SYSTEMIC LUPUS ERYTHEMATOSUS Shreya Roy

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TO BEGIN WITH: TABLE OF CONTENTS.
Introduction
Aetiology
Types
Pathogenesis
Manifestation
Diagnosis
Treatment
Prognosis
References
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INTRODUCTION
The name: Systemic lupus erythematosus.
Systemic lupus erythematosus (SLE) is the prototypic multisystem autoimmune disorder
with a broad spectrum of clinical presentations encompassing almost all organs and
tissues.
The signs and symptoms of SLE vary among affected individuals, and can involve
many organs and systems, including the skin, joints, kidneys, lungs, central nervous
system, and blood-forming (hematopoietic) system.
The extreme heterogeneity of the disease has led some investigators to propose that
SLE represents a syndrome rather than a single disease.

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AETIOLOGY
The causes of SLE are unknown but are believed to be linked to environmental,
genetic, and hormonal factors.
SLE Incidence and Prevalence:
SLE is relatively uncommon and not a reportable disease, so it is relatively expensive
to capture all diagnosed cases reliably for epidemiologic studies.
National incidence data are difficult to obtain because it is relatively expensive to
capture all diagnosed cases reliably and the year of onset is hard to determine
(slowly developing, non-specific symptoms and signs), so resource-intense studies must
be done in small areas.

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TYPES OF LUPUS:
Discoid (Cutaneous)

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TYPES OF LUPUS: (CONTD..)
Drug-induced Lupus Neonatal Lupus

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PATHOGENESIS: KEY EVENTS:
Increased amounts of apoptosis-related endogenous nucleic acids stimulate the
production of IFNα and promote autoimmunity by breaking self-tolerance through
activation of antigen-presenting cells. Once initiated, immune reactants such as
immune complexes amplify and sustain the inflammatory response.
In healthy individuals, immune complexes are cleared by Fc and complement
receptors; failure to clear immune complexes results in tissue deposition and tissue
injury at sites.
Tissue damage is mediated by recruitment of inflammatory cells, reactive oxygen
intermediates, production of inflammatory cytokines, and modulation of the
coagulation cascade.

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MANIFESTATION:11 SIGNS OF LUPUS
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 THE 11 SIGNS: LISTED
Butterfly-shaped rash
Patches of inflamed skin
Photosensitivity
Oral ulcers
Rheumatoid Arthritis
Pleuritis
Seizures
Raynaud’s phenomenon
Kidney damage (Nephritis)
Presence of ANAs in the blood
Low blood cell counts

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DIAGNOSIS:
Serological tests
Prognostic markers and the role of autoantibodies
Diagnosis: typical and atypical presentations

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TREATMENT:
There is no cure for Lupus, it can only be treated, i.e., its symptoms can be controlled
under severe conditions.
Use of non-steroidal anti-inflammatory drugs.
Use of sunblock, with a SPF of more than 30, to reduce photosensitivity.

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PROGNOSIS:
Although current treatment of lupus has improved survival dramatically, prolonged
and complete remission— defined as 5 years without clinical and laboratory
evidence of active disease and on no treatment-has remained elusive for most
patients.
The incidence of flare is estimated to 0.65 per patient-year of follow-up. Moreover,
a significant number of patients do not respond adequately to immunosuppressive
therapies.

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REFERENCES:
Systemic Lupus Erythematosus: Pathogenesis and Clinical Features
George Bertsias, Ricard Cervera, Dimitrios T Boumpas : Eular.
www.lupusuk.org.uk/medical/gp-guide/introduction-to-lupus/epidemiology-of-
lupus/
 https://lupuslinkmn.org/types-of-lupus/

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THANK YOU.

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