Combined pulmonary fibrosis and emphysema (CPFE) is a clinical syndrome characterized by upper lobe emphysema and lower lobe fibrosis manifested by exercise hypoxemia, normal lung volumes, and severe reduction of diffusion capacity of carbon monoxide. It has varying prevalence worldwide with a male predominance, and with smoking history of more than 40 pack-years being a common risk factor. The unique imaging features of CPFE emphasize its distinct entity, aiding in the timely detection of pulmonary hypertension and lung cancer, both of which are common complications. High-resolution computed tomography (HRCT) is an important diagnostic and prognostic tool, while lung cancer is an independent factor that alters the prognosis in CPFE patients. Treatment options for CPFE are limited, but smoking cessation, usual treatments of pulmonary fibrosis and emphysema, and avoidance of environmental exposures are encouraged.

Hypersensitivity pneumonitis (HP) is a complex interstitial lung disease caused by chronic inhalation of a wide variety of antigens in susceptible and sensitized individuals, commonly associated with an occupational exposure. An impressive number of inciting antigens causing hypersensitivity pneumonitis have been found to cover a wide range of occupations. As working practices have changed over time, especially in industrialized countries, new names for occupational HP have emerged. This review emphasizes the main diagnostic issues arising from the high variability of clinical presentation and the broad spectrum of causal antigens. Furthermore, it provides an overview of current methods to unveil possible causes of hypersensitivity pneumonitis, highlights HP’s current diagnostic and treatment challenges and the remaining areas of uncertainty, and presents prevention strategies.

Pulmonary Hypertension (PH) in patients with Interstitial Lung Disease (ILD) is a critical, yet underrecognized, complication that affects patients’ quality of life and increases mortality. Emerging evidence further suggests that PH-ILD is not merely a consequence of hypoxia and parenchymal fibrosis, as the severity of pulmonary vascular disease often correlates poorly with the extent of fibrotic lung involvement, indicating more complex underlying pathophysiological mechanisms. Diagnosis requires a high index of suspicion when symptoms appear “disproportionate” to the degree of parenchymal lung disease. Key indicators include diffusing capacity for carbon monoxide (DLCO) < 45%, a forced vital capacity to diffusing capacity for carbon monoxide ratio (FVC/DLCO) > 1.6, and radiological findings of increased pulmonary artery diameter. While echocardiography and circulating biomarkers serve as useful screening tools, right heart catheterization remains the gold standard for definitive diagnosis. Early identification is essential for risk stratification, lung transplant evaluation, and determining eligibility for targeted pharmacological interventions, as this group of patients remains one of the most therapeutically challenging forms of pulmonary vascular disease. Ongoing research and advances in diagnostic tools are increasingly focused on refining phenotypic classification, identifying valuable biomarkers, and elucidating molecular drivers that may enable personalized treatment strategies in this heterogeneous patient group.

ANCA-associated vasculitides (AAVs) are rare but carry major prognostic significance. Increasing evidence shows that they extend beyond vascular inflammation and frequently involve interstitial lung disease (ILD), most often with a UIP pattern, which is linked to high mortality. The issue is particularly relevant since ILD may precede vasculitis and mimic isolated pulmonary fibrosis, raising the risk of underdiagnosis. Conventional vasculitis therapies have proven ineffective in halting fibrosis and increase infection risk, while antifibrotic agents offer promise but remain insufficiently studied. The absence of clear guidelines and dedicated trials creates clinical uncertainty, making AAV-ILD an emerging field at the crossroads of pulmonology and rheumatology, where urgent research is needed and the potential to improve outcomes is considerable

Aim: To study the anatomical features of bronchial malformations in clinical and imaging context in children. Methods:The study was conducted on a sample of 18 children with congenital bronchial malformations, confirmed by thoracic CT scans (HRCT). There were 15 children with tracheal bronchus, 2 children with bronchial stenosis from vascular rings, 1 child with bridging bronchus. The age of the children from the 2 months to 11 years; 8 boys and 10 girls. Results:In all the children, the tracheal bronchus emerged from the right side of the trachea. Among them, 26.6% showed the bronchus starting from the middle segment of the trachea, in 14.3%:95%CI 1.8-42.8 from the lower segment, in 64.3%:95%CI 35.1-87.2 - near the tracheal bifurcation. Children with a bridging bronchus exhibited the emergence of the right middle and lower lobe bronchi through a common bronchus from the left main bronchus. The children had pneumonic infiltration in 22.2% of cases, changes resembling "ground glass" in 14.3%:95%CI 1.8-42.8, segmental atelectasis in 33.3%, and pulmonary fibrosis in 21.4%:95% CI 4.7-50.8. Children with bronchial malformations exhibited severe symptoms including progressive respiratory failure and recurrent lung infections. These children showed clinical signs of respiratory failure due to the narrow caliber of the trachea and bronchi in their early years, have difficulty tolerating stenotic lesions of the airways, and often require surgical treatment. Conclusions: HRCT imaging research provides valuable information in specifying the anatomical features of bronchial malformations, the type of bronchial anomalies, the degree of stenosis, and pulmonary complications.