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DANGE .SAMIRA. S.
ROLL NO: 18
MSC 1
HISTORY
 Hippocrates (400 B.C) first described
cutaneous ulcers.
 Ferdinand Von Hebra (1816-1880) first
used the term ‘Lupus’.
 Moriz Kaposi (1837-1902) first recognized
Lupus as a systemic disease.
EPIDEMIOLOGY
Women are affected nine times
more frequently than men (9:1)
regardless of race.
SLE has nearly tripled in the last
50 years due to improved diagnosis
of the chronic disease.
 Asian, African and Latin natives
are affected much more frequently
than Caucasians.
ETIOLOGY
Mostly SLE is Idiopathic but there are some predisposing factors:
DRUG-INDUCED LUPUS:
SLE caused by taking
certain prescriptions.
 The most common
culprits are Hydralazine,
Isoniazid, etc.
GENETIC PREDISPOSITION:
 Susceptibility Genes.
The rate of SLE is seen
more in Monozygotic
twins than dizygotic
twins.
Hyper estrogenic.
ENVIRONMENTAL FACTORS:
Photosensitivity.
Air pollution,
cigarette smoking,
vaccines, epigenetic
modifications etc.
SLE is characterized by phases of remission and relapse.
At least 4 of the 11 clinical criteria are usually met for diagnosis given by the
American College of Rheumatology.
The diagnostic criteria:
PATHOPHYSIOLOGY
SLE is an Autoimmune Disease, so it is mediated by Autoimmune Reactions:-
•Type III Hypersensitivity:
Antigen-Antibody complex formation and disposition in tissues thus causing
inflammation.
•Type II Hypersensitivity:
Antibodies against Red and white blood cells and molecules like various phospholipids
which can cause phagocytosis and destruction leading to additional symptoms.
IgG and IgM antibodies attacks self antigens on cells.
SUSCEPTIBILITY
GENES
Diagnosis of SLE must be based on Clinical
features and Antibodies Lab Test.
•HISTORY
•PHYSICAL EXAMINATION
•LABORATORY TEST
HISTORY: Family history related to SLE disease.
P.Examination: Fever, rashes on body, butterfly rash
on face, ulcer in mouth etc.
Laboratory Tests: ANA TEST, LE CELL TEST, CBC,
LFT, RFT, BIOSPY, ESR, ANTI DNA, ANTI
HISTONE, ANTI SMITH etc.
TREATMENT AND PREVENTION:
• SLE treatment with antimalarials is recommended unless there are no
contraindications thus Hydroxychloroquine and chloroquine are licensed
for SLE treatment.
• Glucocorticoids are the local treatment of choice for skin lesions in SLE.
• The FDA approved Belimumab in 2011, the first new drug for SLE in 50
years.
TREATMENT
• Preventing exposure to ultraviolet (UV) light.
• Cigarette smoking cessation.
• Prevent working in crystalline silica work environment (e.g.,
cleaning powders, soil, pottery materials, cement, etc.)
• Moderate alcohol drinking can be effective for SLE.
PREVENTION
REFERENCES
1. George Bertsias, Ricard Cervera, Dimitrios T Boumpas :
“Systemic Lupus Eythematous : Pathogenesis & Clinical
features.” 2010; pp 477.
2. Ghaussy No, Sibbitt WL, Qualls CR (2009). “ Cigarette
smoking, alcohol consumption, and the risk of Systemic
Lupus Erythematous: a case control study”. J. Rheumatol.
28 (11): 2499-53.
3. Kaposi KM. Neue Beitrage Zur Kenntnis des Lupus
Erythematous . Arch Dermatol Syphilis. 1872; 4:36-78.
4. Kuhn A, Aberer E, Bardec. Leitlinien Kutaner Lupus
Erythematous; 2009. PP. 214-257.
5. Ruiz-G, Khamashta MA,. Hydroxychloroquine: the
cornerstone of Lupus therapy. Lupus. 2008; 17: 271-273.
SYSTEMIC LUPUS ERYTHEMATOSUS

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SYSTEMIC LUPUS ERYTHEMATOSUS

  • 1. DANGE .SAMIRA. S. ROLL NO: 18 MSC 1
  • 2.
  • 3. HISTORY  Hippocrates (400 B.C) first described cutaneous ulcers.  Ferdinand Von Hebra (1816-1880) first used the term ‘Lupus’.  Moriz Kaposi (1837-1902) first recognized Lupus as a systemic disease.
  • 4. EPIDEMIOLOGY Women are affected nine times more frequently than men (9:1) regardless of race. SLE has nearly tripled in the last 50 years due to improved diagnosis of the chronic disease.  Asian, African and Latin natives are affected much more frequently than Caucasians.
  • 5. ETIOLOGY Mostly SLE is Idiopathic but there are some predisposing factors: DRUG-INDUCED LUPUS: SLE caused by taking certain prescriptions.  The most common culprits are Hydralazine, Isoniazid, etc. GENETIC PREDISPOSITION:  Susceptibility Genes. The rate of SLE is seen more in Monozygotic twins than dizygotic twins. Hyper estrogenic. ENVIRONMENTAL FACTORS: Photosensitivity. Air pollution, cigarette smoking, vaccines, epigenetic modifications etc.
  • 6. SLE is characterized by phases of remission and relapse. At least 4 of the 11 clinical criteria are usually met for diagnosis given by the American College of Rheumatology. The diagnostic criteria:
  • 7. PATHOPHYSIOLOGY SLE is an Autoimmune Disease, so it is mediated by Autoimmune Reactions:- •Type III Hypersensitivity: Antigen-Antibody complex formation and disposition in tissues thus causing inflammation. •Type II Hypersensitivity: Antibodies against Red and white blood cells and molecules like various phospholipids which can cause phagocytosis and destruction leading to additional symptoms. IgG and IgM antibodies attacks self antigens on cells.
  • 9.
  • 10. Diagnosis of SLE must be based on Clinical features and Antibodies Lab Test. •HISTORY •PHYSICAL EXAMINATION •LABORATORY TEST HISTORY: Family history related to SLE disease. P.Examination: Fever, rashes on body, butterfly rash on face, ulcer in mouth etc. Laboratory Tests: ANA TEST, LE CELL TEST, CBC, LFT, RFT, BIOSPY, ESR, ANTI DNA, ANTI HISTONE, ANTI SMITH etc.
  • 11. TREATMENT AND PREVENTION: • SLE treatment with antimalarials is recommended unless there are no contraindications thus Hydroxychloroquine and chloroquine are licensed for SLE treatment. • Glucocorticoids are the local treatment of choice for skin lesions in SLE. • The FDA approved Belimumab in 2011, the first new drug for SLE in 50 years. TREATMENT
  • 12. • Preventing exposure to ultraviolet (UV) light. • Cigarette smoking cessation. • Prevent working in crystalline silica work environment (e.g., cleaning powders, soil, pottery materials, cement, etc.) • Moderate alcohol drinking can be effective for SLE. PREVENTION
  • 13. REFERENCES 1. George Bertsias, Ricard Cervera, Dimitrios T Boumpas : “Systemic Lupus Eythematous : Pathogenesis & Clinical features.” 2010; pp 477. 2. Ghaussy No, Sibbitt WL, Qualls CR (2009). “ Cigarette smoking, alcohol consumption, and the risk of Systemic Lupus Erythematous: a case control study”. J. Rheumatol. 28 (11): 2499-53. 3. Kaposi KM. Neue Beitrage Zur Kenntnis des Lupus Erythematous . Arch Dermatol Syphilis. 1872; 4:36-78. 4. Kuhn A, Aberer E, Bardec. Leitlinien Kutaner Lupus Erythematous; 2009. PP. 214-257. 5. Ruiz-G, Khamashta MA,. Hydroxychloroquine: the cornerstone of Lupus therapy. Lupus. 2008; 17: 271-273.