systemic lupus erythematous

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!!!