[A case of hard metal lung disease in a man who worked as an iron grinder].

The patient was a man who had suffered from repeated pneumothoraces since August 2003, when he was 16 years old. A right pneumothorax was observed at age 21 years, in April 2008. At the same time, a dry cough began to appear and diffuse small nodular shadows in both lung fields were found on a chest X-ray film. Due to worsening symptoms and the chest X-ray findings, a transbronchial lung biopsy was performed in September 2008. Pathological examination showed mural type organization, and large numbers of multinucleated giant cells that were engulfing nucleated cells and had black pigment in their cytoplasm. Giant cell interstitial pneumonia and hard metal lung disease (HMLD) were suspected because of the patient's occupational history as a metal grinder, which included the use of a hard metal tool for three years since August 2005. In an elementary analysis using an electron probe microanalyzer, tungsten was detected in resected lung tissue obtained in April 2008 which confirmed the diagnosis. His symptoms improved after the initiation of corticosteroid therapy, which continued but with a gradual decrease in the dose. In this case, HMLD developed over a relatively short period despite the low level of dust dispersal of a hard-metal tool, perhaps because of a hypersensitivity of the patient to hard metal.

An observational study of giant cell interstitial pneumonia and lung fibrosis in hard metal lung disease.

BACKGROUND: Hard metal lung disease has various pathological patterns including giant cell interstitial pneumonia (GIP) and usual interstitial pneumonia (UIP). Although the UIP pattern is considered the prominent feature in advanced disease, it is unknown whether GIP finally progresses to the UIP pattern. OBJECTIVES: To clarify clinical, pathological and elemental differences between the GIP and UIP patterns in hard metal lung disease. METHODS: A cross-sectional study of patients from 17 institutes participating in the 10th annual meeting of the Tokyo Research Group for Diffuse Parenchymal Lung Diseases, 2009. Nineteen patients (seven female) diagnosed with hard metal lung disease by the presence of tungsten in lung specimens were studied. RESULTS: Fourteen cases were pathologically diagnosed as GIP or centrilobular inflammation/fibrosing. The other five cases were the UIP pattern or upper lobe fibrosis. Elemental analyses of lung specimens of GIP showed tungsten throughout the centrilobular fibrotic areas. In the UIP pattern, tungsten was detected in the periarteriolar area with subpleural fibrosis, but no association with centrilobular fibrosis or inflammatory cell infiltration. The GIP group was younger (43.1 vs 58.6 years), with shorter exposure duration (73 vs 285 months; p<0.01), lower serum KL-6 (398 vs 710 U/mL) and higher lymphocyte percentage in bronchoalveolar lavage fluid (31.5% vs 3.22%; p<0.05) than the fibrosis group. CONCLUSIONS: The UIP pattern or upper lobe fibrosis is remarkably different from GIP in distribution of hard metal elements, associated interstitial inflammation and fibrosis, and clinical features. In hard metal lung disease, the UIP pattern or upper lobe fibrosis may not be an advanced form of GIP.

Upper lobe-dominant pulmonary fibrosis showing deposits of hard metal component in the fibrotic lesions.

We present a 54-year-old man employed in the field of hard metal manufacturing who complained of progressive dyspnea and weight loss. His chest radiograph showed bilateral fibrosis predominantly distributed in the upper lobes with bilateral pleural effusions, and a strong reduction in lung volume. Lung histopathology showed apical cap-like fibrosis but no giant cell interstitial pneumonia. Electron probe microanalysis detected tungsten deposits in the fibrotic region: we therefore considered this to be a case of hard metal disease. Hard metal disease should be considered as one possibility in the differential diagnosis of upper lobe-dominant pulmonary fibrosis.