Abstract

TOPIC: Pulmonary Manifestations of Systemic Disease TYPE: Medical Student/Resident Case Reports INTRODUCTION: The implication of COVID 19 pneumonia on chronic inflammatory disorders is not clearly known. Due to a lack of data, it is difficult to predict the disease course post-COVID 19 pneumonia. Here, we present a case of stable sarcoidosis that progressed rapidly after COVID 19 pneumonia. CASE PRESENTATION: A 43-year-old male, with a history of sarcoidosis, briefly treated with steroids at initial diagnosis and in remission for the last six years, was admitted for dyspnea and hypoxia (room air oxygen saturation 83%) secondary to COVID 19 pneumonia diagnosed a week prior to admission. Chest X-ray on admission showed diffuse bilateral interstitial and airspace opacities. He was treated with dexamethasone and remdesevir. The clinical status of the patient improved after a week, and he was discharged on prednisone taper (10 mg for 5 days). Four weeks later, the patient had a recurrence of dyspnea on exertion with occasional hemoptysis. Computed Tomography (CT) scan of the chest showed honeycombing and reticulations in bilateral upper lobes, interstitial thickening, and worsening hilar and mediastinal lymphadenopathy (sarcoidosis Scadding stage IV). Labs were significant for elevated serum soluble interleukin-2 (IL-2) receptor and calcitriol levels. Pulmonary function test showed a restrictive defect with reduced diffusion capacity. The patient was started on prednisone. Repeat CT scan after three months showed improvement in ground-glass opacities and stable scarring. Fine needle aspiration biopsy of subcarinal lymph node confirmed non-caseating granulomatous inflammation. The patient was started on mycophenolate mofetil, tapered off prednisone, and is being evaluated for a lung transplant. DISCUSSION: The main pathogenesis related to sarcoidosis is the formation of granulomas due to sustained host immune system stimulation from various known and unknown antigens. Activation of the immune system as evidenced by elevated inflammatory makers in viral infections may in turn precipitate the relapse and progression of inflammatory disorders such as sarcoidosis. It is difficult to distinguish between the sequela of COVID 19 pneumonia and sarcoidosis progression. CT scan findings in fibrotic sarcoidosis have upper lobe predilection. However, the distribution of ground-glass opacities and fibrosis in COVID 19 pneumonia is usually peripheral and may have lower lobe predilection. Close monitoring is important to look for activation of sarcoidosis post COVID 19 pneumonia. CONCLUSIONS: Implications of COVID 19 infection on pathogenesis and progression of sarcoid are important to understand, and more research is required so that clinicians can be vigilant about worsening pulmonary function and intervene in a timely manner. REFERENCE #1: Ramdani H, Benelhosni K, Moatassim Billah N, Nassar I. COVID-19 pneumonia in a patient with sarcoidosis: A case report. Clin Case Rep. 2020 Dec 23;9(2):910-913. REFERENCE #2: Tana C, Mantini C, Cipollone F, Giamberardino MA. Chest Imaging of Patients with Sarcoidosis and SARS-CoV-2 Infection. Current Evidence and Clinical Perspectives. Diagnostics (Basel). 2021 Jan 27;11(2):183. DISCLOSURES: No relevant relationships by Salim Daouk, source=Web Response No relevant relationships by Samiksha Gupta, source=Web Response No relevant relationships by Ahmad Hassan, source=Web Response No relevant relationships by SYED HUSSAIN, source=Web Response No relevant relationships by Miloni Parmar, source=Web Response

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