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Objectives: To analyze computed tomography (CT) characteristics predictive for diagnostic accuracy and pneumothorax in CT fluoroscopy-guided transthoracic biopsy (CTF-TTB) of lung lesions using non-coaxial biopsy needle technique. Methods: Retrospectively 274 lung lesion biopsies with confirmed histology were included in our study. CTF-TTB was done using an 18-gauge non-coaxial cutting needle. Diagnostic accuracy rates were calculated per lesion size and CT and procedural characteristics were evaluated for their predictive value regarding diagnostic accuracy and development of pneumothorax (maximal nodule diameter, distance to pleura, location per lung segment, nodule composition, benign versus malignant histology, and number of specimens). Results: Overall diagnostic accuracy of CTF-TTB was high (93%). Diagnostic accuracy for lesions ≤10 mm was 81%. Maximal nodule diameter was the only predictive CT characteristic for diagnostic success (p = 0.03). Pneumothorax occurred in 27%. Distance of lesion to pleura was the only risk factor for pneumothorax (p < 0.00001). Pneumothorax rates were significantly lower in subpleural lesions (14%) compared to those located 1−10 mm (47%), 10−20 mm (33%), and >20 mm from pleura (29%). Conclusions: High diagnostic accuracy rates were achieved with CTF-TTB using non-coaxial biopsy technique, even for lesions ≤10 mm. Pneumothorax rates were comparable with other studies. Lesion size was the only predictive CT characteristic for diagnostic accuracy. Distance to pleura was the only risk factor for pneumothorax.

Background Pulmonary arterial hypertension (PAH) is hallmarked by the development of neointimal lesions. The transcription factor Egr-1 seems to play a critical role in neointimal formation in experimental PAH and was identified as a putative target for intervention. In this study we investigated whether Egr-1 is also associated with neointimal-type vascular remodeling in different forms of human PAH or pulmonary hypertension. Methods Using immunohistochemistry, we studied Egr-1 expression specifically in a wide morphologic spectrum of pulmonary arteries in the lung tissue of 72 patients with different forms and stages of PAH, specifically idiopathic PAH ( n = 18), advanced-stage congenital heart disease‒associated PAH (PAH-CHD) ( n = 21), early-stage PAH-CHD ( n = 19) and non-neointimal hypoxic pulmonary hypertension (PH) ( n = 4), and controls ( n = 10). Results In PAH patients, pulmonary vascular expression of Egr-1 protein was abundant, whereas it was sporadic in non-neointimal (hypoxic) PH patients and controls. In PAH-CHD, protein expression was more pronounced in patients with advanced vascular lesions compared to those with less advanced lesions, such as medial hypertrophy. Conclusions Pulmonary vascular Egr-1 expression is significantly increased in patients with PAH, appears specifically associated with neointimal-type vascular remodeling, and correlates with disease progression. These data translate the critical role of Egr-1 in the development of experimental PAH to human pulmonary vascular disease forms. [ABSTRACT FROM AUTHOR]

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Immunocytochemical studies of lung biopsies from patients with cryptogenic fibrosing alveolitis and those having fibrosing alveolitis associated with scleroderma show that numerous T-cells occur in the alveolar walls and septa of all patients with these diseases, implying that cell-mediated hypersensitivity reactions are involved in the pathogenesis. However, B-lymphocytes, mainly within lymphoid follicles, are also present and, in the CFA group, such patients, and those with <50% T-suppressor/cytotoxic cells in the diffuse T-cell infiltrates, may have a poorer prognosis. Interleukin-2 receptor expression indicates that T-cell activation is occurring within the lungs, and there is evidence that interstitial monocytes/macrophages and alveolar epithelial cells may play a more important role in antigen presentation than alveolar macrophages. These observations on the features of the inflammatory response in the interstitial tissues of patients with fibrosing alveolitis need to be incorporated into the existing hypothesis on pathogenetic mechanisms based mainly on lavage findings of alveolar macrophages and granulocytes. [ABSTRACT FROM AUTHOR]