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Background and Objective: There is increasing interest in the role of lipids in processes that modulate lung fibrosis with evidence of lipid deposition in idiopathic pulmonary fibrosis (IPF) histological specimens. The aim of this study was to identify measurable markers of pulmonary lipid that may have utility as IPF biomarkers. Study Design and Methods: IPF and control lung biopsy specimens were analysed using a unbiased lipidomic approach. Pulmonary fat attenuation volume (PFAV) was assessed on chest CT images (CTPFAV) with 3D semi‐automated lung density software. Aerated lung was semi‐automatically segmented and CTPFAV calculated using a Hounsfield‐unit (−40 to −200HU) threshold range expressed as a percentage of total lung volume. CTPFAV was compared to pulmonary function, serum lipids and qualitative CT fibrosis scores. Results: There was a significant increase in total lipid content on histological analysis of IPF lung tissue (23.16 nmol/mg) compared to controls (18.66 mol/mg, p = 0.0317). The median CTPFAV in IPF was higher than controls (1.34% vs. 0.72%, p < 0.001) and CTPFAV correlated significantly with DLCO% predicted (R2 = 0.356, p < 0.0001) and FVC% predicted (R2 = 0.407, p < 0.0001) in patients with IPF. CTPFAV correlated with CT features of fibrosis; higher CTPFAV was associated with >10% reticulation (1.6% vs. 0.94%, p = 0.0017) and >10% honeycombing (1.87% vs. 1.12%, p = 0.0003). CTPFAV showed no correlation with serum lipids. Conclusion: CTPFAV is an easily quantifiable non‐invasive measure of pulmonary lipids. In this pilot study, CTPFAV correlates with pulmonary function and radiological features of IPF and could function as a potential biomarker for IPF disease severity assessment. Aberrant cell lipid metabolism has been described in IPF but the underlying mechanisms are underexplored. In this study, chest CT is used to assess pulmonary fat attenuation volume (PFAV) in IPF. CTPFAV correlates with spirometry and IPF radiological markers. With further validation, CTPFAV could be used as a disease severity biomarker. [ABSTRACT FROM AUTHOR]

Objectives: Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH) occurs due to abnormal proliferation of pulmonary neuroendocrine cells. We hypothesized that performing a quantitative analysis of airway features on chest CT may reveal differences to matched controls, which could ultimately help provide an imaging biomarker. Methods: A retrospective quantitative analysis of chest CTs in patients with DIPNECH and age matched controls was carried out using semi-automated post-processing software. Paired segmental airway and artery diameters were measured for each bronchopulmonary segment, and the airway:artery (AA) ratio, airway wall thickness:artery ratio (AWTA ratio) and wall area percentage (WAP) calculated. Nodule number, size, shape and location was recorded. Correlation between CT measurements and pulmonary function testing was performed. Results: 16 DIPNECH and 16 control subjects were analysed (all female, mean age 61.7 +/− 11.8 years), a combined total of 425 bronchopulmonary segments. The mean AwtA ratio, AA ratio and WAP for the DIPNECH group was 0.57, 1.18 and 68.8%, respectively, compared with 0.38, 1.03 and 58.3% in controls (p < 0.001, <0.001, 0.03, respectively). DIPNECH patients had more nodules than controls (22.4 +/− 32.6 vs. 3.6 +/− 3.6, p = 0.03). AA ratio correlated with FVC (R2 = 0.47, p = 0.02). A multivariable model incorporating nodule number, AA ratio and AWTA-ratio demonstrated good performance for discriminating DIPNECH and controls (AUC 0.971; 95% CI: 0.925–1.0). Conclusions: Quantitative CT airway analysis in patients with DIPNECH demonstrates increased airway wall thickness and airway:artery ratio compared to controls. Advances in knowledge: Quantitative CT measurement of airway wall thickening offers a potential imaging biomarker for treatment response. [ABSTRACT FROM AUTHOR]

Background and Objective: There is increasing interest in the role of lipids in processes that modulate lung fibrosis with evidence of lipid deposition in idiopathic pulmonary fibrosis (IPF) histological specimens. The aim of this study was to identify measurable markers of pulmonary lipid that may have utility as IPF biomarkers., Study Design and Methods: IPF and control lung biopsy specimens were analysed using a unbiased lipidomic approach. Pulmonary fat attenuation volume (PFAV) was assessed on chest CT images (CT PFAV ) with 3D semi-automated lung density software. Aerated lung was semi-automatically segmented and CT PFAV calculated using a Hounsfield-unit (-40 to -200HU) threshold range expressed as a percentage of total lung volume. CT PFAV was compared to pulmonary function, serum lipids and qualitative CT fibrosis scores., Results: There was a significant increase in total lipid content on histological analysis of IPF lung tissue (23.16 nmol/mg) compared to controls (18.66 mol/mg, p = 0.0317). The median CT PFAV in IPF was higher than controls (1.34% vs. 0.72%, p < 0.001) and CT PFAV correlated significantly with DLCO% predicted (R 2  = 0.356, p < 0.0001) and FVC% predicted (R 2  = 0.407, p < 0.0001) in patients with IPF. CT PFAV correlated with CT features of fibrosis; higher CT PFAV was associated with >10% reticulation (1.6% vs. 0.94%, p = 0.0017) and >10% honeycombing (1.87% vs. 1.12%, p = 0.0003). CT PFAV showed no correlation with serum lipids., Conclusion: CT PFAV is an easily quantifiable non-invasive measure of pulmonary lipids. In this pilot study, CT PFAV correlates with pulmonary function and radiological features of IPF and could function as a potential biomarker for IPF disease severity assessment., (© 2023 The Authors. Respirology published by John Wiley & Sons Australia, Ltd on behalf of Asian Pacific Society of Respirology.)

Competing Interests: Competing interests: Competing interests The BMJ has judged that there are no disqualifying financial ties to commercial companies. The authors declare the following other interests: none. Further details of The BMJ policy on financial interests are here: https://www.bmj.com/about-bmj/resources-authors/forms-policies-and-checklists/declaration-competing-interests