Ankylosing Spondylitis
Ankylosing Spondylitis is a form of arthritis. Ankylosing Spondylitis (AS) affects certain joints of the spine, which become inflamed, stiffen, become rigid, and then fuse together. If confined to the lower back, AS will cause virtually no limitation of movement. In some cases, however, the entire spine may become rigid and bent. If the joints between the ribs and spine are affected, it will cause severe breathing problems due to limited expansion of the chest wall. Postural deformities are common. Currently 318,000 Americans are afflicted; two and a half times as many men as women have AS.
Essentials of Diagnosis
Chronic low backache in young adults
Progressive limitation of back motion and of chest expansion
Transient (50%) or permanent (25%) peripheral joint involvement indistinguishable from peripheral rheumatoid arthritis
Diagnostic x-ray changes in sacroiliac joints
Uveitis in 20 - 25%
Accelerated erythrocyte sedimentation rate and negative serologic test for rheumatoid factor
HLA-B27 usually positive
General Considerations
Ankylosing spondylitis is a chronic inflammatory disease of the joints of the axial skeleton, manifested clinically by pain and progressive stiffening of the spine. While the synovitis of ankylosing spondylitis is histologically identical with peripheral rheumatoid arthritis, certain features tend to distinguish this disease from rheumatoid arthritis: its preponderance among males; age at onset (usually in late teens or early 20's); the relatively high incidence of uveitis; a pathologically distinctive lesion of the aorta; and absence of rheumatoid factor. In addition to the synovitis, a second pathologic feature of ankylosing spondylitis is reactive periostitis. The annulus fibrosus may gradually ossify, with fusion of vertebral bodies.
Clinical Findings
A. Symtoms and Signs
The onset is usually gradual, with intermittent bouts of back pain radiating down the thighs. As the disease advances, symptoms progress in a cephalad direction and back motion becomes limited, with the normal lumbar curve flattened and the thoracic curvature exaggerated. Atrophy of the trunk muscles is common. Chest expansion is often limited as a consequence of costovertebral joint involvement. Radicular symptoms may occur. Cauda equina syndrome may occur years after onset of the disease and is due to fibrosis of the nerves without bony impingement. In advanced cases, the entire spine becomes fused, allowing no motion in any direction. Transient acute arthritis of the peripheral joints occurs in about 50% of cases, and permanent changes in the peripheral joints - most commonly the hips, shoulders and knees - are seen in about 25%.
When it occurs in childhood, ankylosing spondylitis may, at its onset, mimic pauciarticular juvenile rheumatoid arthritis.
Spondylitic heart disease, characterized chiefly by atrioventricular conduction defects and aortic insufficiency, occurs in 3 - 5% of patients with longstanding severe disease. Amyloidosis may also occur in patients with chronic disease. Nongranulomatous anterior uveitis is associated in as many as 25% of cases and may be a presenting feature. Pulmonary fibrosis of the upper lobe, with progression to cavitation and brochiectasis, may occur, characteristically long after the onset of skeletal symptoms. Constitutional symptoms similar to those of rheumatoid arthritis are absent in most patients.
B. Laboratory Findings
The erthrocyte sedimentation rate is accelerated in 85% of cases, but serologic tests for rheumatoid factor are characteristically negative. There may be leukocytosis and anemia.
HLA-B27 is found in 80 - 90% of patients with ankylosing spondylitis, as opposed to 6 - 8% among normal individuals. These figures must be modified in different racial groups. Although the cellular membrane antigens determined by the major histocompatibility locus in humans (HLA system) are found with greater than normal frequency in some other diseases, the most striking association is between ankylosing spondylitis, Reiter's syndrome, and the sacroiliitis and spondylitis associated with psoriasis and inflammatory bowel disease. Because of the noted incidence of this antigen in the normal population, its use as a diagnostic test is limited.
Persons with other rheumatic diseases such as rheumatoid arthritis, degenerative joint disease (osteoarthritis), and gout do not show a higher than normal incidence of HLA-B27.
C. X-Ray Findings
Early in the course of ankylosing spondylitis, x-ray shows erosion and sclerosis of the sacroiliac joints; later, involvement of the apophyseal joints of the spine, ossification of the annulus fibrosus, calcification of the anterior and lateral spinal ligaments, and squaring and generalized demineralization of the vertebral bodies may occur. The term "bamboo spine" has been used to describe the late radiographic changes.
Additional x-ray findings include periosteal new bone formation on the iliac crest, ischial tuberosities and calcanei, and alterations of the symphysis pubica and sternomanubrial joint similar to those of the sacroiliacs. Radiologic changes in peripheral joints, when present may be differentiated from rheumatoid arthritis by their asymmetry, relative lack of demineralization, smaller erosions and marginal periostitis.
Differential Diagnosis
Although rheumatoid arthritis may ultimately involve the spine, it does so characteristically in the cervical region, usually sparing the sacroiliac joint. Other features differentiating ankylosing spondylitis from rheumatoid arthritis are the rare involvement of the small joints of the hands and feet, the absence of subcutaneous nodules, and the negative serologic tests for rheumatoid factor in spondylotis. The history and physical findings of ankylosing spondylitis serve to distinguish this disorder from other causes of low back pain such as degenerative disc disease, degenerative joint disease, osteoporosis, soft tissue trauma and tumors. The single most valuable distinguishing radiologic sign of ankylosing spondylitis is the appearance of the sacroiliac joints, although a similar pattern may be seen in Reiter's syndrome and in arthritis associated with inflammatory intestinal diseases and psoriasis. In ankylosing hyperostosis (diffuse idiopathic skeletal hyperostosis - DISH, Forestier's disease), there is exuberant osteophyte formation. The osteophytes of are thicker and more anterior than the syndesmophytes of ankylosing spondylitis, and the sacroiliac joints are not affected. The x-ray appearance of the sacroiliac joints in spondylitis should be distinguished from that in osteitis condensans ilii. In some geographic areas and in persons with appropriate occupations, brucellosis and fluoride poisoning may be important in the differential diagnosis.
Treatment
A. Basic Program
In general, treatment is similar to rheumatoid arthritis. The importance of postural and breathing exercises should be stressed.
B. Drug Therapy
The nonsteroidal anti-inflammatory agents are employed in the treatment of this disorder. Of these, indomethacin appears to be the most effective, though it is not unreasonable to begin therapy with aspirin. Although phenylbutazone has been shown to be efficacious, its toxicity in long-term therapy prohibits its use. The dosage of indomenthacin is usually 25 - 50 mg 3 times a day, but the least amount should be used will provide symptomatic improvement. Agents such as naproxen, fenoprofen, tolmetin, sulindac and piroxicam are valuable alternatives and may even be used as primary therapy. Indomethacin may produce a variety of untoward reactions, including headache, giddiness, nausea and vomiting, peptic ulcer, depression and psychosis.
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