RESUMEN
BACKGROUND: Acute autonomic neuropathy (AAN) is rare disorder with anecdotal report, especially for childhood onset patients. Misdiagnosis or delays in treatment can always be found in clinical practice. We conducted this study to give a description of the manifestations and treatment of AAN in children and therefore help clinicians to make the accurate diagnosis early so that the prognosis of the patients can be improved. METHODS: A systematic record from 3 clinical centers was used to identify 11 subject, 3 males and 8 females, with clinical diagnosed AAN. RESULT: The age ranged from 2 years and 4 months to 14 years and 6 months (mean, 9 ± 3.6 years old) and the course from onset to diagnosis ranged from 7 days to 8 months. All children shared prominent initial symptoms, 7 with frequent vomiting and 4 with motor dysfunctions. The condition of 9 patients improved after treatment of IVIg and intravenous glucocorticoid. CONCLUSION: The clinical manifestations of AAN are diverse, generalized, and non-specific. Gastrointestinal disorders were the most common initial symptoms. Symptoms of gastrointestinal system and abnormal secretion of glands were severe and more common than other symptoms. The mechanism of AAN remains unknown. Although IVIg and intravenous glucocorticoid can be used in clinical practice, there is still no treatment recommendation and further study is needed.
Asunto(s)
Enfermedades del Sistema Nervioso Autónomo , Enfermedades Gastrointestinales , Niño , Preescolar , Femenino , Humanos , MasculinoRESUMEN
OBJECTIVE: To explore the signal transduction pathway mediated by thrombopoietin (TPO) in the inflammation model of microglia induced by lipopolysaccharide (LPS). METHODS: The inflammation model of microglia BV2 cells was prepared by LPS of 0.5 and 1.0 µg/mL stimulation. The expression of TPO and ERK mRNA in BV2 cells was detected by real time quantitative PCR. Western blot was used to evaluate the expression of TPO and ERK protein in BV2 cells. TPO and IL-6 contents in the culture supernatant fluid were measured using ELISA. RESULTS: LPS stimulation increased significantly the mRNA and protein expression of TPO and ERK in BV2 cells, especially at the concentration of 1.0 µg/mL for 12 hrs stimulation. There was a significant positive correlation between the mRNA and protein expression of TPO and ERK. CONCLUSIONS: Signal transduction pathway of ERK1/2 participates in the activation of TPO in inflammatory injury of BV2 cells.
Asunto(s)
Inflamación/etiología , Microglía/patología , Transducción de Señal/fisiología , Trombopoyetina/fisiología , Animales , Ensayo de Inmunoadsorción Enzimática , Quinasas MAP Reguladas por Señal Extracelular/genética , Quinasas MAP Reguladas por Señal Extracelular/metabolismo , Ratones , ARN Mensajero/análisis , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Trombopoyetina/análisis , Trombopoyetina/genéticaAsunto(s)
Enfermedades del Sistema Nervioso Autónomo , Enfermedad Aguda , Niño , Humanos , MasculinoRESUMEN
OBJECTIVE: To explore the neuro-protective effect and mechanism of qingkailing injection (QKL) against cerebral injury caused by E. coli-meningitis (CM). METHODS: The CM model rabbits were treated by ampicillin with QKL as adjuvant. The leukocyte count and protein content in cerebral spinal fluid (CSF), the contents of water, sodium, potassium and calcium in cerebral tissues were measured before, 16 h and 26 h after Bacillus coli injection respectively. The expression of matrix metalloproteinase-9 (MMP-9) was determined at the same time. RESULTS: Adjunctive treatment with QKL can not only inhibit the increase of leukocyte cells, protein content in CSF, and water, sodium, calcium content in cerebral tissues, but also the decrease of potassium content revealed during simple antibiotic treatment. It also can decrease the expression of MMP-9 in cerebral tissues of rabbits with CM. CONCLUSION: As an adjunctive treatment, QKL can prevent transient inflammatory reaction and aggravation of brain injury in CM induced by simple antibiotic treatment, its mechanisms might relate with calcium antagonism and attenuation of MMP-9 expression in brain tissues.