Clinical

Glial cell activity involved in hepatic encephalopathy

Last Updated: 2006-04-12 13:03:04 -0400 (Reuters Health)

NEW YORK (Reuters Health) - Patients with hepatic encephalopathy show increased expression of peripheral benzodiazepine binding sites (PBBS) by glial cells, according to a report by Australian researchers in the April issue of Gut.

Previous research has implicated PBBS in the pathogenesis of hepatic encephalopathy, the authors point out. They hypothesized that PBBS-expressing glial cells participate in the general inflammatory response seen in hepatic encephalopathy.

Dr. R. B. Banati from the University of Sydney, Lidcombe and colleagues investigated whether there is a change in PBBS expression in the brains of patients with minimal hepatic encephalopathy and related regional patterns of increased expression to the underlying severity of liver disease and to psychometric test results.

Analysis of PET scans of five patients with hepatic encephalopathy revealed increased PBBS expression bilaterally in the pallidum, in the right putamen, and in the right dorsolateral prefrontal region, the authors report.

Increased PBBS expression was related to the severity of cognitive decline, but it appeared to be unrelated to the etiology of the disease or other clinical characteristics.

The authors suggest that "the apparent link between up-regulation of [PBBS] and cognitive decline, the key symptom for minimal hepatic encephalopathy, supports the hypothesis that PBBS in the brain could indeed participate in the pathogenic mechanism of hepatic encephalopathy."

"This further implies," they conclude, "that glial cell dysfunction is pivotal in this process, as the binding sites... are exclusively non-neuronal and, given an intact blood-brain barrier, have been shown to be expressed only by activated or reactive glia."

Gut 2006;55:547-553.