The mechanism of thrombocytopenia during acute pulmonary hypertension (PH) decompensation may be partly due to platelet aggregation in the lung. Platelet aggregates in explanted lung from 16 lung transplant patients during acute PH decompensation with and without thrombocytopenia were identified by immunohistochemistry. Scanning electron microscopy (SEM) was performed. 7 explant lung controls without PH and thrombocytopenia were also examined. Compared with controls, the median number of platelet aggregates was higher in patients with acute PH decompensation with thrombocytopenia (19.4 [IQR 3.4–38.3] vs 147.5 [IQR 26.5–203.2]). SEM showed capillaries filled with platelet aggregates. Our study suggests that platelets may aggregate in the lungs during acute PH decompensation.

Mesenchymal stem cells (MSC) have immune regulatory properties that may ameliorate pathophysiological processes in sepsis. We determined the effect of allogeneic adipose-derived MSCs (Cx611) on the host response during sepsis due to community-acquired bacterial pneumonia (CABP) by measuring 29 plasma biomarkers and blood transcriptomes at six time points in 82 patients randomised to two intravenous infusions of Cx611 or placebo. Cx611 treatment enhanced several endothelial cell and procoagulant response plasma biomarkers, and led to increased expression of pathways related to innate immunity, haemostasis and apoptosis. Cx611 infusion in sepsis due to CABP is associated with broad host response alterations. RNAseq data are available from the NCBI Sequence Read Archive (SRA) under the BioProject accession PRJNA1097551. Other data generated and/or analysed during the current study are available on reasonable request.

Interstitial lung disease (ILD) is a heterogeneous parenchymal disorder.1 2 Patients with ILD often present with non-specific symptoms such as a non-productive cough and exertional dyspnoea. The differential diagnosis for ILD is broad and includes conditions such as connective tissue disease (CTD), hypersensitivity pneumonitis, drug-associated ILD and granulomatous diseases. Furthermore, the initial management depends on factors such as antigen exposure, causative drugs, inflammation and fibrosis. Accurate diagnosis requires a detailed medical history, chest high-resolution CT (HRCT) and pathology.3 4 From a physiological perspective, ILD manifests as a restrictive disorder with reduced diffusion capacity of the lungs for carbon monoxide (DLco).5–7 Many clinical trials on ILD have used forced vital capacity (FVC) as a surrogate marker for mortality.8 9 Additionally, trends in FVC and DLco have been shown to be useful predictors of mortality, particularly in idiopathic pulmonary fibrosi

Background Lung function testing remains a cornerstone in the assessment and management of interstitial lung disease (ILD) patients. The clinical implications of the Global Lung function Initiative (GLI) reference equations and the updated interpretation strategies remain uncertain. Methods Adult patients with ILD with baseline forced vital capacity (FVC) were included from the Australasian ILD registry and the National Healthcare Group ILD registry, Singapore. The European Coal and Steel Community and Miller reference equations were compared with the GLI reference equations to assess (a) differences in lung function percent predicted values; (b) ILD risk prediction models and (c) eligibility for ILD clinical trial enrolment. Results Among 2219 patients with ILD, 1712 (77.2%) were white individuals. Idiopathic pulmonary fibrosis (IPF), connective tissue disease-associated ILD and unclassifiable ILD predominated. Median FVC was 2.60 (2.01–3.36) L, forced expiratory volume in 1 s was 2.0