Lucia Vietri

Lipid metabolism has been demonstrated to be altered in different interstitial lung diseases (ILDs), including idiopathic pulmonary fibrosis (IPF); it can influence the pathogenesis of fibrotic lung disorders. Serum Amyloid A (SAA) is an acute-phase protein mainly produced by the liver in response to proinflammatory cytokines. Several studies I conducted on Serum Amyloid A (SAA) support the hypothesis that this protein could be considered a potential specific biomarker for Idiopathic Pulmonary Fibrosis (IPF), capable of predicting the clinical course and prognosis of patients. SAA may help discriminate between a pulmonary interstitial disease with an inflammatory substrate and progressive pulmonary fibrosis. The follow-up of serum SAA levels over time could help us monitor the clinical and functional progression of IPF patients, as well as their risk of acute exacerbation, aiming to guide these patients toward antifibrotic therapies and lung transplantation within the appropriate time window. Additionally, my research on Serum Amyloid A reinforces the hypothesis of the role of lipid metabolism in the fibrogenic process. SAA plays a crucial role in regulating lipid metabolism and the production of matrix metalloproteinases (MMPs) in IPF, which are involved in extracellular matrix remodeling. SAA could be considered a potential therapeutic target for IPF, including through apolipoproteins.

Background: Lipid metabolism is altered in different interstitial lung diseases (ILDs). The role of serum amyloid A (SAA) in the pathogenesis of fibrosis it9s unknown, in particular in idiopathic pulmonary fibrosis (IPF). Aims and Objectives: our purpose was to improve the results of our previous study [1] on SAA serum levels in IPF, to define its potential value as clinical biomarker and its specificity in IPF. Methods: We recruited 131 patients, divided in 41 stable IPF, 8 on acute exacerbation (AE) of IPF, 24 chronic sarcoidosis, 24 hypersensitivity pneumonitis (cHP), 17 pulmonary langerhans cell histiocytosis and lymphangioleiomyiomatosis (PLCH-LAM) and 17 healthy controls. SAA levels were determined by an enzyme-linked immunosorbent assay (ELISA) kit. Results: IPF group showed significantly higher levels of SAA than the other ILDs (6418 ng/ml, Figure 1). A cut-off value of 4053 ng/ml of SAA discriminated IPF from AE-IPF and supports our hypothesis of SAA as a marker of fibrosis. SAA levels > 4057.8 ng/mL were associated to a poor prognosis in IPF. Conclusions: SAA could be a potential biomarker of IPF that can predict clinical course, prognosis and survival of IPF patients. Monitoring SAA serum levels could help to identify rapidly progressive phenotype of IPF or at risk of acute exacerbation. References [1] Vietri, L. et al. Respiratory Investigation 2019; 57(5):430-434.

Serum amyloid A (SAA) is an apo‐lipoprotein produced by the liver in response to proinflammatory cytokines. Few data are available on SAA levels in patients with idiopathic pulmonary fibrosis (IPF), the most common idiopathic form of interstitial pneumonitis (ILD). This study compared SAA concentration in IPF patients to other ILD groups to explore its potential use as a clinical biomarker.

Aim: Interstitial lung diseases (ILD) are a group of lung disorders characterized by interstitial lung thickening. Krebs von den Lungen-6 (KL-6) is a molecule that is predominantly expressed by dam...

Introduction Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease often managed with Nintedanib, a tyrosine kinase inhibitor targeting several profibrotic pathways. Although clotting processes are involved in wound healing and repair in the lung, there is no data on the role of antithrombin III on in IPF patients treated with Nintedanib. A previous proteomic analysis of serum of IPF patients before and after one year of Nintedanib treatment showed differential protein expression of antithrombin III. Aims Here we used quantitative methods to evaluate differential ATIII concentrations in IPF patients before and after one year of Nintedanib treatment and to assess the potential of ATIII as a prognostic biomarker in IPF patients. Methods Serum levels of ATIII were measured by ELISA in 14 IPF patients before and after one year of Nintedanib treatment. Results A statistically significant inverse correlation was found between serum ATIII concentrations and PFT s parameters in all patients at baseline and follow up. Baseline serum ATIII and BAL neutrophils proved to be reliable predictors of poor prognosis. A baseline ATIII threshold of 126.5 μg/mL discriminated survivors from non‐survivors. Conclusions After 12 months of antifibrotic treatment, IPF patients with high serum ATIII concentrations and high BAL neutrophil percentages had a poor prognosis and increased survival risk. The results of this preliminary study suggest, that ATIII has potential as a biomarker of IPF severity and in predicting answer to Nintedanib therapy. As a marker, ATIII showed several advantages over BAL neutrophil percentage.

The original version of this article unfortunately contained a mistake. First and last names of the authors were interchanged.

Background: Serum Amyloid A (SAA) is an acute phase protein and we analyzed its concentrations in lung transplantated patients (LTX). Methods: 26 LTX patients (58.6 +/- 11 years) and 11 healthy controls (55 +/- 11.3 years). Three groups of LTX patients: acute rejection (AR, 7) bronchiolitis obliterans syndrome (BOS, 3), acute infection (INF, 9) and stable patients (NEG, 7). Results: In LTX patients SAA concentrations were significantly increased, particularly in AR and INF. In LTX-AR patients were observed a correlation between SAA levels and peripheral CD4+ lymphocyte percentage (r=0.9, p<0.01) and a reverse correlation with FVC percentages (r -0.94, p=0.01). Conclusions: SAA may represent a potential biomarker of LTX acute complications, with a prognostic value in AR.