What
causes AS ?
AS occurs
in people who carry certain genes and who
are exposed to a trigger, thought to be bacteria living in the gut.
The genetics
:
The B27
gene and other genes are needed for the development of AS. [However,
some people develop AS without the B27 gene i.e. in Kuwait and Lebanon
only 25% of people with AS have the B27 gene compared to 95% in Europe]
The
trigger:
Identical
twins both have disease 6 in 10 times. This means that getting AS is
not only due to genetics.
The trigger for AS is thought to be a bowel infection (often without
symptoms). Evidence for this comes from:
- Reiter's
Syndrome (which is related to AS) is triggered by a bowel / urinary
infection
- A rat
which develops AS, develops bowel inflammation and then develops AS.
If the rat is kept in a sterile environment it does not develop bowel
disease or arthritis.
- 50%
of people with AS who had an examination of their gut, had inflammation
of the bowel (without symptoms).
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What
are the main symptoms of AS ?
Back
pain and stiffness
Low back
pain which is felt deep in the buttock region. The back ache and stiffness
tends to worsen after prolonged inactivity (ie sleeping). It tends to
be eased by movement. The symptoms may worsen on exposure to cold and
dampness.
Chest
pain may result from inflammation in the upper spine. This means breathing
and expanding/moving the chest may become painful.
The neck
may be affected resulting in loss of mobility.
However,
loss of movement is often due to pain and muscle spasms. With adequate
drugs and physiotherapy a great deal of movement can be regained.
Tenderness/enthesitis
Inflamation
of the area where muscle inserts into the joint causes pain and tenderness.
Hip
and shoulder
1 in 4
people have inflammation in areas outside the spine. The hips are more
likely to become affected in people who developed symptoms of AS before
the age of 16. If hip disease has not occurred within the first 10 years
of experiencing the symptoms of AS it is unlikely to occur. About 6
in 100 people will go on to need a hip replacement. Shoulder involvement
is less common.
Hands/feet/knees
More women
than men develop AS in their hands and feet. People who experienced
symptoms in childhood may have more problems with their knees, ankles
and feet.
Non-bone
involvement
Inflammation
of the eye occurs in 40% of people with AS. This is iritis.
Inflammation
of the skin occurs in 16% of people with AS. This is psoriasis.
Inflammation
of the bowel occurs in 10% of people with AS. This is inflammatory bowel
disease.
Very rarely
the heart and lungs are affected.
Management
of AS using anti-inflammatories drugs
(NSAIDs) and exercise has been very effective for most people with AS.
However, successful new drugs are currently being developed and investigated
and understanding of AS is improving rapidly.
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What
is the natural course of AS ?
People
show very different levels of severity of AS. The course of the disease
is highly variable and there may be times of remission (ie no disease)
and flares particularly in early disease.
Of 51 Canadian
war veterans with ankylosing spondylitis followed from 1947-1980 (ie
33 years) the disease progressed to severe spinal restriction in 21
(41% or 2 in 5) people. Those people who progressed to severe disease
after 33 years had already got severe disease within the first 10 years
of symptoms. Those who did not develop severe disease did not have severe
X ray changes in the first 10 years. This means the severity of
disease can be predicted in the early years. A predictable pattern of
disease emerges within the first 10 years of disease.
Skeleton
change : The level of change to the bone in general progresses with
time. However, 10% of people show no progression after initial diagnosis
and in the majority of people progression is very slow.
The course
of AS is extremely variable. Some people show very mild disease and
others show very severe disease. It is though that some of this variation
may be due to genetic differences.
Predictors
of prognosis : Good function and the ability to work are maintained
in most people with AS, especially if the person can avoid heavy manual
work, prolonged standing and excessive jarring and twisting. The
people with early hip disease and early changes in the neck bones are
the ones most likely to be disabled by this condition. However,
hip replacement surgery has been very successful and can prevent a great
deal of disability.
It is difficult
to predict the prognosis for an individual but some general comments
are that the severity of the disease early on is a good predictor for
future development ie early fusion, hip disease, and wide spread involvement
predict severe disease in the future. Men have more severe spinal disease
(ie back and neck) than women. Smoking is associated with poor outcome
especially in people who also have psoriasis. People who are very fit
and active maintain better function and have less disease activity (ie
pain and fatigue) than those who do not exercise or have an active life
style.
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References
- Sieper
J, Braun J. New treatment strategies in AS: Proceeding of the Ankylosing
Spondylitis Workshop, Berlin Germany. 18-19 January 2002. Ann
Rheum Dis. 2002; 61(S111):iii1-iii2
- van
der Linden S et al. Evaluation of diagnostic criteria for ankylosing
spondylitis. A proposal for modification of the New York Criteria.
Arthritis Rheum 1984 27;361-8.
- Brewerton
D et al. Ankylosing spondylitis and HLA-27. Lancet 1973; 11: 904-907
- Khan
M. HLA-B27 and its subtypes in world populations. Curr Opinons in
Rheumatol. 1994; 7: 263-269
- Mielants
H et al. Subclinical involvement of the gut in undifferentiated spondyloarthrotpathies.
Clin Exp Rheumatol 1989; 7:499-504.
- Alharbi
S, et al. Association of the MHC class I with spondyloarthropathies
in Kuwait. Eur J Immunogenet 1996; 23(1): 67-70.
- Awada
H. et al. Weak assocations between HLA-B27 and the spondylarhtropathies
in Lebanon. Arthritis Rheum 1997; 40 (2): 388-389.
- Brown
MA, Kennedy LG, MacGregor AJ, Darke C, Duncan E, Shatford JL. Susceptiblity
to ankylosing spondylitis in twins: the role of genes, HLA, and the
environment. Arthritis Rheum 1997; 40: 1823-8.
- Muhammad
Khan. Ankylosing spondylitis : clinical aspects. Ed. Calin A and Tourog
J. The Spondylarthritides. 1998 Oxford University Press.
- Braun
J, Golder W, Bollow M, Sieper J, van der Heijde D. Imaging and scoring
in ankylosing spondylitis. Clin Exp Rheumatol 2002; 20
(Suppl. 28): S178-S184.
- Carette
S, Graham D, Little H, Rubenstein J, Rosen P. The natural disease
course of ankylosing spondylitisl. Arthritis Rheum 1983; 26(2): 186-90.
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