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1.
Neurocrit Care ; 30(3): 601-608, 2019 06.
Artigo em Inglês | MEDLINE | ID: mdl-30430380

RESUMO

BACKGROUND: Noncontrast computed tomography (CT) markers are increasingly used for predicting hematoma expansion. The aim of our study was to investigate the predictive value of expansion-prone hematoma in predicting hematoma expansion and outcome in patients with intracerebral hemorrhage (ICH). METHODS: Between July 2011 and January 2017, ICH patients who underwent baseline CT scan within 6 h of symptoms onset and follow-up CT scan were recruited into the study. Expansion-prone hematoma was defined as the presence of one or more of the following imaging markers: blend sign, black hole sign, or island sign. The diagnostic performance of blend sign, black hole sign, island sign, and expansion-prone hematoma in predicting hematoma expansion was assessed. Predictors of hematoma growth and poor outcome were analyzed using multivariable logistical regression analysis. RESULTS: A total of 282 patients were included in our final analysis. Of 88 patients with early hematoma growth, 69 (78.4%) had expansion-prone hematoma. Expansion-prone hematoma had a higher sensitivity and accuracy for predicting hematoma expansion and poor outcome when compared with any single imaging marker. After adjustment for potential confounders, expansion-prone hematoma independently predicted hematoma expansion (OR 28.33; 95% CI 12.95-61.98) and poor outcome (OR 5.67; 95% CI 2.82-11.40) in multivariable logistic model. CONCLUSION: Expansion-prone hematoma seems to be a better predictor than any single noncontrast CT marker for predicting hematoma expansion and poor outcome. Considering the high risk of hematoma expansion in these patients, expansion-prone hematoma may be a potential therapeutic target for anti-expansion treatment in future clinical studies.


Assuntos
Hemorragia Cerebral/patologia , Progressão da Doença , Hematoma/patologia , Avaliação de Resultados em Cuidados de Saúde , Adulto , Idoso , Idoso de 80 Anos ou mais , Hemorragia Cerebral/diagnóstico por imagem , Feminino , Seguimentos , Hematoma/diagnóstico por imagem , Humanos , Masculino , Pessoa de Meia-Idade , Tomografia Computadorizada por Raios X
2.
Pak J Pharm Sci ; 29(3 Suppl): 1087-93, 2016 May.
Artigo em Inglês | MEDLINE | ID: mdl-27383488

RESUMO

To investigate the effects of the iron chelatordeferoxamine (DFA) on inhibition formicroglia activation and protection of secondary nerve injury after intracerebral hemorrhage (ICH) in rats. The rats were randomly divided into sham operation group, ICH group and DFA treatment group. The collagenase was used to prepare ICH model of basal gangliain rats and 1h after the beginning of the operation, the intraperitoneal injection with DFA was arranged every 12 h and for a total of 7d. The changes of Iron ion concentration were measured at perihematomaat different time points after the medicine was given. OX42 immunohistochemical staining observed microglia change at perihematoma. ELISA method determined the changes of IL-1ß and TNF-ß content of brain tissue. Neurological deficit scores and Nissl staining were used to observe the situation of neurological function and neuronal loss of rats after DFA treatment. 1 d After the start of ICH, the concentration of iron in perihematoma was significantly higher than that of animalsin sham-operated group and could sustain for28 d. At the same time, the quantities of local microglial cells were significantly increased. After applying DFA, the concentration of iron ions in the brain tissue around the hematoma was significantly reduced, so did the number of microglial cells and activation of neurotoxic cytokines (IL-1ß and TNF-α content) secreted by microglial cells was significantly reduced. At the same time, the loss of neurons in the tissue around of the hematoma was significantly reduced and neurological deficit scores were significantly reduced. Iron ions which were sustainedly released by hematoma after ICH can activate the local microglia and cause secondary brain injury. DFA curb excessive activation of microglia and reduce neuronal death of ICH by means of clearinf away iron ions of brain tissue surrounding the hematoma, thus improve secondary neurological dysfunction.


Assuntos
Encéfalo/efeitos dos fármacos , Hemorragia Cerebral/tratamento farmacológico , Desferroxamina/farmacologia , Quelantes de Ferro/farmacologia , Microglia/efeitos dos fármacos , Fármacos Neuroprotetores/farmacologia , Animais , Encéfalo/metabolismo , Encéfalo/patologia , Morte Celular/efeitos dos fármacos , Hemorragia Cerebral/complicações , Hemorragia Cerebral/metabolismo , Hemorragia Cerebral/patologia , Citoproteção , Modelos Animais de Doenças , Interleucina-1beta/metabolismo , Ferro/metabolismo , Masculino , Microglia/metabolismo , Microglia/patologia , Ratos Sprague-Dawley , Fatores de Tempo , Fator de Necrose Tumoral alfa/metabolismo
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