Background/Aims: Secondary infection with influenza virus occurs in critically ill patients and is associated with substantial morbidity and mortality; however, there is limited information about it in patients with severe coronavirus disease 2019 (COVID-19). Thus, we investigated the clinical outcomes of and risk factors for secondary infections in patients with severe COVID-19. Methods: This study included patients with severe COVID-19 who were admitted to seven hospitals in South Korea between February 2020 to February 2021. Multivariate logistic regression analyses were performed to assess factors associated with the risk of secondary infections. Results: Of the 348 included patients, 104 (29.9%) had at least one infection. There was no statistically significant difference in the 28-day mortality (17.3% vs. 12.3%, p = 0.214), but in-hospital mortality was higher (29.8% vs. 15.2%, p = 0.002) in the infected group than in the non-infected group. The risk factors for secondary infection were a high frailty scale (odds ratio [OR], 1.314; 95% confidence interval [CI], 1.123 to 1.538; p = 0.001), steroid use (OR, 3.110; 95% CI, 1.164 to 8.309; p = 0.024), and the application of mechanical ventilation (OR, 4.653; 95% CI, 2.533 to 8.547; p < 0.001). Conclusions In-hospital mortality was more than doubled in patients with severe COVID-19 and secondary infections. A high frailty scale, the use of steroids and application of mechanical ventilation were risk factors for secondary infection.

Capillary hemangioma of the tracheobronchial tree is an extremely rare benign tumor in adults, especially those located in the bronchus. Characteristics and treatment of capillary hemangiomas of adult tracheobronchial trees have not been well known. We present a 61-year-old man with hemoptysis, which was caused by a small tiny nodule in the left lingular segmental bronchus. The nodule was removed by a forcep biopsy, via flexible bronchoscopy, and it was revealed to be capillary hemangioma. A small isolated endobronchial capillary hemangioma can be treated with excisional forcep biopsy, but a risk of massive bleeding should not be overlooked.
Adult ; Biopsy ; Bronchi ; Bronchoscopy ; Capillaries ; Hemangioma, Capillary ; Hemoptysis ; Hemorrhage ; Humans ; Surgical Instruments

BACKGROUND: It is not clear whether microangiopathies are associated with subclinical atherosclerosis in type 2 diabetes mellitus (T2DM). We investigated the relation of cardiac autonomic neuropathy (CAN) and other microangiopathies with carotid atherosclerosis in T2DM. METHODS: A total of 131 patients with T2DM were stratified by mean carotid intima-media thickness (CIMT) > or = or <1.0 mm and the number of carotid plaques. CAN was assessed by the five standard cardiovascular reflex tests according to the Ewing's protocol. CAN was defined as the presence of at least two abnormal tests or an autonomic neuropathy points > or =2. Diabetic microangiopathies were assessed. RESULTS: Patients with CAN comprised 77% of the group with mean CIMT > or =1.0 mm, while they were 29% of the group with CIMT <1.0 mm (P=0.016). Patients with diabetic retinopathy (DR) comprised 68% of the group with CIMT > or =1.0 mm, while they were 28% of the group without CIMT thickening (P=0.003). Patients with CAN comprised 51% of the group with > or =2 carotid plaques, while they were 23% of the group with < or =1 carotid plaque (P=0.014). In multivariable adjusted logistic regression analysis, the patients who presented with CAN showed an odds ratio [OR] of 8.6 (95% confidence interval [CI], 1.6 to 44.8) for CIMT thickening and an OR of 2.9 (95% CI, 1.1 to 7.5) for carotid plaques. Furthermore, patients with DR were 3.8 times (95% CI, 1.4 to 10.2) more likely to have CIMT thickening. CONCLUSION: These results suggest that CAN is associated with carotid atherosclerosis, represented as CIMT and plaques, independent of the traditional cardiovascular risk factors in T2DM. CAN or DR may be a determinant of subclinical atherosclerosis in T2DM.
Atherosclerosis ; Carotid Artery Diseases* ; Carotid Intima-Media Thickness ; Diabetes Mellitus, Type 2 ; Diabetic Angiopathies ; Diabetic Neuropathies* ; Diabetic Retinopathy ; Humans ; Logistic Models ; Odds Ratio ; Reflex ; Risk Factors

BACKGROUND: It is not clear whether microangiopathies are associated with subclinical atherosclerosis in type 2 diabetes mellitus (T2DM). We investigated the relation of cardiac autonomic neuropathy (CAN) and other microangiopathies with carotid atherosclerosis in T2DM. METHODS: A total of 131 patients with T2DM were stratified by mean carotid intima-media thickness (CIMT) > or = or <1.0 mm and the number of carotid plaques. CAN was assessed by the five standard cardiovascular reflex tests according to the Ewing's protocol. CAN was defined as the presence of at least two abnormal tests or an autonomic neuropathy points > or =2. Diabetic microangiopathies were assessed. RESULTS: Patients with CAN comprised 77% of the group with mean CIMT > or =1.0 mm, while they were 29% of the group with CIMT <1.0 mm (P=0.016). Patients with diabetic retinopathy (DR) comprised 68% of the group with CIMT > or =1.0 mm, while they were 28% of the group without CIMT thickening (P=0.003). Patients with CAN comprised 51% of the group with > or =2 carotid plaques, while they were 23% of the group with < or =1 carotid plaque (P=0.014). In multivariable adjusted logistic regression analysis, the patients who presented with CAN showed an odds ratio [OR] of 8.6 (95% confidence interval [CI], 1.6 to 44.8) for CIMT thickening and an OR of 2.9 (95% CI, 1.1 to 7.5) for carotid plaques. Furthermore, patients with DR were 3.8 times (95% CI, 1.4 to 10.2) more likely to have CIMT thickening. CONCLUSION: These results suggest that CAN is associated with carotid atherosclerosis, represented as CIMT and plaques, independent of the traditional cardiovascular risk factors in T2DM. CAN or DR may be a determinant of subclinical atherosclerosis in T2DM.
Atherosclerosis ; Carotid Artery Diseases* ; Carotid Intima-Media Thickness ; Diabetes Mellitus, Type 2 ; Diabetic Angiopathies ; Diabetic Neuropathies* ; Diabetic Retinopathy ; Humans ; Logistic Models ; Odds Ratio ; Reflex ; Risk Factors

Idiopathic interstitial pneumonia (IIP) is a histologically identifiable pulmonary disease without a known cause that usually infiltrates the lung interstitium. IIP is largely classified into idiopathic pulmonary fibrosis, idiopathic non-specific interstitial pneumonia, respiratory bronchiolitis-interstitial lung disease (ILD), cryptogenic organizing pneumonia, desquamative interstitial pneumonia, and acute interstitial pneumonia. Each of these diseases has a different prognosis and requires specific treatment, and a multidisciplinary approach that combines chest high-resolution computed tomography (HRCT), histological findings, and clinical findings is necessary for their diagnosis. Diagnosis of IIP is made based on clinical presentation, chest HRCT findings, results of pulmonary function tests, and histological findings. For histological diagnosis, video-assisted thoracoscopic biopsy and transbronchial lung biopsy are used. In order to identify ILD associated with connective tissue disease, autoimmune antibody tests may also be necessary. Many biomarkers associated with disease prognosis have been recently discovered, and future research on their clinical significance is necessary. The diagnosis of ILD is difficult because patterns of ILD are both complicated and variable. Therefore, as with other diseases, accurate history taking and meticulous physical examination are crucial.
Biomarkers ; Biopsy ; Classification ; Connective Tissue Diseases ; Cryptogenic Organizing Pneumonia ; Diagnosis ; Idiopathic Interstitial Pneumonias ; Idiopathic Pulmonary Fibrosis ; Lung ; Lung Diseases ; Lung Diseases, Interstitial ; Physical Examination ; Prognosis ; Respiratory Function Tests ; Thorax

PURPOSE: The tight junction protein claudin-5 (CLDN5) is critical to the control of endothelial cellular polarity and pericellular permeability. The role of CLDN5 in chronic obstructive pulmonary disease (COPD) remains unclear. The aim of this study was to investigate the association between CLDN5 levels and clinical variables in patients with COPD. METHODS: In total, 30 patients with COPD and 30 healthy controls were enrolled in the study. The plasma CLDN5 level was checked in patients with stable or exacerbated COPD and in healthy controls. RESULTS: The mean plasma CLDN5 level of patients with COPD was 0.63 ± 0.05 ng/mL and that of healthy controls was 6.9 ± 0.78 ng/mL (P = 0.001). The mean plasma CLDN5 level was 0.71 ± 0.05 ng/mL in exacerbated COPD patients and 0.63 ± 0.04 ng/mL in patients with stable COPD (P < 0.05). The plasma CLDN5 level among COPD subjects was correlated with the smoking amount (r = −0.530, P = 0.001). The plasma CLDN5 level in stable COPD patients was correlated with forced expiratory volume in one second (FEV1, %pred.) (r = −0.481, P = 0.037). CONCLUSIONS: The plasma CLDN5 level was not correlated with age. CLDN5 may be involved in the pathogenesis of COPD. Further studies having a larger sample size will be needed to clarify CLDN5 in COPD.
Claudin-5* ; Forced Expiratory Volume ; Humans ; Permeability ; Plasma ; Pulmonary Disease, Chronic Obstructive* ; Sample Size ; Smoke ; Smoking ; Tight Junctions*

A 65-year-old male patient with an end-stage renal disease was diagnosed with coronavirus disease 2019 (COVID-19) by reverse transcription polymerase chain reaction. The patient complained of cough, sputum, and respiratory distress that worsened three days ago. The patient required mechanical ventilation and extracorporeal mentrane oxygenation. On day 9, convalescent plasma collected from a 34-year old man who recovered from COVID-19 45 days ago was administered. The patient showed immediate clinical improvement. However, on day 14, the patient’s clinical course worsened again. On day 19 and day 24, vancomycin-resistant Enterococcus faecium bacteremia and methicillin-resistant Staphylococcus aureus pneumonia were found. After long-term supportive care, he slowly recovered. He was discharged on day 91 without any oxygen requirement. This case report suggests that convalescent plasma therapy might just provide a short-term relief and that persistent effort for critical care is necessary to save patients from severe COVID-19.

Idiopathic interstitial pneumonia (IIP) is a histologically identifiable pulmonary disease without a known cause that usually infiltrates the lung interstitium. IIP is largely classified into idiopathic pulmonary fibrosis, idiopathic non-specific interstitial pneumonia, respiratory bronchiolitis-interstitial lung disease (ILD), cryptogenic organizing pneumonia, desquamative interstitial pneumonia, and acute interstitial pneumonia. Each of these diseases has a different prognosis and requires specific treatment, and a multidisciplinary approach that combines chest high-resolution computed tomography (HRCT), histological findings, and clinical findings is necessary for their diagnosis. Diagnosis of IIP is made based on clinical presentation, chest HRCT findings, results of pulmonary function tests, and histological findings. For histological diagnosis, video-assisted thoracoscopic biopsy and transbronchial lung biopsy are used. In order to identify ILD associated with connective tissue disease, autoimmune antibody tests may also be necessary. Many biomarkers associated with disease prognosis have been recently discovered, and future research on their clinical significance is necessary. The diagnosis of ILD is difficult because patterns of ILD are both complicated and variable. Therefore, as with other diseases, accurate history taking and meticulous physical examination are crucial.

Purpose: Junctional adhesion molecule (JAM)-A is an immunoglobulin-like molecule that colocalizes with tight junctions (TJs) in the endothelium and epithelium. It is also found in blood leukocytes and platelets. The biological significance of JAM-A in asthma, as well as its clinical potential as a therapeutic target, are not well understood. The aim of this study was to elucidate the role of JAM-A in a mouse model of asthma, and to determine blood levels of JAM-A in asthmatic patients. Materials and Methods: Mice sensitized and challenged with ovalbumin (OVA) or saline were used to investigate the role of JAM-A in the pathogenesis of bronchial asthma. In addition, JAM-A levels were measured in the plasma of asthmatic patients and healthy controls. The relationships between JAM-A and clinical variables in patients with asthma were also examined. Results: Plasma JAM-A levels were higher in asthma patients (n=19) than in healthy controls (n=12). In asthma patients, the JAM-A levels correlated with forced expiratory volume in 1 second (FEV1%), FEV1/forced vital capacity (FVC), and the blood lymphocyte proportion. JAM-A, phospho-JNK, and phospho-ERK protein expressions in lung tissue were significantly higher in OVA/OVA mice than in control mice. In human bronchial epithelial cells treated with house dust mite extracts for 4 h, 8 h, and 24 h, the JAMA, phospho-JNK, and phospho-ERK expressions were increased, as shown by Western blotting, while the transepithelial electrical resistance was reduced. Conclusion These results suggest that JAM-A is involved in the pathogenesis of asthma, and may be a marker for asthma.

Background/Aims: For patients hospitalized with coronavirus disease 2019 (COVID-19) who require supplemental oxygen, the evidence of the optimal duration of corticosteroid is limited. This study aims to identify whether long-term use of corticosteroids is associated with decreased mortality. Methods: Between February 10, 2020 and October 31, 2021, we analyzed consecutive hospitalized patients with COVID-19 with severe hypoxemia. The patients were divided into short-term (≤ 14 days) and long-term (> 14 days) corticosteroid users. The primary outcome was 60-day mortality. We performed propensity score (PS) analysis to mitigate the effect of confounders and conducted Kaplan-Meier curve analysis. Results: There were 141 (52%) short-term users and 130 (48%) long-term corticosteroid users. The median age was 68 years and the median PaO2/FiO2 at admission was 158. Of the patients, 40.6% required high-flow nasal cannula, 48.3% required mechanical ventilation, and 11.1% required extracorporeal membrane oxygenation. The overall 60-day mortality rate was 23.2%, and that of patients with hospital-acquired pneumonia (HAP) was 22.9%. The Kaplan-Meier curve for 60- day survival in the PS-matched cohort showed that corticosteroid for > 14 days was associated with decreased mortality (p = 0.0033). There were no significant differences in bacteremia and HAP between the groups. An adjusted odds ratio for the risk of 60-day mortality in short-term users was 5.53 (95% confidence interval, 1.90–18.26; p = 0.003). Conclusions For patients with severe COVID-19, long-term use of corticosteroids was associated with decreased mortality, with no increase in nosocomial complications. Corticosteroid use for > 14 days can benefit patients with severe COVID-19.