Systemic Lupus Erythematosus Causes, SLE Diagnosis, SLE Criteria, SLE Treatment, Systemic Lupus Erythematosus Diagnosis,

Systemic Lupus Erythematosus Causes | SLE Diagnosis Criteria


Systemic Lupus Erythematosus Causes | SLE Diagnosis Criteria: Systemic lupus erythematosus (SLE) is an autoimmune inflammatory connective tissue disease that affects multiple organs in young women. Early, mild, and atypical cases are increasing. Systemic Lupus Erythematosus Causes | SLE Diagnosis Criteria.  Some critically ill patients (except those with diffuse proliferative glomerulonephritis) can sometimes relieve themselves. Some patients have a “transient” episode, and the disease can completely disappear after a short period of several months. Systemic Lupus Erythematosus Causes | SLE Diagnosis Criteria.

We will Learn:

1: Systemic Lupus Erythematosus Causes:

2: Systemic Lupus Erythematosus Pathophysiology and Symptoms:

3: Systemic Lupus Erythematosus Examination:

4: Systemic Lupus Erythematosus (SLE) Diagnosis:

5: Systemic Lupus Erythematosus Differential diagnosis:

6: Systemic Lupus Erythematosus Treatment:


1: Systemic Lupus Erythematosus Causes:

The etiology of this disease has not yet been affirmed, and a large number of studies have shown that genetic, endocrine, infection, immune abnormalities, and some environmental factors are related to the pathogenesis of this disease.
Under the interaction of various factors such as genetic factors, environmental factors, and estrogen levels, it leads to the decrease of T lymphocytes, the decrease of T inhibitory cell function, the excessive proliferation of B cells, the production of a large number of autoantibodies, and the formation of complex antigens in the body. The corresponding immune complex is deposited on the skin, joints, small blood vessels, glomeruli, and other parts. With the participation of complement, causing acute and chronic inflammation and tissue necrosis (such as lupus nephritis), or antibodies directly interact with tissue cell antigens, causing cell destruction (such as red blood cells, lymphocytes and platelet wall specific antigens combined with the corresponding autoantibodies), causing hemolytic anemia, lymphopenia, and thrombocytopenia, respectively, resulting in multiple system damage to the body.

2: Systemic Lupus Erythematosus Pathophysiology and Symptoms:

1: General symptoms:

The ratio of men and women in this disease is 1:7 to 9, and the age of onset is 20 to 40 years old. The child or the elderly can also develop the disease. Weakness, fever, and weight loss.

2: Skin and mucous membranes
The performance is diverse and can be broadly classified into specific and non-specific. 1 specific skin lesions have butterfly erythema, subacute skin lupus erythematosus, discoid erythema. 2 non-specific skin lesions arephotoallergic, hair loss, mouth ulcers, cutaneous vasculitis (purpura), pigment changes (stagnation or loss), reticular bluish, Raynaud’s phenomenon, urticaria-like rash, rare lupus lipid film Inflammatory or deep lupus and bullous lupus erythematosus.

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3: Skeletal muscles
The table shows joint pain, arthritis, joint deformity (10% X-ray damage) and myalgia, muscle weakness, avascular osteonecrosis, osteoporosis.

4: Cardiac involvement
There may be pericarditis (4% of patients have signs of pericardial tamponade), myocarditis mainly manifests as congestive heart failure, heart valve disease, such as Libman-Sacks endocarditis. Coronary arteritis is rare, mainly manifested as chest pain, abnormal ECG and elevated myocardial enzymes.

5: Respiratory system involvement
Pleurisy, pleural effusion, lung reduction syndrome mainly manifested as a hernia and diaphragmatic dysfunction; pulmonary interstitial lesions, pulmonary embolism, pulmonary hemorrhage, and pulmonary hypertension can occur.

6: Kidney
The clinical manifestation is nephritis or nephrotic syndrome. Red blood cells, white blood cells, casts, and proteinuria appear in the urine during nephritis. Renal function tests are normal early, gradually progressing, and uremia can occur later. Nephrotic syndrome and laboratory manifestations of systemic edema, with varying degrees of abdominal cavity, chest and pericardial effusion, large amounts of proteinuria, decreased serum albumin, white globulin ratio inversion and hyperlipidemia.

7: Nervous system involvement
May have convulsions, mental disorders, organic brain syndrome including organic amnesia / cognitive dysfunction, dementia and altered consciousness, others may have aseptic meningitis, cerebrovascular accident, transverse myelitis, and lupus-like sclerosis, as well as peripheral neuropathy.

8: Blood system
Affected can have anemia, decreased white blood cell count, thrombocytopenia, swollen lymph nodes, and splenomegaly.

9: Digestive system
Affected can be anorexia, nausea, vomiting, diarrhea, ascites, liver, abnormal liver function and pancreatitis. Uncommon mesenteric vasculitis, Budd-Chiari syndrome and protein-losing enteropathy.

10: Other
Can be combined with hyperthyroidism or hypotension, Sjogren’s syndrome and other diseases.

3: Systemic Lupus Erythematosus Examination:

1. General inspection:
Because SLE patients often have multiple system involvement, such as abnormal blood system and kidney damage, blood tests can have anemia, decreased white blood cell count, and thrombocytopenia. When the kidney is involved, urine analysis can show proteinuria, hematuria, cells, and particles. Tube type; erythrocyte sedimentation rate (erythrocyte sedimentation rate) increases during the active phase of SLE, and the remission period can be reduced to normal.

2. Immunological examination:
50% of patients have hypoproteinemia, 30% of patients with SLE have hyperglobulinemia, especially elevated gamma globulin, and serum IgG levels increase during disease activity. When the disease is in an active phase, the level of complement is often reduced because the formation of immune complexes consumes a decrease in the ability of complement and liver to synthesize complement, and the individual complement components C3, C4 and total complement activity (CH50) can be reduced during disease activity.

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3. Biochemical examination:
Liver function tests in patients with SLE were mostly mild to moderate abnormalities, and more often occurred during the course of the disease, accompanied by elevated alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Abnormal serum albumin suggests a decompensation of renal function. Quantitative detection of microalbuminuria in urine function tests helps to determine and monitor the extent of kidney damage and prognosis. In the presence of lupus nephritis, serum urea nitrogen (Bun) and serum creatinine (Cr) help to determine the clinical stage and observe treatment effects.

SLE patients have a high risk of cardiovascular disease and have gradually attracted great attention in recent years. Some patients with SLE have severe dyslipidemia, elevated inflammatory markers, and high homocysteine (Hcy). Serum lipid levels, hypersensitive C-reactive protein (hs-CRP) and homocysteinemia are considered to be effective predictors of connective tissue disease (CTD)-associated atherosclerotic cardiovascular disease (ASCVD), regularly Detection can reduce the risk of reducing cardiovascular events.

4. Autoantibody detection:
Currently, clinically conducted SLE-related autoantibody routine detection items mainly include anti-nuclear antibody (ANA), anti-double-stranded deoxyribonucleic acid (anti-dsDNA antibody) antibody, anti-soluble antigen-antibody (anti-ENA antibody) (including anti-Sm, anti-U 1 RNP, anti-SSA/Ro, anti-SSB/La, anti-RNP, anti-Scl-70 and anti-Jo-1, etc.), anti-nucleosome antibodies and antiphospholipid antibodies. For patients with clinically suspected SLE, immunological autoantibody testing should be performed. In the ACR revised SLE classification criteria, immunological abnormalities and autoantibody positives include anti-Sm antibodies, anti-dsDNA antibodies, antiphospholipid antibodies, and ANA positive.

5. Histopathological examination:
Skin biopsy and renal biopsy are also very helpful in diagnosing SLE. The glomerular performance of the skin lupus test positive and “full hall” is highly specific.

4: Systemic Lupus Erythematosus Diagnosis:

The diagnosis of SLE relies mainly on clinical manifestations, laboratory tests, histopathology, and imaging studies. In the SLE classification standard revised by the American College of Rheumatology (ACR) in 1997, laboratory tests such as hematological abnormalities, immunological abnormalities, and autoantibodies were clearly included in the diagnostic criteria. SLE laboratory examinations are important for the diagnosis, differential diagnosis and judgment of activity and recurrence of SLE. ‘Systemic Lupus Erythematosus Causes | SLE Diagnosis Criteria’

5: Systemic Lupus Erythematosus Differential diagnosis:

Fever, rash should be differentiated from dermatomyositis, adult ills (AOSD), systemic vasculitis, infectious diseases, and neoplastic diseases; arthritis should be associated with rheumatoid arthritis, acute Identification of rheumatic fever and other phases; kidney involvement should be differentiated from a primary glomerular disease.

6: Systemic Lupus Erythematosus (SLE) Treatment:

1. General treatment
Suitable for all SLE patients. This includes psychological and mental support, avoiding the sun or ultraviolet radiation, preventing and treating infections or other comorbidities, and choosing appropriate exercise methods depending on the condition.

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2. Drug treatment:

  1. Non-steroidal anti-inflammatory drugs (NSAIDS) are suitable for patients with low fever, joint symptoms, rash, pericardium, and pleurisy, and those with blood system lesions should be used with caution.
  2. Antimalarial drugs chloroquine or hydroxychloroquine, effective for rash, hypothermia, arthritis, mild pleurisy and pericarditis, mild anemia and white blood cell count and combined with Sjogren’s syndrome, those with ophthalmia should be used with caution. A long-term application is helpful to reduce the dose of hormones and maintain the relief of the disease. The main adverse reactions were cardiac conduction disorder and retinal pigmentation. Electrocardiogram and ophthalmologic examination should be performed regularly.
  3. Glucocorticoids are selected according to the condition and dosage form. The adverse reactions of hormones include Cushing’s sign, diabetes, high blood pressure, various infections caused by low resistance, stress ulcers, aseptic osteonecrosis, osteoporosis, and children’s growth retardation or stagnation.
  4. Immunosuppressive agent 1 cyclophosphamide (CTX) is effective for nephritis, pulmonary hemorrhage, central nervous system vasculitis, and autoimmune hemolytic anemia. Adverse reactions include digestive discomfort, myelosuppression, liver damage, hemorrhagic cystitis, alopecia, amenorrhea, and decreased fertility. 2 azathioprine oral, for autoimmune hepatitis, nephritis, skin lesions and arthritis. Adverse reactions include digestive discomfort, myelosuppression, liver damage, and allergic reactions. 3 methotrexate (MTX) is fixed or oral, effective for arthritis, serositis, and fever, renal damage should be reduced, and occasionally adverse reactions to enhance photoallergies. 4 cyclosporine A (CSA) oral, currently used mainly for SLE patients who are ineffective in the treatment of other drugs. effective for thrombocytopenia.

3. Other treatments:
High-dose immunoglobulin shock, plasma exchange, suitable for critically ill patients, conventional treatment cannot be controlled or intolerable, or contraindications.

4. Treatment of lupus nephritis 1 glucocorticoids. 2 immunosuppressants. 3 plasma exchange and immunoadsorption therapy. “Systemic Lupus Erythematosus Causes | SLE Diagnosis Criteria” 4 high-dose immunoglobulin shock therapy is suitable for active lupus nephritis (LN), immunocompromised patients with infection. 5 other such as anticoagulant, systemic lymph node irradiation, and traditional Chinese medicine, renal dysfunction can be dialysis treatment.

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