A hepaticus encephalopathia kóroktana, kórfejlődésének újabb szempontjai Irodalmi összefoglaló

Abstract

Summary In the present literature review the authors discuss the pathophysiology of a neurological syndrome, namely hepatic encephalopathy (HE). HE is a brain disorder that associated with liver failure or porto-systemic bypass in the absence of hepatic disease. The latter cause is a rare case in humans, but it is the most frequent one in dogs. This syndrome is classified into different groups according to the underlying liver diseases and the neurological manifestations, but many of the papers use only the terms “acute HE” and “chronic HE”. The acute HE is a life-threatening form of this syndrome, due to the developing brain oedema. In addition the mildest, subclinical manifestation of HE, namely minimal HE has also great significance, because it has an adverse impact on quality of life in humans. HE was first characterized in the 1890’s, but despite the intensive research the pathophysiology is not fully understood yet. Ammonia has a key role in the pathogenesis of HE due to its elevation in the blood as well as in the brain. Increasingly, systemic inflammation and oxidative stress are being recognized also as etiological factors in HE and act synergistically with ammonia. The cerebral events are also complex, including the alteration of neurotransmitter systems, glutamateglutamine cycle and bioenergetic as well as oxidative stress, neuroinflammation and increasing of the blood-brain barrier permeability. There is a big significance of astrocyte swelling, which is one of the most important cause of cerebral oedema during acute HE. The precise pathomechanism of this event is especially complex and has not been clarified yet. Some new elements of the etiological factors and cerebral pathophysiological events mentioned above will be discussed basis of the scientific literature.