Development Of Sepsis Syndrome Research Articles

Clinic and diagnosis of encephalopathy of critical conditions in children with infectious diseases

Purpose: to assess the functional state of the brain in critically ill encephalopathy in children with infectious diseases.Materials and methods: 75 patients aged from 1 month to 17 years 11 months with infectious diseases, who were in the intensive care unit of the clinic, were examined, divided into two groups: the main group and the comparison group. Exclusion criteria: patients with cerebral palsy, organic lesions of the central nervous system, neuroinfections and epilepsy. Conducted daily clinical and neurological examination; study of the level of neurospecific proteins (NSE, protein S100) in blood serum; electroencephalography; study of evoked potentials of various modalities; ultrasound examination of the optic nerves, neuroimaging.Results: All patients had general infectious manifestations, the development of sepsis syndrome, cerebral systemic disorders with impaired consciousness, as well as convulsive syndrome. In the acute period of the disease in the main group, NSE values in 87.5% of children were within the upper limit of normal, S100 protein levels were many times higher than those in the comparison group. In dynamics, all patients showed an increase in the level of NSE, which correlated with persistent neurological symptoms in the form of irritability, weakness, and cognitive decline. In the comparison group, an increase in NSE occurred in 53% of children, an increase in S100 - in 83%. By the time of discharge, 47% of patients had an increase NSE and S100 protein. Visual evoked potentials in 84% of the children of the main group in the acute period, had a decrease the amplitude of the N2-P2 cortical response was revealed without significant dynamics in the future, which was accompanied by pronounced clinical manifestations, which made it possible to substantiate the expediency of dispensary observation of children who underwent a critical condition against the background of severe infectious pathology.Conclusion: in infectious diseases in children that are not accompanied by inflammatory processes in the nervous system, but proceed with the development of a critical condition, there is a neuropsychiatric deficit in the outcomes, which necessitates follow-up follow-up of such patients in the future.

The novel translocation of t (1;21) in multiple myeloma with poor prognosis

Objective: Multiple myeloma (MM) is characterized as the neoplastic proliferation of plasma cells producing a monoclonal paraprotein. The aim of this paper is to report complex karyotype that leads to a fatal clinical course in a patient with MM. Case: A 48-year-old male patient was diagnosed as MM free lambda. The karyotype of the patient was 46, XY, t(1;21) (p11;p11), del(3) (q25;q29), del(6) (q24;q26), t(11;14) (q13;q32), del(13) (q14;q21) in cytogenetic evaluation. Vincristine, doxorubicin and dexamethasone were started. The creatinine levels increased after the second course of chemotherapy, the chemotherapy protocol was switched to bortezomib and dexamethasone. Patient was admitted to the emergency department with pneumonia after the second chemotherapy cycle. Despite using broad spectrum antibiotics and oxygen support, he died after the development of sepsis syndrome. Conclusion: The anomaly of t (1;21) (p11;p11), that we detected in this case was detected in a case with MM for the first time and this anomaly has not been detected between these breaking points in any malignancies before. Although the prognostic impact of this unique anomaly may be unclear, further studies are needed to evaluate the effect of cytogenetic anomalies on prognosis of multiple myeloma.

Correlation of Cytokines with Outcome in Children with Dengue and Septic Shock

Correlation of Cytokines with Outcome in Children with Dengue and Septic Shock Cytokines are inflammatory mediators responsible for diffuse tissue injury associated with infections. Of the numerous mediators implicated in the development of sepsis syndrome, evidence suggests that cytokines are decisive factors in determining the pathobiology of septic shock.

Posaconazole as successful treatment for fungemia due to Cryptococcus albidus in a liver transplant recipient

A 55-year-old man with Laennec cirrhosis and a MELD score of 24 underwent orthotopic liver transplantation. Post-operatively his recovery was complicated by development of sepsis syndrome with fever and respiratory failure. Antimicrobial coverage with broad-spectrum antibacterials, fluconazole 400 mg IV daily, and prophylactic doses of oral trimethoprim/sulfamethoxazole and valganciclovir as well as immunosuppressive treatment with sirolimus, mycophenolate mofetil and intermittent doses of lymphocyte immune globulin, anti-thymocyte, were begun in the perioperative period. Focus of infection was not identified despite an aggressive evaluation including unremarkable physical examination and computed tomograms of the chest, abdomen, and pelvis, negative cultures of bronchoalveolar lavage fluid, negative stool assay for Clostridium difficile toxin, and multiple negative cultures of blood and urine. Daily fevers in excess of …

Tumor necrosis factor alpha gene variants do not display allelic imbalance in circulating myeloid cells

Carriage of the TNF -308 A allele (rs1800629 A) has been associated with increased serum TNF-alpha levels, the development of sepsis syndrome, and fatal outcome, in severely traumatized patients (Menges et al., 2008 [1]). Herein, we analysed the putative allelic imbalance of TNF-alpha release from myeloid cells. Circulating peripheral blood cells from healthy human blood donors (n=104) and monocyte-derived macrophages (n=158) were analysed for their ex vivo capacity of TNF-alpha expression. Our findings indicate that carriage of the TNF -308 A allele is not associated with high TNF-alpha expression in circulating human leucocytes and monocyte-derived macrophages. Other cellular sources, e.g. tissue-resident cells like mast cells and/or tissue specific macrophages might be the cellular source of high TNF-alpha serum levels shortly after trauma.

Sepsis syndrome and death in trauma patients are associated with variation in the gene encoding tumor necrosis factor*

Patients encountering severe trauma are at risk of developing sepsis syndrome and subsequent multiple organ failure. This is often associated with fatal outcome despite survival of the initial injury. We postulate that variation of the gene coding for tumor necrosis factor (TNF)-alpha is associated with increased occurrence of sepsis syndrome and mortality in trauma patients. Prospective cohort study; validation in an external replication sample. Tertiary academic medical center. We included 159 severely traumatized patients from a single center. Serial blood samples were analyzed for serum concentrations of TNF-alpha and lymphotoxin-alpha (LTA). We genotyped nine polymorphisms in the TNF gene and tested for an association with sepsis syndrome and outcome. Genetic associations were validated in an external replication sample (n = 76). We examined the peripheral blood transcriptome in 28 patients by whole genome-based profiling and validated the results. None. Carriage of the TNF rs1800629 A allele was associated with higher TNF-alpha serum concentrations on the first day after trauma and during follow-up (two-sided p = 5.0 x 10(-5)), with development of sepsis syndrome (odds ratio 7.14, two-sided p = 1.2 x 10(-6); external validation sample [n = 76]: odds ratio 3.3, one-sided p = .03), and with fatal outcome (odds ratio 7.65, two-sided p = 1.9 x 10(-6)). Carriage of the TNF rs1800629 A allele was associated with differential expression of genes representing stronger proinflammatory and apoptotic responses compared with carriage of the wild-type allele. Common TNF gene variants are associated with sepsis syndrome and death after severe injury. These findings are strongly supported by functional data and may be important for developing preemptive anti-inflammatory interventions in carriers of the risk-associated allele.

Vascular access in haemodialysis patients: a modifiable risk factor for bacteraemia and death

Bacteraemia and the development of sepsis syndrome is second only to cardiovascular disease as the leading cause of death in patients on renal replacement therapy. To determine the contributions of laboratory and clinical variables to the risk of bacteraemia and death in haemodialysis patients. Retrospective analysis. We analysed all patients receiving haemodialysis in our renal unit at the beginning of January 2004 (n=263), recording clinical and laboratory variables for each patient at study entry. Bacteraemia and mortality were recorded for the subsequent 18-month period. Multivariate analysis using a Cox proportional hazards model was used to test for independent associations between variables and outcomes. During the study period, 45 patients (17.1%) developed bacteraemia and 65 (24.7%) died. Under multivariate analysis, use of dialysis catheters at study entry was a major factor in the development of bacteraemia and death with hazard ratios (HR) of 5.4 (p<0.001) and 2.8 (p=0.012), respectively, for tunnelled central venous catheters vs. arteriovenous fistulas (AVFs) and 3.1 (p=0.01) and 3.4 (p=0.001), respectively, for non-tunnelled central venous catheters vs. AVFs. Elevated CRP at study entry was independently associated with bacteraemia (HR 1.5 per unit log-CRP, p=0.006). Low serum albumin (HR 0.92, p=0.005) was independently associated with death. Use of synthetic vascular access catheters and heightened inflammatory state both have strong independent associations with subsequent bacteraemia and death. Bacteraemia surveillance strategies should be developed, with consideration of vascular access type and baseline inflammatory state as key components.

Prolonged Exposure to Lipopolysaccharide Inhibits Macrophage 5-Lipoxygenase Metabolism Via Induction of Nitric Oxide Synthesis

LPS from bacteria can result in the development of sepsis syndrome and acute lung injury. Although acute exposure to endotoxin primes leukocytes for enhanced synthesis of leukotrienes (LT), little is known about the effect of chronic exposure. Therefore, we determined the effect of prolonged LPS treatment on 5-lipoxygenase (5-LO) metabolism of arachidonic acid in alveolar macrophages (AM) and in peripheral blood monocytes. Pretreatment of AM with LPS caused time- and dose-dependent suppression of LT synthetic capacity. LPS pretreatment failed to inhibit arachidonic acid (AA) release. The fact that LPS inhibited LT synthesis from endogenous AA more than from exogenous AA suggested an effect on 5-LO-activating protein (FLAP). In addition, an inhibitory effect of LPS treatment on AM 5-LO activity was suggested by cell-free 5-LO enzyme assay. No effect on the expression of either 5-LO or FLAP proteins was observed. New protein synthesis was necessary for LPS-induced reduction of 5-LO metabolism in AM, and immunoblotting demonstrated marked induction of NO synthase (NOS). Inhibition by LPS was reproduced by an NO donor and was abrogated by inhibitors of constitutive and inducible NOS. Compared with AM, peripheral blood monocytes exhibited no suppression by LPS of 5-LO metabolism and no induction of inducible NOS. We conclude that prolonged exposure to LPS impairs AM 5-LO metabolism by NO-mediated suppression of both 5-LO and FLAP function. Because LT contribute to antimicrobial defense, this down-regulation of 5-LO metabolism may contribute to the increased susceptibility to pneumonia in patients following sepsis.