scholarly journals Non-alcoholic fatty liver disease, non-alcoholic steatohepatitis, metabolic syndrome and hepatocellular carcinoma—a composite scenario

2018 ◽  
Vol 7 (2) ◽  
pp. 130-133 ◽  
Author(s):  
Luca Viganò ◽  
Ana Lleo ◽  
Alessio Aghemo
2019 ◽  
Vol 42 (1) ◽  
pp. 78-83
Author(s):  
N. B. Gubergrits ◽  
N. V. Byelyayeva ◽  
G. M. Lukashevich ◽  
P. G. Fomenko ◽  
A. V. Yuryeva

The article provides brief epidemiological data on non-alcoholic fatty liver disease and non-alcoholic steatohepatitis, emphasizing the danger of steatohepatitis, progression of which may cause the development of hepatocellular carcinoma. The properties of ursodeoxycholic acid, which are the basis for its use in a treatment of non-alcoholic steatohepatitis, are analyzed in detail, such as cytoprotective, antioxidant, antifibrotic ones, effects on apoptosis, etc. The authors presented the results of the main evidence-based studies demonstrating the effectiveness of ursodeoxycholic acid and its combinations with other drugs in the treatment of non-alcoholic steatohepatitis.


2012 ◽  
Vol 49 (1) ◽  
pp. 89-96 ◽  
Author(s):  
Mônica Rodrigues de Araújo Souza ◽  
Margareth de Fátima Formiga de Melo Diniz ◽  
José Eymard Moraes de Medeiros-Filho ◽  
Maria Salete Trigueiro de Araújo

CONTEXT: Non-alcoholic fatty liver disease (NAFLD), hepatic manifestation of metabolic syndrome, has been considered the most common liver disease nowadays, which is also the most frequent cause of elevated transaminases and cryptogenic cirrhosis. The greatest input of fatty acids into the liver and consequent increased beta-oxidation contribute to the formation of free radicals, release of inflammatory cytokines and varying degrees of hepatocytic aggression, whose histological expression may vary from steatosis (HS) to non-alcoholic steatohepatitis (NASH). The differentiation of these forms is required by the potential risk of progression to cirrhosis and development of hepatocellular carcinoma. OBJECTIVE: To review the literature about the major risk factors for NAFLD in the context of metabolic syndrome, focusing on underlying mechanisms and prevention. METHOD: PubMed, MEDLINE and SciELO data basis analysis was performed to identify studies describing the link between risk factors for metabolic syndrome and NAFLD. A combination of descriptors was used, non-alcoholic fatty liver disease, non-alcoholic steatohepatitis, metabolic syndrome and risk factors. At the end, 96 clinical and experimental studies, cohorts, meta-analysis and systematic reviews of great impact and scientific relevance to the topic, were selected. RESULTS: The final analysis of all these data, pointed out the central obesity, type 2 diabetes, dyslipidemia and hypertension as the best risk factors related to NAFLD. However, other factors were highlighted, such as gender differences, ethnicity, genetic factors and the role of innate immunity system. How these additional factors may be involved in the installation, progression and disease prognosis is discussed. CONCLUSION: Risk factors for NAFLD in the context of metabolic syndrome expands the prospects to 1) recognize patients with metabolic syndrome at high risk for NAFLD, 2) elucidate pathways common to other co-morbidities, 3) determine risk factors associated with a worse prognosis, 4) develop therapeutic strategies with goal of reducing risk factors, 5) apply acquired knowledge in public health policies focusing on preventive strategies.


2021 ◽  
Vol 8 ◽  
Author(s):  
Jose D. Torres-Peña ◽  
Laura Martín-Piedra ◽  
Francisco Fuentes-Jiménez

Non-alcoholic fatty liver disease (NAFLD) is the primary cause of chronic liver disease. The range is extensive, including hepatocellular carcinoma, cirrhosis, fibrosis, fatty liver, and non-alcoholic steatohepatitis (NASH). NASH is a condition related to obesity, overweight, metabolic syndrome, diabetes, and dyslipidemia. It is a dynamic condition that can regress to isolated steatosis or progress to fibrosis and cirrhosis. Statins exert anti-inflammatory, proapoptotic, and antifibrotic effects. It has been proposed that these drugs could have a relevant role in NASH. In this review, we provide an overview of current evidence, from mechanisms of statins involved in the modulation of NASH to human trials about the use of statins to treat or attenuate NASH.


2021 ◽  
Vol 3 (2) ◽  
pp. 71-80
Author(s):  
Margarita E. Semendyaeva

The article considers the non-alcoholic fatty liver disease as an important medical and social problem. This problem include such questions as metabolic syndrome, essential lipoproteinemia, insulinoresistance. It is possible to consider non-alcoholic steatohepatitis as predictor of liver fibrosis and chirrosis. The questions of diagnosis and treatment are discussed.


2013 ◽  
Vol 154 (29) ◽  
pp. 1124-1134
Author(s):  
Gabriella Pár ◽  
Gábor Horváth ◽  
Alajos Pár

Non-alcoholic fatty liver disease and non-alcoholic steatohepatitis, the hepatic manifestations of metabolic syndrome with close association with inzulin resistance and obesity, are the most common liver diseases, affecting up to a third of the population worldwide. They confer increased risk for hepatocellular carcinoma as well as cardiovascular diseases. The review aims to summarize advances in epidemiology, pathogenesis and clinical management of non-alcoholic fatty liver disease and non-alcoholic steatohepatitis. Besides liver biopsy and biomarkers, a novel non-invasive diagnostic tool the called “controlled attenuation parameter” measuring the attenuation of ultrasound generated by the transient elastography transducer, can quantitatively assess the hepatic fat content and differentiate between steatosis grades. At the same time, liver stiffness (fibrosis) can also be evaluated. The authors present their own results obtained with the latter procedure. In non-alcoholic fatty liver disease, the lifestyle intervention, weight loss, diet and exercise supported by cognitive behavioural therapy represent the basis of management. Components of metabolic syndrome (obesity, dyslipidaemia, diabetes and arterial hypertension) have to be treated. Although there is no approved pharmacological therapy for NASH, it seems that long lasting administration of vitamin E in association with high dose ursodeoxycholic acid may be beneficial. In addition, omega-3 polyunsaturated fatty acid substitution can also decrease liver fat, however, the optimal dose is not known yet. Further controlled clinical studies are warranted to establish the real value of any suggested treatment modalities for non-alcoholic fatty liver disease and non-alcoholic steatohepatitis, although these are in experimental phase yet. Orv. Hetil., 2013, 154, 1124–1134.


2014 ◽  
Vol 23 (4) ◽  
pp. 425-429 ◽  
Author(s):  
Mihai Voiculescu ◽  
Radu M. Nanau ◽  
Manuela G. Neuman

Non-alcoholic fatty liver disease (NAFLD) is by far the most common form of chronic liver disease worldwide, affecting adults as well as children. Under the term of NAFLD there is a wide spectrum of diseases ranging from simple steatosis to the non-alcoholic steatohepatitis (NASH), which can progress to cirrhosis and hepatocellular carcinoma (HCC). Several mechanisms have been described to influence the progression of the disease from the benign NAFL to the aggressive NASH. The imbalance between pro- and anti-oxidant mechanisms and between pro- and anti-inflammatory cytokines is thought to play a pivotal role in the pathogenesis of NAFLD and disease progression toward NASH and fibrosis. The present review intends to look at some of the mechanistic biomarkers to be employed in establishing an early diagnosis in HCC derived from NASH.Abbreviations: ANGPT: angiopoietin-2; AFP: α-fetoprotein; ALT: alanine aminotransferase; AST: aspartate aminotransferase; CI: confidence interval; COL: collagen; DCP: des-carboxyprothrombin; γGT: gamma glutamyl transpeptidase; HBV: hepatitis B virus; HCC: hepatocellular carcinoma; HCV: hepatitis C virus; HR: hazard ratio; ITG: integrin; LAM: laminin collagen genes; MMP: matrix metalloproteinase; MS: metabolic syndrome; NAFLD: non-alcoholic fatty liver disease; NASH: non-alcoholic steatohepatitis; PDGFRA: platelet derived growth factor receptor-α


2016 ◽  
Author(s):  
Κωνσταντίνος Καργιώτης

Προς το παρόν δεν υπάρχει καμία αποτελεσματική θεραπεία για τη μη αλκοολική λιπώδη νόσο του ήπατος (Non Alcoholic Fatty Liver disease, NAFLD) ή την προχωρημένη μορφή της τη μη αλκοολική στεατοηπατίτιδα (Non Alcoholic Steatohepatitis, NASH), η οποία μπορεί να εξελίχθη σε κίρρωση του ήπατος και τελικά σε ηπάτωμα. Σκοπός της μελέτης ήταν να διερευνηθεί η επίδραση της ροσουβαστατίνης σε ασθενείς με μεταβολικό σύνδρομο (Metabolic Syndrome, MetS) και NASH. Καθώς και η πιθανή συσχέτιση των μεταβολών της NASH με τις μεταβολές της αρτηριακής σκληρίας μετά τη χορήγηση υπολιπιδαιμικής αγωγής. Η προοπτική αυτή μελέτη περιελάμβανε 20 ασθενείς με MetS, δυσλιπιδαιμία και αποδεδειγμένη με βιοψία NASH. Οι ασθενείς έλαβαν συμβουλές τρόπου ζωής και έλαβαν θεραπεία για 12 μήνες με ροσουβαστατίνη (10 mg/ημέρα) ως μονοθεραπεία. Επανάληψη βιοψίας και επανάληψη του υπερηχογραφήματος του ήπατος διεξήχθησαν στο τέλος της μελέτης σε όλους τους ασθενείς. Τα ηπατικά ένζυμα, η γλυκόζη πλάσματος νηστείας, τα επίπεδα του ουρικού οξέος, και το προφίλ των λιπιδίων αξιολογούνταν κάθε 3 μήνες. Το πρωτεύον καταληκτικό σημείο ήταν ο βαθμός υποστροφής της μη αλκοολικής στεατοηπατίτιδας σε συνδυασμό με την ελάττωση των τιμών της ταχύτητας του σφυγμικού κύματος (Pulse Wave Velocity, PWV). Η επαναληπτική βιοψία ήπατος και το επαναληπτικό υπερηχογράφημα έδειξε πλήρη υποστροφής της NASH σε 19 ασθενείς καθώς και σημαντική βελτίωση των τιμών της PWV σε διαδοχικές ανά εξάμηνο μετρήσεις. Ο 20ος ασθενής, ο οποίος δεν είχε καμία βελτίωση, αλλά ούτε επιδείνωση, εμφάνισε αρτηριακή υπέρταση και αύξηση των επιπέδων των τριγλυκεριδίων κατά τη διάρκεια της μελέτης, κατά πάσα πιθανότητα λόγω των αλλαγών στον τρόπο ζωής, συμπεριλαμβανομένης και της κατάχρησης αλκοόλ. Οι δραστηριότητες των ηπατικών ενζύμων του ορού αλανινική αμινοτρανσφεράση, ασπαρτική αμινοτρανσφεράση, γάμμα-γλουταμυλοτρανσπεπτιδάση και αλκαλική φωσφατάση ομαλοποιήθηκαν από τον 6ο μήνα της θεραπείας. Η γλυκόζη νηστείας του πλάσματος και η τιμή της γλυκοζυλιωμένης αιμοσφαιρίνης μειώθηκαν στατιστικά. Οι τιμές των λιπιδίων ομαλοποιήθηκαν από τον 3ο μήνα της θεραπείας. Κανένας ασθενής δεν είχε MetS από τον 9ο μήνα της θεραπείας. Ο δείκτης μάζας σώματος και η περίμετρος της μέσης παρέμειναν αμετάβλητες κατά τη διάρκεια της μελέτης. Έτσι, οι μεταβολές στην ηπατική παθολογία και λειτουργία θα πρέπει να αποδοθούν αποκλειστικά στη μονοθεραπεία με ροσουβαστατίνη. Τα ευρήματα αυτά υποδηλώνουν ότι η μονοθεραπεία με ροσουβαστατίνη θα μπορούσε να βελτιώσει την αποδεδειγμένη με βιοψία στεατοηπατίτιδα με παράλληλη ευνοϊκή επίδραση της αρτηριακής σκληρίας και να προκαλέσει σημαντική βελτίωση των παραμέτρων του MetS εντός 12 μηνών. Αυτές οι επιδράσεις αλλά και η μείωση της γλυκόζης νηστείας του πλάσματος και των επιπέδων ουρικού οξέος στον ορό μπορεί να μειώσουν σημαντικά τον κίνδυνο της σχετιζόμενης με το καρδιαγγειακό σύστημα, αλλά και με το ήπαρ, νοσηρότητας και θνησιμότητας σε ασθενείς με μη αλκοολική στεατοηπατίτιδα. Αυτά τα ευρήματα χρειάζονται επιβεβαίωση από μεγαλύτερες μελέτες.


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