OVERVIEW

What kind of disease is systemic lupus erythematosus?

Systemic lupus erythematosus (SLE) is an autoimmune connective tissue disease that affects multiple systems and organs. Patients have various autoantibodies in their serum, and the fundamental pathological change is vasculitis. Simply put, it occurs when the immune system mistakenly attacks the body's own blood vessels as if they were foreign invaders.

The clinical manifestations of SLE are diverse, characterized by "four multiples": multiple systems, multiple organs, multiple autoantibodies, and a higher prevalence among women of childbearing age. Medication is typically used for treatment, and proper drug therapy can alleviate symptoms in most patients ^[1,2]. Without timely and effective treatment, the mortality rate is relatively high, primarily due to infections, kidney failure, and central nervous system damage (such as epilepsy, lupus headaches, cerebrovascular lesions, etc.) ^[1].

Is systemic lupus erythematosus common?

The prevalence of SLE varies among populations. In China, the prevalence is (30.13–70.41) per 100,000 people.

This means approximately 3,013–7,041 out of every 10 million people in China have SLE. It is more common in women, particularly those aged 20–40 in their childbearing years ^[1].

What is the connection between the "wolf" in systemic lupus erythematosus and actual wolves?

Patients with SLE often experience recurrent, stubborn skin lesions on their hands or face. In some cases, these red patches may develop ulcers, atrophy, or scars, resembling wounds caused by a wolf bite—hence the name "lupus" (derived from Latin).

Which department should patients with systemic lupus erythematosus visit?

Rheumatology and Immunology Department. Since SLE is an immune-related disease, patients should generally seek treatment from a rheumatology and immunology specialist.

SYMPTOMS

What are the main clinical manifestations of systemic lupus erythematosus?

The clinical manifestations of systemic lupus erythematosus (SLE) are complex and varied, with early symptoms often being atypical. Most patients have an insidious onset, initially presenting with fever, fatigue, weight loss, hair loss, rash, fingers turning white or purple upon exposure to cold, recurrent oral ulcers, superficial lymphadenopathy, prolonged menstrual bleeding, skin purpura, decreased platelet count, occult nephritis, loss of appetite, nausea, vomiting, and other symptoms. As the disease progresses, patients gradually develop damage to multiple systems, typically characterized by alternating periods of remission and exacerbation^[1].

• Systemic manifestations: Patients may experience various types of fever during the course of the disease, with low to moderate fever being the most common. Fever can be either the initial symptom or an accompanying symptom, often accompanied by fatigue, muscle pain, loss of appetite, and weight loss.
• Skin and mucosal lesions: The most characteristic feature is the butterfly-shaped rash on the cheeks. Other skin manifestations include discoid lupus, alopecia, bullous lesions, vasculitis, livedo reticularis, Raynaud's phenomenon, photosensitivity, oral ulcers, and periungual erythema.

• Joints and muscles: Symmetrical polyarthralgia and swelling, commonly affecting the proximal interphalangeal joints, wrists, knees, and metacarpophalangeal joints, usually without bone destruction. A small number of patients may develop avascular necrosis of the femoral head, though it is unclear whether this is due to the disease itself or a side effect of glucocorticoids. A few patients may develop myositis, mostly in active lupus.
• Renal involvement: Affects the glomeruli, tubules, interstitium, and blood vessels, presenting as nephritis or nephrotic syndrome, potentially progressing to end-stage renal failure.
• Cardiovascular involvement: Includes pericarditis, myocarditis, angina, and even acute myocardial infarction. Patients may also develop Libman-Sacks endocarditis, which typically does not cause symptoms but may lead to valvular vegetations that can embolize or become infected.
• Pulmonary involvement: SLE often affects the lungs, causing pleuritis, lupus pneumonitis, interstitial lung disease, diffuse alveolar hemorrhage, and pulmonary hypertension.
• Neurological involvement: Neuropsychiatric lupus, or lupus cerebritis, occurs mostly during active disease and can affect the central and/or peripheral nervous systems. Symptoms range from anxiety, personality changes, memory loss, and cognitive impairment to severe manifestations like stroke, coma, status epilepticus, paraplegia, and incontinence.
• Gastrointestinal involvement: Symptoms include loss of appetite, nausea, vomiting, abdominal pain, diarrhea, ascites, and melena, which may be the initial presentation in some patients. A few may develop acute abdominal conditions like pancreatitis, intestinal necrosis, or obstruction.
• Hematological involvement: 50%–80% of patients develop anemia (normocytic normochromic), with 10% having hemolytic anemia. Leukopenia (especially lymphopenia) occurs in 50% of patients, while 20% have painless lymphadenopathy and 15% have splenomegaly.
• Antiphospholipid syndrome: Found in 40% of SLE patients, characterized by arterial/venous thrombosis, recurrent miscarriage, and thrombocytopenia.
• Secondary Sjögren's syndrome: Some patients develop dry mouth and eyes due to exocrine gland dysfunction.
• Ocular involvement: Most commonly affects the retina, causing hemorrhages, papilledema, and exudates. Vasculitis may involve the optic nerve, leading to vision loss or blindness. Keratitis and conjunctivitis are also seen, while uveitis or scleritis is rare.

What causes anemia in SLE patients?

Anemia in SLE is usually normocytic normochromic. Sudden severe anemia often indicates autoimmune hemolysis, with reticulocytosis observed on lab tests^[2].

What are butterfly rash and discoid lupus in SLE?

The butterfly rash is a symmetrical erythema across the nose and cheeks, a hallmark of SLE^[1]. It is edematous and typically resolves without scarring, though some patients may develop hyperpigmentation.

Discoid lupus commonly appears on the face, scalp, and ears as round, annular, or irregular plaques with scaling, leaving scars and atrophy after resolution^[3].

What is antiphospholipid syndrome in SLE?

Antiphospholipid syndrome (APS) occurs during active SLE and includes recurrent thrombosis, miscarriages, and thrombocytopenia. Thrombosis is the most prominent feature and a major cause of recurrent pregnancy loss in SLE patients^[1].

APS-positive patients should carefully consider pregnancy, as even in remission, the risk of miscarriage remains high.

What characterizes oral ulcers in SLE?

Approximately 22.1% of Chinese SLE patients develop oral ulcers^[4]. SLE-related ulcers are often painless, unlike typical painful ulcers. Maintaining oral hygiene and avoiding spicy foods is advised. Confirmation by a doctor aids diagnosis^[1,5].

Why do SLE patients experience hair loss?

Necrotizing vasculitis in SLE disrupts follicular blood supply, causing diffuse or patchy alopecia^[1,2]. Hair usually regrows after treatment, but recurrence may indicate disease flare.

Why do female SLE patients often have menstrual irregularities or amenorrhea?

Possible causes include:

1. Disease activity: SLE can affect the reproductive system^[2,3].
2. Medications: High-dose glucocorticoids and immunosuppressants may disrupt menstruation. Older women face higher risks of permanent amenorrhea from immunosuppressants^[6].

Why should SLE patients avoid sun exposure?

Sunlight triggers painful or pruritic rashes, especially on exposed skin^[2]. Sun protection (e.g., long sleeves, hats) is recommended.

What is Raynaud’s phenomenon in SLE?

30%–50% of SLE patients experience Raynaud’s phenomenon—vasospasm-induced color changes (white → purple → red) in extremities upon cold/emotional stress^[3]. It can be primary (idiopathic) or secondary (e.g., due to SLE).

What is subacute cutaneous lupus?

A photosensitive rash on the neck, back, and arms, resolving with hyperpigmentation but no scarring^[2]. Distinct from SLE.

What is lupus nephritis?

50%–70% of SLE patients develop kidney involvement (hematuria, proteinuria >0.5 g/day, edema, hypertension, renal impairment)^[3-5].

What is lupus cerebritis?

Neuropsychiatric lupus, occurring in active/advanced SLE, includes headaches, cognitive decline, seizures, or coma. Diagnosis requires ruling out infections/drug effects^[2,4,5].

What is lupus pneumonitis?

Non-infectious lung inflammation in SLE, presenting acutely (fever, dyspnea) or chronically (interstitial disease). Acute cases have poor prognosis^[1,3,4].

What is neonatal lupus?

A transient condition in infants (especially girls) with annular rash and/or heart block, linked to maternal anti-Ro/SSA antibodies^[2].

What is drug-induced lupus?

Medication-triggered lupus (e.g., hydralazine, procainamide), usually resolving after discontinuation and rarely affecting kidneys/skin^[1,2].

What is lupus crisis?

Life-threatening SLE complications (e.g., rapidly progressive nephritis, severe CNS involvement, hemolytic anemia, pneumonitis)^[2,7].

How to differentiate SLE-related vs. steroid-induced psychiatric symptoms?

SLE neuropsychiatric symptoms (e.g., psychosis, seizures) improve with treatment. High-dose steroids may cause euphoria, insomnia, or psychosis^[7,8]. Timing of seizures and neurological signs aid differentiation.

CAUSES

What are the causes of systemic lupus erythematosus?

The exact cause of this disease is not yet fully understood. Extensive research suggests that systemic lupus erythematosus (SLE) may be related to genetic, environmental, and endocrine factors^[2]:

1. Genetics: SLE is a polygenic inherited disorder, requiring the combined action of multiple genes for its onset. Defects in a single gene are seen in only a very few cases. Currently, HLA class II genes are believed to be more strongly associated with SLE than class I genes.
2. Endocrine factors:
   • Sex hormones and their metabolic abnormalities: Among all SLE cases, the prevalence in women of childbearing age is 9–15 times higher than in men of the same age. The prevalence in prepubertal and postmenopausal women is slightly higher than in men, which is related to an increased estrogen/androgen ratio.
   • Estrogen receptors: Some studies have found that estrogen receptor levels are significantly higher in SLE patients during active disease than in those during remission.
   • Prolactin and growth hormone: Although growth hormone is not a reproductive hormone, it shares many similarities with prolactin in terms of primary structure and immunomodulatory functions. These two hormones may stimulate abnormal immune cells in SLE patients, contributing to the disease.
3. Viral infections: Various viral infections (e.g., Epstein-Barr virus, cytomegalovirus) may be associated with SLE, but the exact mechanism remains unclear.
4. Immune abnormalities: These include impaired macrophage clearance of apoptotic material, dendritic cell overactivation, and excessive B-cell proliferation and activation.

What are the risk factors for systemic lupus erythematosus?

1. Smoking: Smokers have a sevenfold higher risk of developing SLE compared to non-smokers, but early passive smoking does not increase the risk of SLE in adult women^[2].
2. Medications: Certain drugs can induce SLE. High-risk drugs include hydralazine and procainamide; moderate-risk drugs include isoniazid and quinidine; low-risk drugs include carbamazepine and captopril^[2].
3. Ultraviolet (UV) radiation: UV exposure can trigger or worsen skin lesions and systemic involvement in SLE patients^[1,2].

Who is more likely to develop systemic lupus erythematosus?

1. Individuals with a first-degree relative who has SLE: Since SLE is a polygenic disorder, those with affected parents or siblings are at higher risk.
2. Women of childbearing age: SLE predominantly affects women aged 20–40, making this group more susceptible.
3. Pregnant women: Changes in estrogen, progesterone, and prolactin levels during pregnancy increase the risk.
4. Smokers: The longer and heavier the smoking history, the higher the risk.
5. Long-term users of certain medications: Those taking hydralazine, procainamide, isoniazid, quinidine, etc., are at increased risk.
6. Individuals with excessive UV exposure: Long-term sun exposure (e.g., tanning, outdoor work) raises the risk.

Is systemic lupus erythematosus hereditary?

Genetic factors play a significant role in SLE. Human leukocyte antigen (HLA) alleles, particularly HLA-DR2 and HLA-DR3, are closely associated with SLE^[1]. Epidemiological and family studies also show higher prevalence among first-degree relatives and identical twins.

Is systemic lupus erythematosus contagious?

No.

SLE arises from a combination of genetic predisposition, hormonal imbalances, and environmental triggers, which collectively impair immune tolerance and lead to autoimmune dysfunction^[1-3]. Unlike infections caused by pathogens, SLE cannot spread between people. Healthy individuals need not fear contagion, and patients in remission can engage in normal work, study, and social activities without isolation.

DIAGNOSIS

How to Diagnose Systemic Lupus Erythematosus?

Since autoantibodies are important serological markers for systemic lupus erythematosus (SLE), doctors initially assess SLE through autoantibody testing and confirm the diagnosis with general examinations, complement tests, etc.:

General Examinations: Depending on the affected systems, abnormalities may appear in blood tests, urinalysis, liver and kidney function tests. For example, patients with neuropsychiatric lupus (lupus cerebritis) often show increased cerebrospinal fluid pressure and protein levels, while glucose, chloride, and cell counts remain normal ^[1].

Autoantibody Testing: Various autoantibodies can be detected in the serum of SLE patients, serving as key serological markers ^[1,2].

1. Antinuclear Antibody Spectrum
   • Antinuclear Antibodies (ANAs): These target nuclear components. ANA positivity in SLE is as high as 95%, with higher titers (≥1:80) being more diagnostically significant. However, ANAs are not specific to SLE and may appear in other connective tissue diseases like scleroderma or Sjögren’s syndrome, though with lower positivity rates and titers.
   • Anti-dsDNA Antibodies: Highly specific to SLE (50–80% positivity), with titers decreasing as the disease remits.
   • Anti-Sm Antibodies: 99% specific but less sensitive (20–30% positivity), unrelated to disease activity.
   • Other autoantibodies (e.g., anti-RNP, anti-SSA, anti-SSB, anti-histone) may also be positive.
2. Antiphospholipid Antibodies: Including anticardiolipin antibodies, lupus anticoagulant, and false-positive syphilis tests. These antibodies inhibit blood clotting but paradoxically increase thrombosis risk, alongside recurrent miscarriages and thrombocytopenia—collectively termed antiphospholipid syndrome.
3. Other SLE Autoantibodies: Such as anti-erythrocyte, anti-granulocyte, anti-platelet, anti-lymphocyte, anti-ribosomal, and anti-nucleosome antibodies. ~1/3 of cases test positive for rheumatoid factor (RF).
4. Additional Tests:
   • Complement Levels: Low CH50, C3, or C4 often indicate active SLE.
   • Disease Activity Markers: Increased proteinuria, elevated ESR/CRP, or thrombocytosis may suggest active disease.
   • Imaging: CT/MRI helps detect early organ damage (e.g., lung/kidney involvement, lupus cerebritis).

What Are the Diagnostic Criteria for SLE?

SLE diagnosis is complex and requires specialist evaluation. Below are the widely used criteria:

1997 ACR Classification Criteria ^[2]: Patients meeting ≥4 of the following 11 criteria (sequentially or simultaneously) are diagnosed with SLE after excluding infections/tumors/other connective tissue diseases: 1. Malar rash 2. Discoid rash 3. Photosensitivity 4. Oral ulcers 5. Non-erosive arthritis 6. Serositis (pleuritis/pericarditis) 7. Renal disorder (proteinuria/cellular casts) 8. Neurologic disorder (seizures/psychosis) 9. Hematologic disorder (hemolytic anemia/leukopenia/thrombocytopenia) 10. Immunologic disorder (anti-dsDNA/anti-Sm/antiphospholipid antibodies) 11. Positive ANA

2009 Revised ACR Criteria ^[2]: Clinical Criteria (≥1 required): 1. Acute/chronic cutaneous lupus 2. Oral/nasal ulcers 3. Non-scarring alopecia 4. Synovitis 5. Serositis 6. Renal (proteinuria/red cell casts) 7. Neurologic (seizures/psychosis/etc.) 8. Hemolytic anemia 9. Leukopenia/lymphopenia 10. Thrombocytopenia Immunologic Criteria (≥1 required): 1. Positive ANA 2. Anti-dsDNA/Sm antibodies 3. Antiphospholipid antibodies 4. Low complement 5. Direct Coombs’ test (without hemolysis) Definitive SLE: Active nephritis with ANA/anti-dsDNA positivity, OR ≥4 criteria including ≥1 clinical + ≥1 immunologic.

How Is SLE Disease Activity Scored?

Activity assessment guides treatment adjustments. The widely used SLEDAI scoring system ^[2]: - 8 points each: Seizures, psychosis, stroke, vasculitis. - 4 points each: Arthritis, myositis, proteinuria. - 2 points each: Rash, mucosal ulcers, pleuritis, low complement. - 1 point each: Fever, cytopenias. Total score: 0–4 (inactive), 5–9 (mild), 10–14 (moderate), ≥15 (severe).

How to Identify an SLE Flare?

Recurrence lacks strict criteria but may involve: - Clinical signs: Unexplained fever, new rash, joint pain, alopecia, headaches. - Lab changes: Rising anti-dsDNA, falling complement, elevated ESR, proteinuria. Action: Seek immediate medical attention if symptoms reappear.

What Diseases Mimic SLE?

1. Drug-Induced Lupus: - Triggered by medications (e.g., hydralazine, procainamide). - Older age, milder symptoms (rare renal/CNS involvement). - Resolves after drug withdrawal. - High anti-histone antibodies (95%), rare anti-dsDNA/Sm (<5%), normal complement.
2. Subacute Cutaneous Lupus: - Photosensitive, non-scarring rashes (neck/upper back). - May involve oral ulcers, Raynaud’s phenomenon. - Distinguished by biopsy. ^[3]

TREATMENT

What are the treatment principles for systemic lupus erythematosus?

Currently, there is no effective cure for systemic lupus erythematosus. For newly diagnosed cases, if drug-induced factors can be ruled out, early treatment should be initiated upon confirmation. Due to individual differences among lupus patients, treatment cannot be standardized. It is essential to emphasize personalized treatment based on the patient's clinical manifestations, laboratory tests, disease activity, organ damage, comorbidities, and socioeconomic conditions. Additionally, the risks and benefits of treatment must be evaluated to select the optimal treatment plan ^[4].

How is systemic lupus erythematosus treated?

1. General treatment:

   • Patients should maintain an optimistic attitude, seek disease knowledge from healthcare professionals, correctly understand the disease, and eliminate fear. Participating in hospital-organized patient support groups and communicating with other patients is also beneficial [2].
   • Balance work and rest. Patients with severe symptoms should rest in bed, while those with stable conditions can engage in appropriate activities but must avoid overexertion ^[1,2].
   • Avoid self-medication. Consult a doctor before taking any medication, especially contraceptives or antibiotics ^[1,2].
   • Practice sun protection by using sunscreen or protective clothing ^[1,2].
   • Consult a doctor before vaccinations. Vaccinations should only be administered during remission, and live vaccines (e.g., chickenpox or BCG vaccines) should be avoided if possible ^[1].

2. Symptomatic treatment: For fever, patients can first attempt physical cooling (e.g., using a wet towel or cooling patches) before seeking medical help. Doctors may recommend medications like ibuprofen or diclofenac sodium. For lupus encephalopathy with symptoms like confusion or hallucinations, caregivers should protect the patient from falls or accidents. Doctors may administer treatments to reduce intracranial pressure or prevent seizures. Patients with hypertension, diabetes, or dyslipidemia will also receive targeted treatments ^[1].

3. Drug therapy:

   • For mild cases, doctors may prescribe NSAIDs (e.g., aspirin, ibuprofen), antimalarials (e.g., chloroquine, hydroxychloroquine), thalidomide, or low-dose steroids. NSAIDs may cause nausea, vomiting, headaches, or tinnitus; antimalarials may lead to retinal damage; and thalidomide may cause drowsiness, rashes, or nausea ^[7].
   • For moderate cases, glucocorticoids (e.g., prednisone) are used, sometimes combined with immunosuppressants (e.g., methotrexate, azathioprine). Glucocorticoids may cause nausea, vomiting, or moon face, while immunosuppressants may lead to gastrointestinal issues, oral ulcers, or bone marrow suppression ^[7,8].
   • For severe cases, glucocorticoids (e.g., prednisone) are typically the first choice, combined with immunosuppressants like cyclophosphamide, methotrexate, or azathioprine ^[7] (side effects as above).
   • For lupus crisis, the goal is to save lives, protect affected organs, and prevent complications. High-dose glucocorticoid (methylprednisolone) pulse therapy is often used, followed by treatments for severe lupus to induce and maintain remission ^[7].

   Biological agents (e.g., belimumab, rituximab), plasmapheresis, intravenous immunoglobulin, and stem cell transplantation are also used clinically ^[1].

What are the indications and precautions for NSAIDs in systemic lupus erythematosus patients?

NSAIDs are commonly used in both mild and severe lupus for anti-inflammatory, analgesic, and antipyretic effects ^[1]. However, NSAIDs lack immunosuppressive effects, so glucocorticoids or immunosuppressants must be used concurrently. Since lupus often involves multiple organs, especially the kidneys, and NSAIDs inhibit prostaglandins (potentially worsening renal function), caution is needed, particularly in lupus nephritis patients ^[7].

When should systemic lupus erythematosus patients undergo glucocorticoid pulse therapy?

Pulse therapy involves high-dose glucocorticoids (e.g., 500–1000 mg methylprednisolone daily via slow IV infusion) for a short period, typically 3 days ^[7]. It may be considered for severe lupus nephritis, pneumonitis, mesenteric vasculitis, neuropsychiatric lupus, or severe cytopenia. While effective, it is not sustainable long-term and must be combined with other therapies while preventing infections.

What are the side effects of glucocorticoids in systemic lupus erythematosus patients?

Side effects include hypertension, infections, peptic ulcers, osteonecrosis, osteoporosis, delayed wound healing, hyperglycemia, and neuropsychiatric symptoms (e.g., agitation, insomnia, or psychosis) ^[8]. Some patients may even develop suicidal tendencies. Proper dosing, tapering, and preventive measures are crucial to minimize risks.

Can systemic lupus erythematosus patients with diabetes or osteonecrosis still use glucocorticoids?

Yes ^[8]. Glucocorticoids are vital, especially for severe lupus. For diabetic patients, blood glucose must be closely monitored and controlled (with oral agents or insulin). For osteonecrosis, glucocorticoid doses should be minimized, supplemented with circulatory and bone-nourishing therapies ^[7,8].

What should systemic lupus erythematosus patients note when using antimalarials?

Antimalarials (e.g., hydroxychloroquine) help with skin lesions, arthritis, and oral ulcers but may cause retinal damage. Baseline and biannual eye exams are required. They are contraindicated in patients with cardiac conduction disorders ^[2,7].

How effective is hematopoietic stem cell transplantation for systemic lupus erythematosus?

It may alleviate symptoms but is not curative. Due to high costs and risks, it is reserved for select cases and not recommended as routine therapy ^[2].

How should medication be adjusted during delivery for systemic lupus erythematosus patients?

Glucocorticoid doses should be increased (e.g., 60–80 mg methylprednisolone IV during delivery, tapered postpartum). Low-dose aspirin (50–100 mg/day) or heparin during pregnancy may reduce miscarriage risk by 54% ^[1,2,7].

How should systemic lupus erythematosus patients manage medication during breastfeeding?

NSAIDs (e.g., ibuprofen) are generally safe. For glucocorticoids or immunosuppressants, consult a doctor to weigh risks. Hydroxychloroquine and biologics are relatively safe, but cyclophosphamide and methotrexate are contraindicated.

How effective is plasmapheresis for systemic lupus erythematosus?

It removes immune complexes for short-term relief but does not suppress their production. Combined with glucocorticoids and cyclophosphamide, it may achieve long-term remission. High costs and infection risks limit its use ^[2].

What is the prognosis for systemic lupus erythematosus patients?

With early diagnosis and treatment, 10- and 15-year survival rates reach 90% and 80%, respectively. Poor prognosis is associated with renal failure, neuropsychiatric lupus, or infections ^[1].

Can systemic lupus erythematosus patients receive vaccines?

During remission, non-live vaccines (e.g., flu or tetanus) may be given under medical guidance. Live vaccines (e.g., BCG) should be avoided ^[1].

Do systemic lupus erythematosus patients need psychological therapy?

Yes. Patients may experience depression or isolation, but with proper treatment, most can lead normal lives. Support and education are crucial ^[1,2].

Can systemic lupus erythematosus be cured?

No, but remission is possible with treatment. Avoid unverified remedies to prevent harm ^[1,2].

DIET & LIFESTYLE

Can patients with systemic lupus erythematosus get pregnant?

Patients with active systemic lupus erythematosus should not become pregnant. However, if the condition has been stable for more than one year after treatment, with a daily oral prednisone dose of less than 10 mg, no major organ involvement, and no use of immunosuppressants for at least 6 months, pregnancy may be considered^[1,2,7].

The fertility of patients with systemic lupus erythematosus is normal, but pregnancy increases the risk of miscarriage, premature birth, stillbirth, and intrauterine growth retardation, especially in patients with positive anti-cardiolipin antibodies. Pregnancy can worsen the condition or trigger a relapse, and even patients in stable condition may experience disease exacerbation during pregnancy or after delivery.

It is crucial to strictly follow the doctor's instructions regarding medication and receive joint follow-up and treatment from obstetric and rheumatology specialists after pregnancy ^[2].

What dietary precautions should systemic lupus erythematosus patients take?

1. If proteinuria occurs without kidney damage, sufficient protein intake—especially high-quality protein such as eggs, milk, lean meat, and fish—should be ensured;
2. Patients with kidney damage should limit protein and salt intake to avoid increasing the burden on the kidneys ^[5];
3. Patients with skin lesions should avoid photosensitive foods like celery and coriander to prevent worsening skin symptoms ^[5,10];
4. Spicy and irritating foods such as chili and mustard should be avoided ^[5];
5. Patients are encouraged to consume a diet rich in vitamins, such as oranges, apples, and carrots. Reduced intake of vitamin B₆, B₁₂, folic acid, and dietary fiber may contribute to atherosclerosis, accelerating disease progression. Therefore, increasing the intake of these nutrients is recommended ^[10].

In summary, patients should prioritize a light, easily digestible, low-salt, and vitamin-rich diet.

What should systemic lupus erythematosus patients pay attention to after discharge?

1. After discharge, patients must never adjust their medication dosage on their own, especially glucocorticoids, even if their condition changes significantly ^[5]. They should visit a rheumatology clinic for follow-up tests, including liver and kidney function, blood, urine, and stool tests, and only adjust medication under a doctor's evaluation. Additionally, patients must adhere to regular follow-up appointments as advised by their doctor.
2. Maintain a positive mood. After improvement, engage in physical exercise and light household chores, avoiding overexertion. Adopt healthy lifestyle and dietary habits with a regular routine. Use sun protection when going outdoors. Prevent colds to avoid worsening the condition ^[1,2].

PREVENTION

Can systemic lupus erythematosus be prevented? How to prevent it?

Since the exact cause of this disease is not yet fully understood, there is no specific prevention method. However, the following measures may help reduce the risk to some extent:

1. Quit smoking: Smokers have a seven times higher risk of developing systemic lupus erythematosus than non-smokers ^[2]. Quitting smoking can lower the risk of developing the disease.
2. Standardized medication use: Avoid drugs that may trigger the disease, such as hydralazine, procainamide, and isoniazid ^[2]. Always follow medical advice and use medications as prescribed.
3. Sun protection: Use sunscreen daily, wear protective clothing, and avoid direct exposure to strong sunlight ^[2].
4. Early intervention for high-risk groups: Individuals with a family history of the disease, women of childbearing age who smoke, long-term users of hydralazine, procainamide, isoniazid, or quinidine, and those with excessive UV exposure should undergo annual check-ups. Pregnant women should have regular prenatal check-ups for early detection and treatment.

How to prevent the recurrence of systemic lupus erythematosus?

So far, there is no definitive method to completely prevent the recurrence of systemic lupus erythematosus, but this does not mean it cannot be mitigated.

1. In addition to preventing colds, patients should take medications as prescribed by their doctors, avoid self-medication, and refrain from discontinuing treatment based on hearsay about "miracle cures."
2. Ensure adequate rest, avoid overexertion, maintain moderate work levels, engage in appropriate physical activity, and avoid prolonged sun exposure ^[1,2].
3. Maintain a positive mental state, adopt a balanced diet, and schedule regular check-ups with a doctor to monitor test results ^[1,2].