Rhematoid Spondylitis (Bekhterev’s Disease / Ankylosing Spondylitis)
Ankylosing spondylitis is an inflammatory disease that is responsible for fusing of vertebrae in the spin, thus making the spine far less flexible and can result in a hunched-forward posture. It can also be difficult to breathe deeply if the ribs are affected as well.
Ankylosing spondylitis predominantly affects men with signs and symptoms typically beginning during early adulthood. Inflammation also can occur in other parts of your body, such as the eyes.
Treatments can lessen your symptoms and possibly slow progression of the disease despite there being no cure.
What causes ankylosing spondylitis?
It is believed that ankylosing spondylitis is genetically inherited, with nearly 90% of these people being born with a gene known as the HLA-B27 gene. An understanding of the relationship between HLA-B27 and ankylosing spondylitis has bee furthered due to the development of special blood tests. The HLA-B27 gene seems only to increase the tendency of developing ankylosing spondylitis, whereas some additional, possibly environmental factor(s), are necessary for the disease to appear or become expressed fully.
For example, whilst the HLA-B27 gene is present in 7% of the United States population, only 1% of the population actually has the disease ankylosing spondylitis. In northern Scandinavia (Lapland), 1.8% of the population has ankylosing spondylitis while 24% of their general population has the HLA-B27 gene.
Even among individuals whose HLA-B27 blood test is positive, the development of ankylosing spondylitis appears to based more on heredity. In HLA-B27-positive individuals who have relatives with the disease, the risk of developing ankylosing spondylitis is six times greater than for those whose relatives do not have ankylosing spondylitis).
WHAT ARE THE SYMPTOMS OF RHEMATOID SPONDYLITIS?
Pain and stiffness in your lower back and hips, especially in the morning and after periods of inactivity are often early warning signs that ankylosing spondylitis is present or developing. Neck pain and fatigue also are common. Over time, symptoms can worsen, improve or stop at irregular intervals.
The most commonly affected areas are:
- The vertebrae in your lower back
- Sacroiliac -the joint between the base of your spine and your pelvis
- Entheses – The places where your tendons and ligaments attach to bones mainly in your spine, but occasionally along the back of your heel
- The cartilage between the ribs and breastbone
- The shoulder and hip joints
WHAT TREATMENT OPTIONS ARE AVAILABLE TO TREAT RHEMATOID SPONDYLITIS?
Relieving pain and stiffness, whilst preventing or delaying complications of spinal deformity is the main goal of treatment. Treating Ankylosing spondylitis is most successful before the disease causes irreversible damage to the joints.
Nonsteroidal anti-inflammatory drugs (NSAIDs) like naproxen (Naprosyn) and indomethacin (Indocin) are most often used to treat ankylosing spondylitis as they can help to relieve inflammation, stiffness and pain. However, gastrointestinal bleeding can result from taking these medications.
Your doctor might suggest you start taking a biologic medication, such as a tumor necrosis factor (TNF) blocker – medications that target a certain cell protein that causes inflammation in the body – or an interleukin 17 (IL-17) inhibitor, if NSAIDs prove to be ineffective. IL-17 plays an important role in defending your body against infection and also has a role in inflammation.
A reduction in pain, stiffness, and tender or swollen joints can be achieved by taking TNF blockers. They are administered by injecting the medication through an intravenous line or under the skin.
The five TNF blockers approved by the Food & Drug Administration to treat ankylosing spondylitis are:
- Adalimumab (Humira)
- Etanercept (Enbrel)
- Certolizumab pegol (Cimzia)
- Infliximab (Remicade)
- Golimumab (Simponi; Simponi Aria)
Secukinumab (Cosentyx) was the first IL-17 inhibitor approved by the FDA for the treatment of ankylosing spondylitis. Side effects of TNF blockers and IL-17 inhibitors can include reactivating latent tuberculosis and make you more prone to infection.
Physical therapy can provide a number of benefits, from pain relief to improved strength and flexibility is an essential part of treatment. A physical therapist can design specific exercises for your needs.
Flexibility in your joints and good posture can be preserved through the application of range-of-motion and stretching exercises. Getting the right amount of sleep, good walking positions and abdominal and back exercises can help maintain your upright posture.
Most people with this condition don’t require surgery. However, your doctor might recommend surgery if you have severe joint damage or pain, or if your hip joint is so damaged that it needs to replacing.
DIAGNOSING RHEMATOID SPONDYLITIS
- Consult with doctor and physical exam: During the physical exam, your doctor might test the range of motion of your spine by asking you to bend in different directions. He or she might try to reproduce your pain by pressing on specific sections of your pelvis or by positioning your legs in certain ways as well as asking you to breathe deeply to see if you have difficulty expanding your chest.
- Imaging tests: Although the visible signs of ankylosing spondylitis are not always evident early in the disease, X-rays allow your doctor to check for changes in your joints and bones. An MRI uses radio waves and a strong magnetic field to create more-detailed images of bones and soft tissues. MRI scans can reveal evidence of ankylosing spondylitis earlier in the diseases development, however they come with a hefty price tag.
- Lab tests: Certain blood tests can measure and check for markers of inflammation, however inflammation can be caused by so many other health problems. This can make diagnosing ankylosing spondylitis difficult. There are no specific lab tests to identify ankylosing spondylitis. You can be tested for the HLA-B27 gene, however most people who have that gene don’t have ankylosing spondylitis, and fewer black people with the disease have the gene than white people do.