Liver cirrhosis treatment may curb cerebral edema

Reuters Health Information: Liver cirrhosis treatment may curb cerebral edema

Liver cirrhosis treatment may curb cerebral edema

Last Updated: 2015-09-28

By Reuters Staff

NEW YORK (Reuters Health) - Lactulose and rifaximin treatment of cirrhosis patients with minimal hepatic encephalopathy (MHE) reverses low-grade cerebral edema, according to researchers from India.

In a September 17 online paper in Clinical and Translational Gastroenterology, Dr. Radha K. Dhiman and colleagues at the Postgraduate Institute of Medical Education and Research in Chandigarh, observed that as many as 80% of liver cirrhosis patients may have MHE. The condition impairs daily functioning and health-related quality of life and predicts the development of overt HE.

They further noted that, on magnetic resonance imaging (MRI), decreased magnetization transfer ratio (MTR) in the brain characterizes cerebral edema, and to evaluate its reversibility, they studied 23 patients with cirrhosis. Of these, 14 had MHE and nine did not. Also included were six healthy controls.

Patients were followed for eight weeks and seven in each cirrhosis group completed the study. Blood analysis showed that ammonia levels were significantly higher in the cirrhosis group than in controls and in the MHE group compared to non-MHE patients. Ammonia correlated positively with interleukin-1 and interleukin-6 levels.

Among the team's findings were that MTRs in parietal white matter, internal capsule and basal ganglia were significantly lower in the MHE group compared with controls and non-MHE patients. However, following treatment, MHE patients showed significant MTR increase in these areas.

IL-6 and ammonia had significant negative and significant positive psychometric hepatic encephalopathy score (PHES) correlation with MTR in various regions. Nevertheless, there was no significant correlation between changes in MTR values and changes in PHES, ammonia, or inflammatory markers levels after treatment in MHE patients.

However, the team noted that this may have been due to the small number of patients and said these findings suggest "that inflammation and ammonia have a role to play in the genesis of low-grade cerebral edema in patients with MHE with a resultant cognitive decline."

They concluded, "Cerebral edema is reversible after treatment. MTR may be used as an objective surrogate end point in future trials assessing the efficacy of treatment of MHE."

Dr. Dhiman did not respond to a request for comment by press time.

The authors reported no funding or disclosures.


Clin Transl Gastroenterol 2015.

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