| Institution: | 1. Clinical Laboratory, Hirosaki University Hospital, Hirosaki, Japan;2. Department of Clinical Laboratory Medicine, Hirosaki University Graduate School of Medicine, Hirosaki, Japan;3. Aomori Infection Control Netowork, Hirosaki, Japan;1. Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan;2. Center for Education in Medicine and Health Sciences, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan;3. Department of Primary Care and Medical Education, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan;1. Department of Pharmacy, Tsuyama Chuo Hospital, 1756 Kawasaki, Tsuyama, Okayama, 708-0841, Japan;2. Department of General Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan;1. Department of Bacteriology I, National Institute of Infectious Diseases, Tokyo, Japan;2. Division of Environmental and Preventive Medicine, Department of Social Medicine, Graduate School of Medicine, Tottori University, Tottori, Japan;3. Infectious Disease Surveillance Center, National Institute of Infectious Diseases, Tokyo, Japan;4. Osaka City Public Health Office, Osaka, Japan;5. Antimicrobial Resistance Surveillance Center, National Institute of Infectious Diseases, Tokyo, Japan;1. Department of Pharmacy, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, 250021, China;2. Department of Traumatic Orthopaedics, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, 250021, China;1. Virology Laboratory, Basil Hetzel Institute, Department of Surgery, University of Adelaide, Adelaide, Australia;2. Inflammation Biology Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia;3. School of Molecular Biosciences, University of Adelaide, Adelaide, Australia;4. South Australian Health and Medical Research Institute, Adelaide, Australia |
| Abstract: | IntroductionThe aim of this study was to investigate procalcitonin levels according to the causative pathogens of bacteremia. The relationships between the clinical outcomes and procalcitonin levels were also studied.MethodsFrom among 452 patients, 507 cases of positive blood culture were included in the present study. Procalcitonin levels were studied according to the pathogen types. The prevalence of septic shock and the mortality rates were also studied in four groups stratified by the procalcitonin levels (groups 1, 2, 3, and 4 had procalcitonin levels of <0.5 ng/mL, 0.5 ≤ 2.0 ng/mL, 2.0 < 10 ng/mL, and ≥10 ng/mL, respectively).ResultsThe procalcitonin levels were significantly higher in bacteremia cases with Gram-negative rods (19.50 ng/mL), such as Escherichia coli (32.5 ng/mL), than those with Gram-positive rods (8.45 ng/mL) or Gram-positive cocci (9.21 ng/mL) (p < 0.01). The 28-day mortality rates in groups 1, 2, 3, and 4 were 6.0%, 12.0%, 14.9%, and 19.8%, respectively. The procalcitonin levels of samples taken before or on the same day of blood cultures were significantly lower than those taken one day after blood cultures. Multiple logistic regression analysis showed that C-reactive protein and procalcitonin ≥10 ng/mL were independently associated with a higher risk of mortality within 28 days.ConclusionsThe PCT levels were higher in cases of bacteremia caused by GNR than those caused by GPR or GPC. The 28-day mortality rate increased as the PCT levels increased. Clinical importance of early evaluations and appropriate interpretation of procalcitonin levels for bacteremia were indicated. |
