Base de dados : MEDLINE
Pesquisa : C10.228.140.163 [Categoria DeCS]
Referências encontradas : 1897 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 190 ir para página                         

  1 / 1897 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29069042
[Au] Autor:Ren S; Chen Z; Liu M; Wang Z
[Ad] Endereço:aDepartment of Neurology bDepartment of Radiology, Dongfang Hospital, Beijing University of Chinese Medicine, Beijing, China.
[Ti] Título:The radiological findings of hypoglycemic encephalopathy: A case report with high b value DWI analysis.
[So] Source:Medicine (Baltimore);96(43):e8425, 2017 Oct.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Hypoglycemic encephalopathy is a metabolic encephalopathy. Clinical risk is mixed with acute cerebrovascular disease, so it is critical to identify and make the correct diagnosis of the disease as early as possible. PATIENT CONCERNS: Here, we report a case of a 51-year-old male patient with hypoglycemic encephalopathy, who presented confusion and unconsciousness for 1 day. DIAGNOSES: In addition to blood-related indicators and medical histories, magnetic resonance imaging (MRI), especially diffusion-weighted imaging (DWI), can be valuable to the diagnosis of hypoglycemic encephalopathy, which showed diffuse high-signal intensity in the cerebral cortex, and also the hippocampus, head of the caudate nucleus, the lentiform nucleus, and corpus callosum. INTERVENTIONS: Intravenous glucose injection and drip was performed repeatedly. The blood glucose levels were gradually corrected, and the resulting blood glucose was 6.5 mmol/L. OUTCOMES: The prognosis depends on the degree of hypoglycemia, duration, and condition of the organism. Due to the long duration of hypoglycemia, unfortunately, the patient died. LESSONS: It is critical to diagnose hypoglycemic encephalopathy as early as possible. MRI reveals diffuse abnormal intensity in the cortex and basal ganglia region. DWI using high b values provides important information for diagnosis.
[Mh] Termos MeSH primário: Encefalopatias Metabólicas/diagnóstico por imagem
Imagem de Difusão por Ressonância Magnética/métodos
Hipoglicemia/complicações
[Mh] Termos MeSH secundário: Encefalopatias Metabólicas/tratamento farmacológico
Encefalopatias Metabólicas/etiologia
Córtex Cerebral/diagnóstico por imagem
Evolução Fatal
Hipocampo/diagnóstico por imagem
Seres Humanos
Hipoglicemia/tratamento farmacológico
Hipoglicemiantes/uso terapêutico
Masculino
Meia-Idade
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hypoglycemic Agents)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171123
[Lr] Data última revisão:
171123
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171026
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008425


  2 / 1897 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Wajner, Moacir
Texto completo
[PMID]:28762469
[Au] Autor:Vendramin Pasquetti M; Meier L; Loureiro S; Ganzella M; Junges B; Barbieri Caus L; Umpierrez Amaral A; Koeller DM; Goodman S; Woontner M; Gomes de Souza DO; Wajner M; Calcagnotto ME
[Ad] Endereço:Postgraduate Program in Biological Sciences: Biochemistry, Department of Biochemistry, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.
[Ti] Título:Impairment of GABAergic system contributes to epileptogenesis in glutaric acidemia type I.
[So] Source:Epilepsia;58(10):1771-1781, 2017 Oct.
[Is] ISSN:1528-1167
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Glutaric acidemia type I (GA-I) is an inherited neurometabolic disorder caused by deficiency of glutaryl-CoA dehydrogenase (GCDH) and characterized by increased levels of glutaric, 3-OH-glutaric, and glutaconic acids in the brain parenchyma. The increment of these organic acids inhibits glutamate decarboxylase (GAD) and consequently lowers the γ-aminobutyric acid (GABA) synthesis. Untreated patients exhibit severe neurologic deficits during development, including epilepsy, especially following an acute encephalopathy outbreak. In this work, we evaluated the role of the GABAergic system on epileptogenesis in GA-I using the Gcdh mice exposed to a high lysine diet (Gcdh -Lys). METHODS: Spontaneous recurrent seizures (SRS), seizure susceptibility, and changes in brain oscillations were evaluated by video-electroencephalography (EEG). Cortical GABAergic synaptic transmission was evaluated using electrophysiologic and neurochemical approaches. RESULTS: SRS were observed in 72% of Gcdh -Lys mice, whereas no seizures were detected in age-matched controls (Gcdh or Gcdh receiving normal diet). The severity and number of PTZ-induced seizures were higher in Gcdh -Lys mice. EEG spectral analysis showed a significant decrease in theta and gamma oscillations and predominant delta waves in Gcdh -Lys mice, associated with increased EEG left index. Analysis of cortical synaptosomes revealed a significantly increased percentage of glutamate release and decreased GABA release in Gcdh -Lys mice that were associated with a decrease in cortical GAD immunocontent and activity and confirmed by reduced frequency of inhibitory events in cortical pyramidal cells. SIGNIFICANCE: Using an experimental model with a phenotype similar to that of GA-I in humans-the Gcdh mice under high lysine diet (Gcdh -Lys)-we provide evidence that a reduction in cortical inhibition of Gcdh -Lys mice, probably induced by GAD dysfunction, leads to hyperexcitability and increased slow oscillations associated with neurologic abnormalities in GA-I. Our findings offer a new perspective on the pathophysiology of brain damage in GA-I.
[Mh] Termos MeSH primário: Erros Inatos do Metabolismo dos Aminoácidos/genética
Encefalopatias Metabólicas/genética
Encéfalo/efeitos dos fármacos
Epilepsia/genética
Glutaril-CoA Desidrogenase/deficiência
Glutaril-CoA Desidrogenase/genética
Ácido gama-Aminobutírico/efeitos dos fármacos
[Mh] Termos MeSH secundário: Erros Inatos do Metabolismo dos Aminoácidos/metabolismo
Animais
Western Blotting
Encefalopatias Metabólicas/metabolismo
Cromatografia Líquida de Alta Pressão
Epilepsia/metabolismo
Antagonistas GABAérgicos/farmacologia
Glutamato Descarboxilase
Ácido Glutâmico/efeitos dos fármacos
Ácido Glutâmico/metabolismo
Glutaril-CoA Desidrogenase/metabolismo
Camundongos
Camundongos Knockout
Pentilenotetrazol/farmacologia
Sinaptossomos/efeitos dos fármacos
Sinaptossomos/metabolismo
Ácido gama-Aminobutírico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GABA Antagonists); 3KX376GY7L (Glutamic Acid); 56-12-2 (gamma-Aminobutyric Acid); EC 1.3.8.6 (Glutaryl-CoA Dehydrogenase); EC 4.1.1.15 (Glutamate Decarboxylase); WM5Z385K7T (Pentylenetetrazole)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170802
[St] Status:MEDLINE
[do] DOI:10.1111/epi.13862


  3 / 1897 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28704229
[Au] Autor:Achinger SG; Ayus JC
[Ad] Endereço:1Department of Nephrology, Watson Clinic LLP, Lakeland, FL. 2Renal Consultants of Houston, Department of Research, Houston, TX. 3Department of Nephrology, Hospital Italiano, Buenos Aires, Argentina. 4Department of Nephrology, Hospital Austral, Austral University, Buenos Aires, Argentina. 5Department of Nephrology, University of California, Irvine, CA.
[Ti] Título:Treatment of Hyponatremic Encephalopathy in the Critically Ill.
[So] Source:Crit Care Med;45(10):1762-1771, 2017 Oct.
[Is] ISSN:1530-0293
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Hyponatremic encephalopathy, symptomatic cerebral edema due to a low osmolar state, is a medical emergency and often encountered in the ICU setting. This article provides a critical appraisal and review of the literature on identification of high-risk patients and the treatment of this life-threatening disorder. DATA SOURCES, STUDY SELECTION, AND DATA EXTRACTION: Online search of the PubMed database and manual review of articles involving risk factors for hyponatremic encephalopathy and treatment of hyponatremic encephalopathy in critical illness. DATA SYNTHESIS: Hyponatremic encephalopathy is a frequently encountered problem in the ICU. Prompt recognition of hyponatremic encephalopathy and early treatment with hypertonic saline are critical for successful outcomes. Manifestations are varied, depending on the extent of CNS's adaptation to the hypoosmolar state. The absolute change in serum sodium alone is a poor predictor of clinical symptoms. However, certain patient specific risks factors are predictive of a poor outcome and are important to identify. Gender (premenopausal and postmenopausal females), age (prepubertal children), and the presence of hypoxia are the three main clinical risk factors and are more predictive of poor outcomes than the rate of development of hyponatremia or the absolute decrease in the serum sodium. CONCLUSIONS: In patients with hyponatremic encephalopathy exhibiting neurologic manifestations, a bolus of 100 mL of 3% saline, given over 10 minutes, should be promptly administered. The goal of this initial bolus is to quickly treat cerebral edema. If signs persist, the bolus should be repeated in order to achieve clinical remission. However, the total change in serum sodium should not exceed 5 mEq/L in the initial 1-2 hours and 15-20 mEq/L in the first 48 hours of treatment. It has recently been demonstrated in a prospective fashion that 500 mL of 3% saline at an infusion rate of 100 mL per hour can be given safely. It is critical to recognize the early signs of cerebral edema (nausea, vomiting, and headache) and intervene with IV 3% sodium chloride as this is the time to intervene rather than waiting until more severe symptoms develop. Cerebral demyelination is a rare complication of overly rapid correction of hyponatremia. The principal risk factors for cerebral demyelination are correction of the serum sodium more than 25 mEq/L in the first 48 hours of therapy, correction past the point of 140 mEq/L, chronic liver disease, and hypoxic/anoxic episode.
[Mh] Termos MeSH primário: Encefalopatias Metabólicas/etiologia
Encefalopatias Metabólicas/terapia
Estado Terminal
Hiponatremia/complicações
Solução Salina Hipertônica/uso terapêutico
[Mh] Termos MeSH secundário: Fatores Etários
Edema Encefálico/etiologia
Edema Encefálico/prevenção & controle
Doenças Desmielinizantes/etiologia
Doenças Desmielinizantes/prevenção & controle
Esquema de Medicação
Seres Humanos
Hipóxia/complicações
Fatores de Risco
Fatores Sexuais
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Saline Solution, Hypertonic)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170714
[St] Status:MEDLINE
[do] DOI:10.1097/CCM.0000000000002595


  4 / 1897 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28302372
[Au] Autor:Tsai FC; Lee HJ; Wang AG; Hsieh SC; Lu YH; Lee MC; Pai JS; Chu TH; Yang CF; Hsu TR; Lai CJ; Tsai MT; Ho PH; Lin MC; Cheng LY; Chuang YC; Niu DM
[Ad] Endereço:Department of Pediatrics, Taipei Veterans General Hospital, Taipei, Taiwan, ROC.
[Ti] Título:Experiences during newborn screening for glutaric aciduria type 1: Diagnosis, treatment, genotype, phenotype, and outcomes.
[So] Source:J Chin Med Assoc;80(4):253-261, 2017 Apr.
[Is] ISSN:1728-7731
[Cp] País de publicação:China (Republic : 1949- )
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Glutaric aciduria type 1 (GA-1) is an organic acidemia with potentially severe neurological sequelae. In Taiwan, newborn screening (NBS) for GA-1 began in 2001, but large-scale reporting is lacking. This study describes Taiwan's largest newborn screening population to date. METHODS: Between 2001 and 2015, 1,490,636 newborns were screened for GA-1. Confirmatory examinations included the carnitine loading test. Confirmed patients were treated with a low lysine diet, carnitine, and high-energy intake during illness. Clinical, laboratory, and neuroimaging data were analyzed. RESULTS: Fourteen newborns were diagnosed with GA-1 (incidence: 1/106,474). C5DC concentration was clearly increased after carnitine loading in the affected newborns, but not in false-positive newborns (p = 0.004), indicating that this test is useful as an adjuvant diagnostic method. Eleven patients followed in our hospital were enrolled, namely nine NBS patients and two patients diagnosed clinically. IVS10-2A>C was the most common mutation. Two novel mutations (T36fs and N291K) were identified. Pendular nystagmus was found in two pediatric GA-1 patients. The corresponding pathology was optic atrophy in one patient, but remained undetermined in the other patient. The frequency of encephalopathic crisis decreased substantially following NBS. Among patients diagnosed by NBS, cognitive functioning was better among patients with good compliance than patients with poor compliance (p = 0.03). Abnormalities were detected by brain MRI including diffusion-weighted imaging and apparent diffusion coefficient maps; these affected various brain regions at different stages of the disease. Basal ganglion injuries occurred after an encephalopathic crisis. White matter disease was prevalent among older patients, either with or without an encephalopathic crisis. CONCLUSION: Early diagnosis by newborn screening followed by full compliance with treatment guidelines is important to a good outcome.
[Mh] Termos MeSH primário: Erros Inatos do Metabolismo dos Aminoácidos/diagnóstico
Encefalopatias Metabólicas/diagnóstico
Glutaril-CoA Desidrogenase/deficiência
Triagem Neonatal
[Mh] Termos MeSH secundário: Erros Inatos do Metabolismo dos Aminoácidos/complicações
Erros Inatos do Metabolismo dos Aminoácidos/terapia
Encefalopatias Metabólicas/complicações
Encefalopatias Metabólicas/terapia
Feminino
Genótipo
Seres Humanos
Recém-Nascido
Imagem por Ressonância Magnética
Masculino
Fenótipo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 1.3.8.6 (Glutaryl-CoA Dehydrogenase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170318
[St] Status:MEDLINE


  5 / 1897 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:28270654
[Au] Autor:Surjan RC; Dos Santos ES; Basseres T; Makdissi FF; Machado MA
[Ad] Endereço:Department of Surgery, University of São Paulo, São Paulo, SP, Brazil.
[Ti] Título:A Proposed Physiopathological Pathway to Hyperammonemic Encephalopathy in a Non-Cirrhotic Patient with Fibrolamellar Hepatocellular Carcinoma without Ornithine Transcarbamylase (OTC) Mutation.
[So] Source:Am J Case Rep;18:234-241, 2017 Mar 08.
[Is] ISSN:1941-5923
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND Hyperammonemic encephalopathy is a potentially fatal condition that may progress to irreversible neuronal damage and is usually associated with liver failure or portosystemic shunting. However, other less common conditions can lead to hyperammonemia in adults, such as fibrolamellar hepatocellular carcinoma. Clinical awareness of hyperammonemic encephalopathy in patients with normal liver function is paramount to timely diagnosis, but understanding the underlying physiopathology is decisive to initiate adequate treatment for complete recovery. CASE REPORT A 31-year-old male with fibrolamellar carcinoma and peritoneal carcinomatosis presented with rapid onset hyperammonemic encephalopathy. Despite usual treatment for hepatic encephalopathy, his hyperammonemia was aggravated. A physiopathological pathway to encephalopathy resulting from hepatocellular dysfunction or portosystemic shunting was suspected and proper treatment was initiated, which resulted in complete remission of encephalopathy. Thus, we propose there is a physiopathology path to hyperammonemic encephalopathy in non-cirrhotic patients with fibrolamellar carcinoma independent of ornithine transcarbamylase (OTC) mutation. An ornithine metabolism imbalance resulting from overexpression of Aurora Kinase A as a result of a single, recurrent heterozygous deletion on chromosome 19, common to all fibrolamellar carcinomas, can lead to a c-Myc and ornithine decarboxylase overexpression that results in ornithine transcarboxylase dysfunction with urea cycle disorder and subsequent hyperammonemia. CONCLUSIONS The identification of a physiopathological pathway allowed adequate medical treatment and full patient recovery from severe hyperammonemic encephalopathy.
[Mh] Termos MeSH primário: Encefalopatias Metabólicas/etiologia
Carcinoma Hepatocelular/complicações
Carcinoma Hepatocelular/fisiopatologia
Hiperamonemia/etiologia
Neoplasias Hepáticas/complicações
Neoplasias Hepáticas/fisiopatologia
[Mh] Termos MeSH secundário: Adulto
Seres Humanos
Masculino
Ornitina Carbamoiltransferase
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.1.3.3 (Ornithine Carbamoyltransferase)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170403
[Lr] Data última revisão:
170403
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170309
[St] Status:MEDLINE


  6 / 1897 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28062662
[Au] Autor:Schmiesing J; Lohmöller B; Schweizer M; Tidow H; Gersting SW; Muntau AC; Braulke T; Mühlhausen C
[Ad] Endereço:Department of Biochemistry, Children's Hospital, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
[Ti] Título:Disease-causing mutations affecting surface residues of mitochondrial glutaryl-CoA dehydrogenase impair stability, heteromeric complex formation and mitochondria architecture.
[So] Source:Hum Mol Genet;26(3):538-551, 2017 Feb 01.
[Is] ISSN:1460-2083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The neurometabolic disorder glutaric aciduria type 1 (GA1) is caused by mutations in the GCDH gene encoding the mitochondrial matrix protein glutaryl-CoA dehydrogenase (GCDH), which forms homo- and heteromeric complexes. Twenty percent of all pathogenic mutations affect single amino acid residues on the surface of GCDH resulting in a severe clinical phenotype. We report here on heterologous expression studies of 18 missense mutations identified in GA1 patients affecting surface amino acids. Western blot and pulse chase experiments revealed that the stability of half of the GCDH mutants was significantly reduced. In silico analyses showed that none of the mutations impaired the 3D structure of GCDH. Immunofluorescence co-localisation studies in HeLa cells demonstrated that all GCDH mutants were correctly translocated into mitochondria. Surprisingly, the expression of p.Arg88Cys GCDH as well as further substitutions by alanine, lysine, or methionine but not histidine or leucine resulted in the disruption of mitochondrial architecture forming longitudinal structures composed of stacks of cristae and partial loss of the outer mitochondrial membrane. The expression of mitochondrial fusion or fission proteins was not affected in these cells. Bioluminescence resonance energy transfer analyses revealed that all GCDH mutants exhibit an increased binding affinity to electron transfer flavoprotein beta, whereas only p.Tyr155His GCDH showed a reduced interaction with dihydrolipoamide succinyl transferase. Our data underscore the impact of GCDH protein interactions mediated by amino acid residues on the surface of GCDH required for proper enzymatic activity.
[Mh] Termos MeSH primário: Erros Inatos do Metabolismo dos Aminoácidos/genética
Encefalopatias Metabólicas/genética
Estabilidade Enzimática/genética
Glutaril-CoA Desidrogenase/deficiência
Glutaril-CoA Desidrogenase/genética
Mitocôndrias/genética
[Mh] Termos MeSH secundário: Erros Inatos do Metabolismo dos Aminoácidos/patologia
Substituição de Aminoácidos/genética
Encefalopatias Metabólicas/patologia
Regulação Enzimológica da Expressão Gênica/genética
Glutaril-CoA Desidrogenase/química
Células HeLa
Seres Humanos
Mitocôndrias/patologia
Dinâmica Mitocondrial/genética
Mutação de Sentido Incorreto/genética
Conformação Proteica
Multimerização Proteica/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 1.3.8.6 (Glutaryl-CoA Dehydrogenase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170915
[Lr] Data última revisão:
170915
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170108
[St] Status:MEDLINE
[do] DOI:10.1093/hmg/ddw411


  7 / 1897 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28010956
[Au] Autor:Isik U; Dinçer A
[Ad] Endereço:Acibadem University, Department of Pediatrics, Division of Pediatric Neurology, Kozyatagi Acibadem Hastanesi, Inönü Cad. Okur Sok. No: 20, Kozyatagi, Istanbul, Turkey. Electronic address: ugur.isik@acibadem.com.tr.
[Ti] Título:Central tegmentum tract hyperintensities in pediatric neurological patients: Incidence or coincidence.
[So] Source:Brain Dev;39(5):411-417, 2017 May.
[Is] ISSN:1872-7131
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIM: The central tegmental tract hyperintensities (CTTH) have been found in many different pediatric neurological conditions. There is only scarce data about the value of this radiological phenomenon. In this study we aimed to show the neurological conditions associated with this radiological finding. MATERIALS AND METHODS: We performed a retrospective analysis of all pediatric brain MRI's between 2013 and 2015. After finding those patients with CTTH, we evaluated them in the pediatric neurology clinic. RESULTS: There were 41 out of 1464 brain MRI's with CTTH with 2.8% prevalence. Thirty four patients (23 male, age range 3months-98months) were available for evaluation. CTTH were present in mainly younger age group. There were many different neurological conditions associated with CTTH. These included brain tumors, epilepsy, developmental delay, metabolic disorders and genetic syndromes. CONCLUSION: CTTH is found in many different pediatric neurological conditions. Further neuropathological and prospective MRI and clinical studies are needed to better understand this interesting radiological finding.
[Mh] Termos MeSH primário: Deficiências do Desenvolvimento/epidemiologia
Doenças do Sistema Nervoso/diagnóstico por imagem
Doenças do Sistema Nervoso/epidemiologia
Tegmento Pontino/diagnóstico por imagem
[Mh] Termos MeSH secundário: Adolescente
Encefalopatias Metabólicas/diagnóstico por imagem
Encefalopatias Metabólicas/epidemiologia
Criança
Pré-Escolar
Deficiências do Desenvolvimento/diagnóstico por imagem
Epilepsia/diagnóstico por imagem
Epilepsia/epidemiologia
Feminino
Seres Humanos
Processamento de Imagem Assistida por Computador
Incidência
Lactente
Recém-Nascido
Imagem por Ressonância Magnética
Masculino
Prevalência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170417
[Lr] Data última revisão:
170417
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161225
[St] Status:MEDLINE


  8 / 1897 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27765861
[Au] Autor:Van Der Gucht A; Aoun Sebaiti M; Guedj E; Aouizerate J; Yara S; Gherardi RK; Evangelista E; Chalaye J; Cottereau AS; Verger A; Bachoud-Levi AC; Abulizi M; Itti E; Authier FJ
[Ad] Endereço:Department of Nuclear Medicine, H. Mondor Hospital, Assistance Publique-Hôpitaux de Paris/Paris-Est University, Créteil, France axel.vandergucht@gmail.com.
[Ti] Título:Brain F-FDG PET Metabolic Abnormalities in Patients with Long-Lasting Macrophagic Myofascitis.
[So] Source:J Nucl Med;58(3):492-498, 2017 Mar.
[Is] ISSN:1535-5667
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to characterize brain metabolic abnormalities in patients with macrophagic myofascitis (MMF) and the relationship with cognitive dysfunction through the use of PET with F-FDG. F-FDG PET brain imaging and a comprehensive battery of neuropsychological tests were performed in 100 consecutive MMF patients (age [mean ± SD], 45.9 ± 12 y; 74% women). Images were analyzed with statistical parametric mapping (SPM12). Through the use of analysis of covariance, all F-FDG PET brain images of MMF patients were compared with those of a reference population of 44 healthy subjects similar in age (45.4 ± 16 y; = 0.87) and sex (73% women; = 0.88). The neuropsychological assessment identified 4 categories of patients: those with no significant cognitive impairment ( = 42), those with frontal subcortical (FSC) dysfunction ( = 29), those with Papez circuit dysfunction ( = 22), and those with callosal disconnection ( = 7). In comparison with healthy subjects, the whole population of patients with MMF exhibited a spatial pattern of cerebral glucose hypometabolism ( < 0.001) involving the occipital lobes, temporal lobes, limbic system, cerebellum, and frontoparietal cortices, as shown by analysis of covariance. The subgroup of patients with FSC dysfunction exhibited a larger extent of involved areas (35,223 voxels vs. 13,680 voxels in the subgroup with Papez circuit dysfunction and 5,453 voxels in patients without cognitive impairment). Nonsignificant results were obtained for the last subgroup because of its small population size. Our study identified a peculiar spatial pattern of cerebral glucose hypometabolism that was most marked in MMF patients with FSC dysfunction. Further studies are needed to determine whether this pattern could represent a diagnostic biomarker of MMF in patients with chronic fatigue syndrome and cognitive dysfunction.
[Mh] Termos MeSH primário: Encefalopatias Metabólicas/metabolismo
Encéfalo/metabolismo
Transtornos Cognitivos/metabolismo
Fasciite/metabolismo
Glucose/metabolismo
Miosite/metabolismo
Tomografia por Emissão de Pósitrons/métodos
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Encéfalo/diagnóstico por imagem
Encefalopatias Metabólicas/diagnóstico por imagem
Doença Crônica
Transtornos Cognitivos/diagnóstico por imagem
Fasciite/diagnóstico por imagem
Feminino
Fluordesoxiglucose F18/farmacocinética
Seres Humanos
Masculino
Meia-Idade
Miosite/diagnóstico por imagem
Compostos Radiofarmacêuticos/farmacocinética
Reprodutibilidade dos Testes
Sensibilidade e Especificidade
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Radiopharmaceuticals); 0Z5B2CJX4D (Fluorodeoxyglucose F18); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170501
[Lr] Data última revisão:
170501
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161022
[St] Status:MEDLINE
[do] DOI:10.2967/jnumed.114.151878


  9 / 1897 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:27721316
[Au] Autor:Ishige M; Fuchigami T; Ogawa E; Usui H; Kohira R; Watanabe Y; Takahashi S
[Ad] Endereço:Department of Pediatrics and Child Health, Nihon University School of Medicine, Tokyo, Japan.
[Ti] Título:Severe Acute Subdural Hemorrhages in a Patient with Glutaric Acidemia Type 1 under Recommended Treatment.
[So] Source:Pediatr Neurosurg;52(1):46-50, 2017.
[Is] ISSN:1423-0305
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Glutaric acidemia type 1 is a rare autosomal recessive disease caused by a deficiency of glutaryl-CoA dehydrogenase. Previous studies have reported subdural hemorrhage in untreated patients with glutaric acidemia type 1. However, there is only one report of severe acute subdural hemorrhage after minor head trauma in a patient with glutaric acidemia type 1 under guideline-recommended treatment. We report a second case of life-threatening severe acute subdural hemorrhage after a minor head trauma in a patient with glutaric acidemia type 1. This patient was previously diagnosed by newborn screening, and treatment began at 25 days of age. Early diagnosis and guideline-recommended treatment produce better outcomes for patients with glutaric acidemia type 1, although the risk of subdural hemorrhage remains.
[Mh] Termos MeSH primário: Erros Inatos do Metabolismo dos Aminoácidos/cirurgia
Encefalopatias Metabólicas/cirurgia
Traumatismos Craniocerebrais/cirurgia
Glutaril-CoA Desidrogenase/deficiência
Hematoma Subdural Agudo/cirurgia
Índice de Gravidade de Doença
[Mh] Termos MeSH secundário: Erros Inatos do Metabolismo dos Aminoácidos/complicações
Erros Inatos do Metabolismo dos Aminoácidos/diagnóstico por imagem
Encefalopatias Metabólicas/complicações
Encefalopatias Metabólicas/diagnóstico por imagem
Traumatismos Craniocerebrais/complicações
Traumatismos Craniocerebrais/diagnóstico por imagem
Hematoma Subdural Agudo/complicações
Hematoma Subdural Agudo/diagnóstico por imagem
Seres Humanos
Lactente
Masculino
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
EC 1.3.8.6 (Glutaryl-CoA Dehydrogenase)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170314
[Lr] Data última revisão:
170314
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161011
[St] Status:MEDLINE


  10 / 1897 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:25579321
[Au] Autor:Dubey D; Freeman M; Neeley OJ; Carter G
[Ad] Endereço:a Department of Neurology , University of Texas South Western Medical Center , Dallas , TX , USA.
[Ti] Título:Encephalopathy following melphalan administration.
[So] Source:J Chemother;29(1):45-48, 2017 Feb.
[Is] ISSN:1973-9478
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To describe a rare case of encephalopathy following melphalan administration. Presentation and intervention:: A 59-year-old female with multiple myeloma developed encephalopathy following administration of melphalan. After ruling out other aetiologies, we hypothesized elevated cytokines from systemic inflammatory response to melphalan as the likely aetiology. The TNF-alpha level was found to be significantly elevated. Plasmapharesis was performed which reduced the level of cytokines, and also improved the patient's neurological status. CONCLUSION: Melphalan administration, especially in renally impaired patients, may lead to development of encephalopathy. Based on our case report, we suggest that elevated levels of cytokines could be the underlying mechanism of worsening mental status.
[Mh] Termos MeSH primário: Encefalopatias Metabólicas/induzido quimicamente
Melfalan/efeitos adversos
Agonistas Mieloablativos/efeitos adversos
[Mh] Termos MeSH secundário: Transplante de Medula Óssea
Encefalopatias Metabólicas/terapia
Feminino
Seres Humanos
Meia-Idade
Mieloma Múltiplo/terapia
Plasmaferese
Condicionamento Pré-Transplante/efeitos adversos
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Myeloablative Agonists); Q41OR9510P (Melphalan)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170427
[Lr] Data última revisão:
170427
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150113
[St] Status:MEDLINE
[do] DOI:10.1179/1973947814Y.0000000231



página 1 de 190 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde