Eugene Yen, MD, on Diagnosis and Treatment of Microscopic Colitis

Microscopic colitis (MC) was first identified in 1985 and is now considered to be a type of inflammatory bowel disease (IBD). Much remains unclear about the pathogenesis of this disease, its relationship to other types of IBD and to celiac disease, and how it is best managed to achieve optimal treatment outcomes.

Gastroenterology Learning Network reached out to Eugene Yen, MD, who is a gastroenterologist and clinical associate professor at the NorthShore University Health System in Chicago, Illinois, to answer our questions about microscopic colitis, in which he has a particular research interest.¹

GASTROENTEROLOGY LEARNING NETWORK: You have conducted research and written a good bit about the prevalence, pathogenesis, diagnosis, and management of MC. In one article, you commented that physician awareness of MC is important for preventing diagnostic delays. Do you find that some gastroenterologists are still somewhat unfamiliar with MC?

EUGENE YEN, MD: I don’t think that gastroenterologists are unfamiliar with MC, but compared to Crohn’s and ulcerative colitis, there is just much less awareness, not only on the part of referring doctors but also on patients. We just don’t hear enough about this disorder at our national meetings or in the lay press. In addition, there are a lot of overlaps with irritable bowel syndrome, as many of our MC patients fulfill Rome criteria for IBS. Thus, there is often considerable delay in receiving a diagnosis of MC.

GLN: You mention that the lack of robust evidence and societal guidelines to help manage MC “may be due to our lack of understanding of histologic and clinical predictors of disease severity.” Has there been progress in identifying and understanding those predictors? What specific indicators should gastroenterologists look for to help them better predict severity of disease?

EY: Clinically, we know that almost a quarter of patients with MC have >10 bowel movements per day. Usually if a patient shows severe symptoms on presentation (bowel movements, incontinence), this is a predictor of more budesonide-dependent or treatment-refractory disease. However, there needs to be more than clinical criteria to judge severity. Unfortunately, since the mucosa is generally normal in MC, we currently only use histology for a yes/no diagnosis. We are working on finding histologic predictors of severe disease to help to inform our therapies, much like we do in other forms of IBD.

GLN: Some researchers have posited that MC may be caused by certain medications, including nonsteroidal anti-inflammatory drugs (NSAIDS), selective serotonin reuptake inhibitors (SSRIs), and statins. However, you have suggested that there may be another mechanism at work. Would you explain what you think is the more “biologically plausible” explanation for this apparent relationship between certain drugs and the presentation of MC?

EY: This is a challenging topic, as we know that medications can cause diarrhea, and that medication-induced diarrhea as well as MC occur primarily in the elderly. There have been multiple population-based retrospective studies showing an association of these medications with a diagnosis of MC. In our population we have seen an association of NSAID use with the development of MC. Whether meds are causal and involved in the pathophysiology is unclear. To further confuse the situation, we know that meds such as NSAIDs cause histologic changes that appear like collagenous colitis. If it’s NSAID-induced and improves after stopping NSAIDs, it’s shouldn’t be called microscopic colitis. It should be called NSAID-induced colitis.

GLN: You have also said that there could be a relationship between celiac disease and MC. Could you tell us more about the evidence you have seen for this connection and how it can affect diagnosis and management of MC?

EY: Yes, multiple studies have shown an association with other autoimmune disease, particularly celiac disease, which is seen up to 20 times more frequently in the MC population than in controls. However, microscopic colitis is generally not treated successfully with a gluten-free diet. Thus, it’s a matter of awareness, and of the need to evaluate a celiac patient who is not improving on a gluten-free diet for microscopic colitis, and vice versa.

GLN: What other research do you have underway or planned into MC?

EY: There are so many areas of low-hanging fruit for MC research, and we only need to start with existing published data in other forms of IBD. For example, about 10 years ago, we published one of the first papers associating smoking with MC, despite numerous papers already describing this association in ulcerative colitis and Crohn disease. Unfortunately, there are not a lot of centers that focus on MC, despite it being as common as ulcerative colitis and Crohn disease. We are hoping to contribute to a better understanding of this condition. I feel that much can still be learned about maintenance therapy for MC, as well as finding steroid-sparing agents to treat MC. Predicting severity of disease based on clinical or histologic factors would also be useful, as we discussed above.

Reference:

Gentile N, Yen EY. Prevalence, pathogenesis, diagnosis, and management of microscopic colitis. Gut and Liver. 2018;12(3):227-235. https://doi.org/10.5009/gnl17061