BRAIN TISSUE AMMONIA AND ALZHEIMER TYPE 2 ASTROCYTOSIS IN HUMAN LIVER CIRRHOSIS
Abstract
Hepatic encephalopathy (HE) is among key manifestations of decompensated liver cirrhosis (LC) and is typical for 30-45% of patients [1], reducing their survival rate up to 2 years. The neurotoxic effect of ammonia is central in the pathophysiology of HE [2]. In astrocytes, high ammonia concentration with glutamate are metabolized in osmotically active glutamine, accumulation of which causes astrocytes swelling and subsequent generalized brain edema [3]. Despite the high prognostic value of HE in LC, its clinical diagnosis remains insufficient [4], herewith, postmortem determination of hepatogenic brain injury utilizes mainly the fact of the presence of so-called Alzheimer type 2 astrocytes (AA2) which were considered the hallmark of such pathology [5]. It was confirmed by neuroimaging methods earlier, that in patients with chronic and acute liver failure, ammonia brain concentrations increase significantly [6], hence, to our knowledge, there are no postmortem studies on this issue, making our present research very relevant.
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