RESUMO
A 23-year-old Japanese woman presented with abdominal distention following fever, diarrhea, and abdominal pain during a stay in Taiwan. Serology for the detection of amebic-antibodies and stool microscopic examination were both negative. A computed tomography scan showed a 13 cm diameter abscess spreading from the lower abdominal wall to the pelvic retroperitoneal space. Needle aspiration of the abscess was done under computed tomography guidance, and microscopy of the aspirated fluid revealed trophozoites of Entamoeba. The patient was diagnosed as amebiasis with negative serologic markers that caused intra-abdominal abscess. Intravenous metronidazole treatment for two weeks did not result in any improvement of the abscess. After irrigation and drainage of the abscess, her symptoms resolved. This case report highlights that amebiasis should be considered when indicated by patient history, including travelers returning from endemic areas, and that further evaluation is necessary for diagnosis, even if the serology and stool test are negative.
Assuntos
Abscesso Abdominal/parasitologia , Dor Abdominal/parasitologia , Amebicidas/uso terapêutico , Entamebíase/complicações , Febre/parasitologia , Abscesso Abdominal/sangue , Abscesso Abdominal/patologia , Abscesso Abdominal/terapia , Dor Abdominal/sangue , Dor Abdominal/patologia , Dor Abdominal/terapia , Antibacterianos/uso terapêutico , Biomarcadores/sangue , Biópsia por Agulha Fina/métodos , Proteína C-Reativa/análise , Colonoscopia , Drenagem , Entamoeba histolytica/imunologia , Entamoeba histolytica/isolamento & purificação , Entamebíase/sangue , Entamebíase/parasitologia , Entamebíase/terapia , Feminino , Febre/sangue , Febre/patologia , Febre/terapia , Humanos , Imageamento por Ressonância Magnética , Testes Sorológicos , Taiwan , Irrigação Terapêutica , Tomografia Computadorizada por Raios X/métodos , Trofozoítos/isolamento & purificação , Adulto JovemRESUMO
Mutations in methyl-CpG-binding protein 2 (MeCP2) gene cause the neurodevelopmental disorder Rett syndrome (RTT). Here, we describe a new experimental system that efficiently elucidates the role of MeCP2 in neural development. MeCP2-null and control ES cells were generated by adenoviral conditional targeting and examined for maintenance of the undifferentiated ES cell state, neurogenesis, and gliogenesis during in vitro differentiation. In addition, dopamine release and electrophysiological features of neurons differentiated from these ES cells were examined. Loss of MeCP2 did not affect undifferentiated ES cell colony morphology and growth, or the timing or efficiency of neural stem cell differentiation into Nestin-, TuJ- or TH-positive neurons. In contrast, gliogenesis was drastically accelerated by MeCP2 deficiency. Dopamine production and release in response to a depolarizing stimulus in MeCP2-null ES-derived dopaminergic neurons was intact. However, MeCP2-null differentiated neurons showed significantly smaller voltage-dependent Na(+) currents and A-type K(+) currents, suggesting incomplete maturation. Thus, MeCP2 is not essential for maintenance of the undifferentiated ES cell state, neurogenesis, or dopaminergic function; rather, it is principally involved in inhibiting gliogenesis. Altered neuronal maturity may indirectly result from abnormal glial development and may underlie the pathogenesis of RTT. These data contribute to a better understanding of the developmental roles of MeCP2 and the pathogenesis of RTT.