The microscopic colitis (MC) encompasses lymphocytic and collagenous colitis with increasing incidence in Northern Europe. The clinical symptoms of MC and irritable bowel syndrome are similar and often overlap. Diagnosis is made in 10–14% of patients with chronic diarrhea and macroscopically normal colonoscopy; a medication-induced origin (venotonics, proton pump inhibitors, H2 blockers, and selective serotonin reuptake inhibitors) must be systematically investigated.
Inflammatory bowel diseases (IBDs), including Crohn’s disease and ulcerative colitis, are associated with an increased risk of major adverse cardiovascular events (MACE). These events include ischemic heart disease, heart failure, stroke, and cardiovascular mortality; they have been less studied in MC.
Risk of Cardiovascular Complications
A Swedish cohort included 11,018 adults with MC confirmed by biopsies. The participants had no previous cardiovascular disease (CVD). They were matched with 48,371 reference individuals without MC or CVD. Over a mean follow-up period of 6.6 years, 2181 (19.8%) MACE incident cases were confirmed in patients with MC and 6661 (13.8%) in reference individuals.
Compared to reference individuals, patients with MC had an overall higher risk of cardiovascular complications (adjusted Hazard Ratio [aHR], 1.27) and a higher risk for its components: ischemic heart disease (aHR, 1.38), heart failure (aHR, 1.32), and stroke (aHR, 1.12). However, patients with MC did not have a higher risk of cardiovascular mortality (aHR: 1.07). These findings were more related to collagenous colitis than its lymphocytic counterpart.
The known increased risk of MACE in IBD to a lesser extent also applies to patients with collagenous colitis, although usually no obvious inflammatory biomarkers are present intraluminally. The results of the Swedish cohort were in line with those from Danish registries and remained robust after adjusting for cardiovascular risk factors, considering that MC is likely underdiagnosed in the reference population.
However, this Swedish study lacked data on specific MC and cardiovascular risk factors such as body mass index, alcohol, diet, lipid profiles, and potential surveillance biases, which could have influenced the results. The underlying causes of MACE in patients with IBD were multifactorial (e.g. metabolic comorbidities, environmental influences, and lifestyle factors) and likely outweighed the inflammatory aspect.
This observation is consistent with the lack of efficacy of biologics in severe forms of IBD, which generally respond well to budesonide and thiopurines. This increased cardiovascular risk is likely triggered by the release of proinflammatory cytokines into the bloodstream, increasing the formation of atherosclerotic plaques. Nonetheless, it underscores the need to be aware of cardiovascular risk factors in these patients and to conduct personalized assessments.
In summary, in this extensive national cohort study based on 11,018 patients with MC confirmed by biopsy, the risk of MACE was 27% higher than in the general population. This translates to an additional case of MACE per 13 patients with MC observed over a period of 10 years. Beyond discussions about this association, patients with MC could benefit from personalized cardiovascular risk assessment in the presence of confirmed risk factors.
This article was translated by JIM, part of the Medscape Professional Network.