①Fibrinoid necrosis: This is a homogeneous eosinophilic substance, often found in the vessel wall,

①Fibrinoid necrosis: This is a homogeneous eosinophilic substance, often found in the vessel wall,
containing immunoglobulins, fibrinogen, complement, and DNA, representing the deposition of immune complexes,
which causes vasculitis, leading to vascular stenosis or occlusion. ②"Schiff's purple bodies": They are round or oval-shaped,
containing nuclear proteins and antibodies, located in the cytoplasm of macrophages, also known as tissue "LE cells,"
with the same inclusion body characteristics as those found in lupus erythematosus cells, and can be seen in the inflammatory areas of all affected organs.
The most common sites of SLE lesions are blood vessels, kidneys, joints, and skin.

1. Vascular lesions
   Acute necrotizing vasculitis: In the acute phase, it generally affects small arteries and arterioles,
   with fibrinoid-like deposits occurring within the vessels; in the chronic phase, the vessel walls show fibrous thickening and luminal narrowing,
   accompanied by perivascular lymphocytic infiltration, edema, and increased extracellular matrix.
   DNA, C3, and immunoglobulins can also be found in the vessel walls.
2. Renal changes
   SLE renal pathological changes are generally divided into four types: ① Vasculomembranous lupus nephritis: The glomeruli appear normal,
   the degree of lesion is relatively mild, mainly characterized by mild irregular proliferation of the glomerular mesangium,
   with immune complex deposition. ② Membranous lupus nephritis: Histologically similar to idiopathic membranous glomerulonephritis,
   with widespread basement membrane thickening and fine granular immune complex deposition beneath the epithelium. ③ Focal proliferative lupus nephritis:
   Less than 50% of the glomeruli are involved, with segmental proliferation and focal necrosis,
   and immune complex deposition can be seen beneath the epithelium and within the vessels. ④ Diffuse proliferative lupus nephritis:
   This is the most severe form, with more than 50% of the glomeruli affected, irregular proliferation of the basement membrane,
   extensive necrotic areas, accompanied by glomerulosclerosis.
3. Joint lesions
   It presents as non-erosive bursitis with mild deformity; during the acute phase, neutrophils and fibrin are exuded into the synovial fluid,
   and mononuclear cell infiltration occurs around the vessels beneath the synovial tissue.
4. Skin lesions
   In the acute phase, there is liquefaction, degeneration, necrosis, edema, fibrosis of the basal cell layer or dermal basement membrane,
   along with perivascular lymphocyte, monocyte, and plasma cell infiltration;
   in the chronic phase, there is hyperkeratosis and follicular plugging.
   II. Diagnosis and Treatment
   ( --- ) Clinical diagnosis
5. Symptoms
   The onset can vary widely, ranging from acute fulminant to insidious. Generally, one system is initially affected,
   then the disease spreads to multiple systems. Most patients experience fatigue, fever, joint pain,
   rash, and corresponding symptoms related to the involvement of a particular organ. It can occur spontaneously or be triggered by certain factors,
   such as sun exposure, infection, pregnancy, childbirth, certain medications, tuberculosis, surgery, etc.
6. Physical signs
   ① Skin and mucosa: 85% of patients have skin lesions. The most common sites are exposed areas of the skin,
   presenting symmetrical rashes, typically the butterfly-shaped erythema on both cheeks and the bridge of the nose. Among SLE patients, about 19% have discoid lupus erythema,
   whose lesions differ slightly from the butterfly-shaped erythema, often appearing as irregular circles with slightly raised edges,
   marked capillary dilation, enlarged hair follicle openings in the erythema, and slight scaling; in the later stages, skin atrophy and pigment loss may occur,
   but the margins may show significant pigmentation. 15%–20% of patients may have painless ulcers on the oral and nasal mucosa,
   and occasionally some patients have vaginal mucosal ulcers. ② Joints and muscles: Over 90% of cases involve the joints.
   Joint swelling and pain are often the most common initial symptoms, usually affecting the proximal interphalangeal joints of the hands symmetrically,
   as well as the feet, knees, and wrists, but less frequently the elbows, shoulders, ankles, and hips. Generally, there are no bone abnormalities,
   though a few patients may exhibit hyperextension of the proximal interphalangeal joints and flexion of the distal interphalangeal joints, resulting in a "goose-neck" deformity,
   and even obvious ulnar deviation of the fingers. X-ray examinations generally show no evidence of joint space narrowing or bone erosion. About
   12 patients experience myalgia and tenderness, and some have marked muscle weakness. ③ Serous membranes: More than one-third of patients have bilateral or unilateral pleuritis,
   most with small to moderate amounts of pleural effusion, causing chest pain, shortness of breath, and pleural friction rubs.
   LE cells can be found in the pleural effusion, and occasionally there is bloody pleural effusion. 25% of patients have pericarditis,
   and in some cases up to half, with autopsy rates reaching 80%; pericardial friction rubs are more common than radiographic pericardial fluid findings,
   and pericardial friction rubs are often transient, sometimes accompanied by chest pain, cardiac enlargement, diminished heart sounds, ST segment elevation,
   and T wave inversion on ECG—characteristic changes, though typical cases are rare. ④ Lungs: All SLE patients have pulmonary lesions,
   manifesting as acute pneumonia, chronic interstitial pulmonary fibrosis, extensive alveolar hemorrhage, pulmonary edema combined with diffuse pulmonary vasculitis,
   acute lupus pneumonia, etc. Approximately 10% of patients have lupus pneumonia. Clinical manifestations include dyspnea, chest pain, cough, and bilateral basal crackles,
   X-ray examination may show normal lungs or patchy atelectasis, with honeycomb-like or patchy infiltrative shadows in the interstitium.
   S Kidneys: Almost all SLE cases involve the kidneys, but clinically about half have clinical and urine test abnormalities related to kidney disease,
   and if a renal biopsy is performed, the vast majority show abnormalities. Therefore, clinical manifestations, urine abnormalities, and renal biopsy abnormalities often do not match. G Heart: About 10% of SLE cases involve the heart and endocardium. ① Gastrointestinal tract: Most SLE patients may experience gastrointestinal symptoms and signs,
   commonly abdominal pain, nausea, vomiting, anorexia, difficulty swallowing, ascites, etc. ③ Central nervous system: About 50% involve the central nervous system, posing a serious threat to patients' lives,
   with varying degrees of severity; the most common manifestations are epileptic seizures (often grand mal) and organic brain diseases, such as disorientation,
   perceptual disturbances, memory decline or loss, intellectual impairment, behavioral abnormalities, anxiety, overexcitement, depression, hallucinations, obsessive-compulsive ideas, or paranoia, etc. 9 Other: SLE patients may have mild to moderate lymphadenopathy without tenderness. Female patients may experience irregular menstruation and heavy menstrual bleeding,
   which can lead to massive hemorrhage; pregnant women are prone to miscarriage in the first trimester, and postpartum conditions often worsen. About 15% of patients have scleritis. 20%–25% involve the retina and cornea,
   and in severe cases, visual impairment or even blindness may occur.
7. Related examinations
   (1) General examinations: Patients often present with normochromic, normocytic anemia, 5%–10% with hemolytic anemia,
   about 50% with leukopenia <4×10^9/L, and absolute lymphocyte count <1.5×10^9/L. About 30% have thrombocytopenia, and erythrocyte sedimentation rate is often elevated.
   (2) Immunological examinations: ① Antinuclear antibody (ANA) is the most sensitive laboratory indicator for SLE,
   with a positive rate as high as 95%, but poor specificity. ② Lupus cell phenomenon: The positive rate for SLE is 60%. ③ Anti-dsDNA antibody: Systemic lupus erythematosus patients have two types of anti-DNA antibodies in their serum,
   namely anti-single-stranded DNA (anti-dsDNA) and anti-double-stranded DNA antibody (anti-lupus dsDNA),
   with the latter having higher specificity and greater clinical significance, with a positive rate of about 65%. ④ Anti-Sm antibody (Sm antibody): Considered a marker antigen for lupus cells, with high specificity and great diagnostic value,
   but poor sensitivity, with a positive rate of only about 30%. Rheumatoid factor: 50% of SLE patients are rheumatoid factor (RF) positive. Compared with rheumatoid arthritis patients, RF positivity in SLE is often temporary and the titer is not high. G Other: Almost all SLE patients can detect circulating immune complexes (CIC); most have elevated IgG and IgM levels,
   with polyclonal increases in immunoglobulins, mainly IgG. SLE patients often present with hypocomplementemia,
   which is closely related to lupus activity, lupus nephritis, central nervous system lesions, and extensive skin damage,
   with C3 and C4 titers dropping being the most sensitive indicators. SLE patients may also have many other autoantibodies,
   such as anti-cytoplasmic components like anti-Ro and anti-cytoplasmic RNP (La) antibodies,
   anti-lymphocyte antibodies, anti-platelet antibodies, anti-red blood cell antibodies, anti-SSRNA antibodies, anti-dsRNA antibodies,
   anti-organ-specific antibodies, and some patients even have circulating anticoagulant substances,
   which can prolong prothrombin time.
   (3) Pathological examination and immunofluorescence tests: ① Renal biopsy: Under fluorescence microscopy, fluorescently labeled immune complexes can be seen deposited irregularly or in granular form on the glomerular basement membrane
   or mesangium. ② Lupus band test (LBT): Using direct fluorescence on the epidermis-dermis junction of the patient's skin,
   one or more immunoglobulins and complement components can be observed, arranged in bright green fluorescent bands that are granular, spherical, or linear.
   On normal exposed skin areas in SLE, the positive rate is 50%–70%. On lesional areas, it can reach 90%.
8. Diagnostic criteria
   In March 1982, the Chinese Medical Association's Special Academic Conference on Rheumatology held in Beijing formulated the diagnostic criteria for systemic lupus erythematosus (reference):
   (1) Clinical manifestations: ① Butterfly-shaped or discoid erythema. ② Arthritis or joint pain without deformity. ③ Hair loss. ④ Raynaud's phenomenon and/or vasculitis. S Oral mucosal ulcers. G Serous inflammation. ③ Photosensitivity. ③ Neuropsychiatric symptoms.
   (2) Laboratory tests: ① Elevated erythrocyte sedimentation rate (Westergren method >20). ② Leukopenia <4×10^9/L and/or thrombocytopenia <80×10^6/L and/or hemolytic anemia. ③ Proteinuria (persistent + or above) and/or urinary casts. ④ Hypergammaglobulinemia. S Lupus cell positivity (at least 2 per slide or at least twice positive). Antinuclear antibody positivity.
   Those who meet all six clinical and laboratory criteria can be diagnosed. Before confirmation, attention should be paid to excluding other connective tissue diseases, drug-induced lupus syndrome, tuberculosis, and chronic active hepatitis, etc.
   Those who do not meet the above criteria are considered suspected cases and should undergo further laboratory tests; if they meet all six criteria, they can be diagnosed. ① Positive anti-DNA antibody (using isotope-labeled DNA radioimmunoassay, trypanosome smear, or short-flagellate smear immunofluorescence assay). ② Hypocomplementemia and/or positive circulating immune complex test. ③ Positive lupus band test. ④ Positive renal biopsy. S Sm antibody positivity.
   Patients whose clinical manifestations are not obvious but whose laboratory tests are sufficient to diagnose systemic lupus erythematosus can temporarily be called subclinical systemic lupus erythematosus.
9. Differential diagnosis
   Should be differentiated from other connective tissue diseases such as PSS, DM-PM, PN, RA. In addition, it needs to be differentiated from DLE.
   (1) Rheumatic fever: Recent history of streptococcal infection, migratory polyarticular joint swelling and pain,
   with major involvement of large joints in the limbs, elevated serum anti-streptolysin O, no antinuclear antibodies,
   salicylate preparations often provide rapid and significant relief.
   (2) Rheumatoid arthritis (RA): Joints exhibit typical morning stiffness, involving three or more sites,
   such as wrist, palm, finger, or proximal interphalangeal joint swelling and pain, subcutaneous nodules, positive rheumatoid factor,
   X-rays showing typical radiological changes of rheumatoid arthritis.
   (II) Western medical treatment
   (1) Nonsteroidal anti-inflammatory drug therapy: These drugs are mainly used clinically when only fever, rash, hair loss, fatigue, joint soreness, muscle pain, pleural and pericardial inflammation, etc., appear,
   with commonly used drugs being aspirin, 2–4 grams daily, taken in divided doses; high-dose aspirin can easily cause liver damage and elevated transaminases,
   which generally reverse after discontinuation. Indomethacin 25–50 mg, three times daily. Ibuprofen, naproxen 50 mg, twice daily. These drugs can only be used short-term for symptomatic relief in systemic lupus erythematosus,
   not suitable for long-term treatment. For systemic lupus erythematosus rashes, hydroxychloroquine 200–400 mg daily,
   or chloroquine 125–250 mg, three to five times weekly,
   but these antimalarial drugs have adverse reactions such as retinal toxicity, so caution should be exercised when using them. For systemic lupus erythematosus pleural and pericardial inflammation, aspirin or indomethacin alone can achieve good results.
   (2) Glucocorticoids: These are the main drugs for treating systemic lupus erythematosus. More suitable for patients with kidney,
   central nervous system, heart, lung, severe hemolytic anemia,
   thrombocytopenic purpura, and other major organ involvement, especially for acute or fulminant lupus patients. Usually prednisone is used, at a dose of 1 mg/kg daily,
   for milder cases the dose is 0.5 mg/kg daily. If there is no improvement after 24–48 hours,
   the dose can be doubled. For patients with fulminant or severe lupus nephritis and central nervous system lesions,
   high-dose hormone shock therapy can be used: methylprednisolone 1000 mg, intravenous injection or drip, once daily for three days,
   because its efficacy is still controversial and side effects are significant, it is generally not suitable as routine treatment. However, after shock therapy, prednisone should be taken orally daily,
   4–80 mg, gradually reducing the dose, usually by 5 mg per week,
   until the daily dose is reduced to 2–30 mg, with a slower reduction rate,
   so that most patients can maintain treatment at a dose of 10–15 mg daily after one year.
   If there is a rebound during the reduction process, the previous dose plus 5 mg should be tried to maintain the level. But currently, the best approach to hormone use is to start with a small dose, beginning with 20–30 mg of prednisone daily. Adding traditional Chinese medicine warming kidney drugs can prevent hormone side effects. Alternatively, some advocate speeding up the reduction from high to medium dose,
   while slowing down the reduction from medium to low dose. For example, reducing from 200 mg of prednisone to 80 mg daily can usually be completed within a week,
   while reducing from 30–40 mg daily should be done more slowly. As mentioned above, when using traditional Chinese medicine warming kidney methods, the reduction speed can be slightly accelerated,
   which can also prevent the occurrence of hormone withdrawal syndrome.
   (3) Immunosuppressive drug therapy: Immunosuppressants include azathioprine, cyclophosphamide (CTX), chlorambucil (CB), etc. There is considerable controversy over the therapeutic effect of this group of drugs,
   so far there is no standard therapy. Based on clinical experience, these drugs cannot replace hormones,
   and they have significant side effects; after stopping the medication, relapse is easy, and increasing the dose often does not help.
   Therefore, in clinical practice, they are mainly used for disease recurrence after hormone reduction,
   or when excessive hormone use leads to toxic side effects,
   as well as for systemic lupus erythematosus that is difficult to control with hormones. Cyclophosphamide dosage is 1.5–2.5 mg/kg daily,
   azathioprine is 2–3 mg/kg daily, chlorambucil is 0.1 mg/kg daily. Among them, cyclophosphamide has relatively confirmed effects. Azathioprine has no definite effect on systemic lupus erythematosus,
   but it does have some effect on lupus nephritis. When several drugs are used in combination, it is concluded that intravenous cyclophosphamide treatment is superior to hormone plus oral cyclophosphamide,
   or oral azathioprine plus hormone. Intravenous cyclophosphamide can sometimes save the lives of patients with systemic lupus erythematosus.
   (4) Other treatments: ① Levamisole: This drug may have an inhibitory effect on infections in systemic lupus erythematosus,
   but it cannot be used as a routine treatment. The dosage is levamisole 50 mg/d, three times daily, taken continuously for three days,
   followed by an 11-day break and then another three days, or 50 mg daily for five to ten days, depending on the condition and adverse reactions, to decide whether to continue treatment. Its adverse reactions include decreased appetite, leukopenia, and even bone marrow suppression. ② Antiviral drugs: These drugs can treat primary viral infections in systemic lupus erythematosus,
   and prevent the effects of persistent viral infections on the immune system. Clinically, garlic preparations (oral) or traditional Chinese herbal medicines with antiviral effects can be used, which can achieve certain results. ③ Anti-lymphocyte globulin (AIG): This drug provides another immunosuppressive agent for the treatment of systemic lupus erythematosus, with certain efficacy.
   Its dosage varies from person to person, generally 10–20 mg/kg intravenously daily, can be used continuously for 1–2 weeks,
   and allergic reactions should be noted during the course of treatment. ④ Cyclosporine A: This drug has been tested for treating systemic lupus erythematosus and lupus nephritis,
   but it has toxic effects on the kidneys themselves, can cause proteinuria, and its efficacy is uncertain. S calf thymus extract: This drug has been used domestically for treating systemic lupus erythematosus,
   but its efficacy is not yet confirmed, pending further clinical experience. Transfer factor: Has a certain effect on the patient's immunity,
   but it is difficult to use it to control the disease, can only be used as an auxiliary therapy.
   III. Professor Pei Zhengxue's Thinking Method