8 research outputs found
Procalcitonin is not sufficiently reliable to be the sole marker of neonatal sepsis of nosocomial origin
BACKGROUND: It has recently been suggested that serum procalcitonin (PCT) is of value in the diagnosis of neonatal sepsis, with varying results. The aim of this prospective multicenter study was to assess the usefulness of PCT as a marker of neonatal sepsis of nosocomial origin. METHODS: One hundred infants aged between 4 and 28 days of life admitted to the Neonatology Services of 13 acute-care teaching hospitals in Spain over 1-year with clinical suspicion of neonatal sepsis of nosocomial origin were included in the study. Serum PCT concentrations were determined by a specific immunoluminometric assay. The reliability of PCT for the diagnosis of nosocomial neonatal sepsis at the time of suspicion of infection and at 12â24 h and 36â48 h after the onset of symptoms was calculated by receiver-operating characteristics (ROC) curves. The Youden's index (sensitivity + specificity - 1) was used for determination of optimal cutoff values of the diagnostic tests in the different postnatal periods. Sensitivity, specificity, and the likelihood ratio of a positive and negative result with the 95% confidence interval (CI) were calculated. RESULTS: The diagnosis of nosocomial sepsis was confirmed in 61 neonates. Serum PCT concentrations were significantly higher at initial suspicion and at 12â24 h and 36â48 h after the onset of symptoms in neonates with confirmed sepsis than in neonates with clinically suspected but not confirmed sepsis. Optimal PCT thresholds according to ROC curves were 0.59 ng/mL at the time of suspicion of sepsis (sensitivity 81.4%, specificity 80.6%); 1.34 ng/mL within 12â24 h of birth (sensitivity 73.7%, specificity 80.6%), and 0.69 ng/mL within 36â48 h of birth (sensitivity 86.5%, specificity 72.7%). CONCLUSION: Serum PCT concentrations showed a moderate diagnostic reliability for the detection of nosocomial neonatal sepsis from the time of suspicion of infection. PCT is not sufficiently reliable to be the sole marker of sepsis, but would be useful as part of a full sepsis evaluation
Evaluation of procalcitonin for diagnosis of neonatal sepsis of vertical transmission
BACKGROUND: The results of recent studies suggest the usefulness of PCT for early diagnosis of neonatal sepsis, with varying results. The aim of this prospective multicenter study was to determine the behavior of serum PCT concentrations in both uninfected and infected neonates, and to assess the value of this marker for diagnosis of neonatal sepsis of vertical transmission. METHODS: PCT was measured in 827 blood samples collected prospectively from 317 neonates admitted to 13 acute-care teaching hospitals in Spain over one year. Serum PCT concentrations were determined by a specific immunoluminometric assay. The diagnostic efficacy of PCT at birth and within 12â24 h and 36â48 h of life was evaluated calculating the sensitivity, specificity, and likelihood ratio of positive and negative results. RESULTS: 169 asymptomatic newborns and 148 symptomatic newborns (confirmed vertical sepsis: 31, vertical clinical sepsis: 38, non-infectious diseases: 79) were studied. In asymptomatic neonates, PCT values at 12â24 h were significantly higher than at birth and at 36â48 h of life. Resuscitation at birth and chorioamnionitis were independently associated to PCT values. Neonates with confirmed vertical sepsis showed significantly higher PCT values than those with clinical sepsis. PCT thresholds for the diagnosis of sepsis were 0.55 ng/mL at birth (sensitivity 75.4%, specificity 72.3%); 4.7 ng/mL within 12â24 h of life (sensitivity 73.8%, specificity 80.8%); and 1.7 ng/mL within 36â48 h of life (sensitivity 77.6%, specificity 79.2%). CONCLUSION: Serum PCT was moderately useful for the detection of sepsis of vertical transmission, and its reliability as a maker of bacterial infection requires specific cutoff values for each evaluation point over the first 48 h of life
Accuracy of serum procalcitonin for the diagnosis of sepsis in neonates and children with systemic inflammatory syndrome: a meta-analysis
64 PROCALCITONIN AS A SCREENING TEST IN LATE ONSET SEPSIS IN VERY LOW BIRTH WEIGHT PRETERM INFANTS.
A Glutathione Precursor Reduces Oxidative Injury to Cultured Embryonic Cardiomyocytes
BACKGROUND: Newborn infants are highly vulnerable to oxidative stress. Following birth asphyxia, oxidative injury due to ischemia-reperfusion can result in significant brain and heart damage, leading to death or long-term disability.
STUDY QUESTION: The study objective was to evaluate the effectiveness of antioxidant gamma-L-glutamyl-L-cysteine (ÎłGlu-Cys) in inhibiting oxidative injury to cultured embryonic cardiomyocytes (H9c2 cells).
STUDY DESIGN: Control and ÎłGlu-Cys-treated (0.5 mM) H9c2 cells were incubated under 6-hour ischemic conditions followed by 2-hour simulated reperfusion.
MEASURES AND OUTCOMES: To quantify oxidative stress-induced apoptosis sustained by cardiomyocytes, lactate dehydrogenase (LDH) release and the presence of cytosolic cytochrome c were measured, as well as the number of secondary lysosomes visualized under electron microscopy.
RESULTS: Compared to controls, H9c2 cells coincubated with ÎłGlu-Cys during ischemia-reperfusion exhibited a significant reduction in both LDH release into the incubation medium [23.88 ± 4.08 (SE) vs. 9.95 ± 1.86% of total; P = 0.02] and the number of secondary lysosomes [0.070 ± 0.009 (SD) vs. 0.043 ± 0.004 per ÎŒm; P = 0.01]. Inhibition of LDH release with ÎłGlu-Cys was the same (P = 0.67) as that of a caspase inhibitor. The significant increase in cytosolic cytochrome c (P = 0.01) after ischemia-reperfusion simulation further supports ÎłGlu-Cys\u27s role in apoptosis prevention.
CONCLUSIONS: It is concluded that the glutathione precursor ÎłGlu-Cys protects cultured embryonic cardiomyocytes from apoptosis-associated oxidative injury
ÎČ1-Integrin blockade prevents podocyte injury in experimental models of minimal change disease
Introduction: Activation of the focal adhesion kinase (FAK) in podocytes is involved in the pathogenesis of minimal change disease (MCD), but the pathway leading to its activation in this disease is unknown. Here, we tested whether podocyte ÎČ1 integrin is the upstream modulator of FAK activation and podocyte injury in experimental models of MCD-like injury. Methods: We used lipopolysaccharide (LPS) and MCD sera to induce MCD-like changes in vivo and in cultured human podocytes, respectively. We performed functional studies using specific ÎČ1 integrin inhibitors in vivo and in vitro, and integrated histological analysis, western blotting, and immunofluorescence to assess for morphological and molecular changes in podocytes. By ELISA, we measured serum LPS levels in 35 children with MCD or presumed MCD (idiopathic nephrotic syndrome [INS]) and in 18 healthy controls. Results: LPS-injected mice showed morphological (foot process effacement, and normal appearing glomeruli on light microscopy) and molecular features (synaptopodin loss, nephrin mislocalization, FAK phosphorylation) characteristic of human MCD. Administration of a ÎČ1 integrin inhibitor to mice abrogated FAK phosphorylation, and ameliorated proteinuria and podocyte injury following LPS. Children with MCD/INS in relapse had higher serum LPS levels than controls. In cultured human podocytes, ÎČ1 integrin blockade prevented cytoskeletal rearrangements following exposure to MCD sera in relapse. Conclusions: Podocyte ÎČ1 integrin activation is an upstream mediator of FAK phosphorylation and podocyte injury in models of MCD-like injury