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LETTER TO EDITOR  
Year : 2015  |  Volume : 7  |  Issue : 3  |  Page : 120-121
The role of procalcitonin levels in assessing the severity of Clostridium difficile infection


Department of Infectious Diseases, St Michael's Medical Center, Newark, New Jersey, United States

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Date of Web Publication18-Aug-2015
 

How to cite this article:
Dazley J, Shaaban H, Afridi S, Slim J. The role of procalcitonin levels in assessing the severity of Clostridium difficile infection. J Global Infect Dis 2015;7:120-1

How to cite this URL:
Dazley J, Shaaban H, Afridi S, Slim J. The role of procalcitonin levels in assessing the severity of Clostridium difficile infection. J Global Infect Dis [serial online] 2015 [cited 2019 Sep 15];7:120-1. Available from: http://www.jgid.org/text.asp?2015/7/3/120/162229


Sir,

Clostridium difficile-associated disease (CDAD) is the most recognized cause of healthcare-associated infectious diarrhea and a major cause of morbidity and mortality in hospitalized patients. [1],[2] Clinical manifestations range from mild or moderate watery diarrhea to fulminant, pseudomembranous colitis. [3] Because of the heterogeneous presentation of CDAD, early identification of severe illness may be crucial in the institution of prompt and proper management. [4],[5] There is a paucity of research on biomarkers for the diagnosis for CDAD. [6] Procalcitonin (PCT) is a Food and Drug Administration (FDA)-approved biomarker that is produced by numerous cells in the body, specifically in response to bacterial infections (i. e., pneumonia and sepsis). [7],[8] Its role in the identification of severe CDAD has not been validated. [9],[10] This analysis was conducted in order to evaluate the role of PCT levels as a diagnostic adjunct in the identification of severe CDAD.

A retrospective chart review was conducted in two inner city hospitals in New Jersey. All patients > 18 years of age admitted between January 1, 2011 and August 2012 who were diagnosed with CDAD were eligible. CDAD was defined as having diarrhea (i. e., more than watery stools/24 h) plus a positive Clostridium difficile stool assay (positive enzyme immunoassay for toxin A/B test or polymerase chain reaction (PCR) test). Only patients who had a PCT level drawn within 24 h of confirmation of CDAD were included. The following data were collected: A. Markers of CDAD severity - white blood cell (WBC) count, serum creatinine, serum albumin, temperature, and blood pressure. b. Risk factors and other variables - age, gender, residence in a nursing home, concomitant suspected or confirmed acute bacterial infection, and Charlson comorbidity score. Severe CDAD was defined as presence of CDAD plus any one of the following: WBC > 15,000 cells/ml, fever (temperature > 38.2°C), and 50% increase in serum creatinine from baseline or hypotension (systolic blood pressure (SBP) < 90 mmHg or mean arterial pressure (MAP) < 60).

Logistic regression analysis was done to determine the association between severe CDAD and PCT, as well as the risk factors. Receiver operating characteristic (ROC) curve analysis was done to determine the best cutoff point for PCT. [Figure 1] Fifty-three patients were included in the study, and their characteristics included the following: [Table 1] Mean age in years, 69.2 ± 19 (43.4%); male gender 41.5%; and patients with severe CDAD, 62.3%. Age, gender, concurrent bacterial infection, and residence in the nursing home did not affect PCT's association with severe CDAD.
Figure 1: Logistic regression analysis was done to determine the association between severe CDAD and PCT and receiver operating characteristic (ROC) curve analysis was done to determine the best cut-off point for PCT

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Table 1: Patient characteristics

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PCT > 0.5 is a marker to identify severe CDAD; specificity 86.1%, sensitivity 88.2%, positive predictive value (PPV) 93.9%, and negative predictive value (NPV) 75.0%. [Figure 1] [Table 2].
Table 2: Odds ratio for how different variables are associated with severe CDAD

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PCT levels at > 0.5 μg/mL appear to be a good indicator of severe CDAD, with a very high PPV. [Table 3] Prospective, larger studies are needed to validate this finding. Further research is needed as to whether following PCT levels may be helpful in determining resolution of the disease, risk of relapse, or predict mortality.
Table 3: PCT > 0.5 as a marker to identify severe CDAD

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   References Top

1.
Falsey AR, Becker KL, Swinburne AJ, Nylen ES, Formica MA, Hennessey PA, et al. Bacterial complications of respiratory tract viral illness: A comprehensive evaluation. J Infect Dis 2013;208:432-41.  Back to cited text no. 1
    
2.
Redelings MD, Sorvillo F, Mascola L. Increase in Clostridium difficile-related mortality rates, United States, 1999-2004. Emerg Infect Dis 2007;13:1417-9.  Back to cited text no. 2
    
3.
Rao K, Walk ST, Micic D, Chenoweth E, Deng L, Galecki AT, et al. Procalcitonin levels associate with severity of Clostridium difficile infection. PLoS One 2013;8:e58265.  Back to cited text no. 3
    
4.
Scawn N, Saul D, Pathak D, Matata B, Kemp I, Stables R, et al. A pilot randomised controlled trial in intensive care patients comparing 7 days' treatment with empirical antibiotics with 2 days' treatment for hospital-acquired infection of unknown origin. Health Technol Assess 2012;16:i-xiii, 1-70.  Back to cited text no. 4
    
5.
Tokman S, Schuetz P, Bent S. Procalcitonin-guided antibiotic therapy for chronic obstructive pulmonary disease exacerbations. Expert Rev Anti Infect Ther 2011;9:727-35.  Back to cited text no. 5
    
6.
Kuijper EJ, Coignard B, Tüll P. ESCMID Study Group for Clostridium difficile, EU Member States, European Centre for Disease Prevention and Control. Emergence of Clostridium difficile-associated disease in North America and Europe. Clin Microbiol Infect 2006;12:2-18.  Back to cited text no. 6
    
7.
Bartlett JG. Clinical practice. Antibiotic-associated diarrhea. N Engl J Med 2002;346:334-9.  Back to cited text no. 7
    
8.
Dubberke ER, Reske KA, Olsen MA, McDonald LC, Fraser VJ. Short- and long-term attributable costs of clostridium difficile-associated disease in nonsurgical inpatients. Clin Infect Dis 2008;46:497-504.  Back to cited text no. 8
    
9.
McDonald LC, Owings M, Jernigan DB. Clostridium difficile infection in patients discharged from US short-stay hospitals, 1996-2003. Emerg Infect Dis 2006;12:409-15.  Back to cited text no. 9
    
10.
Burckhardt F, Friedrich A, Beier D, Eckmanns T. Clostridium difficile surveillance trends, Saxony, Germany. Emerg Infect Dis 2008;14:691-2.  Back to cited text no. 10
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Correspondence Address:
Hamid Shaaban
Department of Infectious Diseases, St Michael's Medical Center, Newark, New Jersey
United States
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0974-777X.162229

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2008 Journal of Global Infectious Diseases | Published by Wolters Kluwer - Medknow
Online since 10th December, 2008