Avascular necrosis is bone tissue death due to a lack of blood supply. It is not a direct complication of ulcerative colitis but can be connected to the long-term use of steroids, which are often used to treat ulcerative colitis.
Ulcerative colitis (UC) is a type of chronic inflammatory bowel disease (IBD). It causes inflammation and ulcers to develop in the large intestine. It can also cause rectal bleeding, abdominal pain, and cramping, among other symptoms.
UC can also cause several complications. This includes anemia, dehydration, weight loss, and toxic megacolon. However, one potential complication of UC that is less known is avascular necrosis.
Avascular necrosis is the death of bone caused by a loss of blood supply. It is not a complication of UC directly. It is instead a possible side effect, or “adverse event,” caused by a popular treatment for UC, corticosteroids.
Keep reading to learn more about avascular necrosis, its relationship to UC, and how to prevent it.
Avascular necrosis occurs when there is a loss of blood flow to bone tissue. As a result, the bone dies. With time, the bone that is affected can fracture. This often causes significant pain and difficulty with movement and activity.
The bones may eventually collapse, leaving the joint damaged. This can lead to immobility and even disability. In severe cases, the joint may need to be replaced.
Avascular necrosis most commonly occurs in the bones of the hips, knees, shoulders, and ankles. It can also occur in smaller joints, such as the wrist.
Common causes of avascular necrosis are alcohol misuse, joint injuries, and other conditions, such as cancer or arthritis. But it can also be the result of long-term steroid use, which is how it relates to irritable bowel diseases, such as UC.
Corticosteroids, such as prednisone, are sometimes prescribed to people with UC. These medications help the body reduce flare activity. UC flares are instances when the condition becomes more active, and symptoms are more pronounced or problematic.
Avascular necrosis is a possible side effect of long-term steroid use. A 2019 study in the Journal of Clinical Rheumatology noted that an estimated
A 2019 study in Gastroenterology Research and Practice found that
As a result, an avascular necrosis diagnosis often comes several years after UC is diagnosed and treatment begins. A 2022 study in the journal Inflammatory Bowel Diseases found that people receive a diagnosis of avascular necrosis about 12.2 years after an IBD diagnosis.
The amount of avascular necrosis in people with UC is likely underreported. A 2022 study in the Journal of Clinical Rheumatology found that only 59% of radiology reports from people with IBD even commented on the presence of avascular necrosis.
It is possible that people with UC will develop avascular necrosis without ever taking steroids. According to the same 2022 study, 10% of people with UC developed avascular necrosis without taking steroid medication. In those cases, the people that developed avascular necrosis often had a history of joint diseases, such as arthritis.
No, UC does not directly cause avascular necrosis. Instead, it is most likely the result of long-term corticosteroid use.
IBDs, such as ulcerative colitis, are treated with these medications to reduce symptoms of the disease and induce remission, or a period of lower disease activity.
It is unclear precisely how steroids cause this side effect. But a
This loss of blood flow can ultimately cause the bones to become fragile and eventually collapse.
Not everyone with UC will develop avascular necrosis, and not everyone who has both avascular necrosis and UC will have a history of steroid use.
For example, people who have UC and a prior joint disease, such as arthritis, have a 3-fold higher chance of having avascular necrosis compared to people who do not have the joint disease. Osteoporosis increased the risk of developing avascular necrosis by a factor of 6 in people with UC.
Corticosteroids are not the only treatment option for UC. In fact, they are not as frequently used in people with UC as they are in people with other types of IBD, such as Crohn’s disease.
The best way to reduce the risk of avascular necrosis is to avoid steroid use or use it for only short periods of time. Other treatments for UC may be more beneficial with fewer potential complications.
There is no cure for avascular necrosis. Additionally, this condition is often discovered and diagnosed after the damage to the bone and joint is advanced.
However, there are ways to reduce the pain and discomfort caused by avascular necrosis. These treatments may not reverse bone damage, but they may be able to prevent further damage and restore function.
These treatments include:
- anti-inflammatory medications
- cholesterol-lowering medications that can increase blood flow
- activity modification
- joint braces or assistive devices
- physical therapy
- injections
In severe cases, a joint replacement or bone graft may be necessary.
The longer a person uses corticosteroids, the higher their risk of developing avascular necrosis. If a person has UC and uses corticosteroids, a doctor will likely closely monitor for signs of bone damage. Alternative treatments may be suggested to prevent potential joint damage caused by avascular necrosis.
If avascular necrosis is diagnosed and treated early, treatment may help prevent further damage to the joints. Treatments can also help reduce pain, restore function, and regain mobility.
Avascular necrosis is a rare complication of UC. It occurs when the blood flow to bone tissue is cut off, and the bone begins to die. This can lead to bone fractures and eventually collapse.
For people with UC, avascular necrosis is often caused by the long-term use of steroids for treatment. Not everyone who uses steroids for UC will develop avascular necrosis, but it does significantly increase the risk.