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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The well-known coagulation inhibitors antithrombin and protein C, and the more recently described inhibitors, heparin cofactor II and extrinsic pathway inhibitor, were measured in plasma during a 7-day observation period, from patients with pneumonia (n = 13), and in stroke patients with infarction (n = 9) and haemorrhage (n = 9). In patients with pneumonia, elevated fibrinopeptide A levels and subnormal antithrombin and protein C levels suggested some degree of consumption of the inhibitors. Later, an increase was observed for all the inhibitors, but was most conspicuous for heparin cofactor II which reached high normal values. C-reactive protein, initially markedly elevated, decreased rapidly. This finding suggests that heparin cofactor II might act as a delayed acute phase reactant. In stroke patients only small, not statistically significant, changes occurred during the observation period, except for heparin cofactor II which increased in patients with haemorrhagic stroke.
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PMID:Coagulation inhibitor levels in pneumonia and stroke: changes due to consumption and acute phase reaction. 247 68

A 72-year-old man developed a sudden weakness in his left hand on October 5, 1991. He was admitted two weeks thereafter. Physical examination revealed minimal weakness, and clumsiness of the fingers on his left hand. Exaggerated tendon reflexes and spasticity were also noted only on his left upper limb. He had neither dementia nor psychiatric symptoms. Subsequently he developed weakness in his left leg on November 17. Within 12 days he developed left facial weakness, and myoclonic movements on the left side. By December 2, he developed spastic tetraparesis with bilateral facial palsy, and generalized myoclonic jerks. A few days after that he started to show decorticate posture. From December 16, his mental status deteriorated rapidly, and he became mute, and uncooperative within a week. His clinical course can be summarized as stepwise progression similar to a cerebrovascular accident. Electroencephalography was normal on admission, but periodic synchronous discharge developed in January 1992. Brain CT that showed only mild brain atrophy at first was considered to be compatible with his age, changed to have severe brain atrophy in March 1992. He died of pneumonia on May 24, 1992 after eight months of progressive clinical course. Autopsy was done. The brain weighed 930 grams. Macroscopically there was prominent cortical atrophy. Microscopic examination revealed severe spongy state throughout the cerebral cortex. Typical spongiform changes were confined to the hippocampus. The cerebral white matter appeared to be normal. In the cerebellar cortex, the granular cell layer disappeared and Purkinje's cells were reduced in number. Kuru plaques were not seen. The cerebellar white matter, dentate nucleus, and brainstem seemed to be normal. The spinal cord was not examined. There were no pathological changes to indicate cerebrovascular accident, except for a lacuna in the right basal ganglion and a small angionecrosis in the pons. Western blotting test using Anti-APC (amyloid plaque core) antibody was positive. Neuropathological changes of the present case were consistent with those of CJD. However, the sudden onset of monoparesis without dementia or ataxia is rare as the initial symptom of this disease. The subsequent clinical course with stepwise progression of hemiplegia, which was mimicking a progressive stroke, was also rare for CJD. In comparison to typical case of CJD, this case had a different clinical onset as acute monoparesis. We can find such cases of CJD presenting as stroke in 5.6% in the previous English literatures.
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PMID:[A case of Creutzfeldt-Jakob disease (CJD) started with monoparesis of the left arm]. 904 57

Thrombomodulin (TM) plays an important role in anticoagulation by forming a complex with thrombin, which subsequently activates protein C. TM is inactivated and downregulated by inflammatory cell mediators. This study examined whether bronchopneumonia is associated with changes in TM immunoreactivity, and whether a decrease in TM is accompanied by evidence of hypercoagulability, i.e. local deposition of fibrin. Double antibody staining for TM and fibrin was performed on lung tissue sections from patients who had died of pneumonia and from patients who had died rapidly, secondary to trauma. Inflammatory changes were assessed histologically and immunohistochemically using antibodies against interleukin-1alpha, tumor necrosis factor-alpha, and myeloperoxidase. Areas with bronchopneumonia exhibited markedly decreased endothelial TM staining of alveolar walls and small vessels. These changes were associated with prominent fibrin immunoreactivity. Some areas exhibited mild to moderate inflammation with little fibrin deposition and variable amounts of TM in adjacent vessels. This study is the first to relate changes of TM immunoreactivity levels to fibrin deposition in a human disease process. These data may have implications for pulmonary pathophysiology in patients with bronchopneumonia.
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PMID:Association between decreased pulmonary endothelial cell thrombomodulin and local fibrin deposition in pneumonia. 1173 75

At the 2001 Toronto Critical Care Medicine Symposium, exciting new research results were presented, including a randomized trial of peri-operative pulmonary-artery catheter use and evidence-based guidelines for the prevention of ventilator-acquired pneumonia. Presenters reviewed other important recent critical care developments such as (1) activated protein C and low-dose steroids in sepsis, (2) prone positioning and long-term outcomes in patients with adult respiratory distress syndrome, and (3) medical errors in the critical care unit. Along with these new findings, another theme emerged during the symposium. This theme emphasized that research breakthroughs are not sufficient in themselves: outcome studies are needed to learn how new research is applied on a large-scale basis within actual clinical practice. Furthermore, additional study is needed for an understanding of how physicians implement new research findings. Successful methods of enhancing the widespread adoption of new research require further study.
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PMID:Toronto Critical Care Medicine Symposium, 18-20 October 2001, Canada: research breakthroughs are not enough. 1173 21

This article provides a description of the clinical disorders associated with the development of acute noncardiogenic pulmonary edema, better known as clinical acute lung injury (ALI) or the acute respiratory distress syndrome (ARDS). Much has been learned about the mechanisms by which the lung is injured in patients with sepsis, pneumonia, aspiration of gastric contents, and following major trauma. In the last 5 years, major progress has been made in the treatment of patients with ALI/ARDS. A lung protective ventilatory strategy with a low tidal volume (6 mL/kg/predicted body weight) in conjunction with a plateau pressure limit of 30 cm H(2)0 attenuated the severity of clinical lung injury and reduced mortality by 22%. Ironically, after years of searching for anti-inflammatory treatments for ALI/ARDS, it turns out that a lung protective ventilatory strategy has proven to be the most efficacious anti-inflammatory treatment ever discovered for ALI/ARDS. However, it is still possible that pharmacologic treatments also may enhance survival. For example, a recent report that activated protein C reduces mortality in patients with sepsis raises hope that the incidence and severity of sepsis-induced ALI/ARDS may be reduced by treatment with this agent that has both anti-inflammatory and anticoagulant properties. Also, therapy directed at hastening the resolution of lung injury by increasing the functional recovery of the alveolar epithelium may be of value, both in diminishing the fibroproliferative phase of ALI/ARDS as well as accelerating the resolution of alveolar edema.
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PMID:Clinical Acute Lung Injury and Acute Respiratory Distress Syndrome. 1185 76

Acute lung injury (ALI) and its more severe form, the acute respiratory distress syndrome (ARDS), are syndromes of acute respiratory failure that result from acute pulmonary edema and inflammation. The development of ALI/ARDS is associated with several clinical disorders including direct pulmonary injury from pneumonia and aspiration as well as indirect pulmonary injury from trauma, sepsis, and other disorders such as acute pancreatitis and drug overdose. Although mortality from ALI/ARDS has decreased in the last decade, it remains high. Despite two major advances in treatment, low VT ventilation for ALI/ARDS and activated protein C for severe sepsis (the leading cause of ALI/ARDS), additional research is needed to develop specific treatments and improve understanding of the pathogenesis of these syndromes. The NHLBI convened a working group to develop specific recommendations for future ALI/ARDS research. Improved understanding of disease heterogeneity through use of evolving biologic, genomic, and genetic approaches should provide major new insights into pathogenesis of ALI. Cellular and molecular methods combined with animal and clinical studies should lead to further progress in the detection and treatment of this complex disease.
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PMID:Future research directions in acute lung injury: summary of a National Heart, Lung, and Blood Institute working group. 1266 42

Community-acquired pneumonia (CAP) remains an important cause of morbidity and mortality. Streptococcus pneumoniae is the most common pathogen and respiratory syncitial virus the most important viral pathogen in children. The role of urinary antigen testing and PCR for the diagnosis forS. pneumoniae infection has been an important adjunct to clinical examination, showing good sensitivity and specificity. Host-related immune responses play an important role in defining the severity of illness. Other than the use of Activated Protein C and immunization, the clinical use of therapies designed to modulate these abnormal responses remains largely experimental. The 7-valent vaccine represents a major advance in the prevention of invasive pneumococcal disease. The importance of effective triage and the deleterious effects of deviation from protocols are underscored. Continuous positive pressure ventilation and noninvasive mechanical ventilation are available as options for respiratory support in cases of severe CAP and require further evaluation.
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PMID:Community-acquired pneumonia. 1268 61

The thrombomodulin-protein C-protein S (TM-PC-PS) pathway exerts anticoagulant and anti-inflammatory effects. We investigated the role of TM in the pulmonary immune response in vivo by the use of mice with a mutation in the TM gene (TM(pro/pro)) that was earlier found to result in a minimal capacity for activated PC (APC) generation in the circulation. We here demonstrate that TM(pro/pro) mice also display a strongly reduced capacity to produce APC in the alveolar compartment upon intrapulmonary delivery of PC and thrombin. We monitored procoagulant and inflammatory changes in the lung during Gram-positive (Streptococcus pneumoniae) and Gram-negative (Klebsiella pneumoniae) pneumonia and after local administration of lipopolysaccharide (LPS). Bacterial pneumonia was associated with fibrin(ogen) depositions in the lung that colocalized with inflammatory infiltrates. LPS also induced a rise in thrombin-antithrombin complexes in bronchoalveolar lavage fluid. These pulmonary procoagulant responses were unaltered in TM(pro/pro) mice, except for enhanced fibrin(ogen) deposition during pneumococcal pneumonia. In addition, TM(pro/pro) mice displayed unchanged antibacterial defense, neutrophil recruitment, and cytokine/chemokine levels. These data suggest that the capacity of TM to generate APC does not play a role of importance in the pulmonary response to respiratory pathogens or LPS.
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PMID:Thrombomodulin mutant mice with a strongly reduced capacity to generate activated protein C have an unaltered pulmonary immune response to respiratory pathogens and lipopolysaccharide. 1459 28

One of the most outstanding critical care concepts of the last month is the definition of 5 therapy strategies by the Society of Critical Care for treatment of patients in septic shock. These strategies are: Low tidal volume of 6 ml/kg(-1) body weight in patients with ARDS, early goal-directed therapy, activated protein C therapy, moderate-dose corticosteroids, and tight control of blood sugar. Following further review of the main critical care medicine related journals for strategies to reduce mortality, the non-invasive ventilation is worthwhile mentioning. Moreover, this review summarizes articles on the topics of: Low-dose dopamine does not prevent acute renal insufficiency, increase of mortality is not related to albumin infusion, subglottic suctioning prevents early onset of ventilator associated pneumonia, prone position in ARDS patients has no influence on mortality, the safest site for central venous catheterization, and pulmonary-artery catheter directed therapy has no influence on mortality of high-risk surgical patients.
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PMID:[New pathways and current concepts in intensive care medicine--a summary of important articles of the last month]. 1460 Aug 56

Drotrecogin alpha (recombinant human activated protein C, rhAPC; Xigris) is an immune modulating treatment principle that has been shown to significantly reduce mortality in patients with severe sepsis. Currently, the identification of patients in intensive care that may benefit from such a treatment is insufficient. The importance of this evidence-based treatment modality is commonly ignored for reasons of increased cost. A medically justified and economically acceptable strategy with a medico-legal backing would be a procedure based on the design and the results of the PROWESS study. This may benefit patients with severe sepsis of not longer than 48 h duration, an APACHE II score of > or =25 or > or =2 failing organs and no exclusion criteria. Extending the indication beyond this group should be discussed as a last resort in patients with a fulminant clinical course, such as in meningitis, and based on data from retrospective subgroup analyses. Patients with severe sepsis following community-acquired pneumonia with progressive organ dysfunction may also benefit from activated protein C treatment in addition to an otherwise best standard of care.
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PMID:[Identification of patients suitable for therapy with activated Protein C]. 1655 81


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