Encefalopatia hepatică și disfuncția cerebrovasculară cronică (articol de sinteză)

Hepatic encephalopathy (HE) is a frequent and disabling complication of liver cirrhosis and chronic liver failure. While traditionally attributed primarily to hyperammonemia, growing evidence indicates that HE results from the interaction of metabolic disturbances, systemic inflammation, intestinal dysbiosis, and cerebrovascular dysfunction, supporting its reconceptualization as a chronic brain disorder. A narrative review of the international literature published between 2000 and 2025 was conducted using PubMed/Medline, Journal of Hepatology, SpringerLink, and Google Scholar. Human studies relevant to the pathophysiology, diagnosis, and management of hepatic encephalopathy—including randomized controlled trials, observational studies, meta-analyses, and international guidelines—were included and synthesized qualitatively. Contemporary evidence supports an integrative gut–liver–brain model in which hyperammonemia acts synergistically with systemic inflammation, microbiome alterations, and blood–brain barrier dysfunction. These mechanisms converge to induce neuroinflammation, astrocytic dysfunction, and impaired cerebral blood flow autoregulation. Clinically, HE manifests across a broad cognitive, behavioral, and neuromotor spectrum, including minimal and covert forms associated with significant functional impairment. Cerebrovascular dysfunction appears to contribute to persistent cognitive deficits even after metabolic correction. Hepatic encephalopathy should be conceptualized as a metabolic–inflammatory–vascular brain disorder. While established therapies targeting ammonia and precipitating factors remain fundamental, emerging adjunctive approaches aimed at modulating inflammation, microbiome composition, and cerebral microcirculation warrant further investigation within rigorously designed clinical trials.