Gastroparesis is a condition where the stomach empties its contents into the small intestine more slowly than it should. This delay in gastric emptying can lead to various digestive symptoms. A common question arises regarding its nature: Is gastroparesis an autoimmune disease?
Understanding Gastroparesis
Gastroparesis is a disorder impacting the stomach’s ability to move food into the small intestine. The muscles of the stomach, which are responsible for pushing food through the digestive tract, become impaired or weakened. This results in food remaining in the stomach for an extended period, leading to uncomfortable symptoms.
Symptoms include nausea, vomiting, bloating, and feeling full very quickly after starting a meal or long after finishing one. Patients may also experience upper abdominal pain, heartburn, and a poor appetite. Diagnosing gastroparesis involves reviewing symptoms and medical history, followed by tests such as a gastric emptying scintigraphy (GES). This test measures how quickly food leaves the stomach after consuming a meal containing a small amount of radioactive material.
Is Gastroparesis an Autoimmune Condition?
An autoimmune disease occurs when the body’s immune system mistakenly attacks its own healthy tissues, perceiving them as foreign invaders. Normally, the immune system produces antibodies to protect against harmful substances like bacteria and viruses. In an autoimmune disorder, these autoantibodies are directed against the body’s own cells or organs, causing damage.
Gastroparesis is not classified as a primary autoimmune disease like rheumatoid arthritis or lupus. The underlying issue in gastroparesis involves damage to the vagus nerve, which controls the stomach’s muscle contractions and movement of food. While autoimmune processes can contribute to this nerve damage, gastroparesis itself is not considered an autoimmune disorder. Many cases of gastroparesis arise from causes unrelated to an immune system attack on the stomach or its nerves.
Research indicates that autoantibodies may damage the nerves in the stomach, leading to a form of gastroparesis. This suggests that while not all gastroparesis is autoimmune, an autoimmune mechanism can be a factor. However, the exact cause of gastroparesis remains unclear, emphasizing that it is not solely an autoimmune condition.
Gastroparesis and Autoimmune Associations
While gastroparesis is not always autoimmune, it can occur alongside or as a complication of certain autoimmune diseases. In these situations, the autoimmune condition can indirectly affect the vagus nerve or the stomach muscles, contributing to delayed gastric emptying. For example, systemic sclerosis, an autoimmune disease affecting connective tissues, can lead to gastroparesis by degenerating stomach muscles.
Other autoimmune conditions linked to gastroparesis include lupus and Sjögren’s syndrome. Thyroid autoimmune diseases, such as Hashimoto’s thyroiditis and Graves’ disease (causing underactive or overactive thyroid), are also associated with gastroparesis. When gastroparesis is linked to an autoimmune disease, it is called autoimmune gastrointestinal dysmotility (AGID), where the immune response attacks the nerves controlling gastrointestinal movement.
Different Forms of Gastroparesis
Gastroparesis has various origins. The most common identified cause of gastroparesis is diabetes, resulting in diabetic gastroparesis. High blood sugar levels over time can damage the vagus nerve, impairing the stomach’s ability to empty properly. About one-third of people with type 1 and type 2 diabetes develop gastroparesis.
Another significant category is idiopathic gastroparesis, where no clear cause is identified. This form accounts for a substantial portion of all chronic gastroparesis cases. Post-viral gastroparesis can occur following a viral infection, such as norovirus or rotavirus, triggering nerve damage. Additionally, post-surgical gastroparesis can develop after abdominal surgeries, particularly those involving the stomach or esophagus, due to injury to the vagus nerve. Other less common forms result from neurological disorders or medications.