This document provides an overview of systemic lupus erythematosus (SLE). It defines SLE as a chronic autoimmune disease where the immune system attacks its own tissues. Common symptoms include issues affecting the skin, joints, kidneys, brain and other organs. It discusses genetic, environmental, immunological and hormonal factors that can contribute to SLE. The document also outlines several autoantibodies associated with SLE, potential pathophysiological mechanisms, common drug treatments including antimalarials, NSAIDs, DMARDS and corticosteroids, and their mechanisms of action. It concludes by discussing hopes for more targeted biologic therapies in the future to better treat SLE.

1. SYSTEMIC LUPUS ERYTHEMATOSUS
(SLE)
BY
ANKUSH BISWAS
M.PHARM, 1ST YEAR, 2ND SEMESTER
ROLL NO - 19320217007

2. CONTENTS
 INTRODUCTION
 SLE SYMPTOMS
 FACTORS AFFECTED TO SYSTEMIC LUPUS ERYTHEMATOSUS
 AUTOANTIBODIES IN SLE
 PATHOPHYSIOLOGY OF DISEASE
 DRUGS USED IN SLE
 MOA OF SLE DRUGS
 FUTURE PERSPECTIVE
 REFERENCES

3. INTRODUCTION
 SLE:
Systemic lupus erythematosus (SLE)
is a chronic multisystem autoimmune
inflammatory disease. In this disease,
the body's immune system mistakenly
attacks it’s own tissue. It can affect the
skin, joints, kidneys, brain, and other
organs.
 Ages affected:

4. SLE Symptoms

5. Factors affected to systemic lupus
erythematosus
a) Genetic factors
b) Environmental factors
c) Immunologic factors
d) Hormonal factors

6. Autoantibody specificity Prevalence(%)
ANA 98
Anti dsDNA 70
Anti-Sm 25
Anti-RNP 40
Anti-Ro(SS-A) 30
Anti-La(SS-B) 10
Nucleosome 50-90
PL 30-40
Autoantibodies in SLE

7. PATHOPHYSIOLOGY OF SLE

9. Drugs used in SLE
a) Antimalarials - Hydroxychloroquine sulfate (Plaquenil)
b) NSAIDs - Ibuprofen (Advil, Motrin), Naproxen (Aleve,
Anaprox, Naprosyn)
c) DMARDS, Immunomodulators – Cyclophosphamide,
Methotrexate (Otrexup, Rasuvo)
d) Rheumatologics - Belimumab (Benlysta)
e) Corticosteroids - Methylprednisolone (A-Methapred,
Medrol, Solu-Medrol, Depo-Medrol)

10. MOA of SLE drugs:
• Antimalarials:
1) Hydroxychloroquine sulfate (Plaquenil):
Hydroxychloroquine inhibits chemotaxis of eosinophils and locomotion of
neutrophils and impairs complement-dependent antigen-antibody reactions.
• NSAIDs:
1) Ibuprofen (Advil, Motrin):
Ibuprofen is the drug of choice for patients with mild to moderate pain. It inhibits
inflammatory reactions and pain by decreasing prostaglandin synthesis.
2) Naproxen (Aleve, Anaprox, Naprosyn):
Naproxen is used for relief of mild to moderate pain. It inhibits inflammatory
reactions and pain by decreasing activity of the enzyme cyclooxygenase,
resulting in prostaglandin synthesis.
• DMARDS, Immunomodulators:
1) Cyclophosphamide:

11. Cyclophosphamide is used for immunosuppression in cases of serious SLE
organ involvement, especially severe CNS involvement, vasculitis, and lupus
nephritis.
• Rheumatologics:
1. Belimumab (Benlysta):
Belimumab inhibits the biologic activity of B-lymphocyte stimulator (BLyS); BLyS
is a naturally occurring protein required for survival and for development of B-
lymphocyte cells into mature plasma B cells that produce antibodies. In
autoimmune diseases, elevated BLyS levels are thought to contribute to
production of autoantibodies.
• Corticosteroids:
1) Methylprednisolone (A-Methapred, Medrol, Solu-Medrol, Depo-Medrol)
Methylprednisolone is used for acute organ-threatening exacerbations. It
decreases inflammation by suppressing migration of polymorphonuclear
leukocytes and reversing increased capillary permeability.

12. Future Perspective
Although a decade behind the use of biologic drugs in the treatment of
rheumatoid arthritis, there is a realistic expectation that the next decade
will see the widespread acceptance of the use of these drugs in the
treatment of SLE. It will require the optimization of clinical trials to
demonstrate benefit; the recognition that a variety of particular targeted
approaches will be needed to 'capture' the diversity of clinical features in
SLE and a willingness on the part of individual countries/players to cover
the cost of the biologic approaches. With these caveats we eagerly
anticipate a genuine 'new age of therapy' for patients with SLE, in
particular for those who fail to respond adequately to conventional
immunosuppression.

13. REFERENCES
• Tan EM, Cohen AS, Fries JF, et al. The 1982 revised criteria for the classification
of systemic lupus erythematosus. Arthritis Rheum. 1982;25:1271-1277.
• Hochberg MC. Updating the American College of Rheumatology revised criteria
for the classification of systemic lupus erythematosus [letter]. Arthritis Rheum.
1997;40:1725.
• Arbuckle MR, McClain MT, Rubertome MV, et al. Development of autoantibodies
before the clinical onset of systemic lupus erythematosus. N Engl J Med.
2003;349:1526-1533.
• Sestak AL, Fϋrnrohr BG, Harley JB, Merrill JT, Namjou B. The genetics of
systemic lupus erythematosus and implications for targeted therapy. Ann Rheum
Dis. 2011;70(suppl 1):i37-43. doi: 10.1136/ard138057.
• Bernatsky S, Boivin JF, Joseph L, et al. Mortality in systemic lupus
erythematosus. Arthritis Rheum. 2006;54:2550-2557.

14. THANK YOU