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AS – Ankylosing Spondylitis: Causes and Treatment
AS (Ankylosing Spondylitis) is a chronic inflammatory disease of the spine that causes pain and progressive stiffness. It belongs to the group of spondyloarthritides.
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AS (Ankylosing Spondylitis) is a chronic inflammatory disease of the spine that causes pain and progressive stiffness. It belongs to the group of spondyloarthritides.
What is Ankylosing Spondylitis (AS)?
Ankylosing Spondylitis (AS), also known as Bechterew disease or Spondylitis ankylosans, is a chronic inflammatory condition that primarily affects the spine and the sacroiliac joints (the joints between the sacrum and the pelvis). Over time, AS can cause new bone formation (ankylosis) leading to fusion of the vertebrae, progressive stiffness, and a characteristic forward-stooped posture. AS belongs to the group of spondyloarthritides and is considered an autoimmune disease.
Causes
The exact cause of AS is not fully understood, but it is believed to result from a combination of genetic and immunological factors:
- Genetic predisposition: More than 90% of people with AS carry the HLA-B27 gene, which significantly increases the risk of developing the disease.
- Immune system dysfunction: A misdirected immune response causes chronic inflammation of the joints and spine.
- Environmental triggers: Infections or other external factors may act as triggers in genetically predisposed individuals.
Symptoms
Symptoms typically develop gradually in early adulthood, most commonly between the ages of 20 and 30:
- Inflammatory back pain: Chronic lower back pain and morning stiffness that improve with movement are hallmark symptoms.
- Sacroiliac joint pain: Pain in the buttocks and lower back caused by inflammation of the sacroiliac joints.
- Reduced spinal mobility: As the disease progresses, movement of the spine becomes increasingly limited.
- Extra-articular manifestations: Eye inflammation (uveitis), inflammatory bowel disease, psoriasis, and cardiac complications may occur.
- General symptoms: Fatigue, malaise, and occasionally low-grade fever.
Diagnosis
Diagnosis of AS is based on a combination of clinical assessment, laboratory tests, and imaging:
- Clinical examination: Assessment of spinal mobility (e.g., Schober test, chest expansion).
- Laboratory tests: Testing for the HLA-B27 antigen, inflammatory markers such as CRP (C-reactive protein) and ESR (erythrocyte sedimentation rate).
- Imaging: X-rays of the sacroiliac joints and spine; MRI (magnetic resonance imaging) for early diagnosis before structural changes appear.
- Classification criteria: The modified New York criteria are used for formal classification of AS.
Treatment
There is currently no cure for AS, but the disease can be effectively managed to reduce symptoms and slow progression:
Pharmacological Treatment
- Non-steroidal anti-inflammatory drugs (NSAIDs): First-line treatment for pain and inflammation (e.g., ibuprofen, diclofenac, naproxen).
- Biologics (TNF inhibitors): When NSAIDs are insufficient, biologic agents such as adalimumab, etanercept, or infliximab are used.
- IL-17 inhibitors: Newer biologics such as secukinumab or ixekizumab provide an additional treatment option.
- Corticosteroids: May be used locally for inflamed joints via injection.
Non-pharmacological Treatment
- Physiotherapy: Regular physical therapy is essential to maintain spinal mobility and posture.
- Exercise: Swimming, cycling, and targeted stretching exercises are strongly recommended.
- Patient education: Understanding the condition and practicing self-management strategies are key components of care.
Surgical Treatment
In severe cases with significant joint deformity or damage, surgical intervention such as joint replacement (arthroplasty) may be necessary.
References
- Braun J, Sieper J. Ankylosing spondylitis. The Lancet. 2007;369(9570):1379-1390.
- World Health Organization (WHO). Chronic rheumatic conditions. Available at: https://www.who.int/chp/topics/rheumatic/en/
- van der Linden S, et al. Evaluation of diagnostic criteria for ankylosing spondylitis. Arthritis and Rheumatism. 1984;27(4):361-368.
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