Changes of prostaglandin D2,carboxypeptidase A3 and platelet activating factor in guinea pig in anaphylactic shock / 法医学杂志

OBJECTIVE@#To detect the changes of leukotriene E4(LTE4), prostaglandin D2(PGD2), carboxypeptidase A3(CPA3) and platelet activating factor (PAF) in guinea pigs died from anaphylactic shock.@*METHODS@#Guinea pigs were used for establishing anaphylactic shock models. The levels of LTE4, PGD2 and CPA3, and PAF were detected in urine, plasma, and brain tissues with ELISA kit, respectively. The significant biomarkers were selected comparing with control group. The changes of PGD2, CPA3 and PAF in the guinea pigs at time zero, 12 and 24 hours after death were observed and compared respectively. The effect of platelet activating factor acetylhydrolase (PAF-AH) to PAF in guinea pig brain was examined and compared.@*RESULTS@#There were no statistically differences of LTE4 levels in urine observed between experimental group and control group. The levels of CPA3, PGD2 and PAF in the experimental group were significantly higher than that in the control group at 0 h. The levels of PAF at 12 and 24 hours after anaphylactic shock were significantly higher than that in the control group. The levels of PAF decreased significantly after pretreatment with PAF-AH.@*CONCLUSION@#LTE4 in urine cannot be selected as a biomarker to determine the anaphylactic shock. PGD2 and CPA3 in plasma, and PAF in brain tissue may be used as biomarkers to determine the anaphylactic shock. PAF-AH may be potentially useful for clinical treatment of anaphylactic shock.

Urinary leukotriene E[4] in asthmatic children with and without nocturnal exacerbations

Nocturnal exacerbations of bronchial asthma are very common and disturbing signs with serious consequences on patient's quality of life. The exact mechanism of these exacerbations is not known but inflammatory mediators may play an important role. To study the role of leukotriene E[4] [LTE[4]] in the pathogenesis of nocturnal exacerbations of bronchial asthma. The study was conducted on 50 asthmatic children who used to attend the outpatient clinics of the Pediatric and Chest Departments of Tanta University Hospital. Their ages ranged 8-14 years. The study was carried out over 10 months from October 1, 2000 to July 31, 2001. They were classified into two groups. Group A included 25 asthmatic children without nocturnal symptoms, and group B comprised 25 children who used to have nocturnal asthma exacerbations. Twenty non-asthmatic children of comparable ages were included in the study as controls. All of the children were subjected to full history taking, clinical examination, pulmonary function tests [PFTs], methacholine bronchial challenge test, and measurement of LTE[4] in urine. Values of morning drop of peak expiratory flow [PEFR] in children with nocturnal symptoms [Group B] was significantly higher than those in the asthmatic children without nocturnal exacerbations [Group A] [P<0.05]. The PC[20] FEV[1] was significantly lower in group B than in group A [P<0.05]. Urinary LTE4 levels were found to be significantly higher in group B than in group A [P<0.05]. In asthmatic children with nocturnal exacerbations [group B], urinary LTE[4] levels were found significantly higher at night more than at day hours [P<0.05]. Also, in this same group B, there were significant positive correlations between urinary LTE[4] levels and morning drop in PEFR values and significant negative correlation between urinary LTE[4] levels and PC[20] FEV[1] [P<0.05]. There was no significant difference in urinary LTE[4] levels between atopic and non-atopic asthmatic children. Measurement of urinary LTE[4] levels may represent a non-invasive method for assessment of airway inflammation and for predicting the outcome of nocturnal exacerbations that disturb the life of asthmatic children

Asma por ejercicio: utilidad de marcadores en orina / Exercise induced asthma: utility of urinaria markers

Antecedentes: los metabolitos estables de la Prostaglandina D2 (PGD2) mastocitaria 9 Ó11ß Prostaglandina F2 (9 Ó11ßPGF2) y de los cis-leucotrienos (LTE4) medidos en orina reflejan la producción de estos mediadores. Objetivos: determinar el rol de los leucotrienos y de la Prostaglandina D2 a través de la relación existente entre la provocación del asma por ejercicio (AIE) y los niveles urinarios de Laucotrieno E4 (LTE4) y 9 Ó11ßPGF2. Materiales y métodos: fueron estudiados 24 niños con asma (6-14 años) y 9 niños sanos como control. En todos los asmáticos y en 5 controles se evaluó la presencia de AIE mediante prueba de carrera libre durante 7 min, alcanzando el 80 por ciento de frecuencia cardíaca máxima para la edad. Se realizaron espirometrías basales y post prueba (secuenciales) y se colectó orina inmediatamente antes y 45 minutos despues de la prueba. LTE4 y 9 Ó11ßPGF2 fue evaluada por enzimainmunoensayos específicos. Resultados: Los 5 controles normales no presentaron asma por ejercicio, de los 24 pacientes asmáticos 12 no presentaron AIE y en 12 la prueba fue posititva (VEF1s cae > 15 por ciento). Las medias de los valores basales y post ejercicio de LTE4 y 9 Ó11ßPGF2 en pg/mg creatinina se tabulan a continuación: Asma por ejercicio: 9 Ó11ßPGF2: Basal: 3,39; Post: 7,95; p=0,001; LTE4: Basal: 4,00; Post: 9,39; p=0,002. Asma sin ejercicio: 9 Ó11ßPGF2: Basal: 3,98; Post: 6,28; p=0,02; LTE4: Basal: 5,91; Post: 7,04; p=0,242. Los niveles de 9 Ó11ßPGF2 y LTE4 de los controles normales no variaron significativamente post ejercicio. Conclusión: en los pacientes con asma por ejercicio se verifica activación mastocitaria con liberación de PGD2 que se demuestra como aumento de 9 Ó11ßPGF2 urinaria, y de los leucotrienos aumento del LTE4. El aumento de LTE4 es específico para asma por ejercicio en tanto que la 9 Ó11ßPGF2 aumenta en ambos grupos

Cambios metabólicos del ácido araquidónico en la desensibilización a la aspirina / Aspirin, metabolic change in arachidonic acid in the desensitization

La sensibilización de la aspirina se presenta en acerca del 10 por ciento de todos los pacientes asmáticos. En esta clase de asmáticos la congestión nasal y el broncoespasmo ocurren entre los 30 a 180 minutos después de la ingestión de la aspirina. Luego de la reacción respiratoria a la aspirina todos los pacientes pueden ser desensibilizados a la misma mediante la introducción repetida de pequeñas a grandes cantidades de aspirina hasta que los sujetos asmáticos pueden ingerir 650 mg del fármaco sin ningún efecto adverso. Los mecanismos de la sensibilidad a la aspirina no están totalmente esclarecidos, y las razones por las cuales la desensibilización en los pacientes asmáticos sensibles a la aspirina (ASA) ocurre de manera universal se desconocen. En este estudio, pacientes ASA y testigos asmáticos no ASA se expusieron a dosis provocadoras de aspirina. Se colectaron muestras de orina antes, durante el broncoespasmo inducido, y después de la ingestión de 650 mg de aspirina, cuando los efectos adversos habían desaparecido (fenómeno de desensibilización). Se dertminaron los niveles de los productos tipo y cicloxigenados en las muestras de orina. En este trabajo se analizan los resultados y se expone una explicación del probable mecanismo de la desensibilización