Microscopic Colitis

Microscopic Colitis Linked With cardiovascular risk

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Microscopic colitis (MC) encompasses lymphocytic and collagenous colitis, with an increasing incidence in Northern Europe. Clinical presentations of MC and irritable bowel syndrome are similar and often overlapping. Diagnosis occurs in 10%-14% of patients with chronic diarrhea and macroscopically normal colonoscopy; a drug-related 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 for major adverse cardiovascular events (MACE). These events include any ischemic heart disease, congestive heart failure, stroke, and cardiovascular mortality; they have been studied less in MC.

Cardiovascular Complication Risk

A Swedish cohort included 11,018 adults with MC that had been proven through biopsies. Participants had no prior cardiovascular disease (CVD). They were matched with 48,371 reference individuals without MC or CVD. Over a median follow-up of 6.6 years, 2181 (19.8%) incident cases of MACE were confirmed in patients with MC and 6661 (13.8%) in reference individuals.

Compared with reference individuals, patients with MC had an overall higher risk for cardiovascular complications (adjusted hazard ratio [aHR], 1.27) and a higher risk for its components: Ischemic heart disease (aHR, 1.38), congestive heart failure (aHR, 1.32), and stroke (aHR, 1.12). But patients with MC did not have a higher risk for cardiovascular mortality (aHR, 1.07). These findings were related more to collagenous colitis than its lymphocytic counterpart.

Multifactorial Causes

The well-known increased risk for MACE in IBD is also present, to a lesser extent, in patients with collagenous colitis despite the usual absence of overt inflammatory biomarkers, which remain intraluminal. The results of the Swedish cohort aligned 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 certain MC and cardiovascular risk factors, such as body mass index, alcohol, diet, lipid profiles, and potential surveillance biases that may have influenced the results. Underlying causes of MACE in patients with IBD were multifactorial (eg, metabolic comorbidities, environmental exposures, and lifestyle-related factors) and probably outweighed the inflammatory aspect.

This observation aligns with the lack of efficacy of biologics in severe forms of IBD, which generally respond well to budesonide and thiopurines. This heightened cardiovascular risk is likely triggered by the release of proinflammatory cytokines into the bloodstream, which increases atherosclerotic plaque formation. Nevertheless, it underscores the need to be aware of cardiovascular risk factors in these patients and conduct personalized assessments.

In conclusion, in this extensive national cohort study based on 11,018 patients with biopsy-proven MC, the risk for MACE was 27% higher than in the general population. This translates to one additional case of MACE for every 13 patients with MC followed for 10 years. Beyond discussions about this association, patients with MC could benefit from a personalized cardiovascular risk assessment in the presence of confirmed risk factors.

Do Proton-Pump Inhibitors Cause Microscopic Colitis?

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Small studies suggest a link, but the body of research is still inconclusive.

Microscopic colitis (MC) is increasingly diagnosed as a cause of chronic diarrhea. The cause of MC is unknown; however, it has been associated in small studies with the use of proton-pump inhibitors (PPIs).

To examine this possible association further, investigators in the Netherlands retrospectively assessed medical records of 136 patients who received diagnoses of MC at two hospitals during a 4-year period. Pharmacy data from the 2 years prior to diagnoses were available for 95 (70%) of patients (mean age, 58; 66% women); these patients were matched by age and sex with population-based controls who supplied questionnaire data regarding their drug exposure and medical status. Drug exposure for patients and controls was defined as ≥1 PPI prescription or use of nonsteroidal anti-inflammatory drugs (NSAIDs; excluding low-dose aspirin) or other medications ≤180 days before MC diagnosis.

Exposure to PPIs was more common among patients than controls (38% vs. 13%; P<0.001) as was exposure to NSAIDs (20% vs. 5%; P=0.002). Analysis adjusted for exposure to other drugs showed that only PPI use was associated with MC (adjusted odds ratio 4.5, 95% confidence interval, 2.0–9.5).

Comment: The authors conclude that this study confirms the association between MC and PPI use. However, this conclusion is a stretch, given the study’s small size, limited geographic area, and exclusion of 30% of patients because of a lack of drug-exposure data. Ample opportunities for bias exist in the identification of cases, the selection of controls, and the determination of exposure. Much stronger evidence is needed to confirm such an association, let alone identify a mechanism of effect.

Published in Journal Watch Gastroenterology October 22, 2010