Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 5 de 5
Filtrar
1.
Fa Yi Xue Za Zhi ; 35(5): 576-580, 2019 Oct.
Artigo em Inglês, Chinês | MEDLINE | ID: mdl-31833292

RESUMO

ABSTRACT: Objective To explore the change rules of blood ethanol and blood acetaldehyde concentration, the impairment of psychomotor functions of different acetaldehyde dehydrogenase (ALDH) 2 genotype individuals after alcohol consumption and the relationship among them. Methods The ALDH2 genotypes in seventy-nine healthy volunteers were obtained by SNaPshotTM method, then divided into ALDH2*1/*1 (wild type) and ALDH2*1/*2 (mutant type) group. After volunteers consumed 1.0 g/kg of alcohol, blood ethanol concentration and blood acetaldehyde concentration at a series of time points before and after alcohol consumption and psychomotor functions, such as, visual selective response time, auditory simple response time and tracking experiment were detected. Biphasic alcohol response questionnaires were collected. Results After alcohol consumption, ALDH2*1/*2 group's blood ethanol and blood acetaldehyde concentration reached the peak earlier than ALDH2*1/*1 group. Its blood acetaldehyde concentration was higher than that of ALDH2*1/*1 group, 1-6 h after alcohol consumption. The psychomotor functions, such as visual selective response time and auditory simple response time in ALDH2*1/*2 group were more significantly impaired than those in ALDH2*1/*1 group after alcohol consumption. There was no statistical significance between the two groups in excitement or sedation reactions (P>0.05). Pearson correlation coefficient test showed that blood acetaldehyde concentration was related with psychomotor function. Conclusion There are significant differences between the psychomotor function of ALDH2 wild type and mutant type individuals after alcohol consumption estimated to be related to the difference in blood acetaldehyde concentration after alcohol consumption.


Assuntos
Acetaldeído/sangue , Consumo de Bebidas Alcoólicas , Aldeído Desidrogenase/genética , Etanol/metabolismo , Polimorfismo Genético/genética , Desempenho Psicomotor/efeitos dos fármacos , Acetaldeído/metabolismo , Consumo de Bebidas Alcoólicas/efeitos adversos , Consumo de Bebidas Alcoólicas/sangue , Aldeído-Desidrogenase Mitocondrial , Aldeído Oxirredutases , Etanol/administração & dosagem , Etanol/sangue , Genótipo , Humanos , Desempenho Psicomotor/fisiologia
2.
Zhonghua Er Ke Za Zhi ; 54(5): 379-82, 2016 May.
Artigo em Chinês | MEDLINE | ID: mdl-27143082

RESUMO

OBJECTIVE: To explore the pathogenesis, treatment and prognosis of primary hypogammaglobulinemia complicated with liver cirrhosis in a child. METHOD: Pathogenesis, treatment and prognosis of X-linked agammaglobulinemia (XLA ) complicated with liver cirrhosis in a child were analyzed in Shanghai Children's Medical Center.Using"primary hypogammaglobulinemia"and"liver cirrhosis"as keywords, literatures were searched from Pubmed and Chinese data of Weipu and Wanfang data from January 1988 to January 2015. RESULT: The patient was a 12 years old boy with the chief complaint of 3 times hematemesis with diagnosis of XLA in the past 7 years. He received treatment with immunoglobulin (Ig) monthly for 6 years. He had no hepatitis C virus( HCV ) infection and serologic tests for autoantibodies were negative. Anti-HBs, anti-HBe and anti-HBc were positive, which revealed previous hepatitis B virus(HBV) infection. Gastroscopy suggested esophageal gastric varices. Liver pathology showed liver cell degeneration, necrosis, fiber tissue hyperplasia and pseudolobuli. After hospitalization the boy underwent liver transplantation (LT). He was given tacrolimus (3 mg/d), prednisone (5 mg/d), lamivudine (150 mg/d) and acyclovir (900 mg/d) by oral administration after LT. After 3 months follow-up, the boy was alive and well with stable results of liver function tests. There were no report in Weipu and Wanfang data. A total of 19 cases, including 12 cases of common variable immunodeficiency, 3 cases of XLA, 2 cases of Hyper-IgM syndrome and 2 cases of congenital hypogammaglobulinemia were obtained from Pubmed published between January 1, 1988 and January 1, 2015. Seventeen of the cases had HCV infection. Two cases had autoimmune hepatitis. Of the HCV infected patients, 15 were given intravenous gamma globulin. Seven of the 19 cases survived. Among 5 cases who received liver transplantation, 3 cases died. CONCLUSION: In addition to HCV infection and autoimmune hepatitis as causes of liver cirrhosis in primary hypogammaglobulinemia, chronic HBV infection is another cause. Intravenous gammaglobulin is an important way of transmitting HCV and HBV infection. The effect of liver transplantation remains to be evaluated via further follow-up and studies.


Assuntos
Agamaglobulinemia/complicações , Doenças Genéticas Ligadas ao Cromossomo X/complicações , Cirrose Hepática/complicações , Agamaglobulinemia/terapia , Antivirais/uso terapêutico , Criança , China , Doenças Genéticas Ligadas ao Cromossomo X/terapia , Hepatite B/tratamento farmacológico , Humanos , Imunoglobulinas/uso terapêutico , Cirrose Hepática/terapia , Transplante de Fígado , Masculino
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA