RESUMO
We present a 14-day-old premature born girl with a temperature of 37.8°C and a swelling and redness of the right parotid gland. Laboratory tests revealed a CRP of 79 mg/l and ultrasound examination confirmed a parotitis. Treatment with augmentin i.v. resolved the condition.
Assuntos
Combinação Amoxicilina e Clavulanato de Potássio/uso terapêutico , Parotidite/diagnóstico , Inibidores de beta-Lactamases/uso terapêutico , Edema , Feminino , Humanos , Recém-Nascido , Glândula Parótida/patologia , Parotidite/tratamento farmacológico , Resultado do TratamentoRESUMO
Hypoxic ischemic encephalopathy after perinatal asphyxia is a major cause of mortality and morbidity in infants. Here, we evaluated pathologic changes in the hippocampi of a cohort of 16 deceased full-term asphyxiated infants who died from January 2000 to January 2009. Histochemical and immunocytochemical results for glial and neuronal cells were compared between cases with or without seizures and to adult and sudden infant death syndrome cases (n = 3 each). All asphyxiated infants displayed neuronal cell damage and reactive glial changes. Strong aquaporin-4 immunoreactivity was seen on astroglial cells within hippocampi in 50% of cases. In patients with seizures, the expression of metabotropic glutamate receptors was increased in glial cells. Cases with seizures displayed increased microglial activation and greater expression of the inflammatory markers interleukin 1ß and complement 1q compared with those in cases without seizures. All cases with seizures displayed alterations in the blood-brain barrier, as assessed by immunohistochemistry for albumin. These findings confirm the complex cascade of cellular and molecular changes occurring in the human neonatal hippocampus after perinatal asphyxia. These changes may contribute to seizure development leading to secondary brain damage. These data may aid in the development of therapeutic targets for neonatal seizures.