SLE

Question 1

What is the difference between Systemic Lupus Erythematosus (SLE) and Discoid Lupus Erythematosus (DLE)?

Answer 1

SLE
• progressive often severe autoimmune disease characterised by the presence of a large number of autoantibodies, which involves multiple body systems
• it is a chronic, relapsing and remitting illness characterised primarily by injury to the
o skin
o joints
o kidney
o serosal membranes

DLE
• A disease in which skin involvement dominates the clinical picture, usually without systemic disease

Question 2

Describe the “typical” SLE patient.

Answer 2

• F>M, 20-64yo
• Caucasian, Polynesian, African, Asian background
• Typically onset 20-40yo but can onset anywhere from childhood onwards

Question 3

Discuss the mechanism of tissue damage in SLE

Answer 3

Cellular damage in SLE is mediated by:
o immune complex mediated inflammation (via complement activation)
o direct action of autoantibodies on cells eg anti-RBC antibodies → anemia, anti-clotting factors → thrombocytopenia, etc)

• ANAs are not believed to be able to enter intact cells.

→ use examples of clinical pathology to explain Tx mechanism

e. g 1 immune complex deposition in small vessels, leads to inflammation, leads to vasculitis, leads to ischaemia (i.e. ischaemic tissue damage) of any tissue downstream.
e. g 2 immune complex deposition in glomerulus, leads to glomerulonephritis → tissue damage
e. g 3 immune complex deposition in basement membrane (point of attachment for epithelial cells) via small capillaries, activation of complement → inflammation of skin → external rash.

Question 4

Why is the clinical picture of SLE so varied/variable?

Answer 4

A multitude of tissues/organs may be affected → dependent on Pt (i.e. individual’s mix of auto-Ab’s) and degree to which each system is affected.

Also dependent on whether Dz is taking acute or chronic course

Question 5

List the main 6 (six) organs/tissues that are affected in SLE. Briefly discuss the pathology in each case.

Answer 5

Skin
o Immune complexes deposit in the basement membrane of the skin
o This results in complement activation and inflammation
o Sun exposed areas are especially affected

Pleura
o serositis

Heart
o	d/t inflammation from immune complex deposition
•	pericarditis   
•	myocarditis   
•	endocarditis

CNS
o Cerebral vasculitis and ensuing ischaemia occurs - but not to a significant degree.
o Antibody damage to the vascular endothelium results in proliferation which may be responsible for the CNS manifesting

Kidney
o due to immune complex deposition
o immune complex deposition results in glomerulonephritis

GIT
o Serositis → peritonium

Question 6

List the 6 (six) commonest early presenting symptoms of SLE.

Answer 6

Arthritis
Malar rash
Fever
Photosensitivity
Raynaud's phenomenon
Serositis

Question 7

List the 6 (six) commonest overall symptoms which are seen in SLE in the course of time.

Answer 7

Hematologic
Arthritis
Skin
Fever
Fatigue
Weight loss

Question 8

List 6 (six) laboratory investigations that could be employed in the diagnosis of SLE. In each case briefly explain the reasoning behind the test.

Answer 8

• ANA Fluorescent test (against DS DNA=Main test for Dz)
o Seen in 95% of SLE cases

• CRP↑ed
• ESR ↑ed
• Anemia
o Mild normochromic, normocytic anaemia.

• Leukopenia
• Thrombocytopenia

• Serum albumin↓ed
o Due to glomerular damage (glomerulonephritis) leading to incr. albumin leaching through

• Serum gamma globulin↑ed

• Complement ↓ed
o d/t consumption in active phases of Dz

Question 9

Write notes on the clinical course of SLE.

Answer 9

Variable & unpredictable

• Onset: can be
o Abrupt onset + fever
o Insidious

• Course
o Usually chronic
o Can be acute/progressive