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)

Treatment of dementia costs billions of dollars in long-term care and community services every year. Dementia also burdens the acute care system and may contribute to financial problems for hospitals serving large numbers of demented elderly. In a specialized geriatric medical unit devoted to acute care of the frail elderly, Alzheimer's disease and vascular and mixed dementias afflicted 63% of inpatients and were associated with excess consumption of nursing resources, complications of treatment, nosocomial infections, lengthy hospitalizations, and financial losses to the hospital. Due in part to the effects of dementia on mobility, continence, and nutrition, demented patients suffered more frequently from life-threatening infections, sepsis, iatrogenic disease, and prolonged hospital stays. Hospital losses were 75% higher for demented patients than for nondemented patients. Dementia affected the majority of acute care patients in this study. However, it was rarely coded as an admitting diagnosis, even though it may have been the proximate cause of the medical morbidity which led to the acute hospitalization. In addition, despite the significant impact of dementia on the hospital course and costs, it was a factor in hospital reimbursement in less than one third of cases. The results indicate that dementia was not considered to be an acute diagnosis, nor was it recognized as a complex medical illness. The impact of dementia on acute hospitalization, including the mechanisms by which dementia prolongs the hospital stay, requires further investigation.
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PMID:The effect of dementia on acute care in a geriatric medical unit. 147 11

The aim of this study is to sum up our current knowledge on the so-called "normal pressure hydrocephalus" syndrome, revisited by the authors as the "adult chronic hydrocephalus" syndrome (A.C.H.). It is based upon 1) a review of the literature dealing with the subject (518 references) and 2) an original series of 243 cases summarizing a 10 year experience of 2 french neurosurgical teams (Lyon: 123 cases, Clermont-Ferrand: 120 cases). Part I is devoted to the review of pathologic and pathophysiologic data. Both autopsy and microscopic findings clearly show 2 categories of anomalies in the brains of patients showing this condition: "non specific" lesions may be either causative (leptomeningeal thickening, villositar sclerosis) or secondary to hydrocephalus (ependymal wall disruption, sub-ependymal "edema"). Conversely, "specific lesions" are either degenerative (Alzheimer-type) or ischemic in origin. They seem unrelated to hydrocephalus, but may play a role in the ventricular enlargement by favoring changes in brain elastic properties. Data available from brain biopsies (13 cases) have confirmed the high incidence of such "specific lesions" of the parenchyma. Following the Hakim's initial hypothesis, several mechanisms have been proposed to explain the progressive ventricular dilation despite a fall in C.S.F. pressure. Experimental and clinical data (namely those referring to the pathogenesis of secondary A.C.H.) are reviewed. The sequence of events following acute ventricular obstruction is analysed. The ultimate state of chronic uncompensated hydrocephalus involve multiple factors among which a trans-cerebral mantle pressure gradient may play a major role. The intervention of compensatory mechanisms (reduction of C.S.F. production, establishment of alternative pathways of C.S.F. absorption) is also discussed. Part II is devoted to the presentation of the clinical material. Series of the literature including more than 20 surgical cases are briefly reviewed together with the authors' material and methods. Criteria of selection of patients, methods of clinical evaluation and of statistical analysis of results are exposed. Of the 243 patients of the present series, 225 were managed by C.S.F. shunt (V.A.: 137, V.P.:60, L.P.:28). Results were as follows (mean follow-up:31 mths +/- 28): good results (including excellent results): 128 (52.6%), fair: 52 (21.3%), poor and aggravated: 49 (20%), early deaths: 14 (5.7%), 12 of those post-operatively. The rate of surgical complications was 35% (S.D.H.: 16.8%, sepsis: 4%, seizures: 4%, shunt malfunction: 10.6%) leading to reoperation in 25.7%. Long-term survival rate was 75% (172 alive patients and 57 late deaths).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Chronic hydrocephalus in adults]. 219 67

A 60 year-old man was admitted to our hospital because of gait disturbance and dizziness. At 57 years of age, he noticed his walking unstable. After then, he had dizziness due to orthostatic hypotension, urinary difficulty, loss of livid, and forgetfulness. Neurological examination revealed he had severe orthostatic hypotension, cerebellar ataxia, dysarthria, hyperreflexia of four limbs, myoclonus of right leg, and atonic bladder. His brain CT showed cerebellar atrophy. Thereafter he had recurrent syncopic attacks. His gait disturbance progressed steadily, so he became bedridden. In his terminal stage, his limbs showed rigidity. About 3 years later he died of pneumonia and sepsis. At autopsy brain weighted 1,230 g. Glossly the putamens was bilaterally shrunken, the color of the substantia nigra and locus ceruleus became pale. Base of the pons and the cerebellum were atrophic. Microscopical examination confirmed the degeneration of striato-nigral and olivo-ponto-cerebellar systems without Lewy body. In the spinal cord there was depletion of neuronal cells in the intermediolateral nuclei and Onufrowitz nuclei. In addition to the conventional neuropathological staining methods, we performed the immunohistochemical studies using monoclonal antibody against synthetic peptide of beta protein which detected senile plaque of every stages with formic acid pretreatment, and compared to the modified Bielschowsky method and Congo red method. Our case showed many very primitive and primitive senile plaque in neocortices and hippocampal region. A few neurofibrally tangle were seen in hippocampus. We supposed our case might combine multiple system atrophy and Alzheimer' pathology.
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PMID:[An autopsy case of multiple system atrophy with many senile plaques]. 262 28

Thirty-five patients with acute myelogenous leukemia were treated with aclacinomycin A (60 mg/m2/day for 5 days) and VP-16-213 (100 mg/m2/day for 5 days). All were previously treated and had relapsed or were refractory to primary treatment. Most patients (28) had received prior DAT (daunorubicin, cytosine arabinoside, and 6-thioguanine) induction therapy followed by one or more courses of high-dose cytosine arabinoside (HD-Ara C) as consolidation therapy or as treatment for relapse. One patient was in her fourth relapse, one had relapsed acute megakaryoblastic leukemia (following remission with DAT and HD-Ara-C), one had a treatment-induced leukemia, and four patients were treated for primary treatment failures following two induction courses with DAT or a similar regimen. Fourteen patients had infections at start of therapy. Ten patients died within 14 days of treatment, all from sepsis or bleeding, before their marrow could be evaluated for leukemic response. Fourteen patients (40%) responded; 12 (34%) entered complete remission and two (6%) a partial remission (PR). Two of the four patients who were treated for primary treatment failures went into CR. The median CR duration was 99 days (range 30 to 455 days). Side effects from this treatment were similar to the conventional DAT regimen, although the gastrointestinal toxicity and mucositis appeared to be more severe. In addition, two of the patients had severe but reversible ventricular arrhythmias. The overall response (40%) and CR rate (34%) in this group of previously treated AML patients is encouraging, and further studies are needed to evaluate these preliminary findings.
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PMID:Aclacinomycin A and etoposide (VP-16-213): an effective regimen in previously treated patients with refractory acute myelogenous leukemia. 316 95

Two autopsy cases of neonatal argininosuccinate synthetase (ASS) deficiency demonstrating the particular histological changes of the liver are presented. Case 1 was a female infant with elevated blood ammonia and citrulline. The patient died of sepsis at nineteen days after birth. Autopsy revealed hematomas in bilateral cerebral hemispheres and a yellow liver parenchyma. Histologically, the cerebrum showed diffuse astrogliosis with Alzheimer type II cell and swollen cytoplasm. Status spongiosus and gliosis were observed in the subthalamic and pontine nuclei. The liver demonstrated fatty degeneration and wide portal space with bile duct proliferation and inflammatory cell infiltration. The ASS activities in the liver and the kidneys were not detected. Case 2 was a female infant who died of respiratory distress twenty-four days after birth. Autopsy revealed hematomas in the bilateral cerebral ventricles and a liver with yellow parenchyma. Histologically, there was destruction of arrangement in the cerebrum and cerebellum together with marked decrease of nerve cells with gliosis and phagocytosis. The liver showed mild fatty degeneration and wide portal space accompanied by bile duct proliferation and inflammatory cell infiltration. The ASS activities in the liver and kidneys were not detected.
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PMID:Neonatal type of argininosuccinate synthetase deficiency. Report of two cases with autopsy findings. 407 82

This review describes insults to the brain which result in either an increased or decreased mass effect. These mechanisms produce certain derangements in the central nervous system, which can lead to the patient's death. Increased intracranial mass effect characterized by brain tumors may produce lethal brain-stem ischemia. On the other hand, decreased intracranial mass effect as seen in Alzheimer's disease leads to aspiration pneumonia and terminal sepsis.
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PMID:A neuropathologic approach to human disease: the intracranial mass effect. 703 53

The pathophysiology of organ system failure in sepsis, in particular the effects of septic shock on the central nervous system, are still incompletely understood. Lipopolysaccharide (LPS) from Gram-negative bacteria affects the permeability of the blood-brain barrier and causes the activation of brain microglia. A growing body of research supports involvement of activated brain microglia in brain pathologies caused by infectious diseases, trauma, tumors, ischemia, Alzheimer's disease, Parkinson's disease, Down's syndrome, multiple sclerosis and AIDS. Those seminal studies that have contributed to the characterization of the in vivo and in vitro effects of LPS on microglia function, mediator generation and receptor expression are presented within a historical perspective. In particular, all those in vitro studies on O2-, H2O2 and NO. generation by either unprimed or primed microglia have been extensively reviewed. The apparent controversial effect of LPS on microglia O2- is discussed. Because treatment modalities for septic shock have not significantly affected the current high mortality, alternative strategies with antioxidants are currently being investigated. Reduction of microglia O2- generation is proposed as a possible complementary strategy to antioxidative therapy for septic shock and CNS pathologies that involve activated microglia.
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PMID:Therapeutic implications of microglia activation by lipopolysaccharide and reactive oxygen species generation in septic shock and central nervous system pathologies: a review. 981

A stress-activated serine/threonine protein kinase, p38 mitogen-activated protein kinase (p38 MAPK), belongs to the MAP kinase superfamily. Diverse extracellular stimuli, including ultraviolet light, irradiation, heat shock, high osmotic stress, proinflammatory cytokines and certain mitogens, trigger a stress-regulated protein kinase cascade culminating in activation of p38 MAPK through phosphorylation on a TGY motif within the kinase activation loop. p38 MAPK appears to play a major role in apoptosis, cytokine production, transcriptional regulation, and cytoskeletal reorganization, and has been causally implicated in sepsis, ischemic heart disease, arthritis, human immunodeficiency virus infection, and Alzheimer's disease. The availability of specific inhibitors helps to clarify the role that p38 MAPK plays in these processes, and may ultimately offer therapeutic benefit for certain critically ill patients.
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PMID:MAP kinase pathways activated by stress: the p38 MAPK pathway. 1080 18

Low rates of coronary heart disease was found in Greenland Eskimos and Japanese who are exposed to a diet rich in fish oil. Suggested mechanisms for this cardio-protective effect focused on the effects of n-3 fatty acids on eicosanoid metabolism, inflammation, beta oxidation, endothelial dysfunction, cytokine growth factors, and gene expression of adhesion molecules; But, none of these mechanisms could adequately explain the beneficial actions of n-3 fatty acids. One attractive suggestion is a direct cardiac effect of n-3 fatty acids on arrhythmogenesis. N-3 fatty acids can modify Na+ channels by directly binding to the channel proteins and thus, prevent ischemia-induced ventricular fibrillation and sudden cardiac death. Though this is an attractive explanation, there could be other actions as well. N-3 fatty acids can inhibit the synthesis and release of pro-inflammatory cytokines such as tumor necrosis factoralpha (TNFalpha) and interleukin-1 (IL-1) and IL-2 that are released during the early course of ischemic heart disease. These cytokines decrease myocardial contractility and induce myocardial damage, enhance the production of free radicals, which can also suppress myocardial function. Further, n-3 fatty acids can increase parasympathetic tone leading to an increase in heart rate variability and thus, protect the myocardium against ventricular arrhythmias. Increased parasympathetic tone and acetylcholine, the principle vagal neurotransmitter, significantly attenuate the release of TNF, IL-1beta, IL-6 and IL-18. Exercise enhances parasympathetic tone, and the production of anti-inflammatory cytokine IL-10 which may explain the beneficial action of exercise in the prevention of cardiovascular diseases and diabetes mellitus. TNFalpha has neurotoxic actions, where as n-3 fatty acids are potent neuroprotectors and brain is rich in these fatty acids. Based on this, it is suggested that the principle mechanism of cardioprotective and neuroprotective action(s) of n-3 fatty acids can be due to the suppression of TNFalpha and IL synthesis and release, modulation of hypothalamic-pituitary-adrenal anti-inflammatory responses, and an increase in acetylcholine release, the vagal neurotransmitter. Thus, there appears to be a close interaction between the central nervous system, endocrine organs, cytokines, exercise, and dietary n-3 fatty acids. This may explain why these fatty acids could be of benefit in the management of conditions such as septicemia and septic shock, Alzheimer's disease, Parkinson's disease, inflammatory bowel diseases, diabetes mellitus, essential hypertension and atherosclerosis.
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PMID:Beneficial effect(s) of n-3 fatty acids in cardiovascular diseases: but, why and how? 1113 72

Lipoprotein(a) [Lp(a)] is an enigmatic lipoprotein particle present in the plasma from humans, great apes and hedgehogs. Plasma levels of Lp(a) vary widely between individuals and are largely determined by specific sequences within the gene encoding apo(a), the unique highly polymorphic glycoprotein attached to apoB of low density lipoprotein (LDL) to form Lp(a). Elevated plasma concentrations of LP(a) are associated with the premature development of atherosclerosis. A major goal of our laboratory is to better understand the metabolism of Lp(a) and its function in humans. We have identified unexpected and large variations in plasma Lp(a) levels during renal disease, HIV-infection and in sepsis. Moreover, we have observed an association between Lp(a) and Alzheimer disease. Taken together, our observations suggest that Lp(a) may constitute a novel target in our fight against cardiovascular and neurodegenerative disorders.
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PMID:[Lipoprotein (a) in Alzheimer's atherosclerosis]. 1114 Mar 10


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