Unraveling Systemic Lupus Erythematosus: Understanding Its Causes, Symptoms, Diagnosis, and Underlying Pathology

---

Systemic lupus erythematosus (SLE) is a complex autoimmune disease. It affects many organs in the body. The name gives clues. “Systemic” means it spreads throughout the body. “Erythematosus” shows the skin turns red. “Lupus” means wolf in Latin. This name comes from skin lesions that look like wolf bites. Experts do not know the term’s exact start. They do know that lupus acts on skin and organs.

What Causes Lupus?

Lupus is an autoimmune disorder. In a healthy body, immune cells fight viruses and bacteria. In lupus, immune cells attack the body instead. They cause swelling and damage in many tissues. The immune cells can target the skin, joints, kidneys, heart, and nervous system.

Doctors see two key roles: genes and the environment. Genes may make the immune system act wrongly. Certain genes cause immune cells to target self-antigens. Self-antigens come from cell nuclei. When cells die, they release DNA and proteins.

Ultraviolet (UV) light from the sun can trigger cell death. UV light harms cell DNA. Damaged cells die and spill nuclear antigens into the blood. In a healthy person, the body clears these antigens. In lupus, the clearance is slow. The immune system sees the lingering antigens. B cells then produce antinuclear antibodies (ANAs). These antibodies stick to nuclear antigens and form complexes.

Other triggers include cigarette smoke, infections, certain drugs like procainamide and hydralazine, and hormones such as estrogen. Women in their childbearing years have lupus about ten times more than men. This difference shows that hormones play a role.

Pathophysiology: How Does Lupus Cause Damage?

Antibody-antigen complexes group together in small blood vessels. They build up in the kidneys, skin, joints, and heart. These complexes restart inflammation. They also trigger the complement system—a chain of proteins that defends the body. The defense creates pores in cell membranes. The pores kill healthy cells.

This reaction is a type III hypersensitivity response. Lupus patients might also create other autoantibodies. These autoantibodies target red, white, or platelets or phospholipids. Their work marks these cells for destruction. This is known as a type II hypersensitivity response. Doctors still study how these autoantibodies form.

Clinical Presentation and Symptoms

Lupus shows many symptoms. It can change over time and vary by person. It often appears with both general and organ-specific signs. A well-known picture is a woman with fever, joint pain, and a skin rash.

Doctors use eleven criteria to diagnose lupus. They need four or more to confirm the disease. The criteria include:

1. Malar Rash: Red, butterfly-shaped rash on the cheeks that avoids the folds by the nose. It often follows sun exposure.
2. Discoid Rash: Scaly, plaque-like lesions on skin that sees the sun. These lesions may scar.
3. Photosensitivity: Rashes that get worse with sunlight but usually clear up.
4. Oral or Nasal Ulcers: Painful sores inside the mouth or nose.
5. Serositis: Inflammation on organs like the lung lining (pleuritis) or heart lining (pericarditis). Lupus may also affect other heart layers.
6. Arthritis: Pain, swelling, and stiffness in two or more joints.
7. Renal Disorders: Signs include protein in the urine or inflammation in the kidneys.
8. Neurologic Disorders: Seizures or psychosis due to antibodies in the brain.
9. Hematologic Disorders: Anemia, low platelets, or low white blood cells. Here, the immune system attacks its own helpers.
10. Immunologic Abnormalities: The presence of specific autoantibodies.
11. Antinuclear Antibody (ANA) Positivity: Nearly all lupus patients show positive ANA, though it is not unique to lupus.

Diagnostic Antibodies

Testing antibodies is key for diagnosis. The ANA test is very sensitive. It catches most lupus cases. However, a positive ANA can appear in other autoimmune diseases too.

More specific tests check for:

• Anti-Smith (Anti-Sm): This antibody targets small ribonucleoproteins. It is very specific for lupus.
• Anti-double Stranded DNA (Anti-dsDNA): This antibody rises with worsening disease, especially in the kidneys.
• Anti-phospholipid Antibodies: This group includes anticardiolipin, lupus anticoagulant, and anti-beta2 glycoprotein I. These antibodies raise clotting risk. They can lead to blood clots, strokes, deep vein thrombosis, and pregnancy loss.

Treatment and Management

Lupus usually goes through cycles. Flares happen and then quiet periods follow. Treatment aims to stop flares and ease their effects.

• Sun Protection: Sunlight can start flares. Patients wear protective clothing and use sunscreens.
• Corticosteroids: These drugs fight inflammation. They work by calming the immune response during flares.
• Immunosuppressive Drugs: For serious cases, these drugs slow the immune system broadly.
• Anticoagulation: For patients with clotting risks due to antiphospholipid antibodies, blood thinners may be needed for life.

Conclusion

Systemic lupus erythematosus is a multifaceted autoimmune disease. It stems from a mix of genetic factors and environmental triggers. The immune system wrongly attacks the body through both type II and type III hypersensitivity responses. Lupus causes a wide range of symptoms from skin rashes to kidney or nerve problems. Early diagnosis and careful treatment help control the disease and improve life quality.

contact us @mindfulaimedia@gmail.com