The association of silicosis severity with pectoralis major muscle and subcutaneous fat volumes and the pulmonary artery/aorta ratio evaluated by CT.

PURPOSE: Silicosis is an incurable occupational disease that sometimes rapidly progresses with fatal outcomes. We aimed to evaluate the association between disease severity and the change in the pectoralis major muscle volume (PMV), subcutaneous fat volume (SFV), and the pulmonary artery/aorta (P/Ao) ratio in patients with silicosis using computed tomography (CT). METHODS: The study included 41 male silicosis patients and 41 control group subjects with available chest CT images. Using dedicated software, we measured PMV and SFV from the axial CT images. We calculated the P/Ao ratio and obtained body mass index (BMI) and forced expiratory volume/forced vital capacity (FEV1/FVC) results from hospital records. We used the chest X-ray profusion score according to the International Labor Organization (ILO) classification to evaluate the severity of the silicosis. RESULTS: The mean age was 33.5±4.4 and 34.7±4.7 years in the silicotic and control groups, respectively. The mean BMI, PMV, SFV, and P/Ao values significantly differed between the study and control groups (P = 0.0009, P < 0.0001, P < 0.0001, and P = 0.0029, respectively). According to the ILO classification, there were 12 silicosis patients in category 1, 13 in category 2, and 16 in category 3. A significant difference was found between disease categories in terms of PMV, SFV, P/Ao, BMI, and FEV1/FVC values (P = 0.0425, P = 0.0341, P = 0.0002, P = 0.0492, and P = 0.0004, respectively). CONCLUSION: Disease severity had a stronger association with decreased PMV and SFV and increased P/Ao ratios than BMI in patients with silicosis caused by denim sandblasting. Thus, CT evaluation might be a useful indicator of disease severity.

STING-dependent sensing of self-DNA drives silica-induced lung inflammation.

Silica particles induce lung inflammation and fibrosis. Here we show that stimulator of interferon genes (STING) is essential for silica-induced lung inflammation. In mice, silica induces lung cell death and self-dsDNA release in the bronchoalveolar space that activates STING pathway. Degradation of extracellular self-dsDNA by DNase I inhibits silica-induced STING activation and the downstream type I IFN response. Patients with silicosis have increased circulating dsDNA and CXCL10 in sputum, and patients with fibrotic interstitial lung disease display STING activation and CXCL10 in the lung. In vitro, while mitochondrial dsDNA is sensed by cGAS-STING in dendritic cells, in macrophages extracellular dsDNA activates STING independent of cGAS after silica exposure. These results reveal an essential function of STING-mediated self-dsDNA sensing after silica exposure, and identify DNase I as a potential therapy for silica-induced lung inflammation.

Predictive Value of Mean Platelet Volume for Pulmonary Embolism Recurrence.

PURPOSE: Recurrence is a major clinical problem in patients with pulmonary embolism and can affect mortality. The decision to discontinue treatment is important for recurrence and is based on patients' clinical features as well as certain blood parameters. Our aim in this study was to evaluate whether mean platelet volume (MPV) and platelet distribution width (PDW) have utility as new predictive parameters for recurrence and mortality in pulmonary embolism. MATERIALS AND METHODS: A total of 440 patients with pulmonary embolism underwent computed tomography, Doppler ultrasonography, and echocardiography before and at the conclusion of treatment. Thrombocyte count, MPV, PDW, and D-dimer parameters were also evaluated at the same time points. RESULTS: MPV and PDW were significantly higher in deceased patients (8.8 ± 1.2 fl and 17.4 ± 0.8) compared to surviving patients (7.7 ± 0.9 fl and 17 ± 0.9) (p < 0.0001). Initial MPV and PDW were also significantly higher in patients with recurrence (8.4 ± 0.7 vs 7.6 ± 0.8 fl, p < 0.0001 and 17.3 ± 0.8 vs 16.9 ± 0.9, p = 0.002, respectively) than in patients without recurrence. At the end of treatment, MPV was still higher in patients with recurrence compared to patients without recurrence (8.7 ± 0.5 and 7.5 ± 0.7 fl, respectively, p < 0.0001). MPV values over 8.05 fl at the end of treatment predicted recurrence with 91% sensitivity and 77% specificity. CONCLUSION: MPV seems to be an indicator of recurrence in pulmonary embolism and may have utility in the prediction of recurrence. Elevated MPV can also be used to predict mortality in pulmonary embolism.