Lucia Vietri1, David Bennett2, Paolo Cameli3, Laura Bergantini4, Giuseppe Cillis5, Piersante Sestini6, Elena Bargagli7, Paola Rottoli8. 1. Department of Medical and Surgical Sciences and Neurosciences, Respiratory Disease and Lung Transplant Unit, University of Siena, Viale Bracci, 53100 Siena, Italy. Electronic address: lucia.vietri89@gmail.com. 2. Department of Medical and Surgical Sciences and Neurosciences, Respiratory Disease and Lung Transplant Unit, University of Siena, Viale Bracci, 53100 Siena, Italy. Electronic address: david.btt@gmail.com. 3. Department of Medical and Surgical Sciences and Neurosciences, Respiratory Disease and Lung Transplant Unit, University of Siena, Viale Bracci, 53100 Siena, Italy. Electronic address: paolocameli88@gmail.com. 4. Department of Medical and Surgical Sciences and Neurosciences, Respiratory Disease and Lung Transplant Unit, University of Siena, Viale Bracci, 53100 Siena, Italy. Electronic address: laurabergantini@gmail.com. 5. Department of Medical and Surgical Sciences and Neurosciences, Respiratory Disease and Lung Transplant Unit, University of Siena, Viale Bracci, 53100 Siena, Italy. Electronic address: giuseppecillis@hotmail.it. 6. Department of Medical and Surgical Sciences and Neurosciences, Respiratory Disease and Lung Transplant Unit, University of Siena, Viale Bracci, 53100 Siena, Italy. Electronic address: piersante.sestini@unisi.it. 7. Department of Medical and Surgical Sciences and Neurosciences, Respiratory Disease and Lung Transplant Unit, University of Siena, Viale Bracci, 53100 Siena, Italy. Electronic address: bargagli2@gmail.com. 8. Department of Medical and Surgical Sciences and Neurosciences, Respiratory Disease and Lung Transplant Unit, University of Siena, Viale Bracci, 53100 Siena, Italy. Electronic address: paola.rottoli@unisi.it.
Abstract
BACKGROUND: Serum amyloid A (SAA) is an apo-lipoprotein (12-14 kDa) produced by the liver in response to proinflammatory cytokines from activated monocytes. The precursor of SAA is an acute-phase protein involved in the pathogenesis of sarcoidosis and has been found to be increased during exacerbation of chronic obstructive pulmonary disease and lung cancer. However, no data are available on SAA levels in patients with idiopathic pulmonary fibrosis (IPF), the most common and severe idiopathic form of interstitial pneumonitis associated with a usual interstitial histological and radiological pattern. The aim of this preliminary study was to evaluate SAA concentration in patients with IPF and to explore its potential use as a clinical biomarker. METHODS: SAA levels were determined by enzyme-linked immunosorbent assay in a population of 21 patients with IPF (14 male, aged 64.8 ± 8.1 years) and compared with those in 11 healthy controls (3 male, aged 55 ± 11.3 years). Clinical, functional, and immunological data were collected in a database. RESULTS: SAA levels were significantly higher in patients with IPF than in controls (p = 0.03). In patients with IPF, statistically significant correlations were found between SAA and HDL cholesterol levels (r = -0.62, p = 0.05) and FVC % predicted value (r = -0.52, p = 0.01). CONCLUSIONS: SAA is a promising marker of disease severity in patients with IPF. Our preliminary data suggest a potential pathogenetic role of alteration in lipid metabolism in this rare disease.
BACKGROUND:Serum amyloid A (SAA) is an apo-lipoprotein (12-14 kDa) produced by the liver in response to proinflammatory cytokines from activated monocytes. The precursor of SAA is an acute-phase protein involved in the pathogenesis of sarcoidosis and has been found to be increased during exacerbation of chronic obstructive pulmonary disease and lung cancer. However, no data are available on SAA levels in patients with idiopathic pulmonary fibrosis (IPF), the most common and severe idiopathic form of interstitial pneumonitis associated with a usual interstitial histological and radiological pattern. The aim of this preliminary study was to evaluate SAA concentration in patients with IPF and to explore its potential use as a clinical biomarker. METHODS:SAA levels were determined by enzyme-linked immunosorbent assay in a population of 21 patients with IPF (14 male, aged 64.8 ± 8.1 years) and compared with those in 11 healthy controls (3 male, aged 55 ± 11.3 years). Clinical, functional, and immunological data were collected in a database. RESULTS:SAA levels were significantly higher in patients with IPF than in controls (p = 0.03). In patients with IPF, statistically significant correlations were found between SAA and HDL cholesterol levels (r = -0.62, p = 0.05) and FVC % predicted value (r = -0.52, p = 0.01). CONCLUSIONS:SAA is a promising marker of disease severity in patients with IPF. Our preliminary data suggest a potential pathogenetic role of alteration in lipid metabolism in this rare disease.
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