Aims This study aimed to investigate the clinical and chest computed tomography (CT) features associated with clinical parameters for coronavirus disease (COVID‐19) in the capital of Turkey, Ankara. Materials and methods Epidemiological, clinical features, laboratory findings and radiological characteristics of 1563 hospitalised patients with COVID‐19 in Ankara were collected, reviewed and analysed in this study. The risk factors associated with disease severity were investigated. Results Non‐severe (1214; 77.7%) and severe cases (349; 22.3%) were enrolled in the study. Compared with the non‐severe group, the severe group were significantly older and had more comorbidities (ie, hypertension, diabetes mellitus, cardiovascular disease and chronic kidney disease). Smoking was more common in the severe group. Severe patients had higher respiratory rates and higher incidences of cough and dyspnoea compared with non‐severe patients. Compared with the non‐severe patients, the severe patients had increased C‐reactive protein (CRP), procalcitonin, neutrophil to lymphocyte ratio (NLR) and CRP/albumin ratio and decreased albumin. The occurrence rates of consolidation, subpleural sparing, crazy‐paving pattern, cavity, halo sign, reversed halo sign, air bronchogram, pleural thickening, micronodule, subpleural curvilinear line and multilobar and bilateral involvement in the CT finding of the severe patients were significantly higher than those of the non‐severe patients. Conclusions Many factors are related to the severity of COVID‐19, which can help clinicians judge the severity of the patient and evaluate the prognosis. This cohort study revealed that male sex, age (≥55 years), patients with any comorbidities, especially those with cardiovascular disease, dyspnoea, increased CRP, D‐dimer and NLR, and decreased lymphocyte count and CT findings of consolidation and multilobar involvement were predictors of severe COVID‐19.

Background: Coronavirus Disease 2019 Reverse-Transcriptase Polymerase Chain Reaction (COVID-19 RT-PCR) positive predictive value is low. COVID-19 RT-PCR negative patients with pneumonia were not rare. It is difficult to distinguish COVID-19 pneumonia between other viral pneumonias radiologically and clinically. We aimed to find whether there was any different radiological finding in COVID-19 pneumonia with the other viral agents that caused pneumonia. Material and Methods: The study was designed retrospectively. 78 patients who underwent Thoracic Computed Tomography (CT) and COVID-19 RT-PCR were included in the study. Other viral Polymerase Chain Reaction (PCR) tests were performed on 33 patients. Results: 22 patients had COVID-19 PCR positive and 11 patients had non-COVID-19 PCR positive. 8 patients had influenza A and B, and 3 patients had adenovirus. In both groups, lung parenchymal lesions were predominantly located in the upper lobes and peripheral. 31 (93.9%) patients had ground-glass density lesions, 24 (72.7%) patients had consolidation, and 5 (15.2%) patients had crazy paving lesions. 1(3.0%) patient had a halo sign. There was no statistical difference between the two groups in terms of the features of the parenchymal lesions, except for vascular enlargement. Vascular enlargement was only seen in patients with COVID-19 pneumonia (p: 0.019). Conclusion: Radiologically, the vascular enlargement sign seems to be specific to COVID-19 disease and it can be used to differentiate COVID-19 pneumonia from other viral pneumonias.

The role of autoantibodies against granulocyte-macrophage colony-stimulating factor (GM-CSF) in the development of secondary pulmonary alveolar proteinosis (PAP) in patients exposed to occupational and environmental dust remains unclear. Herein, we describe two cases of secondary PAP who had GM-CSF antibodies and absence of STAT5 phosphorylation index, suggestive of a potential relationship between the appearance of GM-CSF antibodies and environmental dust exposure. However, whether the presence of GM-CSF antibodies is a part of the pathological process or represents an epiphenomenon is currently unknown. In this report, we would like to present two cases supporting these new data and briefly discuss the possible role of autoimmune mechanisms in the development of secondary PAP. Am. J. Ind. Med. 60:591-597, 2017. © 2017 Wiley Periodicals, Inc.

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