A 49-year-old male patient who came to our hospital for three weeks of lung shadow found on physical examination had no cough and sputum, no dyspnea, no appetite or weight loss, no fever, chest pain or hemoptysis, no previous diabetes, no history of trauma or radiation exposure. He had surgery for a fracture of the left clavicle five years ago, the pre-operative chest X-ray have not showed any siderosis changes, and postoperative recovery is satisfactory. When he came to our hospital for examination, the patient performed well in all aspects of his body, body temperature: 36.6 C, pulse: 69 times/min, breathing: 20 times/min, blood pressure: 122/82 mmHg. The patient was mind and spirit, with clear breath sounds in both lungs and no obvious rales of dry and wet, and the remaining physical examination revealed no obvious anomalies. There were no significant abnormalities in common laboratory tests. No significant abnormalities were seen in the routine Electrocardiogram (ECG). Examination of epigastric ultrasonography did not suggest abnormalities associated with this disorder. Pulmonary ventilation function measurement: mild obstructive pulmonary ventilation dysfunction, normal lung diffusion function, negative drug relaxation test. The patient has been working as an "electric welder" for more than thirty years and had a history of smoking for well over twenty years, ten cigarettes per day. He quit smoking after lung shadow was revealed in physical examination. Chest CT done three weeks ago suggested diffuse lesions and localized emphysema, thick-walled cavities and multiple nodules seen in both pulmonary and mediastinal windows ( Figures 1A, B ). The diffuse ground-glass changes in two lungs were considered as diffuse alveolar exudation, at the same time under the two pulmonary interstitial changes, combined with occupational history, considering pneumoconiosis may. Although welding-associated pulmonary fibrosis was the most likely diagnosis for this patient, for further differential diagnosis, we communicate with the patient and his family and inform them of the necessity and risks, and after having their consent, we perform a fiberoptic bronchoscopy. We performed fiber bronchoscopy for differential diagnosis and obtained bronchoalveolar lavage fluid from the posterior segment of the right upper lobe and lingual segment of the left upper lobe. Thecell counts and leukocyte classification results: the posterior upper lobe lavage fluid of the right lung had a bloody turbid appearance, a nucleated cell count of 510/mul and neutrophils accounted for 60%, and the appearance of the lingual segment of the left upper lobe is colorless and micro-muted, with a nucleated cell count of 63/mul, neutrophils 6%. The St. Regis staining of Bronohoalveolarlavage (BAL) fluid showed macrophages engulfing a large number of brown-black particles of varying sizes ( Figure 2A ). Positive Prussian blue staining ( Figure 2B ), alveolar lavage fluid pathological fluid base, and lung biopsy ( Figures 2C-E ), is composed of substantial iron particles. Under the electron microscope visible macrophage cytoplasm containing large size, structure, irregular iron particles ( Figure 2F ), which are brown-yellow or brown-black with different sizes, metallic luster, and strong refraction. The patient's macrophage iron particles differ significantly from those in cases of pulmonary hemorrhage, in which the hemosiderin-containing particles are bluish-black, uneven in size, metallic, and non-refractive. According to pneumoconiosis diagnostic criteria, the patient was diagnosed with pneumoconiosis; also chest CT showed wall cavities with mural nodules, multiple nodules around them, and some nodules with calcification, considering the possibility of old TB. Further acid-fast staining of bronchoscopic brush smears and alveolar lavage fluid showed that acid-fast bacilli were positive (6 in 300 fields) ( Figure 2G ). Acid-fast bacilli were also detected by electron microscopy ( Figure 2H ), biopsy of the posterior right upper lobe of the lung is granulomatous inflammation with necrosis, and the patient was diagnosed with siderosis and TB.
The diagnosis of TB in this patient was clear. No obvious abnormalities in Cryptococcus antigen detection, Mycobacterium TB identification, and for rifampicin resistance testing. Mycobacterium tuberculosis and RIF resistance gene testing is detected by the export kit, as long as the sample is added to the kit, and after a period of time, the instrument can display the results. We contacted the patient, learned that he had no family history of TB, and recommended that he go to the local TB hospital for regular chest CT check-ups. The patient also followed our advice to change jobs to avoid further lung damage.