Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To update the clinical profile of pediatric patients hospitalized with RSV infection, we retrospectively reviewed the records of 246 children (male:female ratio 1.44:1) admitted during one season to a tertiary-care hospital. The most common admitting diagnoses were bronchiolitis (37.4%), pneumonia (32.5%), and possible septicemia (13%). Median age was 3 months; median length of stay, three days. Twice as many minorities were admitted with RSV infection as all other admissions during the same year. Family history of asthma, while common (35%), did not affect length of stay or complications. Of the 38 (15%) patients requiring intensive care, 29 (76%) underwent ventilation. Patients with underlying cardiopulmonary disease had more complications, were more likely to require intensive care (about 50%), and had significantly longer hospital stays than others. All three patients (1.2%) who died had congenital heart disease. Common risk factors included young age, chronic cardiopulmonary disease, male sex, and possibly family history of asthma. Although the most typical clinical diagnoses remain bronchiolitis and pneumonia, a systemic illness resembling the sepsis syndrome has emerged at our institution as a significant clinical presentation.
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PMID:Clinical profile of pediatric patients hospitalized with respiratory syncytial virus infection. 840 43

Some conditions that predispose to ventilatory failure increase the work of breathing (chronic obstructive pulmonary disease [COPD], obesity, kyphoscoliosis), whereas others cause severe respiratory muscle weakness. Specific reasons for muscle weakness include critical illness (electrolyte imbalance, acidemia, shock, sepsis), chronic illness (poor nutrition, cachexia), and neuromuscular diseases. Inspiratory muscle weakness from mechanical disadvantage to the diaphragm is characteristic of asthma and COPD. The increased work of breathing combined with muscle weakness increases the pressure needed to inspire a breath and decreases maximal inspiratory pressure. When this pressure exceeds 0.4, dyspnea and inspiratory muscle fatigue ensue. One way to lower this pressure and avert fatigue is to lower the tidal volume. Ventilatory drive is high, not low, in ventilatory failure. Concomitant shortening of inspiration and breath duration cause the small tidal volume and increased respiratory rate. Gas exchange is compromised by ventilation/perfusion imbalance, and the ratio of dead space to tidal volume is also increased by rapid, shallow breathing. Reduction in tidal volume minimizes dyspnea, but the small tidal volume is inadequate for gas exchange. Acute treatment of respiratory muscle failure involves respiratory muscle rest through mechanical ventilation and removal of noxious influences (infection, metabolic disarray), whereas chronic treatment involves rebuilding the contractile apparatus by nutritional repletion and training.
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PMID:Respiratory muscles and ventilatory failure: 1993 perspective. 850 1

Data were analyzed on 290 children admitted consecutively to the pediatric intensive care unit (PICU) of the Postgraduate Institute of Medical Education and Research in Chandigarh, India, in 1993 to examine the frequency, severity, risk factors, and mortality of hypokalemia (3.5 mEq/l serum potassium) and the efficacy of treatment. 43 (14.8%) children had 54 episodes of hypokalemia. Most (68.6%) episodes were moderate. Predisposing factors were the nature of primary disease (renal disease 19%, septicemia 19%, acute diarrhea 14%, and heart disease with congestive failure and meningoencephalitis 12% each), malnutrition (weight for age 80% in 72%), and treatment with drugs (diuretics 20%, beta-agonists 13%, and corticosteroids 11%). Diagnoses most common in hypokalemia cases were acute renal failure (25%), septicemia (22.8%), and acute severe bronchial asthma (20%). The most important predisposing factor for hypokalemia prior to hospitalization was poor oral intake (i.e., inability to replace adequate potassium) (27%). All 43 children received 4-6 mEq potassium/100 ml of intravenous fluids. Clinicians administered an infusion of 0.3 mEq potassium/kg/hour to 7 children (9 episodes) who had ECG changes of hypokalemia until the ECG became normal. Potassium levels returned to normal in all 9 episodes requiring rapid correction and in 40 of 45 episodes requiring slow correction. PICU patients with hypokalemia were more likely to die than PICU patients with no hypokalemia (25.6% vs. 10.9%; p 0.05; odds ratio = 2.34). Hypokalemia patients who received slow correction therapy were more likely to die than those who received rapid correction therapy (31% vs 0; p 0.05). Mortality was lower in PICU patients whose hypokalemia was corrected than in PICU patients whose hypokalemia was not corrected (13.5% vs. 100%; p 0.05). Based on these findings, regular monitoring and rapid correction are recommended to improve the outcome of hypokalemia.
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PMID:Hypokalemia in a pediatric intensive care unit. 877 44

The authors describe the case of a 53-year-old woman who suffered from an Aspergillus fumigatus infection of the L2/3 intervertebral disc space unrelated to previous operations on her lumbar spine. After surgical debridement combined with amphotericin therapy she died on the 23rd postoperative day from a fulminant bacterial sepsis of pulmonary origin. Although she had intermittently used steroids for bronchial asthma, this is an unusual case of fungal infection of the lumbar spine in an apparently immunocompetent patient.
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PMID:Intervertebral disc space infection caused by Aspergillus fumigatus. 883 Nov 27

The availability of potent and stable bradykinin antagonists has had a tremendous impact on kinin research. This article reviews the current status of research on kinin antagonists, describes their chemical properties, and delineates recent advances that have occurred with the advent of the second generation of kinin antagonists. The data collected with these antagonists support the assumption that kinins are implicated in inflammation and tissue injury as endogenous agents. Their importance, however, is not limited to the role as mediators of tissue injury and inflammation, as kinin antagonists have enabled the identification kinins as potential endogenous cardioprotective substances, also contributing to the effects of angiotensin converting enzyme inhibitors. Clinical studies are currently being performed in asthma, postoperative pain, anaphlyactoid reactions during low density lipoprotein apheresis, systemic inflammatory response syndrome, and suspected sepsis, head injury, and hantavirus infections to investigate the utility of kinin antagonists as therapeutic agents.
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PMID:Kinin receptor antagonists: unique probes in basic and clinical research. 884 12

Leukocyte recruitment from the circulation into inflammatory tissues requires a series of soluble and cell-bound signals between the responding leukocyte and vascular endothelial barrier. Chemotactic factors are believed to be responsible for this selective adhesion and transmigration. A superfamily of small, soluble, structurally-related molecules called 'chemokines' have been identified and shown to selectively promote the rapid adhesion and chemotaxis of a variety of leukocyte subtypes both in vivo and in vitro. Chemokines are produced by almost every cell type in the body in response to a number of inflammatory signals, in particular those which activate leukocyte-endothelial cell interactions. These molecules also appear to play important roles in hematopoesis, cellular activation, and leukocyte effector functions. In addition, chemokines have been found in the tissues of a variety of disease states characterized by distinct leukocytic infiltrates, including rheumatoid arthritis, sepsis, atherosclerosis, asthma, psoriasis, ischemia/reperfusion injury, HIV replication, and a variety of pulmonary disease states. This review will primarily focus on the role of chemokines in cell adhesion and trafficking as well as their role as effector molecules.
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PMID:Chemokine-leukocyte interactions. The voodoo that they do so well. 902 58

The measurement of nitric oxide (NO) in expired gas is being increasingly reported in disease states such as sepsis, heart failure, and asthma. However, the effects of changes in ventilatory and cardiac parameters on expired NO are not known. Therefore, we assessed the effects of changes in minute ventilation (VE), ventilatory pattern, and cardiac output on expired gas NO levels in five anesthetized, intubated pigs. The animals were mechanically ventilated at three settings for each of respiratory rate (12 to 14, 16 to 18, and 22 to 24/min) and tidal volume (10, 15, and 20 mL/kg) applied in random sequence, yielding nine ventilatory patterns and a range of VE (3.7+/-0.1 to 13.2+/-0.8 L/min). When VE was increased, expired NO concentration declined slightly (r=-0.40, p<0.01), but the rate of excretion of NO in expired gas increased significantly (r=0.60, p<0.01). In contrast, when cardiac output was increased progressively from 3.6+/-0.1 to 4.7+/-0.3 and 5.8+/-0.4 L/min (p<0.01) by volume loading during constant eucapneic ventilation, there was no change in expired NO. Changes in VE over a physiologic range significantly affect the measurement of NO in expired gas, whereas short-term changes in cardiac output do not. To facilitate comparison between studies, we suggest that the measurement of expired NO should be reported in conjunction with data on VE.
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PMID:The effects of changes in ventilation and cardiac output on expired nitric oxide. 910 87

Nitric oxide (NO) is a gas with diverse biological activities produced from arginine by NO synthases. It is capable of interacting with a number of molecules, most notably superoxide, forming peroxynitrite, which, in turn, can mediate bactericidal or cytotoxic reactions. Nitric oxide also mediates smooth muscle relaxation, neurotransmission, and modulation of inflammation in a number of organ systems and pathophysiologic conditions. Modulation of NO by administration of inhaled NO for respiratory distress syndromes and infusion of NO synthase inhibitors in bacterial sepsis are ongoing. Levels of exhaled NO are being evaluated for their utility in assessing inflammation in respiratory disorders such as asthma.
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PMID:Nitric oxide. 930 99

This review illustrates the changing paradigms in the understanding of the pathogenesis of pneumatosis intestinalis. Although many theories have been evoked, pragmatically there appear to be four major clinical and diagnostic imaging considerations. The most common and most emergent life-threatening cause of intramural bowel gas is the result of bowel necrosis due to bowel ischemia, infarction, necrotizing enterocolitis, neutropenic colitis, volvulus, and sepsis. In the stomach, intramural gas can be caused by emphysematous gastritis or ingestion of caustic agents. These situations represent surgical emergencies. Pneumatosis is found secondary to mucosal disruption presumably due to over-distention from peptic ulcer, pyloric stenosis, annular pancreas, and even to more distal obstruction. Disruption can also be caused by ulceration, erosions, or trauma, including the trauma of child abuse. Disruption can also be iatrogenic from intracatheter jejunal feeding tubes, stent perforation, sclerotherapy, or surgical or endoscopic trauma. In these cases, the gas may be focal or linear. Treatment depends on the extent of the disruption and the underlying cause. A more subtle form of mucosal disruption may occur due to mucosal erosions and also to defects in intestinal crypts secondary to acute and subclinical enteritides that allow intraluminal bacterial gas under pressure to percolate into the bowel wall layers, particularly the submucosa (29). Pneumatosis, often linear or cystic in appearance, is seen with increased frequency in patients who are immunocompromised because of steroids, chemotherapy, radiation therapy, or AIDS. In these cases, the pneumatosis may result from intraluminal bacterial gas entering the bowel wall due to increased mucosal permeability caused by defects in bowel wall lymphoid tissue. Clinical and imaging findings are important in the differentiation of this transient pneumatosis from fulminant life-threatening causes in this subset of patients. A pulmonary cause must still be considered in cases of chronic obstructive pulmonary disease, asthma, and cystic fibrosis. It can occur with barotrauma and after chest tube placement. It may relate to increased intrathoracic pressure associated with retching and vomiting. The possibility remains that occasionally the origin of pneumatosis intestinalis will remain cryptogenic--caused but unexplained.
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PMID:Pneumatosis intestinalis: a review. 953 Feb 94

The production of pro-inflammatory cytokines, such as interleukins 1 and 6 and tumour necrosis factors, occurs rapidly following trauma or invasion of the body by pathogenic organisms. The cytokines mediate the wide range of symptoms associated with trauma and infection, such as fever, anorexia, tissue wasting, acute phase protein production and immunomodulation. In part, the symptoms result from a co-ordinated response, in which the immune system is activated and nutrients released, from endogenous sources, to provide substrate for the immune system. Although the cytokine mediated response is an essential part of the response to trauma and infection, excessive production of pro-inflammatory cytokines, or production of cytokines in the wrong biological context, are associated with mortality and pathology in a wide range of diseases, such as malaria, sepsis, rheumatoid arthritis, inflammatory bowel disease, cancer and AIDS. Cytokine biology can be modulated by antiinflammatory drugs, recombinant cytokine receptor antagonists and nutrients. Among the nutrients, fats have a large potential for modulating cytokine biology. A number of trials have demonstrated the anti-inflammatory effects of fish oils, which are rich in n-3 polyunsaturated fatty acids, in rheumatoid arthritis, inflammatory bowel disease, psoriasis and asthma. Animal studies, conducted by ourselves and others, indicate that a range of fats can modulate pro-inflammatory cytokine production and actions. In summary fats rich in n-6 polyunsaturated fatty acids enhance IL1 production and tissue responsiveness to cytokines, fats rich in n-3 polyunsaturated fatty acids have the opposite effect, monounsaturated fatty acids decrease tissue responsiveness to cytokines and IL6 production is enhanced by total unsaturated fatty acid intake. There are a large number of potential cellular mechanisms which may mediate the effects observed. The majority relate to the ability of fats to alter the composition of membrane phospholipids. As a consequence of alterations in phospholipid composition, membrane fluidity may change, altering binding of cytokines to receptors and G protein activity. The nature of substrate for various signalling pathways associated with cytokine production and actions may also be changed. Consequently, alterations in eicosanoid production and activation of protein kinase C may occur. We have examined a number of these potential mechanisms in peritoneal macrophages of rats fed fats with a wide range of fatty acid composition. We have found that the total C18:2 and 20:4 diacyl species of phosphatidylethanolamine in peritoneal macrophages relates in a positive curvilinear fashion with dietary linoleic acid intake; that TNF induced IL1 and IL6 production relate in a positive curvilinear fashion to linoleic acid intake; that leukotriene B4 production relates positively with dietary linoleic acid intake over a range of moderate intakes and is suppressed at high intakes, while PGE2 production is enhanced. There was no clear relationship between linoleic acid intake and membrane fluidity, however fluidity was influenced in a complex manner by the type of fat in the diet, the period over which the fat was fed and the presence of absence of TNF stimulation. None of the proposed mechanisms, acting alone, can explain the positive effect of dietary linoleic acid intake on pro-inflammatory cytokine production. However each may be involved, in part, in the modulatory effects observed.
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PMID:Modulation of pro-inflammatory cytokine biology by unsaturated fatty acids. 955 30


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