclusions: Confirmation of PH via preoperative cardiac catheterization was associated with the prognosis of the patient after LTX. Clinicians should consider the necessity for early transplantation surgery before the mPAP reaches ≥25 mmHg.