ABSTRACT
Adverse reactions to intravenous immunoglobulin (ivIg) therapy, such as anaphylaxis, acute encephalopathy, aseptic meningitis, or thrombotic phenomena are uncommon. We report a 58-year-old man with hypertension presenting with muscle weakness which led to paraparesia and respiratory failure. With the diagnosis of Guillain-Barré syndrome (GBS), he was treated with ivIg. He developed an acute encephalopathy few hours after the administration of ivIg, with a decreased level of consciousness and agitation. A CT scan revealed moderate and diffuse brain edema. Encephalopathy resolved 96 hours after ivIg withdrawal and use of plasma exchange. A CT scan performed seven days after showed the resolution of brain edema.
Subject(s)
Humans , Male , Middle Aged , Brain Edema/pathology , Guillain-Barre Syndrome/drug therapy , Immunoglobulins, Intravenous/adverse effects , Brain Edema/chemically induced , Brain Edema/therapy , Plasma ExchangeABSTRACT
To investigate the role of AQP9 in brain edema, the expression of AQP9 in an infectious rat brain edema model induced by the injection of lipopolysaccharide (LPS) was examined. Immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR) analysis demonstrated that the expressions of AQP9 mRNA and protein at all observed intervals were significantly increased in LPS-treated animals in comparison with the control animals. Time-course analysis showed that the first signs of blood-brain barrier disruption and the increase of brain water content in LPS-treated animals were evident 6 h after LPS injection, with maximum value appearing at 12 h, which coincided with the expression profiles of AQP9 mRNA and protein in LPS-treated animals. The further correlation analysis revealed strong positive correlations among the brain water content, the disruption of the blood-brain barrier and the enhanced expressions of AQP9 mRNA and protein in LPS-treated animals. These results suggested that the regulation of AQP9 expression may play important roles in water movement and in brain metabolic homeostasis associated with the pathophysiology of brain edema induced by LPS injection.