Published online Jan 14, 2017. doi: 10.3748/wjg.v23.i2.373
Peer-review started: July 25, 2016
First decision: August 22, 2016
Revised: September 6, 2016
Accepted: October 10, 2016
Article in press: October 10, 2016
Published online: January 14, 2017
Processing time: 174 Days and 7.8 Hours
Posterior reversible encephalopathy syndrome (PRES) is a neuro-radiologic diagnosis that has become more widely recognized and reported over the past few decades. As such, there are a number of known risk factors that contribute to the development of this syndrome, including volatile blood pressures, renal failure, cytotoxic drugs, autoimmune disorders, pre-eclampsia, and eclampsia. This report documents the first reported case of PRES in a patient with severe alcoholic hepatitis with hepatic encephalopathy and delves into a molecular pathophysiology of the syndrome.
Core tip: Posterior reversible encephalopathy syndrome (PRES) has been described in a number of settings, but not in the setting of severe alcoholic hepatitis, as is presented in this case report. There are clear molecular relationships between ammonia, which is detoxified to glutamine in the brain, causing astrocytic swelling, cerebral edema, and vasogenic edema. This vasogenic edema is a pivotal component of PRES and accounts for one of the major hypotheses of the syndrome. Thus, though a clear connection between hyperammonemia and PRES has never been documented, there is a theoretical relationship.
