Ankylosing spondylitis and back pain

Ankylosing spondylitis, or Bechterew's disease, is a systemic disease characterized by inflammation of the axial skeleton and large peripheral joints, nocturnal back pain, back stiffness, worsening kyphosis, constitutional symptoms, and anterior uveitis. Diagnosis requires radiographic evidence of sacroiliitis. Treatment includes NSAIDs or tumor necrosis factor antagonists and physical support to maintain joint mobility.

Ankylosing spondylitis is three times more common in men than in women, with onset most often between the ages of 20 and 40 years. It is 10 to 20 times more common in first-degree relatives than in the general population. The risk of developing ankylosing spondylitis in first-degree relatives carrying the HLA-B27 allele is about 20%. An increased frequency of HLA-B27 in whites or HLA-B7 in blacks suggests a genetic predisposition. However, the concordance rate in identical twins is about 50%, suggesting a role for environmental factors. Immune-mediated inflammation is suggested in the pathophysiology of the disease.

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How does ankylosing spondylitis manifest itself?

At the onset, the most common symptom is back pain, but the disease may also begin in the peripheral joints, especially in children and women, rarely with acute iridocyclitis (iritis or anterior uveitis). Other early symptoms and signs may include decreased range of motion of the chest due to generalized damage to the costovertebral joints, subfebrile condition, fatigue, anorexia, weight loss, and anemia.

Back pain often occurs at night and varies in intensity, becoming more constant over time. Morning stiffness, usually relieved by activity, and paraspinal muscle spasm develop gradually. Bending the body or a forward leaning posture relieves pain and paraspinal muscle spasm. Thus, kyphosis is common in untreated patients. Severe arthritis of the hip joint may develop. In the later stages, patients experience increased kyphosis, loss of lumbar lordosis, and a fixed forward leaning posture that impairs the ventilation capacity of the lungs and makes it impossible to lie on the back. Deforming arthrosis and Achilles tendinitis may develop.

Systemic manifestation of the disease occurs in 1/3 of patients. Recurrent acute anterior uveitis is common, but usually self-limited. Less often, it has a protracted course and causes decreased vision. Neurological signs are occasionally caused by compression radiculopathy or sciatica, vertebral fractures or subluxations, cauda equina syndrome. Cardiovascular manifestations may include aortic insufficiency, aortitis, pericarditis, cardiac conduction disturbances, which may be asymptomatic. Dyspnea, cough, and hemoptysis may result from non-tuberculous fibrosis and cavities in the upper lobes of the lungs, secondary infection (aspergillosis) may join this. Rarely, ankylosing spondylitis causes secondary amyloidosis. Subcutaneous nodules do not occur.

Other spondyloarthropathies

Other spondyloarthropathies may develop in association with gastrointestinal diseases (sometimes called gastrointestinal arthritis), such as inflammatory enteritis, surgical anastomosis, and Whipple's disease. Juvenile spondyloarthropathy is asymmetric, most pronounced in the lower extremities, and most often debuts between the ages of 7 and 16. Spondyloarthropathy may develop in patients without characteristic features of other specific spondyloarthropathies (undifferentiated spondyloarthropathy). Treatment of arthritis in these spondyloarthropathies is the same as for reactive arthritis.

How to recognize ankylosing spondylitis?

Ankylosing spondylitis should be suspected in patients, particularly young adults, with nocturnal back pain and kyphosis, decreased thoracic excursion, Achilles tendinitis, or unspecified anterior uveitis. First-degree relatives of persons with ankylosing spondylitis should be of greatest concern. The following tests should be performed: ESR, C-reactive protein, leukocyte formula. Immunoglobulin M, rheumatoid factor, antinuclear antibodies are determined only when peripheral arthritis arouses suspicion of another disease. There are no specific laboratory tests, but the results may strengthen the case or exclude it in favor of diseases that mimic ankylosing spondylitis. If suspicion of the disease remains after investigations, the patient should have a lumbosacral x-ray to establish sacroiliitis and confirm the diagnosis.

Alternatively, ankylosing spondylitis can be diagnosed using the modified New York criteria. According to these criteria, the patient must have radiographic evidence of sacroiliitis and one of the following:

1. limitation of mobility of the lumbar spine both in the sagittal plane (examination from the side) and in the frontal plane (examination from the back);
2. limitation of chest excursion compared to the age norm;
3. History of inflammatory back pain. Anamnestic differences between inflammatory and non-inflammatory back pain are: onset before age 40, gradual increase, morning stiffness, improvement with physical activity, duration of more than 3 months before seeking medical help.

ESR and other acute-phase reactants (eg, C-reactive protein) are inconsistently elevated in patients with active disease. Rheumatoid factor and antinuclear antibody tests are negative. The HLA-27 marker has no diagnostic value.

Early radiographic abnormalities are pseudo-widening due to subchondral erosions, followed by sclerosis or later narrowing and even overgrowing of the sacroiliac joint. The changes are symmetrical. Early changes in the spine are represented by accentuation of the vertebral body boundaries with sclerosis of the angles, spotty calcification of the ligaments and one or two developing syndesmophytes. Late changes lead to the formation of a "bamboo spine" due to prominence of syndesmophytes, diffuse paraspinal calcification of the ligaments and osteoporosis; these changes are noted in some patients who have been ill for more than 10 years.

Changes typical of Bechterew's disease may not be detected on radiographs for several years. CT or MRI detect changes earlier, but there is no consensus on their use in routine diagnostics.

A herniated disc may cause pain and radiculopathy resembling ankylosing spondylitis, but the pain is limited to the spine, is usually more acutely symptomatic, and does not have associated systemic manifestations or laboratory test abnormalities. CT or MRI may be used to differentiate herniated disc from ankylosing spondylitis when needed. Involvement of the sacroiliac joint alone may mimic ankylosing spondylitis when there is infection. Tuberculous spondylitis may mimic ankylosing spondylitis.

Diffuse idiopathic skeletal hyperostosis (DISH) occurs mainly in men over 50 years of age and may have clinical and radiographic similarities to Bechterew's disease. The patient notes spinal pain, stiffness, and latent limitation of motion. Radiologically, DISH reveals massive ossification in front of the anterior longitudinal ligament (calcification resembles melted candle wax drips in front and on the sides of the vertebrae), the appearance of bone bridges between the vertebrae, usually affecting the cervical and lower thoracic vertebrae. However, the anterior longitudinal ligament is intact and often retracted, the sacroiliac and vertebral apophyseal joints have no erosions. Additional differential criteria are stiffness, which is not accentuated in the morning, and a normal ESR.

How to treat ankylosing spondylitis?

Ankylosing spondylitis is characterized by alternating periods of moderate to severe inflammation with periods of little or no inflammation. With proper treatment, most patients experience minimal or no disability and a full life despite back stiffness. In some patients, the disease is severe and progressive, leading to severe, disabling deformities. The prognosis is poor in patients with refractory uveitis and secondary amyloidosis.

The goal of treatment is to reduce pain, maintain the functional state of the joints and prevent visceral complications.

NSAIDs reduce pain, suppress joint inflammation and muscle spasm, thereby increasing range of motion, facilitating exercise therapy and preventing contractures. Many NSAIDs are effective in a disease such as ankylosing spondylitis, but tolerability and toxicity of the drugs dictate the choice. The daily dose of NSAIDs should be the minimum effective, but maximum doses may be necessary if the disease is active. An attempt to discontinue the drugs should be made slowly over several months, provided that joint symptoms and disease activity are absent.

Sulfasalazine may help reduce peripheral joint symptoms and laboratory markers of inflammation. Peripheral joint symptoms may also be reduced by methotrexate. Systemic corticosteroids, immunosuppressants, and other modified antirheumatic agents have no proven efficacy and should generally not be used. There is increasing evidence that biologic agents (eg, etanercept, infliximab, adalimumab) are effective in treating inflammatory back pain.

Correct execution of therapeutic exercise requires exercises for the postural muscles (e.g. postural training, therapeutic gymnastics), maximum activation of muscles that counteract potential deformations (e.g. extensors are preferable to flexors). Reading in a supine position with support on the elbows or a pillow, thus straightening the back, can help maintain back mobility.

Intra-articular depot corticosteroids may be useful, especially when one or two peripheral joints have more severe inflammation than others, thus allowing for exercise and rehabilitation. This may be effective when systemic medications are ineffective. Injections of corticosteroids into the sacroiliac joint sometimes help reduce the severity of sacroiliitis.

Acute uveitis is usually treated with topical corticosteroids and mydriatics. In severe hip arthritis, total hip arthroplasty can dramatically improve motion.