Potential use of procalcitonin as biomarker for bacterial sepsis in patients with or without acute kidney injury.

INTRODUCTION: There are few investigations regarding the relationships between procalcitonin (PCT) and the acute kidney injury (AKI) in the diagnosis of sepsis. The purpose of this study was to clarify the diagnostic accuracy of the use of PCT levels in patients with or without AKI. METHODS: This study was conducted as a single-center retrospective study. We enrolled 393 patients in whom PCT were measured on admission. We grouped the patients into non-AKI and AKI, and those with AKI were classified according to the RIFLE criteria (Risk, Injury, Failure). The patients in each group were further classified into the sepsis and the non-sepsis group. We subsequently investigated the diagnostic accuracy of the PCT for detecting sepsis in these groups. RESULTS: The levels of PCT were significantly higher in the sepsis group than in the non-sepsis group among the non-AKI and each AKI patients (p < 0.0001). The diagnostic accuracy of the PCT for detecting sepsis was determined according to a ROC analysis; AUC value was 0.958 in the non-AKI group, in the Risk, Injury and Failure groups were 0.888 and 0.917, 0.857, respectively. AUC value for non-AKI group was significantly different from that of Failure group (p < 0.05). CONCLUSIONS: In Failure AKI patients, the diagnostic accuracy of the PCT level is significantly lower than non-AKI patients. It is therefore suggested that we should be careful in using PCT value to diagnose sepsis in patients with Failure under RIFLE criteria.

Methicillin-resistant Staphylococcus aureus bloodstream infections in a Japanese University Hospital between 1987 and 2004.

Methicillin-resistant Staphylococcus aureus (MRSA) infections have been the most common cause of nosocomial infections in Japan, but their genetic characteristics related to bloodstream infections have not been well studied. The aim of this study was to investigate a comprehensive molecular characterization of MRSA blood isolates during the historical 18-year study period between 1987 and 2004 in a tertiary care university hospital. A total of 137 MRSA isolates recovered from the blood of inpatients at Fukuoka University Hospital were analyzed. Clinical information and antimicrobial susceptibility profiles were reviewed, and staphylococcal chromosomal cassette mec (SCCmec), accessory gene regulator (agr), and a battery of bacterial genes were tested by PCR-based assays. The relatedness of these isolates was determined by the repetitive sequence-based PCR (rep-PCR) and pulsed-field gel electrophoresis (PFGE). Although low numbers of agr type III/SCCmec type IV isolates circulated between 1987 and 1992, agr type II/SCCmec type II isolates started circulating in 1993 and were responsible for the increased MRSA isolates until 2004. The rep-PCR and PFGE identified 104 epidemic and 33 sporadic isolates. Among the 104 epidemic isolates, six major rep-PCR/PFGE types were identified, which occupied 67.3% of epidemic isolates. The SCCmec type II and agr type II isolates were observed in significantly higher proportion in epidemic isolates than in sporadic isolates (P = 0.0318, P = 0.0123, respectively). In contrast, SCCmec type IV strains were observed in significantly higher proportion in sporadic isolates than in epidemic isolates (P = 0.0494). Although isolates with sec were detected in higher rates in epidemic isolates (P = 0.0397), seh was detected in higher rates in sporadic isolates (P = 0.0350). Multivariate logistic regression analysis with forward stepping revealed that SCCmec type II was independently associated with epidemic isolates (P = 0.0067; odds ratio, 1.75; 95% confidence interval, 1.17-2.64). These data indicated that SCCmec type II MRSA isolates were responsible for the increased MRSA bloodstream infections for inpatients during the 18-year study period in the hospital.

Intravenous immunoglobulin improves sepsis-induced coagulopathy: A retrospective, single-center observational study.

INTRODUCTION: Inflammation and coagulation are closely interrelated processes in the pathogenesis of sepsis. This study aimed to determine whether intravenous immunoglobulin (IVIg) could improve the hyperinflammatory state and coagulation/fibrinolysis abnormalities in patients with sepsis. METHODS: Forty-one patients with sepsis were included. Nineteen patients were treated with IVIg (IVIg group; 5.0 g daily for 3 days within 2 days after hospitalization), and 22 patients were not (non-IVIg group). Inflammatory and coagulation/fibrinolysis molecular markers, Japanese Association for Acute Medicine disseminated intravascular coagulation score, and the Sequential Organ Failure Assessment score were evaluated in each group. RESULTS: On admission, patients in the IVIg group had a significantly more severe condition. In the IVIg group, after treatment, C-reactive protein, procalcitonin, and interleukin-6 levels significantly decreased relative to values on admission. Also, compared with admission, the various coagulation/fibrinolysis molecular markers decreased after treatment. Moreover, the Japanese Association for Acute Medicine disseminated intravascular coagulation score and the Sequential Organ Failure Assessment score also significantly decreased after treatment. In contrast, in the non-IVIg group, only interleukin-6 level and thrombin-antithrombin complex levels significantly decreased. The 28-day mortality rate of the IVIg group was approximately one third of the value of the non-IVIg group (IVIg: 5.3% vs non-IVIg: 18.2%). CONCLUSIONS: Intravenous immunoglobulin treatment significantly improved hemostatic abnormalities along with the hyperinflammatory state in patients with sepsis. Accordingly, IVIg treatment should be classified as an adjunctive therapy for patients complicated with sepsis-induced coagulopathy.