Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Non-alcoholic steatohepatitis (NASH) is a part of the spectrum of non-alcoholic fatty liver disease (NAFLD), which can progress to hepatic cirrhosis and end-stage liver disease or hepatocellular carcinoma (HCC). Its pathogenesis is associated with insulin resistance (IR) and the metabolic syndrome. Hepatic steatosis has also been considered an early marker of IR. It is now accepted that NASH is a multistep process with a prominent role for IR, where oxidative stress and cytokines retain a central role. Markers for predicting NAFLD with advanced fibrosis are needed. Once considered irreversible, liver fibrosis is now recognized a dynamic process with significant prospects for remission. The liver biopsy is still a gold standard in assessment of liver fibro-inflammatory activity in the injured liver, but has its own limitations: invasiveness, small tissue sample and inter- and intra-observer error. The lack of non-invasive tests limits the ability of monitoring progression of hepatic fibrosis and response to treatment. Therefore, clinical trials focused on finding of new non-invasive diagnostic tools giving possibilities of frequent, more accurate and reproducible assessment of hepatic fibrosis are constantly conducted.
Pol Merkur Lekarski 2008 Aug
PMID:[Non invasive markers of non-alcoholic steatohepatitis]. 1894 40

The Budd-Chiari syndrome is a rare pathology resulting from various etiological factors which often contribute to its late diagnosis. Liver cirrhosis, malignant tumors and haematological disorders resulting in hypercoagulability, are the most common reasons of Budd-Chiari syndrome. The syndrome is characterized by portal hypertension and splanchnic congestion due to obstruction of hepatic venous outflow. The first symptoms include pain, ascites and hepatosplenomegaly. The diagnosis of Budd-Chiari syndrome can be achieved by Doppler ultrasonography, Computed Tomography scan, Magnetic Resonance or Single Photon Emission Computed Tomography. In the following article, a case report of a patient with diagnosed Budd-Chiari syndrome as a result of congenital thrombophilia-factor V Leiden gene mutation is presented. Clinical symptoms, diagnostic process, as well as treatment options, were shown in the article.
Ginekol Pol 2008 Oct
PMID:[Budd-Chiari syndrome induced by hormonal oral contraception in the patient with congenital thrombophilia-factor V Leiden mutation--a case report]. 1905 26

Hepatitis C is caused by the hepatitis C virus (HCV) infection. According to World Health Organization data, 3% of the world population (approximately 170 million people) is infected with HCV; in Poland there are over 700,000. Over 70% of those infected manifest no symptoms in the acute phase of the disease, and in about 70-80% the acute phase progresses into a chronic form. Patients with symptoms in the acute phase of HCV infection most commonly present with unspecific signs and symptoms that may develop in other viral liver infections, e.g. malaise, fatigue, abdominal pain, mild hepato- and splenomegaly and arthralgia. These symptoms usually persist for 2 to 12 weeks. In the chronic phase a subset of patients complain of malaise, nausea, abdominal pain and itching. With time, chronic hepatitis C may develop into liver cirrhosis. The basic diagnostic methods in HCV infection involve determination of anti-HCV antibodies using the ELISA immunoassay and examination of HCV-RNA with the RT-PCR method. The current treatment of HCV infection involves administration of pegylated interferon a and ribavirin over a period of 48 weeks in HCV-1 genotype infection, and 24 weeks for HCV-2 and 3 genotypes. Effectiveness of therapy depends on the HCV genotype. HCV elimination can be achieved in 78% of patients with HCV-2 and 3 genotypes, and in 55% of patients with HCV-1 genotype.
Pol Arch Med Wewn 2008 Dec
PMID:Viral hepatitis C. 1920 52

Hepatitis C virus (HCV) causes chronic infection in humans leading to liver cirrhosis and hepatocellular carcinoma. rRNA transcription, catalyzed by RNA polymerase I (Pol I), plays a critical role in ribosome biogenesis, and changes in Pol I transcription rate are associated with profound alterations in the growth rate of the cell. Because rRNA synthesis is intimately linked to cell growth and frequently up-regulated in many cancers, we hypothesized that HCV might have the ability to activate rRNA synthesis in infected cells. We show here that rRNA promoter-mediated transcription is significantly (10- to 12-fold) activated in human liver-derived cells following infection with type 2 JFH-1 HCV or transfection with the subgenomic type 1 HCV replicon. Further analysis revealed that HCV nonstructural protein 5A (NS5A) was responsible for activation of rRNA transcription. Both the NH(2)-terminal amphipathic helix and the polyproline motifs of NS5A seem to be essential for rRNA transcription activation. The NS5A-dependent activation of rRNA transcription seems to be due to hyperphosphorylation and consequent activation of upstream binding factor (UBF), a Pol I DNA binding transcription factor. We further show that hyperphosphorylation of UBF occurs as a result of up-regulation of both cyclin D1 and cyclin-dependent kinase 4 by the HCV NS5A polypeptide. These results suggest that the endoplasmic reticulum-associated NS5A is able to transduce signals into the nucleoplasm via UBF hyperphosphorylation leading to rRNA transcription activation. These results could, at least in part, explain a mechanism by which HCV contributes to transformation of liver cells.
 ...
PMID:Activation of ribosomal RNA transcription by hepatitis C virus involves upstream binding factor phosphorylation via induction of cyclin D1. 1922 38

A case of a 54-year-old female with hepatic cirrhosis, who developed a large thrombus in the inferior vena cava that extended up to the right atrium and was associated with a portal vein thrombosis. She was admitted to our hospital because of symptoms of overt heart failure. A two-dimensional echocardiogram demonstrated a large mass in the right atrium originated from the inferior vena cava system. Computed tomography scans revealed tumor of the liver and a portal vein thrombosis. The patient was discharged on oral anticoagulation. Her remaining 1-year course has been uncomplicated.
Kardiol Pol 2009 Apr
PMID:[A large thrombus in the right atrium and in the inferior vena cava associated with a portal vein thrombosis in a patient with hepatic cirrhosis - a case report]. 1949 55

Technology development in data processing in ultrasonography let new imaging method feasible. New method of imaging is elastography (elastosonography, ultrasonographic elastography). It relays on the presumption that pathologically changed tissues have different elasticity and change their shape in different way than health tissue. Elastography is used in lesions in alimentary tract diagnostics. Sensitivity and specificity in malignant lesions differentiation is 85% and 90%. In elastography there is used conventional ultrasonography device that is equipped with additional transformator that is located in probe. Examination is performed with multiple pressing the organ. Imaging is acquired in real-time regime they are colour-coded and they are created during compression. As a result of computer analysis images are generated in two colours. On the basis of character of normal and increased rigidity images were classified in five point scale from one to five. Indication to elastography is suspicion of malignant lesions in traditional ultrasonography and monitoring of liver cirrhosis and fibrosis. More trials are required to evaluate this method more reliably. Then it could be recommended for everyday clinical use.
Pol Merkur Lekarski 2009 May
PMID:[Ultrasonographic elastography in alimentary tract lesions diagnostics]. 1960 19

Cirrhosis leads to an inability of the liver to perform its biochemical functions. It can also lead to hepatocellular carcinoma in which, as we showed lately, arginase isoenzyme pattern changes. The present work presents our results on arginase isoenzymes and their possible role in liver cirrhosis. The study was performed on tissues obtained during liver transplantation from 60 patients with liver cirrhosis, and on samples of histologically normal liver (control) from 40 patients with benign or colorectal cancer liver metastases removed during surgery, 6-7 cm from the tumor border. Arginase isoenzymes AI (so-called liver-type arginase) and AII (called extrahepatic arginase) were identified by Western blotting and isolated by ion-exchange chromatography. Their expression on mRNA level was studied by RT-PCR. A significant decrease in arginase activity, dependent of the liver clinical stage, was observed in cirrhotic tissue. Arginase AI activity and its mRNA level were significantly decreased in cirrhotic liver, whereas the activity and expression of arginase AII were concurrently raised, as compared to normal liver. Since arginase AI is a key enzyme of the urea cycle, whereas arginase AII most probably takes part in the biosynthesis of ornithine and polyamines, the defective ammonia inactivation and increased collagen biosynthesis observed in cirrhotic liver may be related to the changes in arginase AI and AII levels, respectively.
Acta Biochim Pol 2009
PMID:Arginase isoenzymes in human cirrhotic liver. 1963 40

Nonenzymatic modification of proteins by reducing sugars, a process that is also known as the Maillard reaction, leads to the formation of advanced glycation end products (advanced glycation end-products--AGEs) in vivo. There is a growing body of evidence that formation and accumulation of AGEs progress during normal aging, and at an extremely accelerated rate under diabetes, and are thus involved in the pathogenesis of various diseases such as diabetic vascular complications, neurodegenerative diseases, renal failure, and liver cirrhosis. Therefore, inhibition of AGEs formation may be a promising target for therapeutic intervention in AGEs-related disorders. There is a growing body of evidence that AGEs and their receptor (receptor for advanced glycation endproducts--RAGE) axis are also implicated in the pathogenesis of various diseases. In the former part of this paper, we discuss several types of AGEs inhibitors and their therapeutic implications in diseases. Then we summarize in the latter part of this review recent findings regarding pathophysiological roles in diseases of RAGE and soluble RAGE and discuss their potential usefulness as therapeutic targets.
Pol Merkur Lekarski 2009 Aug
PMID:[Therapeutic intervention in diseases with advanced glycation end products in their pathogenesis]. 1985 85

Serum concentrations of advanced oxidation protein products (AOPPs) and glycation end products (AGEs) were assessed with respect to functional compromise of liver, as determined by the Child-Pugh and MELD scores. Patients with decompensated liver cirrhosis (Child-Pugh B and C) exhibited significantly higher serum concentrations of AOPPs than both patients with compensated liver cirrhosis (Child-Pugh A) and controls. The levels of plasma AGEs in all liver cirrhotic patients were higher when compared with those with the controls and this difference was statistically significant. Plasma total antioxidant status of the patients was significantly lower than that of controls. Significant positive correlations between AOPPs level and the MELD score and between the oxidative stress index and the MELD score were found in all patients with liver cirrhosis. Altered AOPPs levels in decompensated patients may influence the potency of oxidative stress and the progression of liver disease.
Acta Biochim Pol 2009
PMID:Elevated advanced oxidation protein products levels in patients with liver cirrhosis. 1999 55

Liver pathologies have negative influence on numerous organs including pulmonary system. Liver failure, which often results from cirrhosis, may lead to the hepatopulmonary syndrome and portopulmonary hypertension. The hepatopulmonary syndrome is characterized by increased alveolar-capillary oxygen gradient, presence of intrapulmonary leak and diminished retention of the carbon dioxide from arterial blood. Two types of the hepatopulmonary syndrome are distinguished: the type 1 connected with pre-capillary and capillaries extension, what shortens the time of the blood flow by the pulmonary vessels. The type 2 hepatopulmonary syndrome results from the formation of arteriovenous anastomoses and anatomical "shunt" connections. Most patients with hepatopulmonary syndrome demonstrate both types. Patients with liver failure may develop portopulmonary hypertension, independently from hepatopulmonary syndrome. If not treated, hypertension might lead to the death of 50 to 90% patients in the 5-year follow up. The patients with the serious damage of the liver have hiperdynamic circulation with the increased heart capacity and lowered systemic vascular resistance. The hepatopulmonary syndrome is characterized by the growth of the pulmonary artery pressure and the presence of portal hypertension. The mechanism how the portal hypertension leads to the pulmonary hypertension is not clear.
Pol Merkur Lekarski 2010 Apr
PMID:[Respiratory functional impairment in patients with liver cirrhosis]. 2049 46


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