CASE REPORT FDG PET findings in a case with acute pulmonary silicosis Metin O ¨ zkan • Aslı Ayan • Deniz Arik • Arzu Balkan • O ¨ nder O ¨ ngu ¨ru ¨ • Seyfettin Gu ¨mu ¨s ¸ Received: 16 February 2009 / Accepted: 11 September 2009 / Published online: 29 October 2009 Ó The Japanese Society of Nuclear Medicine 2009 Abstract A 21-year-old male having a history of 4 years of working at a denim factory as a sandblaster was diag- nosed with pulmonary silicosis and he was also an active smoker. Productive cough, dyspnea on effort, night sweats, and weight loss in a short period of time were his com- plaints. Chronic occupational exposure to tiny particles of silicon dioxide can stimulate parenchymal inflammation, collagen synthesis and, ultimately pulmonary fibrosis called silicosis. A typical history of exposure and chest X-ray is usually enough for diagnosis. No effective treat- ment exists except supportive care. Although chest X-ray of the patient revealed bilateral disseminated micronodular densities, a peripherally diffuse prominent FDG [(F-18)-2- fluoro-2-deoxy-D-glucose] uptake in both lungs and faint FDG uptake in mediastinal lymph nodes demonstrating active inflammation regions were noted on PET (Positron Emission Tomography) scan. This case was presented to show the active disease discriminated by FDG PET from chronic changes detected by radiological studies. FDG PET can provide additional information to CT regarding the diagnosis of acute silicosis and the rare accelerated silicosis. Keywords Silicosis Á Occupational diseases Á Positron emission tomography Á PET Introduction Silicosis is characterized by nodular pulmonary fibrosis caused by inhalation of tiny particles of silicon dioxide in the form of crystalline ‘‘free’’ silica or, less commonly, by inhalation of silicates, minerals containing silicon dioxide bound to other elements, such as talc. Inhaled free silica particles are engulfed by alveolar macrophages and they cause the release of cytokines (tumor necrosis factor-a, IL-1), growth factors (tumor growth factor-b), and oxi- dants, stimulating parenchymal inflammation, collagen synthesis, and, ultimately, fibrosis. Although silicosis initially causes no symptoms or only mild dyspnea, over years can advance to involve most of the lung and cause dyspnea, hypoxemia, pulmonary hypertension, and respi- ratory impairment. According to the disease’s severity, onset, and rapidity of progression, there are three main types of silicosis acute form usually occurs after heavy exposure to high concentrations of silica and the symp- toms can develop within a few weeks or as long as 5 years after the exposure; Accelerated silicosis is a very rare form that progresses rapidly folllowing intense short- term exposure to silica particles and the disease develops within 5–10 years after exposure, whereas, the most common is the chronic form which occurs after long-term exposure of low concentrations of silica dust stays unde- tected for many years. History and chest X-ray findings are helpful for diagnosis in chronic forms, but FDG PET imaging may be an important tool for the diagnosis of acute silicosis and the rare accelerated silicosis for preventive measures. M. O ¨ zkan Á D. Arik Á A. Balkan Á S. Gu ¨mu ¨s ¸ Department of Pulmonary Medicine, Gu ¨lhane Military Medical Academy and School of Medicine, 06018, Etlik, Ankara, Turkey A. Ayan (&) Department of Nuclear Medicine, Gu ¨lhane Military Medical Academy and School of Medicine, Ankara, Turkey e-mail: drasliayan@yahoo.com O ¨ .O ¨ ngu ¨ru ¨ Department of Pathology, Gu ¨lhane Military Medical Academy and School of Medicine, Ankara, Turkey 123 Ann Nucl Med (2009) 23:883–886 DOI 10.1007/s12149-009-0309-6