COVID-19-induced pulmonary sarcoid: A case report and review of the literature

Abstract

Background: The COVID-19 pandemic has resulted in dramatic loss of life worldwide, but as the large number of acutely ill patients subsides, the emerging group of "COVID-19 long-haulers" present a clinical challenge. Studies have shown that many of these patients suffer long-term pulmonary disease related to residual fibrosis. Prior studies have shown that while many patients have non-specific findings of fibrotic-like changes, others develop specific patterns of interstitial lung disease.

Case report: Here, we present the first case of a patient developing pulmonary sarcoidosis one year after critical illness from COVID-19. He developed numerous non-necrotizing and well-formed granulomas in mediastinal lymph nodes and pulmonary nodules, compatible radiographically and pathologically with sarcoid.

Conclusions: While the pathophysiology of sarcoid is incompletely understood, inflammation is mediated through the dysregulation of a number of different cytokines (IFNγ, IL-2, IL-12, IL-17, IL-22). This case provides valuable clues for better understanding of the shared pathophysiology of cytokine dysregulation seen in COVID-19 and other interstitial lung diseases such as sarcoidosis.

Keywords: COVID-19; Cardiothoracic; Cytokine; Interstitial lung disease; Sarcoid.

Fig. 1

(A) Prior radiograph from 2016 for comparison. (B) Initial chest radiograph for COVID-19-related admission demonstrated mild lower lobe predominant airspace opacities suggestive of COVID-19 infection, (C) which progressed over the first 12 days of the patient's hospital admission.

Fig. 2

Right frontal lobe intracranial hemorrhage on (A) initial imaging and follow-up imaging at (B) 24 and (C) 48 h demonstrates slowly progressive evolution with a decreasing component of acute blood products.

Fig. 3

Serial axial CT images of the chest from CT of the abdomen and pelvis demonstrated prominent peripheral reticulations, traction bronchiectasis, and ground glass opacities, in excess of what is typically seen in the post-COVID-19 setting.

Fig. 4

Progression of pulmonary parenchymal disease at 5-months (A, B) and 14-months (C, D) post admission demonstrated progression from diffuse lower lobe predominant ground glass opacities to mosaic attenuation (A, B), followed by the development of innumerable pulmonary nodules and diffuse reticulation (C, D). Radiographically these findings are compatible with pulmonary sarcoid.

Fig. 5

Extensive mediastinal and hilar adenopathy on CT at 14 months post infection was best seen on abdomen windows (A, B) and prompted FDG-PET-CT which exhibited high FDG avidity in mediastinal and hilar nodes (C, D). The study was also significant for low level FDG uptake in the lung bases suggestive of infection and/or inflammation.

Fig. 6

Endobronchial ultrasound guided fine needle aspiration of a lymph node (A) and core biopsy of the lung with non-necrotizing and well-formed granulomas (B).