Article updated and reviewed by Ariel D. Teitel, MD, MBA, Chief, Division of Rheumatology, St. Vincent’s Hospital, Manhattan on May 12, 2005.
Ankylosing Spondylitis is an inflammatory disease of unknown origin, first affecting the spine and adjacent structures, and commonly progressing to eventual fusion (ankylosis) of the involved joints.
In extreme cases, the patient develops a forward flexion of the spine, called a “poker spine” or “bamboo spine.”
In people with AS, the joints and ligaments that permit normal movement of the back become inflamed, producing pain and stiffness, usually beginning in the lower back, and often progressing into the upper spine, chest, and neck. As a result, the vertebrae may fuse, causing the spine to become rigid. Other joints such as the hips, shoulders, knees, or ankles may also be involved. Up to half of patients have arthritis of peripheral joints (hips, knees). Recent evidence strongly suggests a familial tendency in AS.
Typically, the disease begins slowly in the lower back and progresses up the spine to the neck. Deterioration of bone and cartilage can lead to fibrous tissue formation and eventual fusion of the spine or peripheral joints. AS is diagnosed three times more often in men than in women. Diagnosis is often overlooked or missed in women, who may show more mild disease.
The disease primarily affects males under 40 years of age and generally burns itself out after a course of 20 years. The male: female ratio of the disease is 3:1. Persons with a genetic marker called HLA-B27 have at least a 1% chance of getting AS. This marker is more commonly found in Caucasians than African Americans. The presence of human leukocyte antigen B27 (found in over 90 percent of people with this disease) and circulating immune complexes suggests immunologic activity. However, the actual relationship between the gene and the disease’s development has been difficult to confirm.
The first symptom in 75% of patients is low back pain that is usually most severe in the morning or after inactivity. The pain improves with exercise, as opposed to many other forms of back pain. It should be present for over three months. Other symptoms depend on the disease stage, and may include:
·Stiffness and limited motion of the lumbar spine
·Pain and limited chest expansion caused by involvement of the costovertebral joints
·Arthritis involving shoulders, hips and knees
·Kyphosis (curvature of the spine) in advanced stages, caused by chronic stooping to avoid symptoms
·Hip deformity with limited range of motion
·Tenderness over the inflammation site
·Mild fatigue, fever, loss of appetite or weight
These symptoms progress unpredictably and the disease can disappear temporarily or permanently at any time. Less than 30% of patients have severe disease.
X-rays of the sacroiliac joints are used to help confirm the diagnosis of AS. These may be normal in the first few months of disease. Other forms of arthritis may mimic AS. Rheumatoid arthritis does not involve the low back. Other spondyloarthropathies exhibit features not found in AS. Reiter’s Disease patients often have rashes, ulcers and more peripheral arthritis. Psoriatic arthritis patients usually have longstanding psoriasis. Occasionally, forms of osteoarthritis may mimic the x-ray appearance of AS, but these patients’ back pain may not improve after exercise and they will not have lab tests showing inflammation.
Poor prognostic factors include: hip arthritis, swelling of digits, high ESR in blood, weak response to NSAID’s, and diminished motion of the lumbar spine. Cigarette smoking also correlates with poor outcome.
Physical therapy helps considerably in the treatment of AS to prevent the characteristically stooped posture as the spine begins to fuse. No treatment stops the progression of the disease, so management aims to delay further deformity by enforcing good posture, stretching, and deep-breathing exercises and, in some people, wearing braces and lightweight support.
The pain and stiffness may be relieved by analgesics and nonsteroidal anti-inflammatory drugs (NSAIDS). These may include aspirin, Indocin, Anaprox, Tolectin, and Clinoril. Indocin is often the NSAID of choice. NSAID’s represent the mainstay of treatment but may be discontinued due to adverse reactions or lack of efficacy.
TNF inhibitors are part of a new class of drugs (biologics) that block the body’s inflammatory messengers. These drugs (Enbrel, Humira, Remicade) decrease the inflammation caused by a protein called TNF (tumor necrosis factor). Enbrel or Remicade may help decrease joint and back pain in AS patients with active disease. Good response to TNF inhibitors may be predicted in younger patients, patients with shorter disease duration, patients with elevated blood ESR/CRP, and in patients with a better baseline functional status. 80% of suitable patients respond to a TNF inhibitor; half experience an overall improvement of about 50% in disease control. TNF inhibitors may reactivate tuberculosis and should not be used in patients with recurrent bacterial infections. Other serious side effects can occur with these drugs.
Oral prednisone (a corticosteroid) rarely produces any benefit, but intra-articular (injections into the joints) corticosteroid injections are occasionally helpful. Methotrexate may be helpful for treatment of patients who have prominent extra-spinal involvement, and is also given in combination with infliximab. Sulfasalazine is also helpful for arthritis outside the spine in AS.
Are further diagnostic tests required?
Should any family members be evaluated?
What do you recommend to help with the stiffness and limited motion?
Would physical therapy be helpful?
Will you prescribe anti-inflammatory drugs?
Is there a problem with adverse reactions?
Would other drugs such as methotrexate or TNF-inhibitors be of value?
Editorial review provided by VeriMed Healthcare Network.