Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of suspected or confirmed neonatal sepsis in modifying the risk of atopic disease during childhood was assessed. Children with early-onset neonatal sepsis were identified from a cohort of neonates, hospitalized between 1990 and 1995. Of 196 individuals, 140 were recruited (71.4%). Pre- and postnatal history was ascertained from neonatal medical records. Based on clinical symptoms and a positive blood culture or at least three of initially defined laboratory or bacteriological criteria, they were stratified in either confirmed neonatal sepsis (CS) or suspected sepsis (SS) group. A control group (C) comprised children who were never hospitalized during infancy (n = 696). Primary end-point was the development of atopic dermatitis, bronchial asthma or allergic rhinitis during childhood (mean age 8.4 yr, range 5.7-12.4). CS and SS children had a higher prevalence of atopic dermatitis (CS 15.7%, SS 21.4%) compared with controls (C 5.2%, p < 0.001). Similarly, children with SS (7.1%), but not with CS (4.3%) had significantly more often a doctor's diagnosis of bronchial asthma compared to controls (1.9%, p = 0.02). No difference in the prevalence of allergic rhinitis was observed (CS 4.3%, SS 10%, C 8.3%). After adjusting for parental history of atopic disease and demographic factors, no significant difference for the risk to develop atopic dermatitis, asthma or allergic rhinitis among the groups was calculated in children with normal birth weight (>2500 g). Our data failed to show a possible link between hospital admission with SS and development of atopic disease.
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PMID:Hospital admission with neonatal sepsis and development of atopic disease: Is there a link? 1634 83

A 92-year-old man with a history of bronchial asthma and allergic rhinitis received antibiotics for sepsis by methicillin-resistant Staphylococcus aureus and multidrug-resistant Enterococcus gallinarum. During the antibiotics treatment, skin eruptions, liver dysfunction, and hypereosinophilia developed, followed by dyspnea, congestive heart failure, electrocardiographic abnormalities, and diffuse mild myocardial hypokinesis. After the discontinuation of the antibiotics and the administration of steroid, skin eruptions, liver dysfunction, and hypereosinophilia improved parallel with the improvement of the congestive heart failure. Vancomycin hydrochloride and teicoplanin were suspected as the causative drugs on the basis of the treatment course. Although congestive heart failure is rare in the case of drug-induced hypereosinophilia, it is one of life-threatening complications. We describe herein a case of congestive heart failure associated with hypereosinophilia developed during antibiotics treatment, successfully treated with steroid after the discontinuation of the causative drug.
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PMID:[Case of congestive heart failure associated with hypereosinophilia developed during antibiotics treatment]. 1640 68

Platelet Activating Factor (PAF) is a D-glycerol derived phosopholipid which is a potent endogenous mediator of inflammation. PAF is synthesized and released by a variety of cell types and elicits its biological activity by interacting with specific G-protein coupled receptors found on platelets, neutrophils, and other inflammatory cells. The physiological consequences of the interaction on PAF with its receptor include an increase in vascular permeability, hypotension, bronchoconstriction, and platelet and neutrophil aggregation. These biological effects are consistent with the concept that PAF is involved in a number of inflammatory diseases such as septic shock and asthma (Arimura A., 1998). Given the potent pathophysiological effects of PAF, a great deal of effort has been focused on the discovery of agents which block the action of PAF at its receptor. Within the past 10 years, a wide range of structures have been identified as PAF antagonists. These include not only PAF analogs, but also antagonists derived form natural product as well as non-lipid synthetic compounds. Several theories have been proposed to unify these diverse structural classes, but sophisticated molecular models of the receptor have not been widely employed (Braquet P., 1987). The discovery of new PAF antagonists has relied heavily on traditional medicinal chemistry approaches. A number of PAF antagonists have advanced to clinical evaluation. While several early compounds demonstrated efficacy in animal models of asthma they have failed to provide benefit for this condition in man. The current generation of potent antagonists are being evaluated as therapies for sepsis, pancreatitis and other disorders (Braquet C., 1991).
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PMID:Platelet Activating Factor antagonists. 1641 13

Platelet-activating factor (PAF) is a potent lipid mediator that has been implicated in asthma, sepsis, acute lung injury and ischemia/reperfusion injury. Its actions in the lungs include vasoconstriction, bronchoconstriction, and edema formation. Despite the fact that PAF exerts these actions within minutes, they are mediated by other lipid mediators, in particular eicosanoids generated by cyclooxygenase and lipoxygenase enzymes and sphingolipids generated by acid sphingomyelinase.We will discuss the mechanisms of the PAF-induced pressor responses that are triggered by thromboxane A(2) and leukotrienes, as well the PAF-induced increase in vascular permeability that is mediated by prostaglandin E(2) (PGE(2)) and ceramide.
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PMID:Mechanisms of platelet-activating factor (PAF)-mediated responses in the lung. 1641 1

Toxic neutrophils exhibit a variety of nuclear and cytoplasmic abnormalities in Romanowsky-stained blood smears, and are associated with inflammation and infection. The purpose of the retrospective study reported here was to investigate the association of toxic neutrophils with clinicopathologic characteristics, diseases, and prognosis in cats. Cats with toxic neutrophils (n = 150) were compared with negative-control cats (n = 150). Statistical analyses included Fisher exact, independent t-, nonparametric Mann-Whitney, and chi-squared tests. Cats with toxic neutrophils had significantly (P < .05) higher prevalence of fever, icterus, vomiting, diarrhea, depression, dehydration, weakness, and cachexia, as well as leukocytosis, neutrophilia, left shift, neutropenia, anemia, hypokalemia, and hypocalcemia. The prevalence of shock, sepsis, panleukopenia, peritonitis, pneumonia, and upper respiratory tract diseases was significantly higher among these cats, as were infectious (viral and bacterial) and metabolic disorders. Control cats had a significantly higher prevalence of feline asthma, as well as allergic, idiopathic, and vascular disorders. Hospitalization duration and treatment cost were significantly (P < .001) higher in cats with toxic neutrophils. In 53 and 47% of the cats with toxic neutrophils, the leukocyte and neutrophil counts were normal, respectively, whereas in 43%, both abnormalities and left shift were absent, and toxic neutrophils were the only hematologic evidence of inflammation or infection. In conclusion, toxic neutrophils were found to be associated with certain clinicopathologic abnormalities, and when present, may aid in the diagnosis, as well as the assessment of hospitalization duration and cost. The evaluation of blood smears for toxic neutrophils provided useful clinical information.
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PMID:Toxic neutrophils in cats: clinical and clinicopathologic features, and disease prevalence and outcome--a retrospective case control study. 1649 19

Cytokines regulate cellular immune activity and are produced by a variety of cells, especially lymphocytes, monocytes, and macrophages. Measurement of cytokine levels has yielded useful information on the pathological process of different diseases such as AIDS, endotoxic shock, sepsis, asthma, and cancer. It may also be of use in the monitoring of disease progression and/or inflammation. To determine spontaneous cytokine gene expression in whole blood and PBMCs, whole blood was obtained from healthy volunteers and total mRNA was isolated from PBMCs. The kinetics of response were determined by sequential testing of cytokine gene expression by RT-PCR analysis. Our results demonstrated that isolated and incubated PBMCs expressed TNF-alpha and high levels of IL-1beta, IL-6, IL-8, and IL-10. In contrast, WB only expressed the mRNA cytokines of TNF-alpha and IL-8 (p < 0.05). These results suggest that spontaneous myriad mRNA cytokine expression can be avoided with the use of WB incubation and the rapid collection of PBMCs. Furthermore, this method should be employed in all cases where the levels of cytokine gene expression can be evaluated.
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PMID:Spontaneous inflammatory cytokine gene expression in normal human peripheral blood mononuclear cells. 1656 5

Dyspnea is an alarming symptom for both the patient and the emergency physician. There are many causes of dyspnea, some of which are life-threatening, especially in the elderly patient. In addition to the usual cardiac and pulmonary causes such as congestive heart failure, asthma exacerbation, COPD, pneumonia, and pulmonary embolism, there are less common causes of dyspnea, which if not diagnosed and managed expeditiously may have dire consequences for both the patient and physician. We present a case of an elderly patient with a life-threatening unusual cause of acute shortness of breath, a diaphragmatic hernia with sepsis.
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PMID:An unusual cause of dyspnea. 1679 52

Plasma Platelet-activating-Factor (PAF)-acetylhydrolase (PAF-AH also named lipoprotein-PLA(2) or PLA(2)G7 gene) is secreted by macrophages, it degrades PAF and oxidation products of phosphatidylcholine produced upon LDL oxidation and/or oxidative stress, and thus is considered as a potentially anti-inflammatory enzyme. Cloning of PAF-AH has sustained tremendous promises towards the use of PAF-AH recombinant protein in clinical situations. The reason for that stems from the numerous animal models of inflammation, atherosclerosis or sepsis, where raising the levels of circulating PAF-AH either through recombinant protein infusion or through the adenoviral gene transfer showed to be beneficial. Unfortunately, neither in human asthma nor in sepsis the recombinant PAF-AH showed sufficient efficacy. One of the most challenging questions nowadays is as to whether PAF-AH is pro- or anti-atherogenic in humans, as PAF-AH may possess a dual pro- and anti-inflammatory role, depending on the concentration and the availability of potential substrates. It is equally possible that the plasma level of PAF-AH is a diagnostic marker of ongoing atherosclerosis.
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PMID:Plasma PAF-acetylhydrolase: an unfulfilled promise? 1680 87

Levels of the soluble form of the triggering receptor expressed on myeloid cells (sTREM)-1 are elevated in severe sepsis. However, it is not known whether sTREM-1 measurements can distinguish milder bacterial infections from noninfectious inflammation. The present authors studied whether serum sTREM-1 levels differ in community-acquired pneumonia, exacerbations of chronic obstructive pulmonary disease (COPD), asthma and controls, and whether sTREM-1 may be used as a surrogate marker for the need for antibiotics. Serum sTREM-1 levels in 150 patients with pneumonia, COPD and asthma exacerbations and 62 healthy controls were measured. Serum sTREM-1 levels were significantly elevated in pneumonia (median 295.2 ng x mL(-1)), COPD (280.3 ng x mL(-1)) and asthma exacerbations (184.0 ng x mL(-1)) compared with controls (83.1 ng x mL(-1)). Levels were higher in pneumonia and Anthonisen type 1 COPD exacerbations than in type 2 and 3 COPD and asthma exacerbations. The area under the receiver operating characteristics curve for sTREM-1 as a surrogate marker for the need for antibiotics was 0.77. Serum levels of the soluble form of the triggering receptor expressed on myeloid cells-1 were elevated predominantly in pneumonia and Anthonisen type 1 COPD exacerbations versus type 2 and 3 chronic obstructive pulmonary disease exacerbations, asthma and controls. Serum levels of the soluble form of the triggering receptor expressed on myeloid cells-1 has moderate but insufficient accuracy as a surrogate marker for the need for antibiotics in lower respiratory tract infections.
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PMID:Soluble triggering receptor expressed on myeloid cells-1 in acute respiratory infections. 1683 6

Activated protein C (APC), a plasma serine protease, is best known for its ability to inhibit blood clot formation. APC acts as an anticoagulant by degrading coagulation cofactors Va and VIIIa, thereby attenuating the coagulation cascade. Over the past 15 years, impressive research advances have provided novel insights into the diverse biological activities of this molecule. APC is now viewed not only as an anticoagulant but also as a signaling molecule that provides a pivotal link between the pathways of coagulation, inflammation, apoptosis, and vascular permeability. The protective effect of APC supplementation in patients with severe sepsis likely reflects the ability of APC to modulate multiple pathways implicated in sepsis pathophysiology. This review attempts to summarize key studies that support the therapeutic potential of APC in conditions beyond sepsis such as stroke, ischemia-reperfusion injury, lung injury, asthma, pancreatitis, wound healing, and angiogenesis. A comprehensive PUBMED literature review up to May 2006 was conducted.
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PMID:Activated protein C in sepsis and beyond: update 2006. 1712 35


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