Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is sometimes very difficult to diagnose dissecting aortic aneurysms (DAA), particularly in its early stage, due to manifold signs and symptoms. The purpose of this study is to clarify the reasons for such erroneous diagnoses. A total of 41 patients with DAA were referred to our hospitals for further examination and/or surgery from April 1986 to August 1989. In 18 of these patients, the diagnostic possibility of an underlying DAA was overlooked by the referring physicians. Among these 18 patients, 2 were mistakenly diagnosed as uncomplicated myocardial infarction (MI), one as pneumonia, 2 as cerebral infarction, 6 as acute abdominal disease, one as cholelithiasis, 5 as thrombosis of the lower extremities, and one as malignant metastasis to the pericardium. The following is the detail: In 2 cases thought to be uncomplicated MI, an expanding dissecting ascending aorta had crushed the lumen of the left coronary artery, causing MI, in turn, wasting clinical treatment and consuming precious time. In one case, enlargement of the descending aorta on the chest radiography was overlooked and the patient's symptoms were mistakenly attributed to pneumonia. In 2 cases in which symptoms of cerebral ischemia were thought to be attributed to cerebral thrombosis, the real cause turned out to be occlusion of the brachiocephalic artery following aortic dissection. Among 6 cases which were initially considered to have only acute abdominal disease, 3 presented with symptoms and signs of ileus, and their exploratory laparotomies yielded no positive findings.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The pitfalls in the clinical diagnosis of dissecting aortic aneurysm]. 133 5

Data from 400 consecutive elective ambulatory operations for inguinal hernia under unmonitored local anaesthesia with limited pre-operative testing were prospectively obtained by the use of standardised files and questionnaires to assess the feasibility, patient satisfaction and potential cost reductions for such a technique. The median age of the patients was 59 years, and 29 operations were performed in ASA group III patients. The median postoperative hospital stay was 85 min. Conversion to general anaesthesia was necessary only in two cases, and nine patients needed overnight admission. One week postoperative morbidity was low with one case of transient cerebral ischaemia and one case of pneumonia, but no case of urinary retention. On follow-up, 88% were satisfied with the procedure, including unmonitored local anaesthesia. The cost reduction was at least 160 Pounds per patient compared with general/regional anaesthesia. We conclude that elective inguinal herniorrhaphy may be performed routinely under unmonitored local anaesthesia with a low postoperative morbidity, a high satisfaction rate and significant cost reductions.
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PMID:The feasibility, safety and cost of infiltration anaesthesia for hernia repair. Hvidovre Hospital Hernia Group. 950 39

The function and course of the cortico-respiratory projections in man are not yet well established. In 30 normal volunteers respiratory muscles were activated by magnetic stimulation of the motor cortex and the cervical and thoracic spinal roots with bilateral recordings from the respiratory muscles. Following cortical stimulation contralateral responses were obtained in all subjects during voluntary inspiration showing a mean latency and amplitude of 13.4+/-1.4ms/1.6+/-1.2 mV (stimulation of the left hemisphere) and 13.2+/-1.3ms/2.5+/-2.5 mV (stimulation of the right hemisphere). Ipsilateral responses were obtained in only 18 (right side) and 21 (left side) subjects and had a significantly (p < 0.001) longer mean latency and lower mean amplitude than the contralateral responses. In 31 patients with impairment of the cortico-respiratory projections due to cerebral infarction demonstrated by magnetic resonance imaging studies, the responsible lesion topography was analysed. We found that, 1. the voluntary activation of respiratory muscles is mediated predominantly by the contralateral motor cortex, 2. the descending cortico-respiratory projections are located within the pyramidal tract, and 3. the cortico-respiratory projections to the respiratory muscles are frequently affected in patients with hemiparesis due to acute stroke. These findings might explain the increased incidence of pneumonia at the hemiparetic side in patients with cerebral ischemia as shown in previous studies.
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PMID:Distribution and course of cortico-respiratory projections for voluntary activation in man. A transcranial magnetic stimulation study in healthy subjects and patients with cerebral ischemia. 1211 8

The objective of this study was to assess typical early-onset complications following ischemic stroke in a large, hospital-based cohort to provide clinical data for future randomized trials and quality standards in clinical routine. 3,866 patients with acute ischemic stroke were prospectively documented in 14 Neurology Departments with an acute stroke unit. Within the first week after admission, increased intracranial pressure (7.6%) and recurrent cerebral ischemia (5.1%) were the most frequent neurological complications. Fever >38 degrees C (13.2%), severe arterial hypertension (7.5%) and pneumonia (7.4%) were the most frequent medical complications. Multivariate regression analysis yielded brain stem infarction and large-artery atherosclerosis as independent predictors for early recurrent ischemic stroke. This study provides representative data on onset and severity of early neurological and medical complications as well as possible predictors for early recurrent cerebral ischemia following acute ischemic stroke.
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PMID:Complications following acute ischemic stroke. 1237 29

The duration of inpatient episodes due to COPD and the factors that affect it have recently been an object of increasing attention, as the aim has been to shorten inpatient periods and thereby to cut health-care costs. All hospital episodes of patients aged over 45 for a primary diagnosis of COPD equal or less than 150 days in duration were drawn from the treatment register maintained by the National Research and Development Centre for Welfare and Health. The lengths of these 152569 inpatient periods were analysed for sex, age and secondary diagnoses by covariance analysis. The mean age of men at the beginning of the hospital episode was 70.6 years and that of women 70.1 years. Men accounted for 76.9% of all inpatient episodes. Covariance analysis ofthe data with age standardised as 70.5 years yielded a mean hospital episode length of 8.9 (95% confidence interval (CI) 8.8-9.0) days. The mean length of hospital episodes without a secondary diagnosis was 7.7 (95% CI 7.6-7.7) days and that with a secondary diagnosis was 10.5 (95% CI 10.5-10.6) days. The longest inpatient episodes were recorded for the patients with secondary diagnoses of pneumonia, 14.7 (95% CI 14.2-15.2) days, and cerebral ischaemia, 14.2 (95% CI 13.5-14.9) days. Concurrent diseases prolonged the hospital episodes of COPD patients. At the beginning of a hospital episode, it is possible to estimate its duration and the need for different treatments based on the patients age and secondary diagnoses.
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PMID:Impact of comorbidities on the duration of COPD patients' hospital episodes. 1258 64

Infections are a leading cause of death in stroke patients. In a mouse model of focal cerebral ischemia, we tested the hypothesis that a stroke-induced immunodeficiency increases the susceptibility to bacterial infections. 3 d after ischemia, all animals developed spontaneous septicemia and pneumonia. Stroke induced an extensive apoptotic loss of lymphocytes and a shift from T helper cell (Th)1 to Th2 cytokine production. Adoptive transfer of T and natural killer cells from wild-type mice, but not from interferon (IFN)-gamma-deficient mice, or administration of IFN-gamma at day 1 after stroke greatly decreased the bacterial burden. Importantly, the defective IFN-gamma response and the occurrence of bacterial infections were prevented by blocking the sympathetic nervous system but not the hypothalamo-pituitary-adrenal axis. Furthermore, administration of the beta-adrenoreceptor blocker propranolol drastically reduced mortality after stroke. These data suggest that a catecholamine-mediated defect in early lymphocyte activation is the key factor in the impaired antibacterial immune response after stroke.
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PMID:Stroke-induced immunodeficiency promotes spontaneous bacterial infections and is mediated by sympathetic activation reversal by poststroke T helper cell type 1-like immunostimulation. 3162 20

The current pathophysiological understanding of stroke is substantially based on experimental studies. Brain injury after cerebral ischemia develops from a complex signaling cascade that evolves in an at least partially unraveled spatiotemporal pattern. Early excitotoxicity can lead to fast necrotic cell death, which produces the core of the infarction. The ischemic penumbra that surrounds the infarct core suffers milder insults. In this area, both mild excitotoxic and inflammatory mechanisms lead to delayed cell death, which shows biochemical characteristics of apoptosis. While brain cells are challenged by these deleterious mechanisms, they activate innate protective programs of the brain, which can be studied by means of experimentally inducing ischemic tolerance (i.e., ischemic preconditioning). Importantly, cerebral ischemia not only affects the brain parenchyma, but also impacts extracranial systems. For example, stroke induces a dramatic immunosuppression via an overactivation of the sympathetic nervous system. As a result, severe bacterial infections such as pneumonia occur. Complex signaling cascades not only decide about cell survival, but also about the neurological deficit and the mortality after stroke. These mechanisms of damage and endogenous protection present distinct molecular targets that are the rational basis for the development of neuroprotective drugs.
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PMID:Pathophysiology of stroke: lessons from animal models. 1555 12

Nitric oxide produced by the inducible nitric oxide synthase (iNOS) is believed to participate in the pathogenic events after cerebral ischemia. In this study, we examined the expression of iNOS in the brain after transient focal cerebral ischemia in mice. We detected differential expression of exons 2 and 3 of iNOS mRNA (16-fold upregulation at 24 to 72 h after middle cerebral artery occlusion, MCAO) compared with exons 6 to 8, 12 to 14, 21 to 22, and 26 to 27 (2- to 5-fold upregulation after 72 and 96 h), which would be compatible with alternative splicing. Expression levels of iNOS mRNA were too low for detection by the Northern blot analysis. Using specific antibodies, we did not detect any iNOS immunoreactivity in the mouse brain 1 to 5 days after MCAO, although we detected iNOS immunoreactivity in the lungs of mice with stroke-associated pneumonia, and in mouse and rat dura mater after lipopolysaccharide administration. In chimeric iNOS-deficient mice transplanted with wild-type bone marrow (BM) cells expressing the green fluorescent protein (GFP) or in wild-type mice transplanted with GFP(+) iNOS-deficient BM cells, no expression of iNOS was detected in GFP(+) leukocytes invading the ischemic brain or in resident brain cells. Moreover, both experimental groups did not show any differences in infarct size. Analysis of three different strains of iNOS-deficient mice and wild-type controls confirmed that infarct size was independent of iNOS deletion, but strongly confounded by the genetic background of mouse strains. In conclusion, our data suggest that iNOS is not a universal mediator of brain damage after cerebral ischemia.
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PMID:Inducible nitric oxide synthase does not mediate brain damage after transient focal cerebral ischemia in mice. 1785 54

Pneumonia constitutes a serious medical complication and major cause of death in patients after cerebral stroke. In a mouse model of cerebral ischemia (MCAO), we have recently demonstrated that stroke animals spontaneously develop severe bacterial pneumonia which is preceded by a stress-mediated suppression of cellular immune responses in primary and secondary lymphoid organs. However, little is known about the mechanisms leading to impaired pulmonary antimicrobial immune response after cerebral ischemia. In this study, we demonstrate a rapid up-regulation of the immunomodulatory neuropeptide alpha-melanocyte-stimulating hormone (MSH) in the lung within 24 h after cerebral ischemia. Systemic administration of the naturally occurring alpha-MSH receptor-1 (MC-1R) antagonist agouti immediately after MCAO significantly reduced pulmonary bacterial burden at 72 h. In contrast, administration of recombinant alpha-MSH further increased bacterial load in lungs of MCAO animals. In addition, cerebral ischemia resulted in a strong modulation of local pulmonary immunity with increased production of IL-10 by lung macrophages, reduced pulmonary lymphocyte counts, as well as decreased lymphocytic IFN-gamma but increased IL-4 production. However, alpha-MSH blockade by administration of agouti did not prevent changes in lung immune cell numbers or cytokine production suggesting that suppression of cellular immune responses is not the primary mechanism of alpha-MSH mediated inhibition of pulmonary antibacterial defenses. This study indicates an important role of alpha-MSH for the increased infectious susceptibility after cerebral ischemia and may provide new therapeutic strategies to prevent post-stroke infectious complications.
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PMID:Alpha-MSH promotes spontaneous post-ischemic pneumonia in mice via melanocortin-receptor-1. 1830 33

The interaction between the brain and immune system has been intensely studied in patients with several central nervous system (CNS) disorders including brain trauma and brain tumours. Pioneering studies described cellular immune changes after human stroke more than three decades ago but the potential existence of a CNS- mediated immunodepression syndrome has obtained renewed attention only recently. The CNS and the immune system are extensively interconnected through neural pathways, hormonal cascades and cell-to-cell interactions orchestrated primarily by cytokines. Indeed, the balance between pro- and anti-inflammatory cytokines determines the prowess of the immunological response but could also influence the fate of the injured brain tissue and the threshold to develop complications including systemic infection. Prominent changes in primary and secondary lymphoid organs and increased susceptibility to infections and pneumonia have been described in a mouse model of transient focal cerebral ischemia in support of the existence of a stroke induced immunodepression syndrome. Yet, the intrinsic characteristics of secondary lymphoid organs located in areas that receive direct signals from the CNS could mediate anti-inflammatory responses after stroke. In human stroke, the balance between pro-inflammatory and anti-inflammatory cytokines is an important prognostic clinical factor. Recent data also suggest that the appearance infections early after stroke could be the manifestation of a stroke-induced immunodepression syndrome, characterized by strong adrenergic activity and excessive anti-inflammatory drive. Overall, current research suggests that a better understanding of the reciprocal effects between the CNS and the immune system could pave the way to more effective therapies for this devastating condition.
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PMID:Stroke induced immunodepression syndrome: from bench to bedside. 1927 27


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