A case of broncholithiasis associated with massive silicosis is reported, showing a rare aspect of parenchymal lesions generating broncholiths as well as the presence of recurrent lithoptysis, with subsequent regression of radiological lesions.Aetiological, clinical, physiopathological, and radiological aspects of the disease are discussed, demonstrating the importance of the use of computed tomography in diagnosis. The mineralogical analysis of expectorated fragments is also shown. Eur Respir J 2002; 20: 1057- Broncholithiasis is characterised by bronchial erosion or distortion due to hilar or parenchymatous calcifications and is usually related to infectious aetiologies, such as tuberculosis or histoplasmosis [1]. Its association with silicosis is quite rare, and in the few reports described in medical literature, broncholithiasis has occurred only as a result of disorders of the lymph nodes [2][3][4][5].The present authors report a unique case of a patient with silicosis, who presented parenchymatous calcified lesions that eroded into the bronchial lumen leading to lithoptysis, with elimination of w100 broncholiths and impressive reduction of radiological lesions.
Case reportA 43-yr-old male presented with productive cough with bloody sputum for 5 months, wheezing and dyspnoea on exertion. The patient also reported the expectoration of small calculi of greyish colour and stony consistency, which werey2 mm in diameter and resembled "grape seeds" (fig. 1).The patient had a 28-pack-yr history of cigarette use. Twenty-six yrs before presentation, the patient had worked as a stone crusher in the stone working industry for a 1-yr period, and was exposed to a large amount of granite and quartz dust, but did not use any respiratory protective equipment. The patient had also occasionally crushed stones from a nearby asbestos mine. During his subsequent jobs as a painter and doorman, there was no exposure to silica dust.Physical examination disclosed diminished breath sounds and sparse ronchi, as well as finger clubbing. The spirometry demonstrated severe airflow obstruction with a forced expiratory volume in one second (FEV1) of 1.17 L (41% of predicted) and FEV1/forced vital capacity of 50% pred. The first chest radiograph revealed bilateral calcified apical coalescence areas, compatible with massive silicosis, lung hyperinflation, hilar eggshell calcifications of the lymph nodes and bilateral diaphragmatic, calcified, pleural plaques ( fig. 2a). The patient underwent a fibreoptic bronchoscopy and the endoscopical appearance was normal. Sputum and bronchoalveolar lavage analyses did not reveal