Letter to the Editor

LETTER TO EDITOR: A RESEARCH REPORT

Acute silicosis is a rare occupational lung disease (Banks, 2005), and also, to the best of my knowledge, plaque formation on the visceral layer of pericardium has not been previously reported. I describe unusually acute silicosis with this interesting finding in autopsy. A 19-yr-old man was admitted with loss of appetite, weight loss, and exertional dyspnea. He had worked as a silica powder packer in a stone-grinding workplace from age 17 for 18 mo. His chest x-ray showed small opacities (p/q) with radiological profusion category 1/2 using the ILO classification system. During the next 3 yr he developed orthopnea, paroxysmal nocturnal dyspnea (PND), resting dyspnea, distended neck veins, prominent jugular vein pulses, presystolic gallop sound (S4), significant right ventricular S3 gallop, hepatomegaly, peripheral edema, and ascites. Latest chest x-ray showed small opacities (r/u) with radiological profusion category 3/3, and large opacity with B scale. Pulmonary function test demonstrated very severe restrictive pattern. He died of cardiogenic shock, and autopsy revealed advanced pigmented silicotic masses in the lungs, pericardial effusion, and cardiomegaly associated with a smooth plaque of irregular shape on the visceral layer of pericardium.

Silica deposition, with or without nodule formation, has been reported in the extrapulmonary organs, wherever it is deposited. The nodule formation had been considered in the abdominal peritoneum, bone marrow, extrathoracic lymph nodes, liver, and spleen (Miranda et al., 1996). On the other hand, silica particles may be deposited in the brain, kidney, and skin without nodule formation (Haustein et al., 1990). I have reported this unique case to bring attention to the increasing evidence that intense exposure to silica may cause or stimulate extrapulmonary complications such as pericardial plaque formation.