1. What are the manifestations of pulmonary involvement in SLE? What is the incidence and regression? Pulmonary involvement is much more common in SLE than in other connective tissue diseases, and SLE can involve any part of the respiratory system including the pleura, lung parenchyma, pulmonary vasculature and respiratory muscles. The main manifestations are: lung infection, pleurisy, acute lupus pneumonia, alveolar hemorrhage, interstitial lung disease (interstitial fibrosis), pulmonary hypertension, pulmonary thromboembolism, respiratory muscle weakness, acute reversible hypoxemia, obstructive lung disease, and upper airway dysfunction. Pulmonary involvement in SLE can occur at any stage of the disease, and the incidence has been reported differently, up to 60%, while others have reported pleural involvement in 17% and pulmonary involvement in 3% of cases at the onset of SLE, and pleural involvement in up to 36% and pulmonary involvement in up to 7% throughout the course of the disease. The clinical and imaging manifestations and even histopathological manifestations of various pulmonary lesions in SLE can overlap with each other, and some patients can have more than one pulmonary symptom throughout the course of the disease. pulmonary involvement in SLE often indicates a poor prognosis, and the mortality rate is more than twice as high as that of patients without pulmonary involvement. 2.What are the common clinical manifestations of SLE pleural lesions? Pleural involvement is more common in SLE than in other connective tissue diseases, and pleurisy is also the most common pulmonary manifestation of SLE, with an incidence of 17-60%. Pleurisy can be the first symptom of SLE, with 45-60% of patients presenting with chest pain, often with dyspnea, cough, and low-grade fever, with or without pleural effusion. Pleural effusions due to SLE pleurisy are all exudates. The appearance is usually yellow and clear or pale blood. Protein and lactate dehydrogenase are elevated. ANA, anti-dsDNA and typical lupus cells can be detected in the pleural effusion with relative specificity but not high sensitivity. Reduced complement C3 and C4, increased levels of immune complexes, and positive rheumatoid factor are also seen in pleural effusions. Pleural effusions can be detected by radiograph in 16-50% of SLE patients and are usually small to moderate in volume and distributed bilaterally or unilaterally (50% of each). Large pleural effusions should be noted to exclude other diseases. Diagnostic puncture must be performed for new pleural effusions. A small amount of pleural thickening often remains after the pleural effusion resolves. Patients with SLE with combined cardiac and/or pulmonary pathology are more likely to have recurrence or rapid exacerbation of pleural effusion than those with pleural involvement alone. 3. What is acute lupus pneumonia? What are the clinical manifestations? ALP is a sudden onset of non-infectious pneumonia, often with fever. The incidence rate is 1-4%. The main manifestations are sudden dyspnea, cough (with or without sputum), chest pain, hypoxemia, fever, and some manifestations of hemoptysis. Blood gas analysis suggests hypocapnia and hypoxemia, and in severe cases, respiratory failure may occur. Imaging manifestations are bilateral or unilateral, patchy solid shadow mainly at the base of the lung, focal pulmonary atelectasis, septal elevation, and most of them are accompanied by pleural effusion. ALP may be the first symptom of SLE or may appear at any stage of the course of SLE. Female patients are at high risk for ALP in the days to weeks after delivery. Young women, unexplained pulmonary infiltrates, and those with active lupus should be on high alert for ALP. ALP has a mortality rate of 50%, and a timely and decisive diagnosis is critical. Clinical attention should be paid to the differentiation with SLE combined with pulmonary infection. Active improvement of SLE disease activity assessment, sputum pathogenic examination, bronchoscopy, imaging examination and lung tissue biopsy will be beneficial to the differential diagnosis. 4.What is diffuse alveolar hemorrhage? What are the clinical manifestations? DAH is a serious and often life-threatening complication, characterized by hemoptysis, anemia, diffuse alveolar infiltration or solidity caused by blood entering the alveoli in the pulmonary microvasculature under the action of different etiologies.DAH is rare and its incidence accounts for about 2% of SLE.DAH is a potentially critical complication of SLE, with a mortality rate of more than 50%.In recent years, with the increasing awareness of DAH, timely diagnosis and treatment has led to a higher mortality rate. DAH is a potentially critical complication of SLE with a mortality rate of more than 50%. DAH is most commonly seen in young women and is characterized by hemoptysis, dyspnea, hypoxemia, cough, and anemia, with more than half of the patients requiring mechanical ventilation support. Some of the major symptoms such as hemoptysis and hypoxemia may be absent at presentation, and many severe alveolar hemorrhages may even remain completely free of hemoptysis. Decreased hemoglobin and decreased erythrocyte pressure are characteristic features of alveolar hemorrhage, ANA and anti-dsDNA are useful in confirming the diagnosis, and hypocomplementation is common. The lung shadows are usually bilateral and symmetrical. The lung shadows are usually bilateral and symmetrical, but may be asymmetrical or even unilateral. The lung shadows may improve rapidly after the hemorrhage stops. In acute alveolar hemorrhage, CT shows a fuzzy, hairy glass-like shadow, sometimes with a solid shadow containing the bronchial air phase, while in the chronic phase the changes are mainly thickening of the lobular septa, which may be a sign of early stromal fibrosis. Pulmonary function tests often indicate an increased diffusion rate of carbon monoxide. Alveolar lavage fluid is hemorrhagic or visible with iron-containing heme cells, and large numbers of macrophages filled with iron-containing heme are seen in the alveolar cavity of lung biopsy specimens, without pus or other pathogenic evidence, contributing to the diagnosis of DAH. DAH usually occurs in patients with active SLE, but can be the first symptom of SLE in 20% of cases, so serologic tests related to SLE should be performed in anyone with undiagnosed SLE who presents with DAH. Nearly one-third of patients with DAH may have coexisting pulmonary infections, such as cytomegalovirus, herpes simplex virus, Aspergillus, Staphylococcus, and Legionella. The diagnosis of DAH needs to exclude other causes of alveolar hemorrhage, and attention should be paid to the differentiation of SLE combined with DAH from other common pulmonary complications of SLE such as infection, pulmonary embolism, heart failure, uremia, and blood culture, sputum culture, bronchoscopy or lung biopsy must be actively performed. 5.What are the clinical manifestations of pulmonary thromboembolism? How to diagnose and treat? Pulmonary thromboembolism is a disease caused by obstruction of pulmonary artery or its branches by thrombus from the venous system or right heart, with pulmonary circulation and respiratory dysfunction as its main clinical and pathophysiological features. positive lupus anticoagulant in SLE patients is a risk factor for intravascular thrombosis. Acute and chronic pulmonary embolism is associated with antiphospholipid antibodies (ACL). the incidence of SLE combined with pulmonary embolism is 9-30%. The severity of clinical manifestations of pulmonary embolism varies widely and can range from asymptomatic to hemodynamically unstable and even sudden death. The main clinical manifestations of pulmonary embolism include dyspnea and shortness of breath, chest pain, syncope, irritability or panic and even near-death feeling, hemoptysis, cough, palpitation, fever, etc., often accompanied by deep vein thrombosis in the lower extremities. On examination, shortness of breath, tachycardia, changes in blood pressure, cyanosis, pulmonary rales, and hyperactive second sounds in the pulmonary valve area are seen. The diagnosis of pulmonary embolism can be initially suspected or other diseases can be ruled out based on the clinical manifestations combined with basic tests such as electrocardiogram, X-ray chest film and arterial blood gas analysis. Ultrasonography is valuable in suggesting the diagnosis of pulmonary embolism and excluding other diseases. Echocardiography is also the basis for classifying submassive pulmonary embolism and is a priority test in the suspected diagnosis of pulmonary embolism. Nuclear pulmonary ventilation/perfusion scan is an important diagnostic method for pulmonary embolism. If the result is highly probable, the diagnostic specificity is 96%, and if the result is normal or near normal, pulmonary embolism can be basically excluded. Pulmonary arteriography is the classic reference method for the diagnosis of pulmonary embolism, but its clinical demand has gradually decreased because it is an invasive test with high cost. Spiral CT (CTPA) is one of the means to confirm the diagnosis of pulmonary embolism, and has become an important examination frequently applied in clinical practice. In addition to general management, thrombolytic and anticoagulant therapy should be decided according to the clinical staging of pulmonary embolism (massive, sub-massive and non-massive). Patients with recurrent thromboembolism should be anticoagulated for life. In addition, aggressive hormonal and immunosuppressive therapy should be given simultaneously to control thrombosis. 6.What are the characteristics of SLE combined with pulmonary infection? Respiratory tract infections are highly prevalent in SLE patients for the following reasons: first, immune dysfunction and low antibacterial activity of alveolar macrophages in SLE patients; second, use of hormones and other immunosuppressive agents; and third, pulmonary edema and respiratory muscle weakness that aggravate the infection. Respiratory infections are an important cause of morbidity and mortality in SLE, second only to sepsis and renal failure. Therefore any new pulmonary infiltrates in patients with SLE must first be excluded with a focus on pulmonary infections, especially in those treated with hormones and immunosuppressive agents. Opportunistic infections in SLE patients include Aspergillosis, Cryptococcosis, Pneumocystis carinii infection, cytomegalovirus infection, and Nocardia infection. Particular care should be taken in clinical workup to be alert for fungal and tuberculosis infections. Tuberculosis is a direct cause of death in SLE. Some studies have shown a 5% incidence of TB in SLE patients, but the incidence of cor pulmonale and extrapulmonary TB is higher due to delay in diagnosis.