Guo Xinmei, Department of Internal Tuberculosis, Shandong Chest Hospital Patient, female, 34 years old. History The patient has been experiencing dyspnea with no obvious cause for the past 1 month, with progressive worsening. She felt chest tightness without palpitations. No cough, coughing sputum, low fever and night sweats. There was no pressure or tearing pain in the precordial region. At first, he felt dyspnea, chest tightness and shortness of breath when going up to the third floor, and as his condition progressed, he gradually developed wheezing and dyspnea when walking about 200 meters on flat ground. He was hospitalized in the local county hospital for more than 10 days, and was considered to be transferred to a city hospital for further treatment of tuberculosis (details not available), but his condition did not improve significantly. Since the onset of the disease, the patient had poor mental health, diet and sleep, normal urination and defecation, and physical strength, with a weight loss of about 5 kg. Physical examination: T 36.2℃, P88 times/min, R20 times/min, BP 100/80 mmHg, normal development, good nutrition, independent body position, clear and cooperative, answers to questions. There was no hemorrhage or yellowing of the skin or mucous membranes, no enlargement of superficial lymph nodes, no deformity of the five senses of the head, red pharynx, and first degree enlargement of the thyroid gland bilaterally. The trachea was centered and the thorax had no deformity. The breath sounds of both lungs were coarse, and no dry and wet woven 8 grain ridge was heard in both lungs, the liver and spleen were not reached, and there was no edema in both lower limbs. Physiological reflexes were present and pathological reflexes were not elicited. Tumor markers NSE,CEA,CA12-5,CA15-3,keratin 19 fragment increased diagnosis was first considered PLAM, currently reported in the domestic literature greater than 200 people, consistent with the diagnosis has more detailed information of 160 people. Final diagnosis: 1. pulmonary lymphangioleiomyomatosis 2. bronchoalveolar carcinoma pulmonary lymphangioleiomyomatosis The first person who defined this type of tumor more accurately was Laipply and Sherrick (1958), and later in 1966, Cornog and Enterline first reported such lesions under the term lymphangioleiomyomatosis, and summarized the previously reported by different terms similar cases. This tumor is rare. It is now considered to be a lesion of pulmonary smooth muscle, characterized by nodular and diffuse hyperplasia of smooth muscle in the lung and lymphatic system (including the hilum, abdominal and lower cervical lymph nodes, and thoracic duct). Lymphangioleiomyomatosis (LAM) is a systemic disease of unknown etiology that develops progressively due to abnormal proliferation of smooth muscle leading to obstruction of bronchi, lymphatic vessels, and small blood vessels. The lungs are most susceptible and often present as diffuse interstitial lung disease; therefore, LAM is often referred to as pulmonary lymphangioleiomyomatosis. The disease occurs mainly in menopausal women and often presents clinically with dyspnea, spontaneous pneumothorax, celiac disease, etc. Typical chest imaging reveals thin-walled small cysts diffusely distributed in both lungs. No exact incidence has been reported at home or abroad before the clinical presentation. The disease was first documented in 1937 until 1997, with a cumulative total of more than 300 cases reported worldwide. The Denver Interstitial Disease Research Center in the United States reported only 16 cases in 10 years, accounting for the rate of diffuse interstitial lung disease 1 cm before the chest radiograph can show. The formation of a large number of pulmonary cysts can result in a significant increase in lung volume, similar to emphysema, and lymphatic obstruction can form KeleyB lines. Unilateral or bilateral pleural fluid, often celiac, is also seen in high and recurrent amounts. Celiac pleural fluid can also occur in the absence of pulmonary involvement, with a high incidence of spontaneous pneumothorax. Lymphangiography may reveal posterior abdominal wall lesions. (b) Chest CT and HRCT are important tools for diagnosing pulmonary lymphatic vascular smooth muscle tumor disease. Chest CT, especially HRCT, can clearly show pulmonary cysts that cannot be shown by ordinary chest X-ray. Pulmonary cysts in pulmonary lymphangioleiomyomatosis have distinctive features, being thin-walled cysts of varying sizes uniformly distributed throughout the lung, with diameters ranging from 0.5 to 5 cm, and the thickness of the cyst walls generally