1. doc.MUDr. Želmíra Macejová, PhD III. Internal clinic LF UPJŠ
Rheumatoid arthritis
doc.MUDr. Želmíra Macejová, PhD
III. Internal clinic LF UPJŠ

2. Rheumatoid arthritis Chronic systemic disease Prevalence 1%
More common in women, women: men 3:1
autoimuniy disease- production of rheumatoid factor – antibody agains human IgG
synovitis, deformity, destraction, instability, subluxatio
symetrical involvement of periferial joints
possibility of involvement of all joints in the body

3. Chronical disease
Clinical features: general:
Fatigue, general malaise, subfebrility, weight loss, depression
local:
arthralgia, myalgia, morning stiffness, joint pain,
Pain is the worst in the morning: PIP, MCP, wrist, MTP - symmetrical

4. Pathogenesis of RA unknown Multifactorial:
genetic: associátion with specific type of HLA (HLA DR-4)
pro-inflammatory cytokines:
TNF alfa, IL-17, IL-1, IL-6
hormonal factors: prolactine, lack of testosterone

6. Clinical features
pain and stiffness in the small joints of the hand and feet, chronic bilateral symmetrical peripherial polyarthritis
involvement of all joints in the body: knees, wrists, elbows, etc.
Symptoms:
Joint pain
Morning stiffness: several hours (more than one hour)
General symptoms: fatigue, general malaise
Disability
Non-articular symptoms

7. Sings
Swelling
Warmth
Tenderness
Deformities
Nodules
Involvement of joints is symmetrical

9. Diagnostic criteria of RA
1. Morning stiffness (more than 1 hour)
2. Arthritis of three and more joints
3. Arthritis of hand joints (PIP, MCP, wrist)
4. Symetrical arthritis
5. Rheumatoid nodules
6. Rheumatoid facktor
7. X-ray changes

10. Laboratory findings RF ( Latex, ELISA) – seropositivity : anaemia
trombocytosis
CRP, ESR
gamaglobulins, alfa2globulins
Synovial fluid: aseptic

12. Steinbrocker – X-ray classification
I.st: periartikular osteoporosis
II.st: destruction, loss of joint space, erosions, cysts
III. st.: + subluxation
IV. st.: ankylosis

13. Treatment
NSA
DMARDs
Biologic treatment

14. NSA Fosfolipidy cell membranes fosfolipase inhibition by
corticosteroids
Arachidonic acid
cyklooxygenase inhibition by NSA
Endoperoxids
tromboxane B PGE PG2F prostacykline

15. NSA Cyklooxigenase: NSA clasification
COX-1 :
fyziological effect (stomach, colon, kidney, Trc)
COX-2:
inflammation
NSA clasification
I. Inhibition of both isoforms: COX-1 a COX-2
II. Most inhibition of COX-2
III. Selective inhibition of COX-2

16. DMARDs: disease modifying antirheumatic drugs
Antimalarics
Methotrexate
Sulfasalazine
Gold
Leflunomide
Imunosupressive drugs: cyklosporine
cyklofosfamide

17. Most common combination: metotrexate +sulfasalazine
DMARDs: combination
Most common combination:
metotrexate +sulfasalazine
metotrexate+antimalarics
metotrexate+cyklosporine
Possible combination: NSA, DMARDs, corticosteroids
synergic effect
lower doses
less AE
remission of disease

18. Corticosteroid drugs p.o. Rapid effect i.a.
i.m.
i.v.
lokálne
Rapid effect
Strong antiinflammatory effect
Analgetic effekt
AE, SAE !!

19. Biological treatment Rapid effect Strong effect AE: Activation of TBC
Anticytokine treatment
Anti - TNF alfa: infliximab,adalimumab,etanercept
Anti - IL-1: anakinra
Anti - CD20 B-lymfocyt: rituximab
Many others on clinical trials
Rapid effect
Strong effect
AE:
Activation of TBC