O presente estudo avaliou a autorregulação encefálica (ARE) em doentes com insuficiência hepática fulminante (IHF) antes e após transplante hepático. Foram avaliados 25 pacientes com diagnóstico de IHF, 17 foram avaliados antes e após o transplante hepático, sendo seis (24,0%) do sexo masculino e 19 (76,0%) feminino. A média de idade foi de 33,8 anos, que variou de 14 a 56 anos, com desvio padrão de 13,1 anos. A hemodinâmica encefálica foi avaliada pela velocidade de fluxo sanguíneo encefálico (VFSE) nas artérias cerebrais médias e artéria basilar (AB), que usou o ultrassom Doppler transcraniano (DTC), dispositivo de dois canais, com transdutores de 2 mega Hertz (MHz). A autorregulação encefálica foi mensurada pelo índice de autorregulação (IARE) estática que leva em conta os efeitos do aumento da pressão arterial média (PAM) sobre a VFSE. Para isso, promoveu-se o aumento da PAM (20 mmHg a 30 mmHg) com infusão de noradrenalina.. Ao se avaliar o IARE considerando a velocidade de fluxo sanguíneo em quatro momentos (pré-transplante, 1°, 2° e 3° dia após o transplante), observou-se que houve diferença estatística em artéria cerebral média (ACM) à direita (p=0,008), esquerda (p=0,007), máxima (p=0,005), e AB (p=0,006); assim como na análise em cada tempo do IARE, observou-se diferença estatística em ACM à direita (p=0,012), esquerda (p=0,009), máxima (p=0,006), e AB (p=0,011). A análise categórica do IARE na artéria cerebral média e basilar descreveu que a maioria dos doentes reestabeleceu a AR no 2° dia em ACM e 3° na AB (índice > 0,6), enquanto com o índice > 0,8 em ambas as artérias a ARE reestabeleceu no 2° dia. As variáveis sistêmicas como pressão parcial de CO2 e hemoglobina nos tempos da avaliação não apresentaram diferença estatística p=0,100 e p=0,093 respectivamente. Os resultados obtidos apontam para o comprometimento da ARE antes e após transplante hepático, tanto em circulação anterior como posterior, e que tende a ser reestabelecido entre 48 a 72 horas. Os achados deste estudo favorecem o manejo adequado de doentes nestas fases (antes e após transplante) e podem evitar a evolução para complicações neurológicas, como tumefação encefálica e hipertensão intracraniana, que indicam prognóstico ruim para a evolução clínica destes doentes. Estudos futuros necessitam ser realizados para que se consolide o uso da monitoração contínua com métodos não invasivos como o DTC para direcionar o manejo hemodinâmico encefálico na IHF / This study evaluated cerebral autoregulation in patients with fulminant hepatic failure (FHF) before and after liver transplantation. A total of 25 patients comprising six (24.0%) males and 19 (76.0%) females with FHF were evaluated. Seventeen patients were evaluated both before and after liver transplantation. Mean age of the patients was 33.8 years, with a range of 14-56 years and standard deviation of 13.1 years. Brain hemodynamics was assessed by cerebral blood flow velocity in the middle cerebral arteries (MCA) and basilar artery (BA) using transcranial Doppler ultrasound on a two-channel device with 2 MHz transducers. Cerebral autoregulation was measured by static cerebral autoregulation index (SCAI), which accounts for the effects of increase in mean arterial blood pressure (ABP) on cerebral blood flow velocity. An increase in ABP (20 mmHg to 30 mmHg) was induced with norepinephrine infusion. Evaluation of SCAI based on blood flow velocity (BVF) at four timepoints (pre-transplant and on 1st, 2nd and 3rd days post-transplant) revealed a statistical difference in the MCA right (p = 0.008) left (p = 0.007), maximum (p = 0.005) and the BA (p = 0.006). In addition, analysis by timepoint showed a statistical difference in MCA (p = 0.012), left (p = 0.009), maximum (p = 0.006) and in the BA (p = 0.011). Categorical analysis of autoregulation in the MCA and BA showed that most patients reestablished autoregulation in the MCA on the 2nd day post-transplant and in the BA (index > 0.6) on the 3rd day, while autoregulation was reestablished in both arteries (index > 0.8) on the 2nd day. On the assessment by timepoint, the systemic variables CO2 partial pressure and hemoglobin showed no statistically significant differences (p = 0.100 and p = 0.093, respectively). The results reveal impaired SCAI before and after liver transplantation, both in anterior and posterior circulation, with a tendency to reestablish at 48 to72 hours. The findings of this study can help improve management of patients at these stages (pre and post transplantation), preventing neurological complications such as brain swelling and intracranial hypertension, associated with poor prognosis for the clinical course. Future studies should be conducted to consolidate the use of continuous monitoring with noninvasive method (TCD), to provide more accurate information to guide brain hemodynamic management in FHF

Este estudo caracteriza a intoxicação por Trema micrantha em equinos, até então desconhecida nesta espécie. No primeiro artigo (artigo 1), é descrito um surto espontâneo de intoxicação por T. micrantha em equinos que ocorreu em junho de 2007, no Município de São José do Herval, na região da encosta da serra do Rio Grande do Sul. Dois equinos morreram na propriedade, após uma árvore de T. micrantha ter sido derrubada por um temporal e suas folhas terem sido consumidas pelos animais. O quadro clínico patológico apresentado foi característico de insuficiência hepática aguda, com desenvolvimento de encefalopatia hepática. Subsequentemente, para melhor caracterizar a intoxicação por Trema micrantha em equinos, desenvolveu-se um experimento (artigo 2). Quatro pôneis receberam e consumiram espontaneamente folhas de T. micrantha, em doses únicas de 30, 25 e 20g/kg. Um equino recebeu uma dose de 15 e outra de 25g/kg, 30 dias após. Três animais adoeceram e evoluíram para morte. Os principais sinais clínicos apresentados foram apatia, desequilíbrios, dificuldade de deglutição, decúbito esternal, decúbito lateral, movimentos de pedalagem coma e morte. Os três equinos afetados apresentaram elevação na atividade sérica de gama glutamil transferase (GGT), nos níveis séricos de amônia, além de diminuição da glicemia. Os principais achados patológicos foram encontrados no fígado e no encéfalo dos três animais. O fígado apresentava macroscopicamente acentuação do padrão lobular, enquanto que no encéfalo havia áreas amareladas na superfície de corte, mais evidentes na substância branca do cerebelo. Microscopicamente, o fígado apresentava necrose, predominantemente centrolobular e hemorragia. No encéfalo, havia edema perivascular generalizado e astrócitos Alzheimer tipo II na substância cinzenta. Esses astrócitos apresentaram marcação fraca ou negativa na imuno-histoquímica anti-GFAP e marcação positiva do antígeno S-100. A dose letal mínima de folhas de T. micrantha estabelecida nesse experimento foi de 20g/kg. A maior sensibilidade da espécie equina constatada nesse estudo, a ampla distribuição de T. micrantha, bem como sua palatabilidade reforçam a importância da planta em casos acidentais de intoxicação nessa espécie. / This study characterizes Trema micrantha poisoning in horses, previously unknown in this species. The first article (Article 1) describes an outbreak of T. micrantha poisoning in horses. The disease occurred in June 2007, in the Municipality of São José do Herval, Rio Grande do Sul State. Two horses died after consuming the leaves of the branches from a T. micrantha tree, which had been felled by a storm. Clinical pathology presented by the animals was characteristic of an acute liver failure with development of hepatic encephalopathy. To further characterize the Trema micrantha poisoning in horses, an experiment was carried out (Article 2). Four ponies received and spontaneously consumed green leaves of T. micrantha, at the doses of 30, 25, and 20 g/kg. One horse received two doses, 15 and 25 g/kg, 30 days apart. Three animals were affected and died. The main clinical signs were apathy, equilibrium deficit, deglutition difficulty, sternal or lateral recumbency, paddling, coma and death. These tree diseased ponies had also enhanced seric activity of gamma-glutamyl transferase (GGT), seric ammonia apart of diminished glycemia. The main pathological findings were observed in the liver and encephalon. There were enhanced lobular pattern of the livers and yellowish areas in the cut surface of the encephalon, especially visualized in the cerebral white matter. Microscopically, there was hepatic necrosis predominantly centrilobular apart of hemorrhages. Generalized perivascular edema and Alzheimer type II astrocytes were observed in the encephalon. The Alzheimer type II astrocytes showed weak or absent anti-glial fibrillar acid protein immunostaining associated with positive immunostaining for S-100 protein. The minimal lethal dose of Trema micrantha leaves was established at 20 g/kg. The high sensibility of this species to this plant, its wide distribution, and the high palatability of the plant reinforce the importance of Trema micrantha in accidental episodes of intoxication in horses.

Dentre as manifestações clínicas observadas em pacientes sépticos, as disfunções neurológicas são, provavelmente, as de fisiopatologia mais obscura e pobremente explorada, o que consequentemente as torna de difícil entendimento e tratamento médico. Adicionalmente, estudos epidemiológicos indicam que a síndrome séptica é mais frequente e mais letal em pacientes idosos. Nesse contexto, este trabalho objetivou comparar os efeitos da sepse, induzida pelo modelo de ligadura e perfuração cecal, no encéfalo de ratos jovens e idosos por meio da análise da expressão gênica de larga escala (transcriptoma), a fim de averiguar como as alterações no padrão de expressão podem estar relacionadas a disfunções neurológicas. Os resultados deste estudo indicaram a diminuição da expressão dos genes Bcl-3, S100A8 e uridina fosforilase 1, bem como o aumento da expressão de Stefin A3, sendo tais efeitos característicos das manifestações comuns da sepse no sistema nervoso central, independentemente da idade dos animais; por outro lado, a diminuição da expressão do gene da haptoglobina foi observada apenas nos animais idosos com sepse. De forma geral, na comparação entre animais idosos e jovens, os resultados desta pesquisa apontaram que animais idosos apresentam uma quantidade menor de genes modificados pela sepse, o que sugere menor capacidade de ativar mecanismos neuroprotetores / Among the clinical manifestations observed in septic patients, the neurological dysfunctions are probably the most obscure and poorly explored pathophysiology, which consequently makes them difficult to understand and to treat. Additionally, epidemiological studies indicate that septic syndrome is more frequent and more lethal in elderly patients. In this context, this article is aimed at comparing the effects of sepsis, induced by the ligature model and cecal perforation, on the brain of young and elderly rats by means of the analysis of the large scale gene expression (transcriptome), in order to investigate how the changes in this expression may be related to neurological dysfunctions. The results of this study indicated decreased expression of the Bcl-3, S100A8 and uridine phosphorylase 1 genes, as well as increased expression of Stefin A3, these effects being characteristic of the common manifestations of central nervous system sepsis regardless of the age of the animals; on the other hand, decreased haptoglobin gene expression was observed only in the elderly animals with sepsis. In general, in the comparison between old and young animals, the results of this research indicated that elderly animals present a smaller amount of genes modified by sepsis, which suggests a smaller capacity to activate neuroprotective mechanisms

No description available.

No description available.

In der Pathogenese der hepatischen Enzephalopathie nimmt die systemische Hyperam-moniämie eine zentrale Stellung ein. Es konnte kürzlich gezeigt werden, dass der Dünndarm in der postprandialen Hyperammoniämie bei Patienten mit Leberzirrhose eine wichtige Rolle spielt. Somit wird das über die Pfortader der Leber zugeführte Ammonium nicht ausschließlich von Bakterien im Kolon produziert, sondern entstammt in relevanter Menge, beim Versuchstier zu etwa 50%, dem Glutaminstoffwechsel der Dünndarmmukosa . Unter pathologischen Verhältnissen wie bei einer Leberzirrhose und dem Vorliegen portosystemischer Umgehungskreisläufe führt die intestinale Ammoniogenese zur systemischen Hyperammoniämie und hepatischen Enzephalopathie. Hauptziele dieser Studie waren zu untersuchen, welche Stickstoffgruppe des Glutaminmoleküls der intestinalen Ammoniogenese dient, welche Rolle die zweite Stickstoffgruppe des Glutamins spielt, welche anderen Metabolite als Produkte des intestinalen Glutaminmetabolismus entstehen. Wir untersuchten 2 Gruppen à 4 Patienten mit Leberzirrhose, bei denen zuvor ein transju-gulärer intrahepatischer portosystemischer Stent-Shunt (TIPS) angelegt worden war. Die Patienten erhielten während 240 min über eine nasoduodenale Sonde eine Nährlösung bestehend aus markiertem Glutamin, Kohlenhydraten und Fetten. Entweder die Amino- oder Amid-Gruppe des Glutamins war durch das stabile Stickstoff-Isotope (15 N) markiert. Je drei Blutentnahmen wurden aus einem arteriellen, einem Mesenterialvenen- und einem Hepatalvenenkatheter vor (-10, -5 und 0 min) und während der Nährlösungsapplikation (150, 195 und 240 min) entnommen. Die Messung der quantitativen Ammoniumkonzentration erfolgte enzymatisch. Die Aminosäurenkonzentrationen wurde mittels HPLC bestimmt. Die Anreicherung des markierten Stickstoffs im Ammonium und in den Aminosäuren erfolgte mittels GC-MS. Der Transfer des markierten Stickstoffs aus der Amid-Gruppe des Glutamins auf das Ammonium war signifikant höher als aus der Amino-Gruppe (1.66 +/- 0.15 MPE vs 0.05 +/- 0.15 MPE). Dagegen war der Transfer auf die Amino-Gruppen anderer Aminosäuren wie Ala-nin, Serin, Glycin und Prolin nach der Applikation von Amino-markiertem Glutamin signifikant höher als der nach der Applikation von Amid-markiertem Glutamin. Aus diesen Daten kann geschlossen werden, dass das durch den Dünndarm produzierte Ammonium überwiegend aus der Deamidierung des Glutamins über die Gluaminase-Reaktion entstammt. / Systemic hyperammonemia plays a central role in the pathogenesis of the hepatic encephalopathy. Recently it could be demonstrated, that the small intestine is an important source of postfeeding hyperammonemia in patients with cirrhosis. The portal venous ammonia load forms partly, in animals up to 50 %, from glutamine metabolism in small intestine. Under pathologic conditions as in liver cirrhosis with portal-systemic shunting, however, this ammonia load causes systemic hyperammonemia. The Main goals of our study were to investigate, which nitrogen group of glutamine molecule serves the intestinal am-moniogenesis, what role the secound nitrogen group of glutamine plays, and which metabolites are produced within the intestinal glutamine metabolism. We investigate 2 Groups of 4 patients each with liver cirrhosis who had received a transjugular intrahepatic porto-systemic stent-shunt (TIPS) before. The patients got a nutrient solution containing labelled glutamine, carbohydrate and fat over 240 min via a nasoduodenal tube. The glutamine molecule was labelled on its amid or amino group respectively with the stable 15 N-isotope. Blood was taken from an arterial, a mesenterial venous and a hepatic venous catheter before (-10, -5 and 0 min) and during (150, 195 and 240 min) application of the nutrient solution. Ammonia concentrations were measured enzymatically, the concentration of the amino acids by HPLC. The enrichment of the labelled nitrogen in ammonia and amino acids was measured by GC-MS. The amount of labelled nitrogen of the amid group which was transferred to ammonia was significantly higher than the labelled nitrogen transferred from amino group (1.66 +/- 0.15 MPE vs 0.05 +/- 0.15 MPE). In contrast the amino nitrogen was significantly transferred to the amino acids such as alanine, serine, glycine and proline. We conclude that the ammonia produced by small intestine predominantly originates from The amid nitrogen of glutamine by deamidation via glutaminase pathway.

Η ηπατική εγκεφαλοπάθεια είναι ένα σύνθετο νευροψυχιατρικό σύνδρομο το οποίο εκδηλώνεται κυρίως σε συνθήκες ηπατικής κίρρωσης. Διάφορες παθολογικές και τοξικές καταστάσεις μπορεί να επηρεάσουν την ηπατική λειτουργία σε τέτοια βαθμό ώστε να προκληθεί ηπατική εγκεφαλοπάθεια. Το οξειδωτικό στρές έχει ενεπλακεί σε διάφορες μελέτες στην παθογένεση της ηπατικής εγκεφαλοπάθειας. Επιπλέον, η ανάπτυξη αυξημένου οξειδωτικού στρές υπό την επίδραση αποφρακτικού ικτέρου έχει μετρηθεί σε διάφορα όργανα πειραματοζώων, συμπεριλαμβανομένου και του εγκεφάλου. Ο σκοπός της παρούσας μελέτης ήταν να ανιχνεύσει της αλλαγές στις αποφρακτικές συνδέσεις των τριχοειδικών αγγείων του εγκεφάλου που συσχετίζονται με την οκκλουδίνη. Για να το επιτύχουμε αυτό χρησιμοποιήσαμε ένα μοντέλο απολίνωσης του κοινού χοληδόχου πόρου (BDL) σε πειραματόζωα (αρουραίους). Στο πείραμα 1 η έκφραση της οκκλουδίνης εκτιμήθηκε μέσω της μεθόδου ποσοτικοποίησης κατά Westernblot. Σε αυτό το πείραμα χρησιμοποιήθηκαν πέντε (BDL) και πέντε ψευδώς χειρουργηθέντα πειραματόζωα (sham). Τα πειραματόζωα θανατώθηκαν δέκα ημέρες μετα το χειρουργείο. Στην κατά Westernblot ποσοτικοποίηση παρατηρήθηκε μεγάλη μείωση της ποσότητας της οκκλουδίνης στα BDL πειραματόζωα σε σχέση με τα sham. Στο πείραμα 2 χρησιμοποιήθηκαν εννέα BDL και εννέα sham πειραματόζωα. Τρία πειραματόζωα από τις δύο παραπάνω ομάδες θανατώθηκαν την πρώτη, την πέμπτη και τη δέκατη μετεγχειρητική ημέρα. Τα επίπεδα οκκουδίνης σε αυτά τα πειραματόζωα συσχετιστήκαν με τις τιμές τηςinvivo μέτρησης των ελευθέρων ριζών οξυγόνο. Τα αποτελέσματα ανέδειξαν ότι η τιμή της οκκλουδίνης στα BDL ζώα ήταν σημαντικά μειωμένη σε σχέση με τα sham όλες τις χρονικές στιγμές που έγιναν οι μετρήσεις, ενώ οι χαμηλότερες τιμές καταγράφηκαν στα πειραματόζωα που παρέμειναν υπό αποφρακτικό ίκτερο για δέκα ημέρες. Επιπλέον καταδείχθη ότι η χρονικά συσχετιζόμενη μείωση των επιπέδων της οκκλουδίνης στα ενδοθηλιακά κύτταρα του εγκεφάλου συσχετίζεται με τα αυξανόμενα επίπεδα ελευθέρων ριζών οξυγόνου της ημέρες μετά το χειρουργείο, φανερώνοντας τη σχέση μεταξύ αυτών των δύο φαινομένων. Συμπερασματικά, η παρούσα μελέτη πρώτη παραθέτει στοιχεία που προτείνουν την εμπλοκή της οκκλουδίνης στην παθοφυσιολογία της ηπατικής εγκεφαλοπάθειας σε συνθήκες εξωηπατικής χολόστασης. Αυτό γίνεται μέσω της μείωσης των επιπέδων τις οκκλουδίνης στις αποφρακτικές συνδέσεις των ενδοθηλιακών κυττάρων του εγκεφάλου υπο την επίδραση του χολοστατικού ικτέρου, η οποία οδηγεί σε άρση του αιματο-εγκεφαλικού φραγμού. / Hepatic encephalopathy in a complicate neuro-psychiatric syndrome which is common under hepatic cirrhosis. Various pathological and toxic lesions can deteriorate liver function in such way, so hepatic encephalopathy can be inflicted. Oxidative stress is involved in pathogenesis of hepatic encephalopathy in several protocols. Moreover the development of increased oxidative stress in the context of obstructive cholestasis has been proven in various rats' organs including the brain. The present study aimed to detect alterations of tight junction-associated occludin in rat brain capillaries. To accomplish that we have used a rats bile duct ligation experimental model (BDL). In experiment 1, occludin expression was evaluated by Western blot analysis. In this experiment were used five BDL and five sham rats. The experimental animals were sacrificed ten days after the operation. Western blot analysis revealed significant decrease of occlidins amount in BDL rats compared to the sham rats. In experiment 2, nine BDL and nine sham animals were used. Three animals from each group were sacrificed during the first, fifth and tenth post-operate day. The results of occludin level to these animals were associated with the in vivo superoxide radical production. The results indicated that occludin level in BDL animals, as opposed to sham-operated, was significantly reduced at every time point studied, being lowest in the rats remaining on BDL condition for 10 days. Moreover, it was demonstrated that the time-dependent reduction of occludin level in the brain endothelial was significantly correlated with the time dependent increase of brain superoxide radical level, implying a relationship between these two abnormalities. In conclusion, the evidence presented herein suggests for first time the implication of occludin in pathophysiology of hepatic encephalopathy under extra-hepatic cholestasis. This phenomenon occur due to the reduce of occludin level to cerebral endothelial cells’ tight junctions under cholestatic jaundice, which drives to lift of brain-blood barrier.

No description available.

Darbo tikslas – nustatyti kompiuterizuoto inhibicinio kontrolės testo (IKT), IL-6, amoniako bei įprastinių kraujo rodiklių vertę diagnozuojant kognityvinius sutrikimus sergantiems lėtinėmis kepenų ligomis. Darbo uždaviniai: nustatyti kognityvinių sutrikimų dažnį, galimus rizikos veiksnius, palyginti IKT ir kraujo testų rezultatus lėtinio hepatito ir kepenų cirozės grupėse; nustatyti IKT bei IL-6, įprastinių kraujo testų vertę minimaliai hepatinei encefalopatijai (MHE). Iki šiol netirta ar pacientai, sergantys lėtiniu hepatitu ir kognityviniais sutrikimais, neturi analogiškų IKT rodiklių pakitimų, IL-6 koncentracijos padidėjimo kaip sergantieji kepenų ciroze ir MHE. Netirta kokie kraujo ar IKT rodikliai kognityvinius sutrikimus prognozuoja geriausia. Į tyrimą įtraukti 62 sergantieji kepenų ciroze be hepatinės encefalopatijos, 73 lėtiniu hepatitu bei 53 sveiki asmenys. Tą pačią dieną buvo atliekami kraujo tyrimai, psichometriniai testai ir IKT. Lėtinio hepatito grupėje kognityviniai sutrikimai nustatyti 54,8 %, о kepenų cirozės grupėje MHE ¬ 71,0 % tiriamųjų asmenų. Kognityvinius sutrikimus predisponuoja trumpesnė mokymosi trukmė, fibrozės laipsnis, dvigubas etiologinis veiksnys, amžius ir lytis įtakos neturi. Lėtinio hepatito grupėje kognityviniai sutrikimai koreliuoja su IKT rodikliais ir kepenų fermentų koncentracijos padidėjimu, o kepenų cirozių grupėje su IKT rodikliais ir IL-6 koncentracija kraujyje. Išvados: Kognityvinius sutrikimus sergant lėtiniu hepatitu ar... [toliau žr. visą tekstą] / The aim of the study was to ascertain a value of computerized inhibitory control test (ICT), routine blood tests, peripheral blood ammonia and IL-6 concentration for diagnosis of cognitive disorders in patients with chronic liver diseases. Tasks: to assess a frequency of cognitive impairments and associated risk factors and to compare ICT and blood tests results in chronic hepatitis and cirrhotic patients; to ascertain ICT, IL-6 and routine blood tests values for diagnosis of minimal hepatic encephalopathy (MHE). Until now there were no studies performed whether chronic hepatitis patients with cognitive disorders have analogous ICT, IL-6 and other tests abnormalities as cirrhotic patients with MHE. It has not been studied which ICT and other tests results predict best the cognitive disorders in such patients. 62 cirrhotic patients without overt hepatic encephalopathy, 73 chronic hepatitis and 53 healthy individuals were enrolled. On the same day blood tests, psychometric and ICT tests were performed by every participant. Cognitive disorders were detected in 54,8% of chronic hepatitis patients. In cirrhotic patients MHE was found in 71,0%. Cognitive disorders predispose shorter study time, the fibrosis score, double etiologic factor, while age and gender has no influence. In chronic hepatitis patients the cognitive impairments correlate with ICT and elevated liver enzymes. In cirrhotic patients cognitive disorders correlate with ICT and IL-6 concentration. Conclusion: the... [to full text]

The aim of the study was to ascertain a value of computerized inhibitory control test (ICT), routine blood tests, peripheral blood ammonia and IL-6 concentration for diagnosis of cognitive disorders in patients with chronic liver diseases. Tasks: to assess a frequency of cognitive impairments and associated risk factors and to compare ICT and blood tests results in chronic hepatitis and cirrhotic patients; to ascertain ICT, IL-6 and routine blood tests values for diagnosis of minimal hepatic encephalopathy (MHE). Until now there were no studies performed whether chronic hepatitis patients with cognitive disorders have analogous ICT, IL-6 and other tests abnormalities as cirrhotic patients with MHE. It has not been studied which ICT and other tests results predict best the cognitive disorders in such patients. 62 cirrhotic patients without overt hepatic encephalopathy, 73 chronic hepatitis and 53 healthy individuals were enrolled. On the same day blood tests, psychometric and ICT tests were performed by every participant. Cognitive disorders were detected in 54,8% of chronic hepatitis patients. In cirrhotic patients MHE was found in 71,0%. Cognitive disorders predispose shorter study time, the fibrosis score, double etiologic factor, while age and gender has no influence. In chronic hepatitis patients the cognitive impairments correlate with ICT and elevated liver enzymes. In cirrhotic patients cognitive disorders correlate with ICT and IL-6 concentration. Conclusion: the... [to full text] / Darbo tikslas – nustatyti kompiuterizuoto inhibicinio kontrolės testo (IKT), IL-6, amoniako bei įprastinių kraujo rodiklių vertę diagnozuojant kognityvinius sutrikimus sergantiems lėtinėmis kepenų ligomis. Darbo uždaviniai: nustatyti kognityvinių sutrikimų dažnį, galimus rizikos veiksnius, palyginti IKT ir kraujo testų rezultatus lėtinio hepatito ir kepenų cirozės grupėse; nustatyti IKT bei IL-6, įprastinių kraujo testų vertę minimaliai hepatinei encefalopatijai (MHE). Iki šiol netirta ar pacientai, sergantys lėtiniu hepatitu ir kognityviniais sutrikimais, neturi analogiškų IKT rodiklių pakitimų, IL-6 koncentracijos padidėjimo kaip sergantieji kepenų ciroze ir MHE. Netirta kokie kraujo ar IKT rodikliai kognityvinius sutrikimus prognozuoja geriausia. Į tyrimą įtraukti 62 sergantieji kepenų ciroze be hepatinės encefalopatijos, 73 lėtiniu hepatitu bei 53 sveiki asmenys. Tą pačią dieną buvo atliekami kraujo tyrimai, psichometriniai testai ir IKT. Lėtinio hepatito grupėje kognityviniai sutrikimai nustatyti 54,8 %, о kepenų cirozės grupėje MHE ¬ 71,0 % tiriamųjų asmenų. Kognityvinius sutrikimus predisponuoja trumpesnė mokymosi trukmė, fibrozės laipsnis, dvigubas etiologinis veiksnys, amžius ir lytis įtakos neturi. Lėtinio hepatito grupėje kognityviniai sutrikimai koreliuoja su IKT rodikliais ir kepenų fermentų koncentracijos padidėjimu, o kepenų cirozių grupėje su IKT rodikliais ir IL-6 koncentracija kraujyje. Išvados: Kognityvinius sutrikimus sergant lėtiniu hepatitu ar... [toliau žr. visą tekstą]