Systemic lupus erythematosus (SLE) is a complex autoimmune disease where the immune system attacks the body's own cells and tissues, causing inflammation and damage. It most often affects the heart, joints, skin, lungs, blood vessels, liver, and kidneys. SLE prevalence is highest in women aged 15-65 years old. While the cause is unknown, genetic and environmental factors like UV light, infections, and smoking may play a role. Symptoms include rashes, fatigue, joint pain, and organ involvement. Treatment focuses on controlling symptoms with drugs like NSAIDs, antimalarials, corticosteroids, and immunosuppressants to minimize long-term damage. With effective treatment

1. SYSTEMIC LUPUS
ERYTHEMATOUS
By Rodnishwar Prasad
Group 23

2. WHAT IS LUPUS?
 Systemic Lupus Erythematous (SLE) is a complex autoimmune disease
The immune system attacks the body’s cells and tissue, resulting in inflammation
and tissue damage.
SLE can affect any part of the body, but most often harms the heart, joints, skin ,
lungs , blood vessels , liver, kidneys, and nervous system.
Over 40 different genes predispose to SLE
Characterized by remissions and exacerbations

3. PREVALENCE
90% of cases are of women
Prevalence rate is between 15 and 65 years of age
Symptoms occur between 15 and 25 years
Prevalence in general population is 1 in 1000

4. ETIOLOGY
The cause of SLE is currently unknown but there may be environmental and genetic
factors to it.
Environmental Factors:
UV lights, certain chemicals(hydrazine), drugs, infections and smoking.
B Cell Activation:
Results in autoantibody(IgG) production to a variety of antigen.
Impaired T cell regulation of immune system

5. SIGNS & SYMPTOMS
 Achy joints / arthralgia
 Fever of more than 38 ° C
 Arthritis / swollen joints
 Prolonged or extreme fatigue
 Skin Rashes
 Anaemia
 Kidney Involvement
 Pain in the chest on deep breathing / pleurisy
 Butterfly-shaped rash across the cheeks and nose
 Sun or light sensitivity / photosensitivity
 Hair loss / Alopecia
 Abnormal blood clotting problems
 Fingers turning white and/or blue in the cold
 Mouth or nose ulcers

7. PATHOPHYSIOLOGY
The plasma cells are producing antibodies that are specific for self proteins, ds-DNA
Overactive B-cells which are stimulated by estrogen.
Suppressed regulatory function in T-cells.
IL-10, also a B-cell stimulator is in high concentration in lupus patient serum.
High concentration linked to cell damage caused by inflammation
Increased levels of Ca2+ leads to spontaneous apoptosis.

8. PATHOPHYSIOLOGY
RBCs lack CR1 receptor which decreases the affective removal of complexes
IgG is the most “pathogenic” because it forms intermediate complexes that can get
to the small places and block them.
DNA is the main antigen for which antibodies are formed.
Extracellular DNA has an affinity for basement membrane where it is bound by
auto-antibodies.
Classical thickening of the basement membrane

9. DIAGNOSIS
Complete blood count(CBC)
Erythrocyte sedimentation rate
Creatine phosphokinase – usually elevated in SLE myositis.
Renal biopsy – indicates of lupus nephritis.
Serology – antinuclear antibody (ANA) test. Positive confirms SLE

10. TREATMENT
Treatment goals
Use of drugs with:
-least side effects
-lowest dosage to control disease
-long term damage control
Mild case : avoid use of steroids
Severe case : aggressive treatment

11. DRUGS TO USE
Non Steroidal Anti Inflammatory Drugs (NSAIDS) :
• NSAIDS have analgesic, antipyretic, and anti-inflammatory properties.
• Drugs include:
-ibuprofen
-naproxen
Antimalarial :
• Hydroxychloroquine used as an adjunct to corticosteroid therapy.
• Plaquenil can be used alone or with other drugs.
Corticosteroids suppress the immune system and reduce inflammation caused
by lupus.
-prednisone

12. DRUGS TO USE
Immunosuppressive drugs for patients whose kidneys and CNS is affected by lupus.
• Cytoxan – restrain the overactive immune system by blocking the production of immune
cells.
Other therapies include:
• Plasma exchange
• Intravenous immunoglobin
• Stem cell transplantation
• Immune therapy

13. PROGNOSIS
Usually chronic, relapsing, and unpredictable. Remissions may last for years.
If initial acute phase is controlled, even if very severe ( with cerebral thrombosis or
severe nephritis), the long-term prognosis is usually good.
The 10-yr survival in most developed countries is 95%. Improved prognosis is in part
due to earlier diagnosis and more effective therapies.
More severe disease requires more toxic therapies, which increase risk of mortality.

14. PATIENT EDUCATION
Minimize appearance of lesions.
Alleviate discomfort
Minimize fatigue.
 Maintain weight at optimal range
Teach the patient to recognize fever
and signs and symptoms of infection.
Maintain joint function and increase
muscle strength.
Recognize anaemia and develop a plan
of care
Minimize episodes of bleeding.
Minimize incidence of infection.
Educate the patient about
immunizations
Educate patient nutritional status.

15. REFERENCE
1. Kim, JM. (2014). Simultaneous presentation of acute disseminated encephalomyelitis
(ADEM) and systemic lupus erythematosus (SLE) after enteroviral infection: can ADEM
present as the first manifestation of SLE. Available:
http://www.ncbi.nlm.nih.gov/pubmed/25488421. Last accessed 16th Dec 2014.
2. Klinik für Kinder und Jugendmedizin. (2014). Pathogenesis and new therapeutic
approaches for systemic lupus erythematosus. Available:
http://www.ncbi.nlm.nih.gov/pubmed/25479933. Last accessed 16th Dec 2014.
3. Leal, GN. (2014). Subclinical right ventricle systolic dysfunction in childhood-onset systemic
lupus erythematosus: insights from two-dimensional speckle-tracking echocardiography.
Available: http://www.ncbi.nlm.nih.gov/pubmed/25492941. Last accessed 16th Dec 2014.

16. THANK YOU!!!