| Abstract | Hepatalna encefalopatija (HE) je neuropsihijatrijski sindrom uzrokovan jetrenom insuficijencijom i/ili porto-sistemnim šantom. Može se prezentirati širokim spektrom neurokognitivnih abnormalnosti, od subkliničkih poremećaja pa sve do komatoznog stanja. Prema težini kliničke slike, HE se dijeli u dvije kategorije, prikrivenu i očevidnu. Prikrivena se HE prezentira suptilnim subkliničkim simptomima koji uključuju promjene osobnosti, poremećaje spavanja, smanjenu koncentraciju i usporene psihomotorne funkcije. Ovi poremećaji značajno utječu na kvalitetu života i obavljanje svakodnevnih aktivnosti. S druge strane, očevidna se HE prezentira očitim kliničkim znakovima i simptomima uključujući poremećaje svijesti, promjene ponašanja, ekstrapiramidne simptome, dezorijentaciju, stupor pa čak i komu. I prikrivena i očevidna HE imaju lošu prognozu i povezane su s povećanim rizikom od hospitalizacije i smrtnog ishoda. Etiopatogeneza HE je kompleksna i uključuje brojne čimbenike koji mogu djelovati zasebno i u kombinaciji. Amonijak i drugi crijevni neurotoksini, upalni citokini i benzodiazepinski-GABAergički sustav imaju važnu ulogu u patogenezi ove bolesti. Ipak, mnogi patofiziološki mehanizmi uključeni u razvoj HE još su uvijek nepoznati. Očevidna se HE može dijagnosticirati na temelju kliničkih znakova i simptoma, dok prikrivena HE zahtijeva provođenje specifičnih psihometričnih ili neurofizioloških testova. Postavljanje dijagnoze HE podrazumijeva isključenje drugih alternativnih uzroka promijenjenog mentalnog statusa i neurokognitivnih deficita. Osnovne terapijske strategije u liječenju epizode HE su pronalaženje i korekcija precipitirajućih čimbenika te snižavanje razine amonijaka i drugih crijevnih toksičnih supstanci u krvi. Trenutno, okosnicu liječenja HE čini primjena neapsorbirajućih disaharida poput laktuloze i antibiotika poput rifaksimina i neomicina. Druge terapijske opcije uključuju primjenu L-ornitin L-aspartata, aminokiselina razgranatih lanaca, cinka, probiotika i albumina. Njihova učinkovitost u liječenju HE treba se detaljnije istražiti. U pojedinih se pacijenata treba razmotriti i transplantacija jetre. |
| Abstract (english) | Hepatic encephalopathy (HE) is a neuropsychiatric syndrome caused by liver insufficiency and/or portal-systemic shunting. HE can be manifested as a wide spectrum of neurocognitive abnormalities ranging from subclinical alterations to coma. Based on its severity, HE is divided into two categories, covert and overt. Covert HE is presented with subtle subclinical symptoms including personality changes, sleep problems, decreased concentration and slowing psychomotor functioning. These abnormalities significantly affect quality of life and activities of daily living. On the other hand, overt HE is presented with obvious clinical signs and symptoms including impairment of consciousness, behaviour changes, extrapyramidal symptoms, disorientation, stupor and even coma. Both covert and overt HE have poor prognosis and are associated with increased hospitalization and death risks. Etiopathogenesis of HE is complex and involves multiple factors, which act alone or in combination. Ammonia and other intestinal neurotoxins, inflammatory cytokines and benzodiazepine-GABAergic system play an important role in the pathogenesis of this disease. However, many pathophysiological mechanisms involved in its development are still unknown. Overt HE can be diagnosed on the basis of clinical signs and symptoms, whereas covert HE requires specific psychometric or neurophysiologic testing. Diagnosis of HE requires the exclusion of alternate causes of altered mental status and neurocognitive deficits. The main treatment strategies for managing an HE episode are detecting and correcting precipitating factors and lowering ammonia and other gut-derived toxic substances in the blood. Currently, the use of non-absorbed disaccharides, such as lactulose and antibiotics, such as rifaximin and neomycin, represent the mainstay of the treatment. Other treatment options include the use of L-ornithine L-aspartate, branched-chain amino acids, zinc, probiotics and albumin infusion. Their effectiveness in the HE management requires further research. In certain patients, the liver transplantation should be considered. |
