RA Symposia

Question 1

How do most therapies aim to work in RA?

Answer 1

Decrease macrophage cytokine production

Question 2

What is the major pathogenic subset in RA?

Answer 2

Th17

IL-17- known to activate synovial fibroblasts and osteoclasts, favours cartiliage resorption

Question 3

Role of B cells in RA

Answer 3

Autoantibodies usually present before onset of disease

Forms diffuse or follicular infiltrates

Question 4

What do cytokines do in RA?

Answer 4

• osteoclast differentiation and activation

- inhibits differentiation of osteoblasts

Question 5

Clinical markers of RA

Answer 5

Elevated ESR

Elevated CRP

Rheumatoid factor

Cyclic citrullinated peptide (CCP) antibodies

Question 6

Rheumatoid factor in RA

Answer 6

These are antibodies against Fc portions of other antibodies

present in 60-70% of pts with RA

not all RA have RF

but those with RF have more severe RA

Question 7

CCP antibody

Answer 7

60-70% of RA have anti-CCP +ve

high specificity of 98%

Anti-CCP +ve have more aggressive disease course

Question 8

Role of anti-CCP in pathogenesis of RA?

Answer 8

enhances inflammation if mild synovitis is already present

Question 9

Effect of smoking on RA

Answer 9

Some people with certain alleles have an increased risk of developing RA if they smoke

TCDD in smoke cigarette found to activate synovial fibroblasts

Question 10

Methotrexate

Answer 10

DMARD, Gold Standard therapy

• inhibits cell proliferation
• Induces apoptosis of activated CD4+ and CD8+ T-cells
• anti-inflammatory

Question 11

How is MTX administered?

Answer 11

Administered between 7.5 and 25mg weekly per os or s.c

“Anchor drug” in combination therapies

Question 12

Rituximab

Answer 12

B cell depleting agent

• complement mediated cytotoxicity
• antibody dependent cell mediated cytotoxicity
• apoptosis