The patient was admitted to the hospital on March 8, 2006 with the main reason of “intermittent cough for 2 years, coughing up large amount of white foamy sputum for 1 month”. 2 years ago, the patient developed cough, coughing sputum, low fever and night sweats without any cause, accompanied by chest pain on the left side, chest CT showed right pleural effusion and small lamellar exudate shadow in the lower lobe of the right lung near the oblique fissure. The patient was diagnosed with pulmonary infection in the hospital, and was treated with anti-infection treatment of Bafil (moxifloxacin) for 2 weeks, and the above symptoms disappeared without re-examination of the chest CT. 9 months ago, he developed cough, sputum and chest pain again, and re-examination of the chest CT showed right pleural effusion again, and the exudate shadow in the lower lobe of the right lung was significantly larger than before, and bronchial air phase and pavement-like changes were seen. The patient refused bronchoscopy. Auxiliary examination: blood sedimentation (ESR) 45 mm/1h, PPD (+), yellow appearance of pleural effusion, specific gravity 1.030, positive Leigh test, total cell count 8.31×109/L, nucleated cell count 0.46×109/L; mononuclear cells 0.90, multinucleated cells 0.10. Total protein of pleural effusion 47.0 g/L, albumin 23.2 g/L, glucose 4.2 mmol/L, lactate dehydrogenase (LDH) 200 IU/L, adenosine deaminase (ADA) 80 U/L, carcinoembryonic antigen 5.0 ng/ml, negative pleural fluid culture, negative pleural fluid for tuberculosis bacilli and tumor cells. The diagnosis of tuberculous pleurisy was made, and the patient was given triple anti-tuberculosis treatment of isoniazid, rifampin and ethambutol for 2 months, and the right pleural effusion disappeared, and the total course of treatment was 6 months. During the anti-tuberculosis treatment, the patient’s coughing sputum volume gradually increased from about 100 ml/d at the beginning to 300-400 ml/d in the last month, and a repeat chest CT showed that the right pleural effusion had disappeared, and the lesion in the lower lobe of the right lung had further increased in size, and CT angiographic signs were seen. He was admitted to our hospital for further diagnosis and treatment. He had a history of 40 years of old tuberculosis, 30 years of radical right breast cancer, 3 years of chronic urinary tract infection, and no history of smoking. Physical examination: right lower lung breath sounds were diminished, and wet rales could be heard in the right lower lung. Preliminary diagnosis: pulmonary shadow to be investigated, alveolar carcinoma is more likely, tuberculosis is not excluded. After admission, sputum was repeatedly checked for negative antacid staining, sputum was negative for tumor cells, and blood carcinoembryonic antigen (CEA) was 1.13 ng/ml. arterial blood gas analysis: pH 7.432, partial pressure of carbon dioxide 32.7 mmHg, partial pressure of oxygen 59 mmHg, oxygen saturation 90%. Bronchoscopy: trachea, bronchi and their branches were patent, with more plasma-like secretions from the right lower lobe bronchi, and transbronchial lung biopsy (TBLB) of the lower lobe of the right lung. Histopathology showed that the alveolar surface was covered with a single layer of high columnar mucus epithelium, partly with papillary hyperplasia, and a large amount of secretion was seen in the alveolar lumen with widened alveolar septa. Electron microscopy showed short microvilli on the cell surface and the cytoplasm contained abundant round mucus granules. The pathological diagnosis was fine bronchoalveolar carcinoma, mucinous type. The patient refused surgical treatment and took 0.25g/d of oral ERSA (gefitinib), which significantly reduced the sputum volume to 50-100 ml/d. After 1 year and 3 months of self-medication discontinuation, the sputum volume increased to 500 ml/d. A repeat chest radiograph in July 2007 showed that the lung lesions had progressed bilaterally. Treatment with gefitinib and azithromycin was added and the sputum was slightly reduced compared to the previous one. The total duration of the patient’s disease has been nearly 4 years, and she is currently in good general condition and under follow-up treatment. Discussion Bronchioloalveolar carcinoma (BAC) is characterized by the growth of tumor cells along the original alveolar structure without interstitial, vascular and pleural invasion, and can be divided into three subtypes: mucinous, non-mucinous and mixed. The first feature is bronchorrhoea, which refers to a daily sputum volume of more than 100 ml. mucinous BAC consists of malignant mucous cells that can secrete large amounts of mucus on their own. bac rarely invades the large bronchi, so mucus is easily eliminated through the bronchi. Especially when the patient’s position changes (e.g. from upright to forward leaning or from sitting to lying), there is often a large amount of sputum coming out of the mouth and nose. The sputum has no special odor and can be divided into two layers at rest, with white foamy sputum in the upper layer and clear water-like or plasma-like mucus in the lower layer. The amount of sputum in BAC patients reflects the load of malignant mucus cells in the lung to a certain extent, such as in this case, in the early stage of the disease, because the lesions in the lung are small, the number of malignant mucus cells is small, so the amount of sputum produced is also small; with the expansion of the lesions in the lung and the progress of the disease, the amount of sputum gradually increases; in some advanced patients, the amount of sputum is even as much as 9L/d, and serious dehydration and electrolyte The second feature is solid lung lesions (p.l.). The second feature is pulmonary consolidation, which can involve one lung segment or the entire lobe, or one or both whole lungs. The imaging sometimes resembles that of lobar pneumonia, hence the name lobar or pneumonic alveolar carcinoma. BAC does not invade blood vessels or large bronchi, so the bronchial gas phase and CT angiogram sign can be seen in solid lungs, which is specific for the diagnosis of BAC. Of course, these signs can also be seen in pneumonia, tuberculosis and pulmonary lymphoma, which can be misdiagnosed. However, patients with BAC (as in this case) often have progressive development of intrapulmonary lesions, ineffective anti-inflammatory and anti-TB treatment, and no cavities or abscesses, which, combined with clinical manifestations such as bronchial mucus overflow, are not difficult to diagnose. If the lesion involves both lungs, it should be differentiated from other diffuse alveolar filling diseases (alveolar filling diseases) such as pulmonary alveolar proteinosis (PAP), Pneumocystis carinii pneumonia (PCP), and diffuse alveolar hemorrhage (DAH). A third feature is intrapulmonary shunt (intrapulmonary shunt), which can lead to intractable hypoxemia. In advanced mucinous BAC, the alveoli are filled with a large number of malignant cells and mucus, but the corresponding pulmonary vasculature is not invaded, resulting in an imbalance of the pulmonary ventilation/blood flow ratio and intrapulmonary shunt, causing uncorrectable hypoxemia. The fourth characteristic is low-grade malignancy with a relatively good prognosis. According to the definition of WHO, simple mucinous BAC should be in situ cancer. The 5-year survival rate after surgery can be 64-100%. For advanced BAC, epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKI) can be used as first-line chemotherapeutic agents with an efficiency of 24% and a median survival of more than 12 months, which is much better than other types of lung cancer; for bronchial mucus overflow, macrolides and EGFR-TKI may be effective.