Objects Invasive pulmonary mold infection usually has devastating outcomes. Timely differentiation between invasive pulmonary aspergillosis (IPA) from pulmonary mucormycosis (PM) is critical for treatment decision-making. However, information on IPA and PM differentiation is limited. Methods We conducted a retrospective, multicenter, observational study, with proven and probable IPA and PM patients from January 2004 to December 2017. Demographics, clinical manifestations, image reports, histopathological findings and outcomes were analyzed. Results A total of 47 IPA (34 proven and 13 probable) and 22 PM (21 proven and 1 probable) cases were analyzed. The majority of tissues (80% in IPA and 67% in PM) were obtained using bronchoscopy. While influenza infection was independently correlated to IPA, prior voriconazole exposure was independently associated with PM (p=0.036, p=0.043, respectively). The positive culture rate for PM was lower than that for IPA (41% vs. 69%, p=0.0363). The galactomannan (GM) level from serum and bronchoalveolar lavage (BAL) fluid was higher in IPA than in PM (3.1 ± 0.5 vs 0.7 ± 0.6, p=0.0313; 4.3 ± 0.6 vs. 1.5 ±1.0, p=0.0375, respectively). The overall mortality rate was 64%, which was similar among IPA and PM groups. Systemic steroid exposure and high Acute Physiology and Chronic Health Evaluation II (APACHE II) scores on admission were independently correlated to mortality in IPA (p=0.024), and concurrent bacterial sepsis predicted the in-hospital mortality among PM patients (p=0.029). Conclusions Influenza infection and prior exposure to voriconazole may help physicians to differentiate IPA and PM. Bronchoscopy-guided biopsy and lavage specimen provide timely and definite diagnosis. While the prognosis of IPA is associated with systemic steroid exposure and higher APACHE II scores on admission, concurrent bacterial sepsis is the only independent predictor for mortality in PM.

Objects: Invasive pulmonary mold infection usually has devastating outcomes. Timely differentiation between invasive pulmonary aspergillosis (IPA) from pulmonary mucormycosis (PM) is critical for treatment decision-making. However, information on IPA and PM differentiation is limited. Methods: We conducted a retrospective, multicenter, observational study, with proven and probable IPA and PM patients from January 2004 to December 2017. Demographics, clinical manifestations, image reports, histopathological findings, and outcomes were analyzed. Results: A total of 46 IPA (33 proven and 13 probable) and 19 PM (18 proven and one probable) cases were analyzed. The majority of tissues (81% in IPA and 61% in PM) were obtained using bronchoscopy. Prior influenza infection was a predisposing factor for IPA, and abscess formation in CT scan was associated with PM (p = 0.0491, p = 0.0454, respectively). The positive culture rate for PM was lower than that for IPA (37% vs. 67%, p = 0.0294). The galactomannan (GM) level from serum and bronchoalveolar lavage (BAL) fluid was significantly higher in IPA than in PM (3.3 ± 0.5 vs. 0.8 ± 0.6, p = 0.0361; 4.0 ± 0.6 vs. 0.59 ± 0.1, p = 0.0473, respectively). The overall mortality rate was 65%, which was similar among IPA and PM groups. Systemic steroid exposure and high Acute Physiology and Chronic Health Evaluation II (APACHE II) scores on admission were independently correlated to mortality in IPA (p = 0.027, p = 0.026, respectively). However, there was no predictor for mortality found in PM patients. Conclusions: Influenza infection, abscess formation in CT scan, and GM level may help physicians to differentiate IPA and PM. Bronchoscopy-guided biopsy and lavage specimen provide timely and definite diagnosis. The prognosis of IPA is associated with systemic steroid exposure and higher APACHE II scores on admission.

Study Objectives: Previous research revealed a positive correlation between endothelial cell injury (indicated by albuminuria) and obstructive sleep apnea (OSA). However, little else has been revealed about acute kidney injury (AKI) in patients with OSA. Methods: This prospective study recruited consecutive patients undergoing overnight polysomnography for evaluation of sleep apnea. Patients in whom any major disease or recent infection had been previously diagnosed were excluded. Ultimately, data from 75 patients with apnea-hypopnea indices of 5 or more were analyzed. Baseline values for the urinary albumin-creatinine ratio (UACR), serum levels for three markers of AKI (cystatin C, neutrophil gelatinaseassociated lipocalin [NGAL], interleukin-18 [IL-18]), and polysomnography data were recorded and analyzed. Patients then were followed for 6 months of continuous positive airway pressure (CPAP) treatment. Results: At baseline, UACRs were greater in patients with more severe OSA (P = .005, r = .329). All three serum markers of AKI (cystatin C, NGAL, and IL-18) studied were positively correlated with OSA severity, and two (cystatin C and IL-18) were positively correlated with the frequency of oxygen desaturation during sleep. However, none of the AKI markers had positive correlations with UACR. After 6 months of CPAP treatment, UACR and IL-18 were decreased significantly in patients with good adherence. Conclusions: Albuminuria and levels of three serum markers of AKI (cystatin C, NGAL, IL-18) were positively correlated with OSA severity, and good adherence with CPAP treatment decreased albuminuria and interleukin-18 levels. These results may provide additional tools for assessing early renal injury in patients with OSA.

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Background and Objectives: We studied whether the extent of exertional oxygen desaturation and emphysema could cause greater mortality in COPD and asthma independent of airflow obstruction. Materials and Methods: We performed a 5-year longitudinal observational study in COPD and asthma patients who matched for airflow obstruction severity. All subjects performed a 6-min walk test (6MWT) and high-resolution computed tomography (HRCT) and followed spirometry and oxygen saturation (SpO2) during the 6MWT every 3–6 months. Overall survival was recorded. Cumulative survival curves were performed according to the Kaplan–Meier method and compared with the log-rank test. Results: The COPD group had higher emphysema scores, higher Δinspiratory capacities (ICs) and lower SpO2 during the 6MWT, which showed a greater yearly decline in FEV1 (40.6 mL) and forced vital capacity (FVC) (28 mL) than the asthma group (FEV1, 9.6 mL; FVC, 1.2 mL; p < 0.05). The emphysema-predominant COPD group had an accelerated annual decline in lung function and worse survival. The nadir SpO2 ≤ 80% and a higher emphysema score were the strong risk factors for mortality in COPD patients. Conclusions: The greater structural changes with a higher emphysema score and greater desaturation during the 6MWT in COPD may contribute to worse yearly decline in FEV1 and higher five-year mortality than in asthma patients with a similar airflow obstruction. The lowest SpO2 ≤ 80% during the 6MWT and emphysema-predominant COPD were the strong independent factors for mortality in chronic obstructive airway disease patients.