Latent TB Doesn’t Raise Key Inflammation Markers in Crohn’s

Crohn’s disease is an inflammatory condition of the gut in which doctors often measure blood and stool markers to track inflammation. Some of the same immune pathways that drive Crohn’s—particularly cytokines such as IL12, IL23, and TNF-α—also play roles in infections caused by mycobacteria, including tuberculosis. This overlap makes it important to consider latent tuberculosis infection when planning immune-suppressing treatments. JabbarSalman Hassan and colleagues set out to see whether latent tuberculosis changes the inflammatory fingerprint seen in people with Crohn’s disease. They focused on a set of commonly tested signals of inflammation: the cytokines TNF-α, IL-12, and IL-23; the blood protein CRP; and fecal calprotectin, which comes from gut immune cells and is used to monitor bowel inflammation. The study compared people with Crohn’s who tested positive for latent tuberculosis to those who did not, and it examined how existing immune-based treatments related to these biomarkers. The goal was to clarify whether latent infection itself might skew the very tests clinicians use to judge disease activity and treatment choices.

The research enrolled 100 patients with inflammatory bowel disease. Of these, 25 patients were diagnosed with latent tuberculosis infection (LTBI) using the Gold-Gold-interferon-gamma release assay (IGRA). The other 75 patients were IGRA negative and later received immunotherapy; they were treated with drugs that included aminosalicylates (5-ASA), corticosteroids, and immunomodulators and were classified as the treated group. The team measured CRP, fecal calprotectin and the cytokines TNF-α, IL-12, and IL-23 and compared levels between the treated group (n=75) and the untreated LTBI group (n=25). The study found no significant correlation between the IGRA test result and the different cytokine levels. Smokers had higher biomarker levels than non-smokers. Patients who received treatment including aminosalicylates (5-ASA), corticosteroids, and immunomodulators showed statistically significant differences in inflammatory markers—especially calprotectin, IL-23, and IL-12—compared to untreated patients, with markedly higher markers in the untreated group. Fecal calprotectin correlated positively with all measured inflammatory biomarkers.

Taken together, these findings show two clear points for clinicians and patients. First, in this study LTBI did not significantly change levels of TNF-α, IL-12, IL-23, CRP, or fecal calprotectin in people with Crohn’s, suggesting that a positive Gold-Gold-interferon-gamma release assay (IGRA) alone may not distort these routine inflammation tests. Second, whether a patient has received immune-based therapy matters a great deal: treated patients had different—and generally lower—levels of calprotectin and some cytokines compared with untreated patients, indicating that aminosalicylates (5-ASA), corticosteroids, and immunomodulators have a measurable impact on these biomarkers. The higher markers seen in smokers highlight an additional factor that can affect test interpretation. While screening for LTBI remains important before starting immunotherapy for safety reasons, these results suggest that latent infection may not be a major confounder of the specific inflammatory markers measured in this study. Clinicians can use this information when interpreting CRP, fecal calprotectin and cytokine data in Crohn’s care.