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E Guidelines A-Z Index A B C D E F G H I J K L M N O P Q R S T U V W X Y Z
Entitlement Eligibility GuidelinesAnkylosing Spondylitis
DefinitionAnkylosing Spondylitis is a chronic, progressive, inflammatory disease of unknown etiology. It mainly involves the sacroiliac joints, and the axial skeleton. It may also involve peripheral joints and extra-articular structures. Extraarticular manifestations include the following:
Ankylosing Spondylitis is also known as Marie-Strumpell Disease, or Bechterew's Disease. Diagnostic StandardDiagnosis by a qualified medical practitioner is required, including copies of relevant test reports and other supporting documentation. Although no laboratory test is specific for, or diagnostic of, Ankylosing Spondylitis, investigations are necessary as the diagnosis cannot be made on clinical grounds alone. X-ray findings usually demonstrate sacroiliitis. The changes seen on x-ray begin with blurring of the cortical margins of the subchondral bone, followed by bone erosions, and eventually by sclerosis. The HLA-B27 gene is found in approximately 90% of persons with Ankylosing Spondylitis. Elevated erythrocyte sedimentation rate (ESR) and an elevated level of C-reactive protein, both of which are not specific for Ankylosing Spondylitis, are often present when the disease is active. Individuals with severe disease may have elevated serum alkaline phosphatase. Rheumatoid factor and antinuclear antibodies are negative unless coexistent disease is present. When Ankylosing Spondylitis results in restricted chest wall motion, pulmonary function studies show decreased vital capacity and increased functional residual capacity. Anatomy and PhysiologyAnkylosing Spondylitis has distinct pathological changes at the enthesis, i.e. the area in which a ligament or joint capsule attaches to bone. The inflammatory component of this disease causes bony erosions at the enthesis. The body seeks to repair these erosions, and this repair activity results in ossification at these sites. It is this inflammation-repair process that is the basis for many of the findings in Ankylosing Spondylitis. Ankylosing Spondylitis is usually diagnosed during the second to fourth decade of life. It is more common in first degree relatives of those with Ankylosing Spondylitis. While a strong affiliation with the HLA-B27 antigen supports a genetic predisposition, the evidence suggests that other factors also play a role in susceptibility to Ankylosing Spondylitis. The HLA-B27 antigen is a generic maker found in 8% of North Americans of European (white) heritage. Of those who are HLA-B27 positive, the actual risk of developing Ankylosing Spondylitis is estimated to be 1 to 2 %. Only 20% of HLA-B27 positive first degree relatives of individuals with Ankylosing Spondylitis and who are positive for HLA-B27 will develop the disease. Clinical FeaturesAnkylosing Spondylitis is a progressive disorder, characterized by alternating flare-ups of active spondylitis and periods of inactive inflammation. Occasionally, the course is severe and unremitting. The most frequent presenting complaint is recurrent low back pain which has persisted more than 3 months. It is often nocturnal in nature. Individuals will develop early morning lumbar spine stiffness, which is typically relieved by activity. The hallmark of Ankylosing Spondylitis is sacroiliitis; it is often bilateral. Sacroiliitis develops early in the progression of the disease but, although symptomatic, changes may not become evident on x-ray for 7 to 10 years. Spinal deformities related to Ankylosing Spondylitis may evolve for up to 10 years. They result in marked immobility and, subsequently, generalized osteoporosis. In extreme cases the entire spine may become fused in a forward flexed position. Untreated persons may develop kyphosis due to the flexed posture assumed because of pain. Spinal stiffening may produce the characteristic manner of body movement, where the torso is moved as one block. Decreased chest expansion (< 4cm) may result as the axial skeleton becomes involved. The chest restriction results in a restrictive lung disease. This does not include asthma, as a restrictive lung disease is due to an abnormality of the chest wall which limits expiratory and inspiratory movements. In some cases, Ankylosing Spondylitis also involves the peripheral joints. This involvement is typically asymmetric and usually affects the large joints of the lower limbs. Peripheral joint disease may be readily apparent from the onset and, in some cases, may dominate the clinical picture. Approximately one-third of those with Ankylosing Spondylitis also develop systemic manifestations, of which uveitis is most common. Pension Considerations
References for Ankylosing Spondylitis
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