A biomarker panel of C-reactive protein, procalcitonin and serum amyloid A is a predictor of sepsis in severe trauma patients.

Severe trauma could induce sepsis due to the loss of control of the infection, which may eventually lead to death. Accurate and timely diagnosis of sepsis with severe trauma remains challenging both for clinician and laboratory. Combinations of markers, as opposed to single ones, may improve diagnosis. We compared the diagnostic characteristics of routinely used biomarkers of sepsis alone and in combination, trying to define a biomarker panel to predict sepsis in severe patients. This prospective observational study included patients with severe trauma (Injury severity score, ISS = 16 or more) in the emergency intensive care unit (EICU) at a university hospital. Blood samples were collected and plasma levels of procalcitonin (PCT), C-reactive protein (CRP), interleukin-6 (IL-6) and serum amyloid A (SAA) were measured using commercial enzyme linked immunosorbent assay (ELISA) kits. A total of 100 patients were eligible for analysis. Of these, 52 were diagnosed with sepsis. CRP yielded the highest discriminative value followed by PCT. In multiple logistic regression, SAA, CRP, and PCT were found to be independent predictors of sepsis. Bioscore which was composed of SAA, CRP, and PCT was shown to be far superior to that of each individual biomarker taken individually. Therefore, compared with single markers, the biomarker panel of PCT, CRP, and SAA was more predictive of sepsis in severe polytrauma patients.

Autophagy participates in the protection role of 1,25-dihydroxyvitamin D3 in acute myocardial infarction via PI3K/AKT/mTOR pathway.

Vitamin D deficiency is associated with acute myocardial infarction (AMI); thus we aimed to explore improvement effects of 1,25-dihydroxyvitamin D3 (VD3) on the AMI and its potential mechanism. AMI models were constructed using male C57/BL6J mice and randomly treated with normal saline or VD3, using sham rats as control. Heart functions, myocardial damage, apoptosis, and inflammation were evaluated. Cardiomyocytes isolated from 3-day-old suckling mice were used for in vitro verification. After VD3 treatment, AMI-induced cardiac dysfunction was reversed with better cardiac function parameters. VD3 treatment reduced inflammatory cell infiltration and myocardial infarction area accompanied by the reduction of inflammatory factors and myocardial infarction markers compared with the AMI group. VD3 treatment obviously alleviated AMI-induced myocardial apoptosis, along with Bcl-2 upregulation and downregulation of caspase-3, caspase-9, and Bax. Both in vivo and in vitro experiments revealed that VD3 enhanced the expression of LC3II and Beclin-1 and decreased soluble p62. Furthermore, VD3 enhanced the AMI-caused inhibition of PI3K, p-AKT, and p-mTOR expression, which was conversely reversed by the addition of 3-methyladenine in vitro. The study highlights the improvement effects of VD3 on cardiac functions. We proposed a potential mechanism that VD3 protects against myocardial damage, inflammation, and apoptosis by promoting autophagy through PI3K/AKT/mTOR pathway.

Cardioprotective effect of erythropoietin on sepsis-induced myocardial injury in rats.

BACKGROUND: Sepsis-induced myocardial injury is one of the major predictors of morbidity and mortality of sepsis. The cytoprotective function of erythropoietin (EPO) has been discovered and extensively studied. However, the cardioprotective effects of EPO on sepsis-induced myocardial injury in the rat sepsis model has not been reported. METHODS: The rat models of sepsis were produced by cecal ligation and perforation (CLP) surgery. Rats were randomly (random number) assigned to one of three groups (n=8 for each group): sham group, CLP group and EPO group (1000 IU/kg erythropoietin). Arterial blood was withdrawn at 3, 6, 12, and 24 hours after CLP. cTnI, BNP, CK-MB, LDH, AST, TNF-α, IL-6, IL-10, and CRP were tested by the ELISA assay. Changes of hemodynamic parameters were recorded at 3, 6, 12, 24 hours after the surgery. Histological diagnosis was made by hematoxylin and eosin. Flow cytometry was performed to examine cell apoptosis, myocardium mitochondrial inner membrane potential, and NF-κB (p65). Survival rate at 7 days after CLP was recorded. RESULTS: In the CLP group, myocardial enzyme index and inflammatory index increased at 3, 6, 12 and 24 hours after CLP compared with the sham group, and EPO significantly blocked the increase. Compared with the CLP group, EPO significantly improved LVSP, LV +dp/dt max, LV -dp/dt min, and decreased LVEDP at different time. EPO blocked the reduction of mitochondrial transmembrane potential, suppressed the cardiomyocyte apoptosis, inhibited the activation of NF-κB, and reduced the production of proinflmmatory cytokines. No difference in the survival rate at 7 days was observed between the CLP group and the EPO group. CONCLUSION: Exogenous EPO has cardioprotective effects on sepsis-induced myocardial injury.

[Effects of fluid resuscitation on myocardial injury in patients with severe sepsis and septic shock].

OBJECTIVE: To observe the influence of fluid resuscitation on patients suffered from myocardial injury with severe sepsis and septic shock, and to evaluate the markers of myocardial injury during fluid resuscitation. METHODS: Acute physiology and chronic health evaluation II (APACHE II) score of 78 patients with severe sepsis and septic shock induced by combined injuries was 18-35. Serum cardiac troponin I (cTnI), N-terminal-ventricular natriuretic peptide precursor (NT-proBNP) and the hemodynamic parameters were recorded before, 3 days, and 5 days after treatment, and correlative analysis was conducted. RESULTS: Serum cTnI was increased in 62.8% (49/78) patients with severe sepsis and septic shock, and in 73.5% of patients (36/49) the increase was greater than 2-fold of the borderline value, and in 30.6% of patients (15/49) was greater than 4-fold of the borderline value. The patients with elevated serum NT-proBNP at admission accounted for 46.2% (36/78), and after fluid resuscitation treatment, patients with continuously rising value accounted for 74.4% (58/78). The serum cTnI, NT-proBNP, pulmonary arterial wedge pressure (PAWP) and cardiac index (CI) after treatment in survival group (55 cases) were obviously improved, and changes in them in non-survival group (23 cases) was not obvious. The serum cTnI (µg/L) and NT-proBNP (ng/L) levels in the non-survival group were distinctly higher than those of the survival group (cTnI 3 days: 2.09 ± 1.00 vs. 1.57 ± 0.93, 5 days: 1.78 ± 0.67 vs. 0.72 ± 0.51; NT-proBNP 3 days: 3.52 ± 0.73 vs. 3.16 ± 0.65, 5 days: 3.21 ± 0.66 vs. 2.66 ± 0.58), and CI [ml·s(-1)·m(-2)] was obviously lower than that of the survival group (3 days: 57.6 ± 6.2 vs. 68.3 ± 5.6, 5 days: 40.5 ± 4.7 vs. 80.7 ± 6.8, all P < 0.05). The cTnI level (µg/L) of 46 patients whose fluid resuscitation achieved the target was lower than that of the 32 cases without achieving the target (1.16 ± 0.62 vs. 1.97 ± 0.76, P < 0.05), and the CI [ml·s(-1)·m(-2)] was obviously increased (61.2 ± 6.4 vs. 49.3 ± 6.1, P < 0.05). The results suggested that whether the fluid resuscitation achieved the target or not was not related to changes in serum NT-proBNP and PAWP. A positive correlation was found between serum cTnI and NT-proBNP (r = 0.865, Y = 2.069 + 0.695X, P < 0.01), also between NT-proBNP and PAWP (r = 0.762, Y = 1.125 + 4.929X, P < 0.01), and a negative correlation was found between cTnI and CI (r = -0.891, Y = 50.623 - 6.114X, P < 0.01). CONCLUSIONS: There is an obvious myocardial injury in the patient with severe sepsis and septic shock, and fluid resuscitation can improve the myocardial injury; the serum levels of cTnI and NT-proBNP are related to the prognosis of patients, but the significance of NT-proBNP guiding the fluid resuscitation can not be ascertained.

[The influence of intensive insulin therapy on hemodynamics in patients with septic shock].

OBJECTIVE: To elucidate effects of intensive insulin therapy and target glucose control on hemodynamics and cardiac function in patients with septic shock. METHODS: Twenty-seven patients of septic shock with myocardial depression were divided into routine group (14 cases, level of blood glucose was 4.1 to 6.1 mmol/L) and target group (13 cases, level of blood glucose was 6.2 to 8.3 mmol/L). Hemodynamics and cardiac function parameters were obtained via pulmonary artery catheter after 48 hours. RESULTS: Mean blood glucose level in target group was lower than that in routine group [(6.0+/-1.5) mmol/L vs. (8.2+/-1.9) mmol/L, P<0.05], with dosage of insulin infusion in target group increased as compared with that of routine group [(10.3+/-3.7) U/h vs. (7.5+/-3.0) U/h, P<0.05]. Furthermore, oxygenation index (PaO(2)/FiO(2)), stroke volume index (SVI), cardiac index (CI) and oxygen delivery index (DO(2)I) were increased 20.2%, 23.3%, 15.1% and 11.7%, respectively (all P<0.05). On the other hands, there was no significant difference between target and routine group in mean artery pressure, acute physiology and chronic health evaluation II (APACHEII) score, blood lactic acid (all P>0.05), although the incidence of severe hypoglycemia was higher in target group than the routine group (38.5% vs. 28.6%, P>0.05). CONCLUSION: Intensive insulin therapy and blood glucose control may improve hemodynamic status and enhance cardiac function in patients with septic shock and myocardial depression.