Abstract
Damage to the small intestine in rheumatological diseases The immune system of the small intestine influences immune processes of the whole organism, including pathological autoimmune processes. This occurs on levels from the generally increased association with diseases with an autoimmune nature to evidence of a shared genetic basis, which has been discovered within the whole histocompatible system in idiopathic intestinal inflammations and spondylarthrosis and in celiac disease, in association with rheumatoid arthritis.
An association between infectious intestinal inflammations and enteropathic spondylarthroses is known as well. The small intestine can also be affected as a result of the primary rheumatoid disease.
The blood vessels supplying the small intestine can be affected by some form of vasculitis, vasculopathy (in cases of systemic sclerodermia) or thrombosis occurring as a result of an associated antiphospholipid syndrome. A direct damage to the small intestine can be observed in cases of systemic lupus erythematodes or in the form of exsudative enteropathy.
Systemic sclerodermia associated with intestinal motility disorders leads to overgrowth of bacteria in the small intestine, which can lead to malabsorption syndrome. Heavy damage to the small intestine can also be a cause for changes in pharmacotherapeutic response to treatment of rheumatoid diseases.
On the other hand, drugs used to treat rheumatoid diseases can cause damage to both structure and function of the small intestine, such as enteropathy caused by non-steroidal anti-inflammatory drugs. We present an overview of the issues with changes to the small intestine, which can be encountered in cases of rheumatologic symptoms or a diagnosed rheumatologic disease.