XXIV National Congress of Italian Pulmonology - XLVII ITS-AIPO Congress

Abstract

Background: COVID-19 leads to a wide spectrum of respiratory diseases ranging from mild upper respiratory tract symptoms to severe acute respiratory distress syndrome. Idiopathic pulmonary fibrosis (IPF) is a rare and progressive interstitial lung disease in which lung function inexorably declines, leading to respiratory failure. Severe COVID-19 and IPF shares major risk factors such as increasing age, male sex, and comorbidities such as hypertension and diabetes.[1] Some recent studies showed that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections and idiopathic pulmonary fibrosis (IPF) disease might stimulate each other through the shared genes [2]. Case report: We report the case of an 83-year-old male patient, a 50 packs/year former smoker, affected by IPF on treatment with Nintedanib since 2019 and home oxygen therapy and chronic kidney disease stage IIIC. A.O.R.N. Antonio Cardarelli. The patient joined the emergency department in serious clinical conditions with worsening dyspnea, fever, chest pain and hypotension. ABGA showed moderate respiratory insufficiency (P/F 150). Therefore, he began supportive therapy with HFNC with ROX index >4.88 after 2, 6 and 12 hours. His blood chemistry tests showed increased inflammation indexes: CRP 75 mg/l, ESR 45 mm/h, leukocytes increase with relative lymphocytosis. He performed SARS-CoV-2 molecular swab which was positive. HRCT showed honey combing, traction bronchiectasis prevailing in the middle and lower fields bilaterally, already present on the previous control imaging and bilateral and peripheral ground glass opacities of new finding. A diagnosis of COVID-19 pneumonia was therefore made. He practiced antibiotic and corticosteroid therapy, without suspending Nintedanib, for 10 days with progressive improvement of symptoms, reduction of inflammation indices and improvement of respiratory insufficiency verified by serial ABGA. As the antigenic swab turned negative, the patient performed HRCT again which showed attenuation of previously observed ground glass pattern. The patient was discharged for improvement and stabilization of the clinical conditions. Checkup a 3 months and 12 months showed no worsening respiratory symptoms, no physiological evidence of disease progression (absolute decline in FVC of ≥ 5%, absolute decline in DLCO of ≥ 10%) and no radiological evidence of disease progression (UIP pattern superimposable on his pre- COVID CTs). Conclusions: This case suggests the efficacy of treatment with Nintedanib in preventing the progression of fibrosis after SARSCoV- 2 infection in patients with IPF. Therefore, its use could also be considered in other non-progressive ILDs and not in antifibrotic treatment in patients with SARS-CoV-2 pneumonia. (Table Presented).