Ermanno Puxeddu1, Alessia Comandini1, Francesco Cavalli2, Gabriella Pezzuto3, Claudio D'Ambrosio2, Lucia Senis3, Maurizio Paci4, Giacomo Curradi5, Gian Luigi Sergiacomi1, Cesare Saltini6. 1. Department of Biomedicine and Prevention, Tor Vergata University Hospital, Roma, Italy. 2. Postgraduate School in Pulmonary Medicine, Tor Vergata University Hospital, Roma, Italy. 3. Pulmonary Fibrosis Clinic, Division of Respiratory Diseases, Tor Vergata University Hospital, Roma, Italy. 4. Department of Chemical Science and Technology, University of Rome "Tor Vergata", Italy. 5. Doctorate School in Medical Sciences, University of Bologna, Bologna, Italy. 6. Department of Biomedicine and Prevention, Tor Vergata University Hospital, Roma, Italy; Postgraduate School in Pulmonary Medicine, Tor Vergata University Hospital, Roma, Italy; Pulmonary Fibrosis Clinic, Division of Respiratory Diseases, Tor Vergata University Hospital, Roma, Italy. Electronic address: cesaresaltini@med.uniroma2.it.
Abstract
RATIONALE: A number of observations suggest that iron accumulates in the lungs of patients with idiopathic pulmonary fibrosis (IPF) with vascular abnormalities, including pulmonary hypertension. OBJECTIVES: The aim of this study was to determine the prevalence and intensity of accumulation of alveolar epithelial lining fluid (ELF) iron and of alveolar macrophage hemosiderin in IPF and its relationship with disease severity. METHODS: Forty seven IPF patients and 14 healthy controls were retrospectively evaluated for iron accumulation in the lower respiratory tract using total iron spectrophotometric measures and for hemosiderin accumulation using the Perls' stain with the Golde score. MEASUREMENTS AND MAIN RESULTS: Total iron levels in ELF were significantly increased in IPF patients compared to non-smoking controls (p < 0.05); there were no differences with healthy smokers (p = 0.2). Hemosiderin accumulation in alveolar macrophages was similar in never smoking and ever smoking IPF patients (p = 0.5), was significantly higher in IPF patients than in both smoking and non-smoking healthy controls (p < 0.05, all comparisons) and was positively correlated with echocardiographic estimates of pulmonary artery systolic pressure (p < 0.05) and with increasing disease severity scores (p < 0.05). CONCLUSIONS: The data show exaggerated accumulation of iron in IPF broncho-alveolar ELF and alveolar cells with no association with tobacco smoke, thus suggesting, occult pulmonary hemorrhage as a likely cause.
RATIONALE: A number of observations suggest that iron accumulates in the lungs of patients with idiopathic pulmonary fibrosis (IPF) with vascular abnormalities, including pulmonary hypertension. OBJECTIVES: The aim of this study was to determine the prevalence and intensity of accumulation of alveolar epithelial lining fluid (ELF) iron and of alveolar macrophage hemosiderin in IPF and its relationship with disease severity. METHODS: Forty seven IPFpatients and 14 healthy controls were retrospectively evaluated for iron accumulation in the lower respiratory tract using total iron spectrophotometric measures and for hemosiderin accumulation using the Perls' stain with the Golde score. MEASUREMENTS AND MAIN RESULTS: Total iron levels in ELF were significantly increased in IPFpatients compared to non-smoking controls (p < 0.05); there were no differences with healthy smokers (p = 0.2). Hemosiderin accumulation in alveolar macrophages was similar in never smoking and ever smoking IPFpatients (p = 0.5), was significantly higher in IPFpatients than in both smoking and non-smoking healthy controls (p < 0.05, all comparisons) and was positively correlated with echocardiographic estimates of pulmonary artery systolic pressure (p < 0.05) and with increasing disease severity scores (p < 0.05). CONCLUSIONS: The data show exaggerated accumulation of iron in IPF broncho-alveolar ELF and alveolar cells with no association with tobacco smoke, thus suggesting, occult pulmonary hemorrhage as a likely cause.
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