The epidemiology of SLE in the United States reported a prevalence of 14.6-122/100,000 in a multi-regional survey; a large series of one-time surveys conducted in Shanghai among textile workers in China showed that the prevalence of SLE was 70/100,000, and among women it was as high as 113/100,000. /The clinical manifestations of SLE are complex and varied. Most of the patients have insidious onset and start to involve only one to two systems, showing mild arthritis, rash, occult nephritis, thrombocytopenic purpura, etc. Some patients are stable in subclinical state or light lupus for a long time, some patients can suddenly change from light to severe lupus, and more patients gradually develop multi-system damage from light; some patients have multiple systems involved in one disease and even show lupus crisis. The natural course of SLE is mostly characterized by alternating exacerbation and remission of the disease. 1. Systemic manifestations: Patients often have fever, which may be a manifestation of SLE activity, but infectious factors should be excluded, especially when fever occurs during immunosuppressive therapy, which requires more vigilance. Fatigue is a common but easily neglected symptom of SLE, and is often a precursor of lupus activity. 2. skin and mucous membranes: erythema distributed in a butterfly shape on the bridge of the nose and cheeks of both cheekbones is a characteristic change of SLE. skin damage of SLE includes photosensitivity, alopecia, palmar and perineural erythema, discoid erythema, nodular erythema, lipofuscinosis, reticular bruising, Raynaud’s phenomenon, etc. SLE rash without obvious pruritus, obvious pruritus suggests allergy, and pruritic rash after immunosuppressive therapy should be noted for fungal infection. SLE patients receiving hormonal and immunosuppressive therapy with unexplained localized burning skin pain may be a precursor to herpes zoster. oral ulcers or mucosal erosions are common in SLE. In oral erosions after immunosuppressive and/or antimicrobial therapy, oral fungal infections should be noted. histopathological manifestations of lesions in SLE are epidermal atrophy, liquefied degeneration of the basal layer, colloid vesicles visible in the epidermis, superficial dermal edema and extravasation of erythrocytes, and deposition of fibrin-like material visible in the dermal capillary wall. 3. Joints and muscles: symmetrical multi-joint pain and swelling are often seen, which usually do not cause bone destruction. SLE patients on hormone therapy with vague pain and discomfort in the hip region need to be excluded from aseptic femoral head necrosis. myalgia and muscle weakness may occur in SLE, and a few may have an increase in muscle enzyme profile. For patients taking hormones for a long time, hormone-induced myopathy should be excluded. The kidney damage: also known as Lupus nephritis (LN), manifests as proteinuria, hematuria, tubular urine, and even renal failure. 50% to 70% of SLE cases have clinical renal involvement, and renal biopsy shows renal pathological changes in almost all SLE. Renal failure is one of the major causes of death in SLE. The World Health Organization (WHO) classifies LN pathology as: type I normal or microscopic lesions, type II thylakoid proliferative, type III focal segmental proliferative, type IV diffuse proliferative, type V membranous, and type VI glomerulosclerotic. Pathological staging has positive implications for estimating prognosis and guiding treatment, usually with a better prognosis for types I and II and a worse prognosis for types IV and VI. However, the pathological types of LN are convertible, with the possibility of conversion to worse types for types I and II and a good prognosis for types IV and V with immunosuppressive therapy. Renal pathology also provides indicators of LN activity, such as proliferative glomerular cell changes, fibrinoid necrosis, nuclear fragmentation, cellular crescent, hyaline emboli, metallic rings, inflammatory cell infiltration, and inflammation of the tubular interstitium are indicative of LN activity; while glomerulosclerosis, fibrous crescent, tubular atrophy, and interstitial fibrosis are indicators of chronic LN. Those with high activity indexes have faster progression of kidney damage, but active treatment can still be reversed; chronic indexes suggest irreversible degree of kidney damage, and drug treatment can only slow down but not reverse the continued rise of chronic indexes. 5. Neurological damage: also known as neuropsychiatric lupus, SLE can involve multiple aspects of the nervous system, including the central nerves of the brain and spinal cord, cranial nerves and peripheral nerves of the spinal nerves, neuromuscular junction, and muscles, and can be manifested as neurological damage or mental or emotional cognitive impairment; according to the criteria of the American College of Rheumatology for neuropsychiatric lupus (ACR, 1999): where one or more of the following manifestations are present According to the criteria of the American College of Rheumatology for neuropsychiatric lupus (ACR, 1999), neuropsychiatric lupus can be diagnosed by combining imaging, cerebrospinal fluid, electroencephalography and other tests if one or more of the following manifestations are present and secondary factors such as infection and drugs are excluded. Its 19 manifestations include: headache, psychosis, acute psychosis, anxiety, cognitive disorders, mood disorders, seizures, aseptic meningitis, cerebrovascular disease, demyelinating syndrome, motor disorders, myelopathy, cranial neuropathy, Guillain-Barré syndrome, disorders of the vegetative nervous system, mononeuropathy, myasthenia gravis, plexiform lesions, and polyneuropathy. The onset of the disease can be acute, subacute or chronic, and the severity of the disease can be mild or severe, and the clinical presentation is complex and varied. Lumbar puncture CSF examination is an irreplaceable test to rule out CNS infection. Neuropsychiatric lupus with diffuse higher cortical dysfunction is mostly associated with anti-neuronal antibodies and anti-ribosomal P protein (Ribsomal P) antibodies; psychiatric neurological lupus with focal neurolocalization signs can be further divided into two conditions: one with positive antiphospholipid antibodies; the other often has systemic vasculitis manifestations and obvious disease activity. The former should be treated with enhanced anticoagulation and the latter should be treated according to the heavy SLE activity. 6. Hematologic manifestations: anemia and/or leukopenia and/or thrombocytopenia are common. Anemia may be chronic disease anemia or nephrogenic anemia. SLE may present with leukopenia, but cytotoxic drugs used to treat SLE also often cause leukopenia and need to be differentiated. Leukopenia due to this disease usually occurs before treatment or at disease relapse, and most are sensitive to hormonal therapy; whereas leukopenia due to cytotoxic drugs occurs in association with drug use and recovery is somewhat regular. Thrombocytopenia is associated with the presence of anti-platelet antibodies and antiphospholipid antibodies in the serum as well as impaired maturation of bone marrow megakaryocytes. Some patients have lymph node enlargement and/or splenomegaly at the beginning of the disease or during active disease. 7. Pulmonary manifestations: SLE often presents with pleurisy, and if combined with pleural effusion its nature is exudate. The radiological features of SLE lung parenchymal infiltrates are more widely distributed and variable shadows, and the cough symptoms of SLE lung damage are relatively mild compared to those of infectious pneumonia with the same degree of radiographic manifestations. or yellow sputum, suggesting a bacterial infection of the respiratory tract. Tuberculosis infection often presents atypically in SLE. Patients with persistent fever should be alerted to the possibility of hematogenous disseminated pulmonary tuberculosis and should undergo weekly chest radiographs and, if necessary, high resolution CT lung examination (HRCT), combined with sputum, broncho-alveolar lavage fluid smear and culture, to clarify the diagnosis and provide timely treatment. Fibrosis, manifested as shortness of breath after activity, dry cough, hypoxemia, and pulmonary function tests often show decreased diffusion function. SLE may also present with pulmonary hypertension, pulmonary infarction, and shrinking-lung syndrome. The latter manifests as a reduction in lung volume, diaphragm elevation, discoid pulmonary dystrophy, respiratory muscle dysfunction, without involvement of the lung parenchyma, pulmonary vascularity, or systemic muscle weakness, myositis, vasculitis. 8. Cardiac manifestations: Patients often present with pericarditis, manifesting as pericardial effusion, but pericardial tamponade is rare. In most cases, the myocardial damage in SLE is less severe, but in severe SLE, it can be accompanied by cardiac insufficiency, which is an indication of poor prognosis. The difference between this and infective endocarditis is that warty endocarditis is most commonly seen on the ventricular side of the posterior mitral leaflet and does not cause a change in the nature of the murmur. SLE can have coronary artery involvement, manifesting as angina and ST-T changes on the electrocardiogram, or even acute myocardial infarction. In addition to the possible involvement of coronary arteritis in the pathogenesis, long-term use of glucocorticoids accelerates atherosclerosis and antiphospholipid antibodies lead to arterial thrombosis, which may be the other two main causes of coronary artery lesions. 9, digestive system manifestations: manifested as nausea, vomiting, abdominal pain, diarrhea or constipation, of which diarrhea is more common, may be accompanied by protein-losing enteritis and cause hypoproteinemia. In the active stage of SLE, mesenteric vasculitis may appear, and its manifestation is similar to acute abdomen, and it may even be misdiagnosed as gastric perforation or intestinal obstruction and surgically explored. The disease should be considered when SLE has significant systemic activity, gastrointestinal symptoms and positive abdominal signs (rebound pain, pressure pain), after excluding secondary factors such as infection, electrolyte disorders, medications, and the combination of other acute abdominal conditions, etc. SLE mesenteric vasculitis is still lacking strong auxiliary examination, and abdominal CT may show indirect signs such as thickening of the small intestinal wall with edema and dilated intestinal collaterals with mesenteric vascular enhancement. SLE can also be complicated by acute pancreatitis. Increased liver enzymes are common, with only a few cases of severe liver damage and jaundice. 10. Other: Ocular involvement includes conjunctivitis, uveitis, fundus changes, optic neuropathy, etc. SLE is often accompanied by secondary dry syndrome with exocrine gland involvement, manifested as dry mouth and dry eyes, and often positive serum anti-SSB and anti-SSA antibodies. 11. Immunological abnormalities: mainly reflected in the anti-nuclear antibody profile (ANAs). Immunofluorescent anti-nuclear antibodies (IFANA) is a screening test for SLE. The diagnostic sensitivity for SLE is 95%, and the specificity is relatively low at 65%. In addition to SLE, ANAs are often present in the sera of other connective tissue diseases, and low titers of ANAs can also be seen in some chronic infections. ANAs include a range of autoantibodies directed against antigenic components of the cell nucleus. Among them, anti-double-stranded DNA (ds-DNA) antibodies in SLE have a specificity of 95% and a sensitivity of 70%, and are associated with disease activity and prognosis; anti-Sm antibodies have a specificity of 99% but a sensitivity of only 25%, and their presence is not significantly associated with disease activity; anti-ribosomal P protein antibodies are associated with psychiatric symptoms in SLE; anti-single-stranded DNA, anti-histone, anti anti-single-stranded DNA, anti-histone, anti-u1RNP, anti-SSA and anti-SSB antibodies can also be found in the serum of SLE, but their diagnostic specificity is low because they are also seen in other autoimmune diseases. Anti-SSB is associated with secondary dry syndrome. Other autoantibodies are antiphospholipid antibodies (including anticardiolipin antibodies and lupus anticoagulant) associated with antiphospholipid antibody syndrome; anti-erythrocyte antibodies associated with hemolytic anemia; anti-platelet antibodies associated with thrombocytopenia; and anti-neuronal antibodies associated with neuropsychiatric lupus. In addition, patients with SLE often present with positive serum rheumatoid factor, hypergammaglobulinemia and hypocomplementemia.Immunopathological examination of SLE includes the cutaneous lupus band test, which shows deposits of immunoglobulins (IgG, IgM, IgA, etc.) and complement (C3c, C1q, etc.) at the superficial dermal junction of the skin and is specific for SLE.Renal immunofluorescence in LN mostly shows A variety of immunoglobulin and complement components are deposited, which is called “full brightness”.