Background: Interstitial lung diseases (ILDs) are chronic, parenchymal lung diseases with a variable clinical course and a poor prognosis. Within various clinical courses, acute exacerbation (AE) is a devastating condition with significant morbidity and high mortality. The aim of this study was to investigate the role of interleukin-6 (IL-6) to predict AE and prognosis in patients with ILD. Methods: Eighty-three patients who were diagnosed with ILD from 2016 to 2019 at the Haeundae Paik Hospital, Busan, South Korea, were included and their clinical data were retrospectively analyzed. Results: The median follow-up period was 20 months. The mean age was 68.1 years and 65.1% of the patients were men with 60.2% of patients being ever-smokers. Among ILDs, idiopathic pulmonary fibrosis was the most common disease (68.7%), followed by connective tissue disease-associated ILD (14.5%), cryptogenic organizing pneumonia (9.6%), and nonspecific interstitial pneumonia (6.0%). The serum levels of IL-6 were measured at diagnosis with ILD and sequentially at follow-up visits. During the follow-ups, 15 (18.1%) patients experienced an acute exacerbation (AE) of ILD and among them, four (26.7%) patients died. In the multivariable analysis, high levels of IL-6 (OR 1.014, 95% CI: 1.001–1.027, p = 0.036) along with lower baseline saturations of peripheral oxygen (SpO₂) were independent risk factors for AE. In the receiver operating characteristic curve analysis, the area under the curve was 0.815 (p < 0.001) and the optimal cut-off value of serum IL-6 to predict AE was 25.20 pg/mL with a sensitivity of 66.7% and specificity of 80.6%. In the multivariable Cox analysis, a high level of serum IL-6 (HR 1.007, 95% CI: 1.001–1.014, p = 0.018) was only an independent risk factor for mortality in ILD patients. Conclusions: In our study, a high level of serum IL-6 is a useful biomarker to predict AE and poor prognosis in patients with ILD.

Background: Anticoagulation during extracorporeal membrane oxygenation (ECMO) usually is required to prevent thrombosis. The aim of this study was to investigate the usefulness of nafamostat mesilate (NM) as a regional anticoagulant during veno-arterial ECMO (VA-ECMO) treatment. Methods: We retrospectively reviewed the medical records of 16 patients receiving VA-ECMO and NM from January 2017 to June 2020 at Haeundae Paik Hospital. We compared clinical and laboratory data, including activated partial thromboplastin time (aPTT), which was measured simultaneously in patients and the ECMO site, to estimate the efficacy of regional anticoagulation. Results: The median patient age was 68.5 years, and 56.3% of patients were men. Cardiovascular disease was the most common primary disease (75.0%) requiring ECMO treatment, followed by respiratory disease (12.5%). The median duration of ECMO treatment was 7.5 days. Among 16 patients, seven were switched to NM after first using heparin as an anticoagulation agent, and nine received only NM. When comparing aPTT values in the NM group between patients and the ECMO site, that in patients was significantly lower than that at the ECMO site (73.57 vs. 79.25 seconds; P=0.010); in contrast, no difference was observed in the heparin group. Conclusions: NM showed efficacy as a regional anticoagulation method by sustaining a lower aPTT value compared to that measured at the ECMO site. NM should be considered as a safer regional anticoagulation method in VA-ECMO for patients at high risk of bleeding.

We evaluated the prognostic value of C-reactive protein (CRP), albumin, CRP clearance (CRPc) and CRP/albumin ratio (CAR) in neurocritically ill patients with acute stroke. This is a retrospective, observational study. We included acute stroke patients who were hospitalized in the neurosurgical ICU from January 2013 to September 2019. The primary outcome was in-hospital mortality. A total of 307 patients were enrolled in the study. Among them, 267 (87.0%) survived until discharge from the hospital. CRP and CAR were significantly higher in non-survivors than in survivors (both p < 0.001). Serum albumin levels were significantly lower in the non-survivors than in the survivors (p < 0.001). In receiver operating characteristic curve analysis for prediction of in-hospital mortality, the area under the curve of CRP (C-statistic: 0.820) and CAR (C-statistic: 0.824) were greater than that of CRPc (C-statistic: 0.650) and albumin (C-statistic: 0.734) (all p < 0.005). However, there was no significant difference in the predictive performance between CRP and CAR (p = 0.287). In this study, CRP and CAR were more important than CRPc and albumin in predicting mortality of neurocritically ill patients with stroke. Early CRP level and CAR determination may help to predict the in-hospital mortality of these patients.

Interstitial lung disease (ILD) encompasses a heterogeneous group of more than 200 diffuse parenchymal lung diseases with various clinical courses. Disease progression is one of the most important prognostic factors, and, the definition of progressive pulmonary fibrosis (PPF) has recently been established. This study aimed to estimate the prevalence, risk factors, and prognosis of PPF among patients with non-idiopathic pulmonary fibrosis (IPF) in real-world practice. A total of 215 patients were retrospectively analyzed between January 2010 and June 2023 at the Haeundae Paik Hospital in the Republic of Korea. According to the criteria proposed in 2022 by Raghu et al, PPF defined as a condition that satisfies 2 or more of the following in the past year: worsening of respiratory symptoms, physiological evidence of disease progression, and radiological evidence of disease progression. The median age of the subjects was 67 years and 63.7% were female. A total of 40% was diagnosed with PPF and connective tissue disease-associated ILD (52.3%) was the most common type, followed by nonspecific interstitial pneumonitis (NSIP) (25.6%) and cryptogenic organizing pneumonitis (16.3%). In multivariate logistic regression for predicting PPF, both the use of steroids and immunosuppressants (OR: 2.57, 95% CI: 1.41–4.67, P = .002) and home oxygen use (OR: 25.17, 95% CI: 3.21–197.24, P = .002) were independent risk factors. During the follow-up period, the mortality rate was significantly higher in the PPF group than in the non-PPF group (24.4% vs 2.3%, P < .001). In the survival analysis using the Cox proportional hazard regression model, disease progression, older age and lower forced vital capacity (FVC) were independent risk factors for mortality. Our study demonstrated that the prevalence of PPF was 40%. Concomitant therapy of steroids with an immunosuppressants and home oxygen use are risk factors for PPF. PPF itself was significantly associated with high mortality rates. Risk factors for mortality were disease progression, older age, and lower FVC.

Connective tissue disease-associated interstitial lung disease (CTD-ILD) represents a significant cause of morbidity and mortality. It is characterized by the progressive convergence of chronic inflammation, immune dysregulation, and fibrotic remodeling in the lung parenchyma. While often conceptualized through a model of idiopathic pulmonary fibrosis (IPF), CTD-ILD is fundamentally an immune-driven pathology with distinct inflammatory mechanisms in which adaptive immunity plays a profound role. This narrative review explores the “inflammation–immunity–fibrosis continuum” in CTD-ILD, elaborating the intricate cellular and molecular pathways that distinguish it from IPF. We highlight the central role of persistent T-cell responses and B-cell dysregulation, which often occur within organized tertiary lymphoid structures in the lung. This review examines how these immune processes are propagated by multiple cytokine pathways, including the TGF-β/SMAD, JAK/STAT, and phosphodiesterase-4 signaling pathways, which serve as crucial links between inflammation and fibrosis. This distinct immune mechanism in CTD-ILD explains why immunomodulatory agents are a cornerstone of CTD-ILD treatment, in contrast to their limited efficacy in IPF, and emphasizes the current paradigm of combining immunosuppression with antifibrotic drugs to target the dual drivers of the disease.

Our aim is to assess the optimal levels of oxygen and carbon dioxide for the prognosis of favorable neurologic outcomes in survivors after extracorporeal cardiopulmonary resuscitation (ECPR). We obtained the mean levels of PaCO₂ and PaO₂ in arterial blood gas samples 72 h after ECPR. The primary outcome was the neurological status, according to the Cerebral Performance Categories (CPC) scale, upon discharge. Of 119 (48.6%) survivors, 95 (38.8%) had favorable neurologic outcomes (CPC 1 or 2). There was a U-shaped relationship between mean arterial blood gas tensions and poor neurological outcomes. The risk of poor neurological outcome was lowest in patients with the second tertile of mean PaCO₂ (30–42 mm Hg) and PaO₂ (120–160 mm Hg). In a multivariable analysis, third tertile of mean PaCO₂, third tertile of mean PaO₂, age, shockable rhythm, out of hospital cardiac arrest, duration of cardiopulmonary resuscitation, and ECPR at cardiac catheterization lab were found to be significantly associated with poor neurologic outcomes. Additionally, hypercapnia and extreme hyperoxia were found to be significantly associated with poor neurological outcomes after ECPR. Therefore, maintaining adequate arterial levels of oxygen and carbon dioxide may be important for favorable neurological prognoses in survivors after ECPR.