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Reactive Psoriatic
Arthritis Arthritis
Ankylosing
Spondylitits
Enteropathic Enthesitis-
Arthritis Related JIA
Clinical Features 1
Clinical features
AS common to all
seronegative
spondarthritis
1) Familial aggregation.
2) Seronegative RF.
3) Asymmetrical inflammatory
oligoarthritis (lower>upper limbs) &
PsA episodic.
4) Inflammatory sacroiliitis &
ReA
spondylitis.
5) Inflammatory Enthesitis.
6) Absence of nodules & other extra
articular features of RA.
Enteropathic
Arthritis
Spondarthritis & HLA-B27
Approximate
Disease prevalence
of HLA-B27
Ankylosing spondylitis (AS) 90 %
HLA-B27 is an
Reactive arthritis (ReA) 40-80% HLA Class I
molecule
Juvenile spondyloarthropathy 70% found in 8% of
healthy white
Enteropathic spondyloarthropathy 35-75% Caucasians
Psoriatic arthritis 40-50%
Epidemiology
• Ranges from 1-6% across different populations.
• The peak onset is in the 2nd &3rd decades.
• Male to female ratio is 3:1.
Etiology
Genetic
• Human leukocyte antigen (HLA)-B27 is a strong
genetic risk factor for .
• 90% persons of affected persons in Europe are
HLA B 27+ve.
Environmental
• Infective triggers have not clearly been linked to
cause AS.
• Increased fecal carriage of Klebsiella aerogenes
was found in AS.
Etiology
Immunological:
• TNF alpha, interferon gamma and IL-6, 17 & 23 play a
role in pathogenesis of AS
• Their role is not fully understood yet.
• Abnormal IL-23 and its receptor (IL-23R) was detected
in AS patients.
• Higher serum levels of IL-6 were demonstrated in
patients with active AS.
Role of HLA B27 in Pathogenesis
4 Theories:
• The arthritogenic peptide hypothesis: HLA-B27
binds a unique set of antigenic peptides, bacterial or
self activate cytotoxic T-cell arthritis
• Self-association of the HLA-B27 molecule: HLA-B27
binds to itself homodimers intracellular stress
activation of immune system
• Alteration of intracellular handling of microbes due
to HLA-B27: e.g.; Salmonella cytokines
• Recognition of HLA-B27 as an autoantigen: HLA-B27
presented by APC to T-helper lymphocyte
Role of HLA-B27
Dactylitis
Clinical Features 5
Early physical signs include:
Time (years)
Investigations
1. ESR & CRP are usually raised.
2. S.alkaline phosphatase is raised in 50%
3. RF, ANA, ACPA is –ve.
4. IgA levels are usually elevated.
5. Radiographic signs:
i. Sacroiliitis is the 1st abnormality: starts in lower synovial
parts of the joints.
ii. Anterior squaring of the vertebrae in lateral views of
thoracolumbar spine.
iii. Bridging syndesmophytes.
iv. Ossification at antero-longitudinal ligament with
bamboo spine formation.
v. Osteoporosis & atlanto-axial dislocation can occur.
Imaging 1
Imaging 2
Imaging 3
Imaging 4
Imaging 5
Imaging 6
Shiny corner sign (Romanus lesion)
Inflammatory
vertebral entheses
result in sclerosis of
superior and inferior
margins of the
vertebral bodies.
Dagger sign
Dense line
caused by
ossification of
supraspinous
and interspinous
ligaments in AS.
Management
The aim is to relieve pain & stiffness while
maintaining skeletal mobility & avoiding
deformity.
Education & appropriate physical activity are
the corner stones of management.
Regular daily chest and back extension
exercises
Swimming, yoga and deep breathing exercises
Baseline ROM exercises
Management
• NSAIDs (especially indomethacin) for
symptoms especially stiffness but they do not
alter the natural course of the disease.
• Pain management by heat, massage.
• Excessive physical exertion, flexion and heavy
lifting should be avoided.
• Proper positioning at rest.
• Avoid poor bed & chair posture.
• The mattress should be firm at sleep, pillows
should be avoided.
Management
Sulfasalazine with /without Methotrexate may
be effective for peripheral joints synovitis but
not useful for axial disease.
Local steroid injection for planter fasciitis &
enthesopathy.
Oral steroid for anterior uveitis.
Biologic agents (TNF alpha blockers):
Etanercept.
Infliximab.
Adalimumab.
BEST CLINICAL PRACTICE GUIDELINES FOR THE USE OF
ANTI–TUMOR NECROSIS FACTOR AGENTS IN
ANKYLOSING SPONDYLITIS:
Clinical presentation and extra-articular features
Peripheral
Enthesitis
Axial arthritis
(excluding hip)
• In contrast to RA,
pregnancy does not
improve the
symptoms of AS.
• In the majority of
patients disease
activity is not
substantially altered
during pregnancy.
REACTIVE ARTHRITIS
Reactive arthritis
• Reactive arthritis is an acute aseptic arthritis
that develops in response to an extra –
articular infection ,typically originating from
gastrointestinal or genitourinary tract.
• It is a seronegative spondyloathropathy
classically presenting with asymmetrical
oligoarthritis, usually in the lower limbs.
Pathophysiology
• Aortic Incompetence.
• Conductive Defect.
• Pleuro-pericarditis.
• Peripheral Neuropathy.
• Seizures.
• Amyloidosis.
ReA, Investigations
• ESR and CRP are raised.
• RF and ANA are negative.
• Normochromic normocytic anaemia.
• Sterile and inflammatory synovitis.
• Stool culture.
• Urine culture.
• Urethral culture.
• High vaginal swab.
• Radiological, the most important findings are:
– Fluffy calcaneal spur.
– Asymmetrical and unilateral sacroiliac joint involvement.
ReA, Treatment
• NSAIDS.
• Local and intra-articular steroid injection.
• Topical and systemic steroids for anterior
uveitis.
• Sulfasalazine and Methotrexate are used in
persistent chronic symptoms or recurrent
arthritis and in severe keratoderma
blennorrhagica.
• Antibiotics for infections.
• Anti-TNF-a therapy.
ReA, Prognosis
• The first attack of arthritis is self-limiting with
spontaneous remission within 2-4/12 of onset,
representing (60%) of patients.
• 15% of patients of ReA relapse.
• 15% of patients of ReA continue to a chronic
state.
• 10% of patients develop ankylosing
spondylitis.
• Mortality in ReA results from cardiac
complications and amyloidosis.