Complicated silicosis due to engineered stone: High metabolic activity in positron emission tomography and systemic inflammation years after exposure cessation

Engineered stone silicosis is an interstitial lung disease that progresses rapidly causing, in many cases, respiratory insufficiency and death. Metabolic activity in lungs and adenopathies and its relationships with systemic inflammation are unknown. Patients with complicated silicosis were enrolled. All had worked for at least 5 years in finishing and installing engineered stone and had ceased exposure for at least 7 years. Clinical data, positron emission tomography/computed tomography using ¹⁸ F-fluorodeoxyglucose ( ¹⁸ F-FDG PET/CT), respiratory function tests and blood samples were collected. Patients’ mean age was 44 ± 5.4 years. The average exposure duration was 10.94 ± 3.2. Years from cessation of exposure was 11.6 ± 1.6. The average maximum standardized uptake value (SUVmax) of large opacities was 6.32 ± 3. All patients presented hypermetabolic mediastinal lymphadenopathies and 88.2% also extrathoracic lymphadenopathies. SUV max of large opacities was correlated with Fibrinogen (ρ = 0.717, P = 0.001), lymphocyte-to-monocyte ratio (ρ = -0.506, P = 0.038), systemic inflammatory response index (ρ = 0.559, P = 0.02) and CD4 + NKT cells. Large lung opacities and lymphadenopathies showed high metabolic activity even years after silica exposure ended. The relationships between metabolic activity and some inflammatory factors open a pathway for exploring new therapeutic targets.