Serum Procalcitonin Is a Candidate Biomarker to Differentiate Bacteremia from Disease Flares in Patients with Inflammatory Bowel Disease

In patients with inflammatory bowel disease (IBD), discriminating between bacterial infections and disease flares is often difficult due to the similar clinical presentations and laboratory findings. The differentiation in patients with IBD is important because treatments for each clinical condition are different and commonly opposite. Especially, early detection and treatment of infection in the disease state requiring immunosuppression have very significant impacts on good prognosis. The white blood cell count, erythrocyte sedimentation rate, and C-reactive protein (CRP) level are not always helpful in distinguishing between the clinical conditions in IBD patients because these markers are elevated not only in infectious conditions , but also when the underlying disease flares. 1-3 Moreover, inflammatory signs can be masked and the CRP level decreased with corticosteroid therapy or immunosuppression, making CRP inconsistently reliable as a biomarker for bacterial infection in these clinical conditions. 4 Recently, procalcitonin has been focused as a new biomarker to distinguish between bacterial infections and another inflam-matory process. Procalcitonin is a precursor protein of calcito-nin with a molecular weight of 13 kDa, produced by the C cells of the thyroid gland. During infection, procalcitonin is known to be synthesized and secreted from extrathyroidal area such as lung, liver, pancreas, and colon. Recently, the level has been measured routinely in some intensive care and surgery units to detect rapid evidence of bacteremia or to differentiate pancre-atitis with infected necrosis from noncomplicated pancreatitis more easily. 5 The reason why procalcitonin is worthy of more attention than other acute phase proteins is that the level is increased by infection stimuli, not by abacterial inflammatory stimuli such as IBD flares. The more usefulness of procalcitonin to differentiate bacterial infections, compared to CRP, has also been proved in other study of various autoimmune diseases. The CRP level had no additive value when combined with the procalcitonin level to determine bacterial infections. 6 Considering the mechanism of increasing serum procalcito-nin, the role of bacterial endotoxin and mediators released in response to bacterial infections (that is, interleukin-1b [IL-1b], tumor necrosis factor α [TNF-α], and IL-6) is important. 7 And procalcitonin strongly correlates with extent and severity of bacterial infections. During infections associated with marked TNF-α release, such as Gram-negative infections, the highest procalcitonin levels were seen. Meanwhile, procalcitonin levels do not increase in mycobacterial infections and viral illness. 1,5 Because upregulation of procalcitonin is attenuated by interferon γ, a cytokine released in response to viral infections, …