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Dissertations / Theses on the topic 'Liver Cirrhosis'
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1
Gunnarsdóttir, Steingerður Anna /. "Liver cirrhosis : epidemiological and clinical aspects /." Göteborg : Section of Gastroenterology and Hepatology, Department of Internal Medicine, Sahlgrenska University Hospital, Göteborg University, 2008. http://hdl.handle.net/2077/10132.
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Gregory, Wendy L. "The genetic epidemiology of primary biliary cirrhosis." Thesis, University of Newcastle Upon Tyne, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.359212.
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Shmueli, Ehoud. "Glucose metabolism and insulin resistance in cirrhosis." Thesis, University of Newcastle Upon Tyne, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308777.
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Mathur, Sachin. "Studies of prognosis and nutritional intervention in liver cirrhosis and liver transplantation." Thesis, University of Auckland, 2010. http://hdl.handle.net/2292/6892.
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In patients with chronic liver disease protein-energy malnutrition (PEM) is a common finding. These patients are predisposed to higher rates of in-hospital mortality, hepatic encephalopathy and infectious complications. In cirrhotic patients awaiting orthotopic liver transplantation (OLT), a strong correlation is noted between worsening PEM and higher post-transplant complications and reduced survival. Some gaps in the literature exist with regard to PEM in cirrhosis. This thesis aimed to address some of these issues: the prognostic utility of markers of PEM; the therapeutic benefit of a specialised immunonutritional supplementation in the peri-OLT setting; and whether PEM returns to normal in the long term, following successful OLT. To assist with these aims, accurate assessment of PEM is required. The body composition laboratory (BCL) offers state of the art methods to assess nutritional status. Dual-energy x-ray absorptiometry (DXA) and in vivo neutron activation analysis (INAA) allow for accurate assessment of body weight, fat, protein and water content, all of which are deranged in cirrhotic patients. In a longitudinal analysis of cirrhotic patients’ serum sodium, hydration state and resting energy expenditure (REE) independently predicted transplant-free survival (TFS) when compared to the Child-Pugh and MELD scores, which are the established prognostic tools in liver cirrhosis. Impact (Nestle), a form of immunonutrition (IN) containing omega-3 fatty acids, arginine and nucleotides, was provided to cirrhotic patients awaiting liver transplantation in a double-blind randomised controlled trial (RCT). When compared to an isocaloric isonitrogenous control feed, pre-OLT body protein gain, post-OLT body composition changes and clinical outcomes were similar. A sub-group of patients also underwent whole-body protein turnover measurements to establish any underlying mechanism of action for IN. Patients were catabolic, which did not improve significantly after fourteen days of IN. Finally, in a cohort of patients followed for three or more years after OLT, body composition had returned to normal, although quality of life (QOL) was reduced when compared to the normal population. In conclusion, the studies from this thesis have shown serum sodium, hydration and REE to be significant predictors of TFS in cirrhotic patients. IN was not superior to an iso-caloric iso-nitrogenous control feed in the peri-OLT setting, and long-term survivors after OLT were restored to normal nutritional status.
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Slyvka, Nataliia Oleksyivna, Y. B. Yakubovska, and A. O. Zakrutko. "Early detection of hepatorenal syndrome in liver cirrhosis." Thesis, Збірник тез наукових робіт учасників міжнародної науково-практичної конференції. "Сучасні тенденції розвитку медичної науки та медичної практики". - м. Львів, 25-26 грудня 2015 р, 2015. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/11346.
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Slyvka, Nataliia Oleksyivna, Y. B. Yakubovska, and A. O. Zakrutko. "Early detection of hepatorenal syndrome in liver cirrhosis." Thesis, Збірник тез наукових робіт учасників міжнародної науково-практичної конференції. "Сучасні тенденції розвитку медичної науки та медичної практики". - м. Львів, 25-26 грудня 2015 р, 2015. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/11328.
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Schafroth, Urs. "Aminopyrine N-demethylation by rats with liver cirrhosis /." [S.l : s.n.], 1986. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.
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Palmer, Jeremy M. "Primary biliary cirrhosis : an immunological study." Thesis, University of Newcastle Upon Tyne, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300194.
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Yasuda, Katsutaro. "A nonhuman primate model of liver fibrosis towards cell therapy for liver cirrhosis." Kyoto University, 2020. http://hdl.handle.net/2433/258975.
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Freeman, J. G. "Therapeutic modalities in liver disease." Thesis, University of Newcastle Upon Tyne, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.378854.
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Dillon, John Francis. "Autonomic nervous system function in cirrhosis of the liver." Thesis, St George's, University of London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266063.
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Egger, Bernhard. "A morphometric analysis of experimental cirrhosis in rat liver /." [S.l : s.n.], 1986. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.
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Chang, Ping. "Quantitative evaluation of hepatic morphological alterations and pharmacokinetic changes of cationic drugs in fibrosis-inducing hepatic diseases /." St. Lucia, Qld, 2001. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16767.pdf.
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Li, Xiangnong. "The role of intrahepatic shunts in the normal and cirrhotic rat liver." Thesis, King's College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271055.
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Le, Moine Olivier. "Interleukin-10 in liver ischaemia-reperfusion injury and alcoholic cirrhosis." Doctoral thesis, Universite Libre de Bruxelles, 1996. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/212296.
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Thomson, Richard Kerr. "Immunogenetic analysis of anti-mitochondrial antibodies in primary biliary cirrhosis." Thesis, University of Southampton, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.323789.
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Collier, Jane Davina. "Molecular mechanisms in human hepatocellular carcinoma." Thesis, University of Newcastle Upon Tyne, 1993. http://hdl.handle.net/10443/693.
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Hepatocellular carcinoma (HCQ is one of the commonest cancers worldwide. There is, however, a marked geographical variation in incidence and it has been suggested that the pathogenesis may vary in different parts of the world. A retrospective analysis of 110 HCC patients was initially undertaken which confirmed that only 29% of British patients had markers of hepatitis B infection, suggesting a possible role for other environmental agents in the pathogenesis, and that 80% of patients had underlying cirrhosis. The nature of the strong relationship between HCC and cirrhosis has not been established but it has been postulated that increased hepatocyte turnover in the cirrhotic liver may predispose to DNA damage by environmental mutagens. Cell proliferation is required to express the strongly promutagenic DNA base lesion 0'-methylguanine, produced by alkylating agents, as a mutation. &- methylguanine is repaired by the DNA repair enzyme 06-methylguanine-DNA methyltTansferase (06-MT). A microassay was developed which could reliably measure 06-MT levels in liver biopsy samples. Using this approach 06-MT levels were found to be significantly lower in cirrhotic liver when compared to non-cirrhotic and normal liver tissue. No correlation was found between lymphocyte and liver levels from individual patients with liver disease indicating that the deficiency in DNA repair is disease-a nd tissue-specific. Three polyclonal antibodies were subsequently raised to 06-MT peptides and characterised by immunoblotting in an attempt to establish the tissue distribution of the enzyme in liver. Although none of the antisera were able to detect &-MT in tissue sections they were used to analyse structural differences in the enzyme between cirrhotic and non-cirrhotic liver using SDS-PAGE followed by immunoblotting and fluorography. A band of M, 24,000r,e presentingn ative enzyme, was visualised by fluorography in all liver extracts. Densitometry of these bands correlated with the enzyme activity determined by the direct enzyme assay, validating the assay findings. Other small molecular weight bands were seen in all liver extracts and comparison with immunoblots suggested that these bands represent C-terminal truncated enzyme. The spectrum of smaller molecular weight enzyme forms was similar in cirrhotic and non-cirrhotic liver. It was, thus, concluded that although 06-MT levels were lower in'cirrhosis this was not accounted for by structural differences in the enzyme. DNA mutations (G to A) produced by the failure to repair 06-methylguanine are known to activate oncogenes and turnour suppressor genes such as p53. However only 5/55 (9%) of HCC expressed mutant p53. Other factors potentially involved in hepatocarcinogenesis include the growth factor TGF-a and a growth factor receptor encoded by the c-erb B-2 proto-oncogene. Expression of TGF-a and the C-erbB -2 oncoprotein were seen in 8/28 (28%) and 2/26 (8%) of HCC respectively, findings which differ from those observed in HCC from the Far East. Deficient DNA repair by &-MT provides one possible reason why cirrhosis is an important risk factor for the development of HCC. However, failure to repair 06-mothylguanine does not result in mutations within the p53 gene in British HCC. Furthermore, the finding of low expression of mutant p53, TGF-a and the c-erb B-2 oncoprotein in HCC from Britain compared to HCC from the Far East and Africa suggests geographical differences in the molecular mechanisms involved in hepatocarcinogenesis between areas of high and low HCC prevalence.
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Горбачевський, Артем Олександрович, Артем Александрович Горбачевский, Artem Oleksandrovych Horbachevskyi, Микола Дмитрович Чемич, Николай Дмитриевич Чемич, and Mykola Dmytrovych Chemych. "Characteristic clinical and diagnostic features of liver cirrhosis associated with viral hepatitis." Thesis, Sumy Sumy State University, 2019. http://essuir.sumdu.edu.ua/handle/123456789/75358.
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Серед опитаних переважно чоловіки середнього віку, які проживають в місті. Найбільш поширений ймовірний шлях зараження під час медичних маніпуляцій. Мінімальна активність і вираженість цирозу (по Чайлд-П'ю) А і В. Найчастіше переважають астено-вегетативний синдром, гепатомегалія, субектерічність склер, підвищення ехогенності жовчного міхура, гиперспленізм, портальна гіпертензія і розширення варикозних розширених вен стравоходу.Среди опрошенных преимущественно мужчины среднего возраста, проживающие в городе. Наиболее распространенный вероятный путь заражения во время медицинских процедур. Минимальная активность и выраженность цирроза (по Чайлд-Пью) А и В. Чаще всего преобладают астено-вегетативный синдром, гепатомегалия, субэктеричность склер, повышение эхогенности желчного пузыря, гиперспленизм, портальная гипертензия и расширение варикозно расширенных вен пищевода.
Among the surveyed are predominantly middle-aged men who live in city. The most common likely route of infection during medical procedures. The minimal activity and expressiveness of cirrhosis (by Child-Pugh) A and B. Prevails most often are astheno-vegetative syndrome, hepatomegaly, sub- icteric sclera, increase of echogenicity of the gallbladder, portal hypertension hypersplenism and varicose esophageal veins enlargement.
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Macnaughtan, J. S. "Modulation of the gut-liver axis in cirrhosis with activated carbon." Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/1547585/.
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Introduction: A substantial body of evidence now exists to implicate bacterial products such as endotoxin in the pathogenesis of cirrhosis and determinants of outcome, most markedly in advanced disease. Strategies to modulate this process clinically are currently limited to antibiotics with the attendant risk of superinfection and resistance. Yaq-001, a new, synthetic non-absorbable carbon, has been shown to exhibit a high adsorptive capacity for bacterial toxins and thus represent a novel strategy to modulate the gut-liver axis. Methods: Neutrophil function, cytokine profile and endotoxin concentrations were determined in the splanchnic circulation of cirrhotic patients. Gut barrier integrity, innate immune function and microbiome analysis was performed in bile duct ligated (BDL) rats treated with or without oral Yaq-001. Ob/ob and MCD mice were treated with or without Yaq-001. Effects on liver injury, immune function and metabolomic profile were determined. Results: Portal compartmentalisation of neutrophil dysfunction and endotoxaemia was observed and associated with an anti-inflammatory cytokine profile. In vitro Yaq-001 exhibited a high adsorptive capacity for endotoxin and acetaldehyde without any effect on bacterial growth kinetics. Yaq-001 administration in BDL rats significantly improved organ injury, portal pressure and innate immune profile along the gut-liver axis. In vivo and in vitro endotoxin sensitivity was improved. Oral Yaq-001 was found to significantly improve liver injury, Kupffer cell function and metabolomic profile in NASH models. Conclusions: Defects at the gut barrier interface play a key role in driving bacterial translocation rates with preserved integrity of hepatic immune surveillance despite advanced disease. Oral administration of Yaq-001 in models of cirrhosis and NASH is safe and associated with a significant improvement in organ injury, portal pressure, innate immune function and endotoxin sensitivity. These studies suggest Yaq-001 represents a promising new strategy for the management of liver disease.
20
Noiret, L. "Development of a mathematical model of ammonia metabolism in liver cirrhosis." Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1367070/.
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Hepatic encephalopathy is a neuropsychiatric syndrome, which affects most patients with advanced cirrhosis. Development of the syndrome has been associated with the accumulation of ammonia (a neurotoxin) in the brain, resulting from abnormally high levels of ammonia in the bloodstream (hyperammonaemia). Blood ammonia concentration increases with the grade of cirrhosis. Hyperammonaemia has also been linked with immune dysfunctions, making the control of toxin levels in cirrhosis essential. Yet current strategies to lower ammonia concentrations are not fully effective. Elevation of blood ammonia level has been suggested to result from deranged metabolism and the development abnormal connections between gastrointestinal blood vessels and the systemic circulation (portosystemic shunting). Most of the research on hyperammonaemia has dealt with the study of metabolic derangements. On the other hand, very few studies have tried to quantify the role of portosystemic shunting. In the first part of this thesis, we test the hypothesis that haemodynamic disturbances associated with cirrhosis are sufficient to cause hyperammonaemia. As standard distributions of organ blood flow at differing grades of cirrhosis do not exist, we develop a methodology to simulate the distribution of organ blood flow. Then we construct a theoretical model, which combines distribution of organ blood flow with individual organ fluxes of ammonia. The model is used to predict arterial ammonia levels when organ blood flow is modulated. This model demonstrates that metabolic derangements are not necessary to develop hyperammonaemia, and that the development of portosystemic shunting associated with the grade of cirrhosis is sufficient to precipitate it. The model also emphasises the importance of renal ammonia production, and suggests that limiting the renal vein flux may slow down the elevation of blood ammonia concentration. Ammonia flux in the kidney depends on both the rate of ammonia production and on the balance between urinary excretion and renal vein reabsorption. In the last part of this thesis, we develop a mathematical model to investigate which transport components within the renal medulla control the rate of urinary ammonia excretion. We suggest a mechanism by which pH environment in the outer medulla could increase the rate of urinary excretion.
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Seymour, Keith. "A contribution to the study of liver metastases and experiments on modification of the metastatic cascade." Thesis, University of Newcastle Upon Tyne, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268456.
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Jones, David E. J. "T-cell responses to the 2-oxo acid dehydrogenases in primary biliary cirrhosis." Thesis, University of Newcastle Upon Tyne, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246087.
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AOKI, KUNIO, RYUICHIRO SASAKI, and ZHU-MIN HUANG. "Trends in Mortality from Primary Liver Cancer, Cirrhosis of the Liver, Virus Hepatitis, and Other Liver Diseases 1968-1984 in Japan." Nagoya University School of Medicine, 1987. http://hdl.handle.net/2237/17497.
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Stokkeland, Knut. "Studies on alcoholic liver disease /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-853-3/.
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Du, Plessis Johannie. "Bacterial translocation : cause of activated intestinal macrophages in decompensated liver disease." Diss., University of Pretoria, 2011. http://hdl.handle.net/2263/31134.
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Background and Aim: Bacterial infections are a well described
complication of cirrhosis and occur in 37% of hospitalized patients. Culture
positive infections in addition to the presence of bacterial products and
DNA lead to loss of liver function and decompensation in cirrhosis. The
mechanisms and molecular pathways associated with Bacterial
Translocation (BT) are unknown. The aims of this study were to determine:
i. macrophage phenotype and molecular pathways associated with
bacterial translocation ii. if intestinal macrophages in liver cirrhosis are
capable of modulating intestinal permeability.iii. structural integrity of the
epithelial barrier.
Methods: Duodenal biopsies and serum samples were collected from 29
patients with decompensated cirrhosis, 15 patients with compensated and
19 controls. Duodenal macrophages were characterized by means of flow
cytometry and IHC. Gene expression analysis was performed to determine
molecular pathways involved in BT. Inflammatory cytokine determination
was done in serum and culture supernatant by means of customized
cytometric bead arrays.
Results: Patients with decompensated cirrhosis demonstrated: increased
frequency of CD33+/CD14+/TREM-1+ and iNOS+ macrophages in their
duodenum, elevated mRNA levels of nitric oxide synthase 2 (NOS2),
chemokine ligand 2 (CCL2), chemokine ligand 13 (CCL13) and interleukin
8 (IL8) and increased serum levels of interleukin 6 (IL6), IL8 and
lipopolysaccharides (LPS). Additionally, patients with decompensated
cirrhosis showed an increase in NO, IL6, IL8 and CCL2 levels in culture
supernatant after short term duodenal biopsy culture. Although the
epithelial barrier on EM seemed intact, significantly increased expression of
the “pore” forming tight junction claudin 2 was observed.
Conclusion: This study showed the presence of activated CD14+Trem-
1+iNOS+ intestinal macrophages and increased levels of NO, IL-6 and
claudin-2 levels in the duodenum of patients with decompensated liver
cirrhosis, suggesting that these factors enhance intestinal permeability to
bacterial products.Afrikaans: Inleiding: Bakteriele infeksie is ‘n beskryfde komplikasie van lewersirrose wat in 37% van gehospitaliseerde pasiente voorkom. Kultuur positiewe infeksies asook die teenwoordigheid van bakteriele produkte en DNA lei tot verlies van lewerfunksie en dekompensasie. Die molekulere meganismes wat verband hou met bakteriele translokasie is nog onbekend. Die doel van hierdie studie was om: i. Makrofaag fenotipe en molekulere meganismes geassosieerd met bakteriele translokasie te beskryf, ii. te bepaal of intestinale makrofage dermdeurlaatbaarheid beinvloed, asook iii. om die struktruele integriteit van die dermwand te bepaal. Methods: Serum en dunderm biopsies was verkry van 29 pasiente met gedekompenseerde lewer sirrose, 15 pasiente met gekompenseerde sirrose en 19 kontroles. Dunderm makrofage was gekarakteriseer met behulp van vloeisitometrie en immunohistochemie. Molekulere meganisms belangrik tydens bakteriele translokasie was bepaal met behulp van geneekspressie. Serum en selkultuur supernatant sitokien bepalings was met Bioplex assays gedoen. Resultate: Pasiente met gedekompenseerde sirrose demonstreer: ‘n verhoogde frekwensie van CD33+/CD14+/TREM-1+ en iNOS+ makrofage in hul dunderm, verhoogde mRNA vlakke van NOS2, CCL2, CCL13 en IL8 asook verhoogde serum vlakke van IL6, IL8, LPS. Addisioneel het pasiente met gedekompenseerde sirrose vehoogde supernatant vlakke van NO, IL6, IL8 and CCL2 na kort termyn dunderm biopsie kulture. Alhoewel elekronmikroskopie gewys het dat die dundermwand intak is, was daar statisties-beduidend verhoogde ekspressie van die “porie” vormende vasteaansluitings- proteien, claudin 2 sigbaar. Gevolgtrekking: Gesamentlik het die studie gewys dat geaktiveerde CD14+/Trem-1+/iNOS+ intestinale makrofage asook verhoogde vlakke van NO, IL-6 en claudin-2 teenwoordig is in die dunderm van pasiente met gedekompenseerde sirrose. Dit dui daarop dat diè faktore derm deurlaatbaarheid vir bakteriele produkte kan verhoog.
Dissertation (MSc)--University of Pretoria, 2011.
Immunology
MSc
Unrestricted
26
Richardson, Rosemary Ann. "Effect of liver cirrhosis and transplantation on fuel metabolism and macronutrient preference." Thesis, University of Edinburgh, 2000. http://hdl.handle.net/1842/22581.
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This study examined factors associated with the anorexia of chronic liver disease and obesity following liver transplantation. Sixty-seven patients with chronic liver disease and a group of 18 healthy volunteers were recruited. A sub-group of 23 patients who underwent liver transplantation were reviewed every three months on three occasions. Nutritional status was determined using body habitus measurements and multi-frequency impedance analysis. Indirect calorimetry was used to determine energy and substrate metabolism in the fasted and fed state. Basal and post-prandial insulin and glucose concentrations were measured. Diet diaries were used to estimate energy and macronutrient intake and macronutrient preference was identified using a single food varying in fat and carbohydrate content. Patients with cirrhosis of hepatocellular origin (alcoholic liver cirrhosis, cryptogenic cirrhosis) had the greatest disturbances in substrate metabolism, depressed dietary intakes and poorest nutritional status when compared with patients with biliary cirrhosis and control subjects. These findings suggest that aberrant metabolism may contribute to anorexia and impact on nutritional status in patients with hepatocellular cirrhosis. No differential effect was observed when patients were stratified for severity of disease. Following liver transplantation, patients weight exceeded pre-illness values by 7% and this increase in body weight was accounted for by fat mass but not lean tissue. A decrease in resting energy expenditure was observed and a 5% increase in the dietary intake of fat derived energy. No association between immunosuppressive medication and body weight was seen. Multiple regression analysis revealed that the strongest predictor of weight gain was resting energy expenditure. These findings suggest that the liver transplant procedure per se is implicated in the energy economy and fat hyperphagia observed following liver transplantation which may be a result of denervation and the loss of afferent input and efferent outflow.
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Mitchison, Harriet Caroline. "Primary biliary cirrhosis : studies in prognosis, early diagnosis, bone disease and treatment." Thesis, University of Newcastle Upon Tyne, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.241281.
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Snowdon, Victoria Katherine. "Relaxin as a therapeutic haemodynamic modulator in liver disease." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/23508.
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Introduction: Hepatorenal syndrome (HRS) is a common complication of advanced cirrhosis with a high mortality rate and limited treatment options. Central to its pathogenesis is severe, but potentially reversible, renal vasoconstriction leading to functional renal failure. Current pharmacological treatment using splanchnic vasoconstrictors is suboptimal and prognosis without liver transplantation is dismal. The peptide hormone relaxin (RLN) mediates haemodynamic adaptations to pregnancy including increased renal blood flow (RBF) and glomerular filtration rate (GFR). I hypothesised that exogenous RLN could be used therapeutically to improve RBF and renal function in the context of experimental cirrhosis and HRS. Methods: To address this I generated pathologically distinct rat models of liver cirrhosis with features of human HRS including renal vasoconstriction and renal failure. Compensated cirrhosis was induced in male rats by 16 weeks of i.p. carbon tetrachloride (CCl4) and decompensated cirrhosis by bile duct ligation (BDL). I studied the effects of acute i.v. or sustained (72 hr) s.c. infusion of RLN compared with vehicle on systemic haemodynamics, RBF, GFR and kidney histology. I used blood oxygen dependent-magnetic resonance imaging (BOLD-MRI) to detect changes in kidney parenchymal oxygenation and Doppler ultrasound to monitor changes in RBF (velocity time integral, VTI) and renal arterial resistance (resistive index, RI). Hepatic and renal expression of the relaxin receptor RXFP1 was determined by quantitative polymerase chain reaction (qPCR) and immunohistochemistry (IHC). Vascular functional responses in isolated renal arteries were assessed by wire myography. Relaxin mediated changes in key vaso-regulatory signalling pathways in the kidney and renal vessels were analysed by qPCR, IHC and ELISA. Results: I showed using in vitro myography that the pathophysiological mechanism that underlies renal vasoconstriction in experimental cirrhosis models is an impairment of endothelium-dependent vasodilatation. Selective targeting of renal vasoconstriction using relaxin improved renal blood flow, tissue oxygenation, and normalized glomerular filtration rate in both compensated and decompensated rat cirrhosis. Furthermore, relaxin treatment restored endothelium-dependent vasodilation in isolated renal vessels from CCl4 cirrhotic rats. Relaxin-induced effects on renal blood flow and glomerular filtration rate were mediated though activation of the AKT/eNOS/nitric oxide signalling pathway in kidney, though systemic nitric oxide levels were unaffected. Crucially for human translation, relaxin did not reduce mean arterial blood pressure even in advanced cirrhosis. Conclusion: My findings identify relaxin as the first potential targeted treatment reversing the vascular dysfunction which causes HRS and directly improving renal function in HRS. Clinical translation in carefully selected populations is warranted.
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Gullstén, H. (Harriet). "Significance of polymorphisms in CYP2A6 gene." Doctoral thesis, Oulun yliopisto, 2000. http://urn.fi/urn:isbn:9514258576.
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Abstract
Cytochrome P450 2A6 (CYP2A6) is involved in the 7-hydroxylation of coumarin, C-oxidation of nicotine, and the metabolism of tobacco specific nitrosamines. Initially in 1995 Fernandez-Salguero et al. reported a genotyping method for three alleles: CYP2A6*1 (wild-type), CYP2A6*2 (variant 1), and CYP2A6*3 (variant 2). Later studies presented in this thesis indicated that the original genotyping method produces erroneous results for the CYP2A6*3 allele due to unspecific PCR conditions and previously unknown CYP2A6*1B allele. Furthermore, the CYP2A6*2 allele genotyping caused erroneous genotypes (CYP2A6*2/*2 was misclassified as CYP2A6*1/*2).
In this work, new PCR based genotyping methods were developed for CYP2A6*2 and for several new alleles (CYP2A6*1B, CYP2A6*4A/*4D and CYP2A6*5). In population-based studies, the deletion alleles (pooled as CYP2A6*4) turned out to be more prevalent among Asians (15.1%) than Caucasians (0.5%). The frequencies of the other inactive alleles varied within 0–3% in both populations. Asians totally lacked the CYP2A6*2 allele, whereas Caucasians lacked the CYP2A6*5 allele. The frequencies of two wild-type alleles, CYP2A6*1A and CYP2A6*1B alleles were 66.5% and 30.0% in Caucasians, and 43.2% and 40.6% in Asians, respectively.
Correlation studies between the phenotype, as tested by the administration of coumarin, and the genotype demonstrated that individuals with the CYP2A6*2/*2 genotype were totally defective, while CYP2A6*1/*2 subjects exhibited intermediate and CYP2A6*1/*1 subjects full capablility of producing 7-hydroxycoumarin. Upon phenotyping with nicotine, individuals with the CYP2A6*1/*2 or CYP2A6*1/*4 genotype were shown to have a lower enzyme activity (one fourth of the normal activity), compared to those with the CYP2A6*1/*1 genotype.
Defective CYP2A6 activity has been hypothesised to reduce the risk of environmentally (especially tobacco smoke) induced diseases either by decreasing production of genotoxic metabolites or by preventing addiction to tobacco smoking. However, in our case-control studies on Spanish patients with liver cirrhosis (n = 83) and liver cancer (n = 90) and their controls (n = 237) no significant association between the CYP2A6 genotypes and disease proneness was found. The odds ratio (OR) for developing liver cancer was was 1.4 (95% confidence interval [CI] 0.5–3.7) for genotypes containing at least one CYP2A6*2 allele. For liver cancer the respective OR was 1.3 (95% CI 0.4–4.5). Similarly, no statistically association between CYP2A6 alleles and the risk of lung cancer was observed in our Finnish study population cinsisting of 177 cases and 1089 controls; the OR for combined CYP2A6 variant allele containing genotypes (CYP2A6*1/*2 and CYP2A6*1/*4) was 1.19 (95% CI 0.56–2.45). Our studies therefore do not indicate any major modifying role for the CYP2A6 genotypes in individual susceptibility to environmentally induced diseases.
30
Wang, Xin Maggie. "Fibroblast activation protein in cell biology and liver fibrosis." Thesis, The University of Sydney, 2007. https://hdl.handle.net/2123/28106.
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Fibroblast activation protein (FAP) is a type 11 cell surface protein of the dipeptidyl
peptidase IV (DPIV) gene family. FAP has two peptidase activities, DP activity and a
recently reported narrow prolyl endopeptidase activity, which is restricted to Gly-Pro
derived substrates. The only known natural substrate of FAP is a collagen type I (CN-I)
specific gelatinase activity. In contrast, as the closest relative of PAP, DPIV has only
DP activity. Nine chemokines, including CXCL12, are DPIV substrates and DPIV binds
to fibronectin (FN). The natural ligands of FAP are unknown. FAP is not detectable in
most normal adult tissue whereas DPIV expression is ubiquitous. In chronic liver injury,
FAP is selectively expressed by activated hepatic stellate cells (HSC) and
myofibroblasts, the major cell types that contribute to fibrosis, while DPIV is mainly
expressed by hepatocytes and also by T cells, endothelium, and bile duct cells.
To investigate the relationship of F AP with fibrillar extracellular matrix (ECM) in
cirrhotic liver, frozen sections of human cirrhotic livers were examined using twocolour
immunofluorescence and the novel technique of second harmonic generation
(SHG) microscopy, which specifically detects fibrous collagen. Collagen fibrils were
visualised at high resolution by SHG and were thereby seen to lie alongside FAP positive
HSC. All FAP-positive HSC were also strongly immunopositive for CN—I and
FN.
Cell adhesion and migration are essential in pathologic processes that involve wound
healing, such as chronic liver disease. To examine the effects of FAP on in vitro cell
adhesion, wound healing, transwell cell invasion, proliferation and apoptosis, green
fluorescent protein (GFP) fusion proteins of FAP and DPIV were expressed in a human
epithelial cell line 293T. The FAP fusion protein was also expressed in the human
activated HSC cell line LX-2. In epithelial cells, cells overexpressing FAP showed
reduced adhesion to plates coated with CN-I, FN or Matrigel (P<0.05). In contrast,
DPIV overexpression increased cell adhesion to FN (P<0.01) but had no effect on
adhesion to CN-I or Matrigel. In a cell monolayer wound healing assay, cells
overexpressing either FAP or DPIV exhibited less migration into the wound on plastic
coated with CN-I, FN or Matrigel (P<0.05). Concordantly, cells overexpressing FAP or
DPIV exhibited reduced migration towards CN-I, FN or Matrigel in the absence or
presence of TGF-B] in transwells. Cells overexpressing either protein enhanced
staurosporine streptomyces (STS)-stimulated apoptosis. DPIV and FAP overexpression
increased cell proliferation. Ablating the enzyme activity of FAP by point mutations at
Ser624 or Glu203/Glu204 did not influence any of the results. Neither DPIV nor FAP
co-localized with the actin cytoskeleton, or altered cytoskeletal morphology.
Overexpressing DPIV or F AP increased expression levels of tissue inhibitor of matrix
metalloproteinase (TIMP) 1 and CD44 and depressed B—catenin and discoidin domain
receptor (DDR) 1 expression. In stellate cells, cells overexpressing FAP showed
enhanced adhesion to plates coated with CN-I, FN or Matrigel (P<0.05) and exhibited
more migration into the wound (P<0.05) on plastic coated with CN-I, FN or Matrigel in
a wound healing assay, and enhanced migration towards CN—I or FN in the absence or
presence of TGF-Bl in transwells. Overexpression of FAP did not trigger apoptosis, but
did enhance STS-stimulated apoptosis. FAP overexpression increased LX-2 cell
proliferation. Removal of the enzyme activities of FAP by point mutation did not
influence the results.
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Fassnacht, Ryan. "Molecular Mechanisms Involved Involved in the Interaction Effects of HCV and Ethanol on Liver Cirrhosis." VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/2246.
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The leading causes of liver disease are Hepatitis C virus infection and chronic alcohol abuse. Alcohol accelerates liver disease in HCV but the mechanisms are poorly understood. The identification of molecular gene expression profiles on human liver tissue was performed using microarrays. Samples were obtained from alcoholic-cirrhotic, HCV-cirrhotic, HCV/alcohol-cirrhotic and control non-cirrhotic liver tissue. Probe set expression summaries were calculated using RMA. Probe set level linear models were fit where probe set expression was modeled by HCV status, alcohol status, and the interaction between HCV and Alcohol. HCV cirrhosis was associated with up-regulation of genes related to viral and immune response, apoptosis and inflammation. There were down-regulation of genes in the ubiquititin-proteasome system in alcoholic cirrhosis. The interaction of HCV and alcohol revealed negative interaction for genes involved in apoptosis and immune response. There was a negative estimate for genes involved in class II restricted antigen presentation.
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SAKUMA, SADAYUKI, HIDEHITO ICHIHASHI, TAKEO NAKAGAWA, YOSHINAO KATSUMATA, and KAZUO KATSUMATA. "Studies on the Computed Tomography of the Pancreas in Patients of Liver Cirrhosis." Nagoya University School of Medicine, 1985. http://hdl.handle.net/2237/17480.
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Virstiuk, N. O., I. Kobitovuch, Nataliia Oleksyivna Slyvka, and O. V. Virstiuk. "N-terminal pro-brain natriuretic peptide and prognosis of alcoholic liver cirrhosis course." Thesis, The international liver congress. - Barselona, Spain, 13-17.04.2016, 2016. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/11745.
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Горбачевський, Артем Олександрович, Артем Александрович Горбачевский, Artem Oleksandrovych Horbachevskyi, Микола Дмитрович Чемич, Николай Дмитриевич Чемич, and Mykola Dmytrovych Chemych. "Variability of complications of liver cirrhosis associated with hepatitis B and C viruses." Thesis, Lithuanian University of Health Sciences, 2020. https://essuir.sumdu.edu.ua/handle/123456789/81411.
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Серед обстежених 84% випадків були розподілені наступним чином: вірусний гепатит С, вірусний гепатит В 7,4% супутня інфекція В + Г 5,6%. В обстеженій групі переважали чоловіки (62,9%) та жителі міста (70,4%), середній вік пацієнтів становив 44,2 ± 0,2 року. Ймовірний шлях зараження: під час медичних втручань (18,5%); вживання внутрішньовенних препаратів, донорство (по 7,4%); стоматологічні процедури (11,1%); переливання крові або його складові (5,5%); професійна діяльність (медичні працівники) (1,8%); не визначено - у 48,3% опитуваних. Пацієнти з мінімальною активністю (68,5%) були в 3,7 рази рідше - середні (18,5%), у 6,2 рази - виражений (11,1%). Декомпенсований цироз (за класифікацією Чайлда П'ю) зареєстрований у 3,7% людей, субкомпенсований - у 37% та компенсований - у 59,3% пацієнтів. Супутня патологія була виявлена у всіх хворих, кожен третій хворий мав метаболічну кардіоміопатію (40,7%), гіпертонію (35,1%), жовчнокам’яну хворобу (31,5%), тоді як серцева недостатність та енцефалопатія були менш поширеними (відповідно - 29,6% та 14,8%). Ультразвукове дослідження органів черевної порожнини виявило: збільшення розміру печінки (29,6%), збільшення ехогенності (77,7%), збільшення розміру ворітної вени (31,4%), ущільнення судин (38,8%), ущільнення стінки жовчного міхура (57,4%); збільшення селезінки (53,7%) та збільшення селезінкової вени (77,7%); ознаки портальної гіпертензії (70,4%). Варикозне розширення вен стравоходу діагностовано у 31,5% хворих, набряково-асцитичний синдром - у 24,1%. Цироз супроводжувався тромбоцитопенією (33,3%), анемією (14,8%) та лейкопенією (9,3%).Среди обследованных 84% случаев были распределены следующим образом: вирусный гепатит С, вирусный гепатит В 7,4% сопутствующая инфекция В + Г 5,6%. В обследованной группе преобладали мужчины (62,9%) и жители города (70,4%), средний возраст пациентов составил 44,2 ± 0,2 года. Вероятный путь заражения: при медицинских вмешательств (18,5%); употребление внутривенных препаратов, донорство (по 7,4%); стоматологические процедуры (11,1%); переливания крови или его составляющие (5,5%); профессиональная деятельность (медицинские работники) (1,8%); не определен - у 48,3% опрошенных. Пациенты с минимальной активностью (68,5%) были в 3,7 раза реже - средние (18,5%), в 6,2 раза - выраженный (11,1%). Декомпенсированный цирроз (по классификации Чайлд Пью) зарегистрирован в 3,7% людей, субкомпенсированный - в 37% и компенсированный - в 59,3% пациентов. Сопутствующая патология была выявлена у всех больных, каждый третий больной имел метаболическую кардиомиопатию (40,7%), гипертонию (35,1%), желчнокаменную болезнь (31,5%), тогда как сердечная недостаточность и энцефалопатия были менее распространенными ( соответственно - 29,6% и 14,8%). Ультразвуковое исследование органов брюшной полости показало: увеличение размеров печени (29,6%), увеличение эхогенности (77,7%), увеличение размера воротной вены (31,4%), уплотнения сосудов (38,8%), уплотнение стенки желчного пузыря (57,4%); увеличение селезенки (53,7%) и увеличение селезеночной вены (77,7%); признаки портальной гипертензии (70,4%). Варикозное расширение вен пищевода диагностирован у 31,5% больных, отечно-асцитический синдром - в 24,1%. Цирроз сопровождался тромбоцитопенией (33,3%), анемией (14,8%) и лейкопения (9,3%).
Among the surveyed, 84% of cases were divided, as follows: viral hepatitis C, viral hepatitis B 7.4 % co-infection B+D 5.6 %. In the surveyed group prevailed men (62.9 %) and city residents (70.4 %), the average age of patients was 44.2 ± 0.2 years. Probable pathway of infection: during medical interventions (18.5 %); use of intravenous drugs, donation (7.4 % each); dental procedures (11.1 %); blood transfusion or its constituents (5.5 %); professional activity (medical workers) (1,8%); not found – in 48.3 % of the surveyed. Patients with minimal activity (68.5 %) were 3.7 times less frequent – moderate (18.5 %), 6.2 times – expressed (11.1 %). Decompensated cirrhosis (according to Child Pugh’s classification) is registered in 3.7 % of people, subcompensated – in 37 %, and compensated – in 59.3 % of the patients. Comorbidity was detected in all the patients, every third patient had metabolic cardiomyopathy (40.7 %), hypertension (35.1 %), gall-stone disease (31.5 %), whereas heart failure and encephalopathy were less common (respectively – 29.6 % and 14.8 %) in the patients. Ultrasound examination of abdominal organs revealed the following: increase in liver size (29.6 %), increase in echogenicity (77.7 %), increase in portal vein size (31.4 %), vascular compaction (38.8 %), sealing of the gallbladder wall (57.4 %); enlargement of the spleen (53.7 %) and enlargement of the splenic vein (77.7 %); the signs of portal hypertension (70.4 %). Varicose veins of the oesophagus were diagnosed in 31.5 % of the patients, oedema-ascitic syndrome – in 24.1 %. Cirrhosis was accompanied by thrombocytopenia (33.3 %), anaemia (14.8 %) and leukopenia (9.3 %).
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Jobara, Kanta. "Whey-hydrolyzed peptide-enriched immunomodulating diet prevents progression of liver cirrhosis in rats." Kyoto University, 2014. http://hdl.handle.net/2433/189665.
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George, Stephanie Marie. "Hemodynamic investigation of the liver using magnetic resonance imaging and computational fluid dynamics." Diss., Atlanta, Ga. : Georgia Institute of Technology, 2008. http://hdl.handle.net/1853/24803.
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Thesis (Ph.D.)--Biomedical Engineering, Georgia Institute of Technology, 2009.Committee Chair: Giddens, Don; Committee Member: Heffron, Thomas; Committee Member: Martin, Diego; Committee Member: Oshinski, John; Committee Member: Vito, Raymond.
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Huaringa-Marcelo, Jorge, Mariella R. Huaman, Ana Brañez-Condorena, Pamela Villacorta-Landeo, Diego F. Pinto-Ruiz, Diana Urday-Ipanaqué, David García-Gomero, Pedro Montes-Teves, and Adelina Lozano Miranda. "Vasoactive agents for the management of acute variceal bleeding: A systematic review and meta-analysis." Romanian Society of Gastroenterology, 2021. http://hdl.handle.net/10757/655881.
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Background & Aims: Vasoactive agents with endoscopic therapy are used to treat acute variceal bleeding (AVB). There are two main groups of vasoactive agents: terlipressin and vasopressin (T-V), and octreotide and somatostatin (O-S). However, the benefit/harm balance is unclear. Our aim was to assess the efficacy and safety of T-V versus O-S for the management of AVB. Methods: We performed a systematic search for randomized controlled trials (RCTs) in PubMed, Scopus, and CENTRAL. Our main outcomes were mortality and adverse events. Secondary outcomes were bleeding control, rebleeding, blood transfusion, hospital stay. We evaluated the certainty of evidence using GRADE methodology. Results: We included 21 RCTs. The risk of mortality (RR: 1.01; 95%CI: 0.83-1.22), bleeding control (RR: 0.96; 95%CI: 0.91-1.02; I2=53%), early rebleeding (RR: 0.91; 95%CI: 0.66-1.24: I2=0%), late rebleeding (RR: 0.94; 95 CI: 0.56-1.60; I2=0%), blood transfusion (MD: 0.04; 95%CI:-0.31-0.39; I2=68%) and hospital stay (MD:-1.06; 95%CI:-2.80-0.69; I2=0%) were similar between T-V and O-S groups. Only 15 studies reported adverse events, which were significantly higher in the T-V compared to the O-S group (RR 2.39; 95%CI: 1.58-3.63; I2=57%). The certainty of evidence was moderate for the main outcomes, and low or very low for others. Conclusions: In cirrhotic patients with AVB, those treated with T-V had similar mortality risk compared to O-S. However, the use of T-V showed an increased risk of adverse events compared to O-S.Revisión por pares
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Koyama, Yukinori. "Effects of oral intake of hydrogen water on liver fibrogenesis in mice." Kyoto University, 2014. http://hdl.handle.net/2433/185194.
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Fleming, Catherine Mary. "The epidemiology of cirrhosis and abnormal liver function in the general population of the UK." Thesis, University of Nottingham, 2010. http://eprints.nottingham.ac.uk/11371/.
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Background Liver disease is a serious problem both in the UK and globally. While the incidence and mortality from several chronic diseases are decreasing, mortality from liver disease is increasing. As well as the medical sequelae for an individual with liver disease, in the UK the increase in chronic liver disease poses particular problems with respect to increasing hospital admissions, mortality and significant costs to the public both in terms of treatment and in loss of productivity. The increase in society of several risk factors for chronic liver disease, notably alcohol intake, obesity and type 2 diabetes, mean that these problems are likely to increase in the future. Despite these apparent problems there are surprisingly few reliable sources of data on the occurrence of chronic liver disease (cirrhosis) in the general population of the UK and the rate and consequence of disease progression particularly among ambulatory patients. Nor are their robust estimates of the prevalence of abnormal liver function tests (which may represent undiagnosed liver disease) and their associations with mortality. This thesis utilises two distinct datasets to examine separate areas of interest in the epidemiology of liver disease in the UK. The first three studies contained within this thesis are concerned with the epidemiology of cirrhosis in the general population of the UK. The second group of three studies focuses on the prevalence of elevated liver function tests in a population of older people in the UK, the demographic, clinical and lifestyle factors associated with such and the mortality following an elevated liver function test. Objectives 1. To estimate the incidence and prevalence of cirrhosis in the population of the UK 2. To describe the mortality associated with cirrhosis compared with the general population and the disease progression of cirrhosis 3. To estimate the prevalence of elevated liver function tests among people aged 75 and over in the UK 4. To describe the association between elevated liver function test and demographic, lifestyle, clinical characteristics and mortality among people aged 75 and over. Methods To examine objectives 1 and 2 I utilised the General Practice Research Database (GPRD) constructing a population based cohort of 4537 subjects with cirrhosis and 44,403 age, sex and practice matched controls. I used Poisson regression to estimate incidence rate ratios and describe trends in alcoholic and non-alcohol-related cirrhosis. Using Cox regression within an historical matched cohort design I estimated the absolute excess mortality rates and hazard ratios for mortality in people with cirrhosis compared to the general population. I described the probability of progressing from one disease state to another. To examine objectives 3 and 4 I accessed data from one arm of the Medical Research Council (MRC) Trial of Assessment and Management of Older People in the Community, a representative sample of community dwelling people aged 75 and over, totalling 15,308 participants. The prevalence of abnormal liver function was described as the proportion of study participants with elevated aspartate transaminase, alkaline phosphatase or serum bilirubin. Associations between elevated liver function and demographic, lifestyle and clinical factors were examined using multivariable logistic regression. I determined the absolute mortality rates and hazard ratios for all-cause and cause-specific mortality using a Cox proportional hazards model. Findings Epidemiology of cirrhosis (GPRD) These studies have shown an increasing trend in both the incidence and prevalence of cirrhosis in the UK with an estimated 45% increase in incidence of cirrhosis in the 10-year period studied. I estimate that 76 per 100,000 people were living with cirrhosis in 2001. Just over half of all cirrhosis was associated with alcoholism. Disease progression with cirrhosis among this mainly ambulatory population was rapid with a rate of decompensation in people with compensated disease of 5% per year and 1 in 10 dying in the first year following diagnosis. This figure increased to 25% of people dying within one year for those with decompensated disease. Mortality in subjects with compensated and decompensated cirrhosis was 93.4 and 178.0 per 1000 person years compared with only 19.2 per 1000 person years in the general control population. Following adjustment for age and sex people with compensated and decompensated disease were respectively 5 and 10 times more likely to die than the general population. Epidemiology of abnormal liver function tests (MRC cohort) Abnormalities in liver function were common with roughly 1 in 6 people aged 75 and over having at least one elevated liver enzyme, although most of these elevations were mild. A single elevated measurement of aspartate transaminase was associated with an increased consumption of alcohol and a lower age in contrast with that of a single measurement of alkaline phosphatase which showed an association with higher age and lower alcohol consumption. An elevated bilirubin measurement was strongly associated with being male. Having a single elevated liver function test was associated with a modest increase in the hazard of death compared with people with normal liver function tests (adjusted hazard ratio for death 1.27 (95% CI[1.19, 1.36]). As well as an unsurprising increase in the hazard ratio for death from liver disease, elevated aspartate transaminase or alkaline phosphatase were both associated with modest increases in the hazard of death from cancer (adjusted hazard ratios of 1.56 (95%CI[1.21, 2.01]) and 1.61 (95%CI[1.39, 1.86]) respectively). Elevated alkaline phosphatase was additionally associated with increases in the hazard of death from respiratory disease (adjusted hazard ratio 1.58 (95%CI[1.32, 1.90])) and cardiovascular disease (adjusted hazard ratio 1.34 (95%CI[1.17, 1.55])). Conclusions From my work on the incidence and prevalence of cirrhosis I estimate that a minimum of 31,000 people in the UK are living with cirrhosis, a figure which is likely to rise given increasing trends in the incidence of cirrhosis described in this thesis. The significant mortality and disease progression associated with cirrhosis means that more needs to be done to combat both the incidence and progression of this disease both on an individual and population level. Elevations in enzymes regarded as reflecting liver function are common in people aged 75 and over and in most people these abnormalities are less than 2x the upper limit of normal for the assays used. These elevations I observed are associated with both a modest increase in all-cause mortality and also with an increase in death due to specific causes. Rather than simply a marker of liver function the investigation of people with elevated liver function tests, particularly those with severely elevated tests, may lead to the identification of potentially treatable conditions that underlie death.
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Mandel, David Walter. "Comparison of Targeted Lower Extremity Strengthening and Usual Care Progressive Ambulation in Subjects Post-Liver Transplant: A Randomized Controlled Trial." Scholarly Repository, 2009. http://scholarlyrepository.miami.edu/oa_dissertations/333.
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Individuals with chronic liver disease experience progressive muscle wasting, weakness, fatigue, and decreased quality of life. Liver transplantation is the only treatment for end-stage liver disease with cirrhosis; however, muscle wasting, strength impairments, activity limitations, and health related quality of life do not return to the level of healthy adults. Currently there is no plan of care for rehabilitation of individuals post-liver transplantation. These individuals are only instructed to gradually increase walking and activity. Walking may increase lower extremity muscle strength; however, walking at a self-selected pace is less effective than resistance exercise. The purpose of this dissertation was to compare the benefits of a home exercise program of targeted lower extremity resistance exercise with benefits of progressive walking in individuals who have undergone liver transplantation. In Chapter 2 we performed a study to validate the ability of several outcome measures to detect changes in strength and activity performance in the population with liver disease and post-liver transplantation. The strength impairment measures of Grip Strength, Heel Rising, and Bridging along with activity limitation measures 30 Second Chair Stand and Six Minute Walk Test (6MWT) were able to differentiate strength and activity performance across levels of liver disease severity including post liver transplantation. Liver disease severity was moderately correlated with the strength impairment measures Bridging and Heel Rising but was not correlated with Grip strength. Liver disease severity was moderately correlated with 6MWT and 30-Second Chair-Stand but was not correlated with the SF-36 physical function scale. Strength impairment measures were strongly correlated with the activity limitation measures. Heel Rising and Bridging were strongly correlated with 30-Second Chair-Standing and 6MWT. Grip strength was moderately correlated with 30-Second Chair-Standing. In Chapter 3 we conducted a randomized controlled trial to assess the benefits of resistance exercise to progressive walking as a treatment plan for improving strength and activity performance in individuals post liver transplantation. We also examined the relationships of the change in muscle strength to the change in activity performance. Both the exercise and walking groups improved in strength and activity performance; however, the group performing the resistance exercise improved more. Bridging, 30 Second Chair Standing, Heel Rising, and 6MWT increased more for the exercise group than the walking group. Additionally, changes in strength were related to the changes in activity performance and health related quality of life. Bridging was correlated with Heel Rising, 30 Second Chair Standing, 6MWT, and the Chronic Liver Disease Questionnaire. In Chapter 4 we discuss the clinical relevance of the results of the studies described in the above chapters. We conclude Bridging, Heel Rising, 30 Second Chair Standing, and 6MWT are valid outcome measures to measure changes in strength and activity performance in the population with liver disease. Individuals post liver transplantation improve in strength and activity performance through progressive walking; however, the addition of resistance exercise to the current treatment plan is necessary for greater improvement. Additionally it is clinically relevant that this population was adherent to a home exercise program. Subjects adherent to the exercise program increased in strength and activity performance greater than subjects who were non-adherent.
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Ishigami, Masatoshi, Yoshiaki Katano, Kazuhiko Hayashi, Akihiro Ito, Yoshiki Hirooka, Yasuharu Onishi, Taro Nakamura, Tetsuya Kiuchi, and Hidemi Goto. "Risk Factors of Recipient Receiving Living Donor Liver Transplantation in the Comprehensive Era of Indication and Perioperative Managements." Nagoya University School of Medicine, 2010. http://hdl.handle.net/2237/14173.
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Cruz, Cristiane Kibune Nagasako Vieira da 1976. "Avaliação da função autonomica e do transito intestinal em pacientes com cirrose hepatica de etiologia não alcoolica." [s.n.], 2007. http://repositorio.unicamp.br/jspui/handle/REPOSIP/310802.
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Orientador: Maria Aparecida MesquitaDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
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Resumo: A disfunção autonômica (DA) parece ser freqüente na cirrose hepática (CH) de etiologia alcoólica, enquanto que os dados referentes à prevalência e repercussões clínicas desta complicação na cirrose de etiologia não alcoólica são controversos. Existem evidências na literatura de que o método da análise da variabilidade da freqüência cardíaca (VFC) em 24 horas é mais sensível que a pesquisa dos reflexos cardiovasculares para a avaliação da função autonômica. Esta técnica foi pouco utilizada na investigação de pacientes com CH. Estudos prévios em cirróticos demonstraram a presença de alterações da motilidade intestinal que predisporiam à ocorrência de supercrescimento bacteriano. Os mecanismos responsáveis por estas alterações não foram ainda esclarecidos. Considerando que o sistema nervoso autônomo (SNA) participa do controle da motilidade intestinal, parece provável que a DA esteja associada com as alterações da motilidade intestinal na CH. Os objetivos deste estudo foram investigar a presença de alterações do SNA parassimpático e simpático em pacientes com CH de etiologia não alcoólica, utilizando os métodos dos testes de reflexos cardiovasculares e da análise da VFC em 24 horas, e avaliar a associação das alterações autonômicas encontradas com a gravidade da disfunção hepática, com alterações do trânsito intestinal, e com o aparecimento de complicações da CH. Foram estudados trinta e quatro pacientes com diagnóstico de CH de etiologia não alcoólica, divididos em Child-Pugh A (13) e Child-Pugh B/C (21). A atividade autonômica foi avaliada através dos testes de reflexos cardiovasculares e da análise da VFC em 24 horas. O estudo do tempo de trânsito orocecal (TTOC) foi realizado pelo teste do H2 no ar expirado, após ingestão de lactulose. De acordo com os testes de reflexos cardiovasculares, a presença de disfunção parassimpática foi encontrada em 4 pacientes Child A (30,8%) e em 6 pacientes Child B/C (28,4%; p>0,05). A análise da VFC em 24 horas mostrou que os parâmetros relacionados com a atividade parassimpática (LF, lnLF, pNN50) e simpática (LF, lnLF) estavam significativamente (p<0,05) diminuídos nos pacientes Child B/C, tanto em relação ao grupo controle, como também em relação aos pacientes Child A. A avaliação individual mostrou a presença de disfunção parassimpática em 3 pacientes Child A (23,1%) e em 12 (57%; p=0,07) Child B/C. A diminuição da atividade simpática concomitante foi encontrada em 8 dos 12 pacientes Child B e C, com lesão parassimpática. Em relação ao TTOC, não houve diferença estatística entre os valores do TTOC no grupo Child A (52±17 minutos) e no grupo controle (52±13 minutos). Em contraste, os pacientes Child B/C apresentaram valores mais altos do TTOC (71±34minutos) em relação aos controles (p=0,02). Apenas dois pacientes apresentaram resultados sugestivos de supercrescimento bacteriano. O tempo de seguimento foi de 19±12 meses. Ao final do estudo, cinco pacientes (24%) Child B/C evoluíram para óbito. Os valores dos parâmetros representativos da atividade parassimpática (HF, lnHF) nesses pacientes foram significativamente (p=0,04) menores que os encontrados nos pacientes do grupo Child B/C que continuavam vivos. A encefalopatia foi a complicação mais freqüente, acometendo 42,8% dos pacientes durante o período de seguimento. Houve associação estatística entre a presença de DA e a incidência de encefalopatia hepática (p<0,05). Não houve correlação entre os parâmetros da atividade autonômica com os valores do TTOC. Também não houve associação entre TTOC prolongado e complicações da CH. Em conclusão, nossos resultados demonstraram que a DA é achado freqüente nos pacientes com CH de etiologia não alcoólica e está associada com o grau de disfunção hepática, sendo mais freqüente nos pacientes com CH Child B e C. Nossos dados não demonstraram associação entre a alteração da função autonômica e o prolongamento do trânsito intestinal observado nesses pacientes. A presença da DA é um fator predisponente para a ocorrência de encefalopatia hepática, e parece influir no prognóstico da doença
Abstract: Autonomic dysfunction (AD) is common in patients with alcoholic hepatic cirrhosis but information on its occurrence and clinical relevance in patients with non-alcoholic liver disease is contradictory. 24-hour heart rate variability (HRV) is considered to be more sensitive than the cardiovascular reflexes to detect autonomic damage. Only a few studies used this technique in the investigation of autonomic function in cirrhotic patients. Previous studies have demonstrated that intestinal transit is delayed in patients with cirrhosis, and that this alteration predisposes to bacterial overgrowth, bacterial translocation and risk of infections. The reasons for that remain unclear. Since the autonomic nervous system participates in the regulation of gastrointestinal motility, it seems likely that AD may play a role in the intestinal motility alterations observed in cirrhosis. Therefore, our aims were to assess autonomic function in patients with non-alcoholic hepatic cirrhosis, and to investigate the relationship of AD with severity of disease, delayed intestinal transit and the clinical outcome. Thirty four patients with non-alcoholic hepatic cirrhosis classified as Child¿s A (n=13) and Child¿ B/C (n=21) were studied. Autonomic function was assessed by using standard cardiovascular reflexes tests and 24- hour HRV analysis. Orocaecal transit time (OCTT) was measured using the lactulose hydrogen breath test. According to cardiovascular reflexes tests, 4 patients Child A (30.8%) and 6 patients Child B/C (28.4%), were found to have evidence of parasympathetic damage. The 24-hour HRV analysis showed that parameters reflecting parasympathetic (HF, lnHF, pNN50) and sympathetic (LF, lnLF) function were significantly decreased (p<0,05) in comparison with both controls and Child¿s A patients. Individual analysis showed parasympathetic damage in three patients Child A (23,1%) and in 12 (57%) Child B/C (p=0.07). Eight patients had combined sympathetic damage. No diference was found in OCTT values between Child¿ A patients (52±17 minutes) and controls (52±13 min). In contrast, OCTT values were significantly higher in Child¿ B/C patients (71±34minutes) than in controls. Bacterial overgrowth occurred in only two patients. The mean follow-up time was 19±12 months. At the end of the study, five Child¿s B/C patients (24%) have died. The values of parameters representative of parasympathetic function (HF, lnHF) were significantly lower (p<0.05) in these patients in comparison with survivors of Child¿s B/C group. Hepatic encephalopathy was the most frequent complication during follow-up, occurring in 42.8% of Child¿s B/C patients. AD was significantly associated with encephalopathy (p<0.05), but did not correlate with OCTT values. In conclusion, our study showed that autonomic dysfunction in common in patients with non-alcoholic liver disease and is related to the severity of hepatic dysfunction. Our results did not show a relationship between delayed intestinal transit and AD. The presence of autonomic damage predisposes these patients to the development of encephalopathy and may be associated to higher mortality
Mestrado
Clinica Medica
Mestre em Clinica Medica
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Chung, Sau-yu. "The progression of CCI4-induced liver cirrhosis of rats and the protective effects of colchicine and green tea polyphenols /." Hong Kong : University of Hong Kong, 2001. http://sunzi.lib.hku.hk/hkuto/record.jsp?B25018498.
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Ayres, Reuben Christopher Simon. "In vitro investigation into the role of human intrahepatic biliary epithelial cells as targets in primary biliary cirrhosis." Thesis, University of Southampton, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.296245.
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Moser, Michael A. J. "Effect of preoperative interventions on the outcome following liver resection in a rat model of cirrhosis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0001/MQ34395.pdf.
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Marcinczak, Jan Marek [Verfasser]. "Image Analysis of Mini-Laparoscopic Sequences for Computer Aided Diagnosis of Liver Cirrhosis / Jan Marek Marcinczak." München : Verlag Dr. Hut, 2015. http://d-nb.info/1079768440/34.
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Slyvka, N. O., N. G. Virstiuk, I. A. Plesh, and V. A. Gaidukov. "Low cardiac output predicts development of hepatorenal syndrome and survival in patients with alcoholic liver cirrhosis." Thesis, Матерiали 97-ї пiдсумковоi' наукової конференцiї професорсько-викладацького персоналу вищого державного навчального закладу України «Буковинський державний медичний унiверситет» (Чернiвцi, 15, 17 ,22 лютого 2016 р.) - Чернiвцi: Медунiверситет, 2016, 2016. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/10380.
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Zaccherini, Giacomo <1985>. "Clinical and pathophysiological characterization of patients with acutely decompensated cirrhosis and acute-on-chronic liver failure." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2022. http://amsdottorato.unibo.it/10083/1/Zaccherini%20-%20Tesi%20PhD.pdf.
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In the last decade, our understanding of the pathophysiological mechanisms underlying decompensated cirrhosis has greatly increased. Moreover, acute-on-chronic liver failure (ACLF) was defined as a distinct syndrome with specific features. Our research activities aimed to provide a contribution in characterizing patients with acutely decompensated cirrhosis and ACLF from a clinical and a pathophysiological perspective. As a first project, we addressed the clinical issue of predicting in-hospital development of ACLF in patients hospitalized for acute decompensation of cirrhosis. As a second contribution, we performed a reassessment of the whole metabolomic dataset obtained from 831 patients enrolled in the CANONIC study, focusing on amino acids, with the aim to uncover alterations in amino acids metabolic pathways. As a third perspective, we performed a GWAS on 270 patients with acute decompensation and ACLF included in the first clinical study. We categorized patients in 4 groups, according to their clinical presentation and their clinical course. We then performed two comparisons: group 1 vs group 4 (i.e., the most severe vs the mildest clinical courses), and group 1 vs group 2 (i.e., patients with different 1-year outcomes from a common clinical presentation with ACLF or bacterial infection). Three SNPs (rs9354118 on chromosome 6q16.1; rs1146878 on chromosome 13q22.2; rs6479397 on chromosome 9q22.31) were significantly associated with the selected phenotypes, but all of them were located in non-codifying DNA regions. However, their potential role as candidate Cis-Regulatory Elements (cCREs) opened interesting hypotheses on effects on the expression of neighboring genes. Indeed, four of them (FUT9 and UFL1 for SNP rs9354118, LMO7 and ACOD1 for rs1146878) are involved in the modulation of immune system activation and systemic inflammation. The results of the GWAS did not confirm previous findings reported in literature and presented some limitations. However, it provided the basis for further research in this still open issue.
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Chu, Shu-Chi, and 朱書志. "Ultrasonic image analysis of liver cirrhosis." Thesis, 2007. http://ndltd.ncl.edu.tw/handle/53106557323580667699.
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碩士臺灣大學
應用力學研究所
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In this study, the gray level B-mode ultrasound image analysis of liver parenchyma and hepatic vein and portal vein Power Doppler Vascular Index (PDVI) analysis was used to differentiate liver cirrhosis. The characteristic parameters extracted from grey-level co-occurrence matrix was statistical significant in differentiating the normal liver and the cirrhotic liver. The PDVI waveforms measured from hepatic vein is more regular or periodic in the normal livers than in the cirrhotic livers. The ratio of maximum PDVI to minimum PDVI ( PDVImax : PDVImin ) for hepatic vein were 2.44 ± 0.85 in control normal, and 1.52 ± 0.26 in patients with liver cirrhosis, and is statistical significant. ( p = 0.007, with threshold of 1.8, sensitivity 93.75%, specificity 80%). Such a difference of PDVI ratio in the portal vein was not as significant as in the hepatic vein. The hepatic vein for normal control subjects can be considered as an elastic vessel. When the liver becomes fibrosis, the vessel would lose its elasticity. Therefore, the pulsation of PDVI of blood vessel decreases, and such the difference would be easily detectable in the hepatic vein than the portal vein. Generally, use the PDVI ratio as an clinical index for differentiating normal livers and cirrhotic livers would to be meaningful.
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WAN, ZI-NAI, and 王姿乃. "Epidemiological study of liver cirrhosis and chronic liver disease in TaiwanMultifactorial study of liver cirrhosis among hepatitis B surface antigen carriers." Thesis, 1992. http://ndltd.ncl.edu.tw/handle/49022884064833851032.
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