Abstract
Procalcitonin has been shown to be useful in separating infection from non-infective disorders. However, infection is often paralleled by tissue inflammation. Most studies supporting the use of procalcitonin were confounded by more significant inflammation in the infection group. Few studies have examined the usefulness of procalcitonin when adjusted for inflammation.Pleural inflammation underlies the development of most exudative effusions including pleural infection and malignancy. Pleurodesis, often used to treat effusions, involves provocation of intense aseptic pleural inflammation. We conducted a two-part proof-of-concept study to test the specificity of procalcitonin in differentiating infection using cohorts of patients with pleural effusions of infective and non-infective etiologies, as well as subjects undergoing pleurodesis.MethodsWe measured the blood procalcitonin level (i) in 248 patients with pleural infection or with non-infective pleural inflammation, matched for severity of systemic inflammation by C-reactive protein (CRP), age and gender; and (ii) in patients before and 24–48 hours after induction of non-infective pleural inflammation (from talc pleurodesis).Results1) Procalcitonin was significantly higher in patients with pleural infection compared with controls with non-infective effusions (n = 32 each group) that were case-matched for systemic inflammation as measured by CRP [median (25–75%IQR): 0.58 (0.35–1.50) vs 0.34 (0.31–0.42) µg/L respectively, p = 0.003]. 2) Talc pleurodesis provoked intense systemic inflammation, and raised serum CRP by 360% over baseline. However procalcitonin remained relatively unaffected (21% rise). 3) Procalcitonin and CRP levels did not correlate. In 214 patients with pleural infection, procalcitonin levels did not predict the survival or need for surgical intervention.ConclusionUsing a pleural model, this proof-of-principle study confirmed that procalcitonin is a biomarker specific for infection and is not affected by non-infective inflammation. Procalcitonin is superior to CRP in distinguishing infection from non-infective pleural diseases, even when controlled for the level of systemic inflammation.
Highlights
Procalcitonin, a precursor of calcitonin manufactured in the thyroid, is significantly elevated during many types of bacterial infection [1,2,3,4,5]
1) Procalcitonin was significantly higher in patients with pleural infection compared with controls with noninfective effusions (n = 32 each group) that were case-matched for systemic inflammation as measured by C-reactive protein (CRP) [median (25– 75%IQR): 0.58 (0.35–1.50) vs 0.34 (0.31–0.42) mg/L respectively, p = 0.003]
Procalcitonin is superior to CRP in distinguishing infection from non-infective pleural diseases, even when controlled for the level of systemic inflammation
Summary
Procalcitonin, a precursor of calcitonin manufactured in the thyroid, is significantly elevated during many types of bacterial infection [1,2,3,4,5]. Controversies exist over the benefits of procalcitonin over conventional inflammatory markers [2] and a recent meta-analysis concluded that evidence supporting the use of procalcitonin remains inadequate [7]. In certain areas, such as ventilatorassociated pneumonia, atypical pneumonia and tuberculosis, the clinical studies on the role of procalcitonin were mixed [1]. Most published studies supporting the use of procalcitonin over conventional inflammatory markers (eg Creactive protein, CRP) have compared procalcitonin in patients with bacterial infection and those with non-infective diseases or other non-bacterial infections [1] These studies are often confounded by differences in the degree of inflammation between the bacterial infection group and the controls. Without adjusting for inflammation, it is not clear if procalcitonin captures signals of infection or of inflammation associated with the more severe infection
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