Microscopic colitis is a chronic inflammatory condition affecting the large intestine. It is characterized by persistent watery diarrhea and abdominal pain, but unlike other inflammatory bowel diseases, the inflammation is only visible when colon tissue samples are examined under a microscope. This distinct feature gives the condition its name.
There are two primary subtypes of microscopic colitis: collagenous colitis and lymphocytic colitis. In collagenous colitis, a thicker-than-normal layer of collagen forms beneath the lining of the colon. Lymphocytic colitis is identified by an increased number of white blood cells, specifically lymphocytes, within the colon’s epithelial lining. Both types share similar symptoms and treatments. While the exact cause of microscopic colitis is often not fully understood, research points to several strong theories and contributing factors.
Medications as Triggers
Certain medications are strongly implicated in triggering microscopic colitis. Nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen and naproxen sodium, are frequently associated with the condition. These drugs may directly irritate the colon lining or alter its permeability, potentially allowing substances to trigger an inflammatory response.
Proton pump inhibitors (PPIs), commonly used to reduce stomach acid, have also been linked to microscopic colitis. Mechanisms include changes in the gut microbiome or increased susceptibility to bacterial toxins. Selective serotonin reuptake inhibitors (SSRIs), such as sertraline, can also contribute to the development of this condition.
Other medications, including statins, have been reported in some cases, although the evidence may be less consistent compared to NSAIDs and PPIs. These medications are thought to induce mucosal damage, disrupt the gut barrier, or initiate an immune response within the colon. Avoiding or discontinuing these trigger medications often leads to an improvement in symptoms for affected individuals.
Immune System Involvement
Microscopic colitis is often considered an autoimmune condition. This theory suggests that the body’s own immune system mistakenly attacks the healthy lining of the colon, leading to the characteristic inflammation. The immune system, designed to protect the body, can become dysregulated and target its own tissues.
There is a strong association between microscopic colitis and other autoimmune diseases, lending support to the idea of immune system dysfunction. Individuals diagnosed with microscopic colitis frequently also have conditions such as celiac disease, thyroid disorders, or rheumatoid arthritis. For instance, histologic features of microscopic colitis are present in a notable percentage of patients with celiac disease, sometimes as high as 30%.
This co-occurrence indicates a shared underlying predisposition to immune system imbalances. The inflammatory process in microscopic colitis involves an increase in immune cells, particularly lymphocytes, within the colon tissue. This cellular infiltration is a hallmark of an immune-mediated response, where the body’s defense mechanisms are actively engaged against its own intestinal cells.
Other Potential Factors and Theories
Several other factors and theories are considered potential contributors to microscopic colitis. Genetic predisposition plays a role, as a family history of irritable bowel syndrome or other autoimmune conditions can increase an individual’s risk. Specific genetic markers, such as certain human leukocyte antigen (HLA) types, have also been associated with the condition.
Infections, both bacterial and viral, are another area of investigation. Pathogens might initiate or exacerbate inflammation in the colon. The toxins produced by certain bacteria could irritate the colon lining, contributing to the inflammatory process.
Bile acid malabsorption is also recognized as a potential factor. When bile acids are not properly absorbed in the small intestine, excess amounts can reach the colon and irritate its lining, leading to symptoms similar to microscopic colitis. Imbalances in the gut microbiome, the complex community of bacteria, fungi, and viruses residing in the digestive tract, are being explored. Disruptions in this microbial balance may contribute to inflammation and altered gut barrier function, potentially influencing the development or progression of the condition. Smoking is another identified risk factor, particularly in younger individuals.