Enteropathic Arthritis: Inflammation That’s Hard to Stomach

Enteropathic Arthritis: Inflammation That’s Hard to Stomach

1 of
  • Enteropathic Arthritis

    Enteropathic Arthritis

    Inflammatory bowel disease (IBD) causes a number of digestive problems and other symptoms. These include abdominal pain, bloody diarrhea, cramps, and weight loss. For some IBD patients, joints throughout the body can be adversely affected by inflammation in a condition known as enteropathic arthritis (EA).

    The additional setback of joint pain that comes with EA can be confusing, because it may seem unrelated to the digestive symptoms of IBD. The two really are related, however, as is discussed in the following slides.

  • The Origin of the Problem: IBD

    The Origin of the Problem: IBD

    Inflammatory bowel disease (IBD) is the chronic inflammation of your digestive tract. The most common forms of IBD are ulcerative colitis (UC) and Crohn’s disease (CD). UC is the inflammation of the lining of your colon. CD, on the other hand, is deeper inflammation that can occur anywhere in the digestive tract.

    The high levels of inflammation may be due to the body’s overreaction to bacteria or viral toxins. It can also be an autoimmune response that causes the body to attack itself. Whatever the cause, the high level of inflammation means that the digestive system doesn’t function correctly. Some theories suggest that gut bacteria may leak out into the bloodstream. This can cause immune responses in other areas of the body, such as the skin, nail beds, eyes, and joints. This has not yet been confirmed by research, however.

  • What Joints are Affected

    What Joints are Affected

    EA has two main forms: peripheral and axial.

    Peripheral EA involves joints in the arms and legs, most often in the lower legs. Multiple joints are often involved. Statistics show that 17 to 20 percent of patients with IBD have some form of peripheral arthritis. It’s slightly more common in those with CD than UC.

    Joint inflammation tends to come in flare-ups with a rapid onset, often within 48 hours. Symptoms usually begin to reduce within about six months, but inflammation may become chronic in some people.

    As the IBD becomes more and less active in cycles, peripheral EA may also occur in these cycles. Symptoms get better or worse depending on the overall level of inflammation.

  • Spondylitis


    The other form of EA is axial. One in six people with IBD also has spinal inflammation, with arthritis developing in the spinal joints. Axial EA is also more common in patients with CD (up to 22 percent of patients) than those with UC (only six percent).

    This axial form of EA can involve arthritis in the sacroiliac joints at the pelvis. In a few patients, the axial form involves the entire spine in a type of arthritic inflammation called ankylosing spondylitis. The spinal joints can become increasingly immobile over time with arthritis.

    It should be noted that the axial form of EA does not follow the cycles of the IBD symptoms.

  • Which Comes First?

    Which Comes First?

    In patients with the axial form of EA, joint symptoms and joint damage may occur before any intestinal symptoms begin at all. Diagnosis of spinal arthritis may happen before the underlying IBD is detected.

    Initial symptoms of peripheral EA include joint pain and arthritis that doesn’t cause deformation or joint erosion (unlike osteoarthritis).

    Symptoms of axial EA include low back pain (especially in younger people), morning stiffness, and pain with extended sitting or standing.

  • Risk Factors

    Risk Factors

    Genetics play a role in the development of EA. Having the gene for the HLA-B27 protein makes you more likely to develop EA and other spondylitis diseases. This protein is part of the surface of macrophages, which is a type of immune cell that may migrate from the IBD-affected digestive system to attack joints.

    Having the HLA-B27 gene may make your immune system attack proteins within your joints, thinking that they are from bacteria. Additionally, infection with certain bacteria—such as Salmonella, Shigella and others—may trigger joint inflammation, especially in those with genetic risk factors.

  • Suppressing the Immune System

    Suppressing the Immune System

    The main method of treatment for EA involves suppressing inflammation. Initially, nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen, naproxen, and stronger prescription anti-inflammatory NSAIDs may be used. These drugs may have long-term side effects on the stomach and digestive system, however, which can be a big problem for IBD patients.

    Drugs that suppress inflammation and the immune system are normally used next. These include corticosteroids such as prednisone, as well as other antirheumatic drugs like sulfasalazine and methotrexate.

    Biologics are a new type of drug that block an inflammatory signal chemical in the body known as TNF. Blocking TNF can suppress inflammation. There are risks, however, of infection due to immune suppression. Examples include etanercept (Enbrel), adalimumab (Humira), infliximab (Remicade), and golimumab (Simponi).

  • Other Treatments

    Other Treatments

    Exercise and physical therapy are important treatments for relieving the pain of arthritis, as well as building and maintaining muscle strength.

    With EA and the IBD factor, probiotics may actually help. Taking probiotics allows you to ingest “good” bacteria to counter the damaging gut bacteria that may be triggering gut and joint inflammation. There still need to be studies to show that probiotics can effectively treat IBD and EA. There are some encouraging studies in development that are taking a close look at the benefits of probiotics.

    Cardiovascular problems are a risk in patients with IBD and EA, and treating heart and blood vessel problems need to be a priority as well.