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

Proteoglycans are macromolecules containing a core protein to which glycosaminoglycan chains are covalently attached. The family contains several members with different structures and various functions. Some of them are elements of the extracellular matrix, while others are located to the cell surface playing important role in cell-cell and cell-extracellular matrix interactions. Present paper discusses the possible consequences of the alterations of proteoglycans observed in liver cirrhosis and liver tumors. It has to be emphasized however, that they are also involved in the pathomechanism of arteriosclerosis, Alzheimer-disease, immune diseases, arthritis, tumor progression and metastasis formation.
 ...
PMID:[Proteoglycans (their structure, function and role in liver diseases)]. 841 46

In the present review piece, we analyze the formation of free radicals as a consequence of the cellular metabolism in aerobe organism, and the beneficious and harmful actions thereof on cellular structures. The balance existing between free radicals and the so-called antioxidant defenses, is a key factor for preventing the development of noxious processes at the cellular and tissue level. In accordance with the present scientific knowledge, the excessive production of free radicals in the organism, and the imbalance between the concentrations of these and the antioxidant defenses, may be related to processes such as aging and several diseases, among which we find cancer, ischemic processes, senile dementia, diabetes, pulmonary and pancreatic diseases, lupus erythematosus, cirrhosis, intestinal inflammatory disease, multiple sclerosis, arthritis, arteriosclerosis, cardiovascular disease, diseases of the central nervous system and the brain. According to the results of numerous research works conducted with the administration of several molecules with an antioxidant activity, one is beginning to see what their role will be in the pharmacological therapeutics for the treatment of a large number of patients such as those with burns, traumas, septics, shock, surgery, transplantation, radiation or chemotherapy, respiratory distress syndrome, AIDS, etc. We may possibly be facing a therapeutic tool which is of great interest in the clinical area, which shall be developed in the near future, as clinical trials which permit confirmation of their efficacy are conducted.
 ...
PMID:[Antioxidants: the therapy of the future?]. 961 71

Hepatocyte growth factor (HGF) was purified as a potent mitogen for rat hepatocytes in primary culture and is believed to be the most physiological hepatotrophic factor that triggers liver regeneration. HGF is one of the largest disulfide-linked cytokines, consisting of a 60-kDa heavy chain and a 35-kDa light chain. Human HGF is synthesized as a single polypeptide chain precursor of 728 amino acid residues that has an appreciable homology with plasminogen, and it is processed proteolytically to release an N-terminal signal peptide of 31 amino acids and to generate an active heterodimer after secretion. The novel serine protease HGF activator and urokinase-type plasminogen activator (u-PA) are responsible for the latter extracellular processing. HGF stimulates the proliferation of rat hepatocytes in primary culture at concentrations as low as 10 pM. It also stimulates the growth of various epithelial cells, endothelial cells, and some kinds of mesenchymal cells. HGF inhibits the proliferation of several tumor cell lines and induces apoptosis of some of them. It also has motogenic, morphogenic, anti-apoptotic, angiogenic, and immunoregulatory activities. The receptor of HGF is the product of c-met proto-oncogene with tyrosine kinase activity that mediates the transduction of multiple biological signals of HGF. During liver regeneration, HGF gene expression in the liver, spleen, and lung and HGF levels in the blood and liver increase prior to the induction of liver DNA synthesis. Liver regeneration is markedly inhibited by continuous administration of a neutralizing anti-HGF antibody. HGF production in cultured cells is induced by PKC-activating agents, cAMP-elevating agents, PKA-activating agents, growth factors, and inflammatory cytokines; and it is inhibited by TGF-beta, glucocorticoids, 1,25-dihydroxyvitamin D3, and retinoic acid. There are many reports on potential application of HGF as a therapeutic agent for organ diseases that are difficult to cure such as liver cirrhosis, chronic renal failure, pulmonary fibrosis, myocardial infarction, and arteriosclerosis obliterans utilizing its potent growth-stimulating activity for a wide variety of cells. ELISA kits for assays of serum and plasma HGF levels are clinically used to prognosticate the development of fulminant hepatic failure.
 ...
PMID:[Function and regulation of production of hepatocyte growth factor (HGF)]. 1206 Nov 40

The aim of this analysis was to observe the pathologic changes in the kidney in 23 children dying of cirrhosis, including five children with renal failure. Besides these pathologic changes, glomerular cellularity and arteriolar wall thickness of these patients were compared with 18 age matched autopsy controls dying of nonhepatic and nonrenal causes. Histologic examination of the kidneys in these cirrhotic children showed significant tubular changes in five patients, diffuse glomerulosclerosis in five, only one child had membranous glomerulopathy or glomerulonephritis and one cirrhotic with serum hepatitis B surface antigen positivity had polyarteritis nodosa. No statistically significant changes were observed in the glomerular cellularity and the arteriolar wall thickness in these cirrhotic children as compared to the controls. However, medial proliferation and hyaline arteriolosclerosis were observed in four cirrhotic children. Tubular bile casts and nephrocalcinosis were the sole lesions causing renal failure in two cases. A combination of glomerulosclerosis, cast formation and arteriolosclerosis was seen in the remaining three patients. Thus the kidney showed a spectrum of pathology in pediatric cirrhosis. The tubular lesions causing renal failure represent acute treatable lesions whereas glomerulosclerosis and arteriosclerosis stand for a more chronic and less reversible renal damage.
 ...
PMID:The renal pathology in children dying with hepatic cirrhosis. 1259 62

Event-related P300 potentials that closely reflect cognitive brain functions show significant age-related latency prolongations. This aging-P300 interaction can best be approximated by third-order polynomial regressions. To delineate the clinical impact this special kind of regression function may have on detecting early cognitive dysfunction, we applied visual P300 potential data of healthy subjects (n = 344; age range, 18-98 years) to nondemented patients with either (i) chronic liver disease (n = 104; age range, 19-74 years) or (ii) cerebral arteriosclerosis (n = 80; age range, 38-80 years). As compared with linear regressions, third-order polynomial regressions for the age-related changes in P300 potential latencies showed a smaller latency increase during middle age, with an accelerating latency prolongation from age 60 onward. In patients with liver cirrhosis, third-order polynomial regressions yielded a rate of abnormal P300 potential latencies exceeding that of linear regressions absolutely by 17-21%, and relatively by 67-71%. Although the rate of P300 abnormalities was much lower in the CAD patients with either regression model, the relative increase in P300 abnormalities due to third-order polynomial regressions was 40-112.5%. In conclusion, normal data for the latencies of P300 potentials based on third-order polynomial regressions result in a higher sensitivity of P300 potentials for detecting early cognitive dysfunction. This gain in diagnostically important information is not offset by a loss in specificity, and may depend on the kind as well as stage of the disease, the age distribution of the patients and the degree of the P300 potential abnormalities.
 ...
PMID:The impact of age-related changes in event-related P300 potentials on detecting early cognitive dysfunction. 1537 98

Anastomotic stricture of the hepatic vein is an annoying complication, especially in living donor liver transplantation. Balloon dilation has been utilized but is sometimes associated with recurrences. Recently, a cutting balloon was invented for treatment of arteriosclerosis. Herein we report the results of application of this device for treatment of anastomotic strictures of the hepatic vein in two living donor liver transplant recipients who underwent percutaneous dilation of the hepatic vein with a cutting balloon (8 x 10 mm, Atherotome, Boston Scientific). Case 1, a 26-year-old woman transplanted for subacute fulminant hepatitis, had been treated for an anastomotic stricture by balloon dilation on 15 occasions over a 2- to 3-month interval. Case 2, a 13-year-old boy transplanted for cryptogenic liver cirrhosis, had been treated for an anastomotic stricture by balloon dilation biannually. The cutting balloon was applied safely without severe complications. The first case showed a recurrent anastomotic stricture at 6 months after dilation. Follow-up at 6 months in the second case revealed a mild recurrence of the stricture. Anastomotic stricture of the hepatic vein jeopardizes the graft and the recipient. The reported treatments involve venoplastic surgery and expandable metallic stents. Application of a cutting balloon seemed to be a safe, convenient modality. However, its effect was not indefinite, so a cutting balloon of greater diameter or application of an expandable metallic stent may be considered for patients with multiple recurrences of their anastomotic stricture.
 ...
PMID:Efficacy of cutting balloon for anastomotic stricture of the hepatic vein. 1568 3

The most frequent etiology of visceral artery aneurysms is arteriosclerosis, but vascular manipulation during hepatic transplantation may also cause a mycotic pseudoaneurysm. Treatment with embolization, stents or percutaneous thrombin injection have been recommended but surgical revascularization is indicated when interventional techniques fail. A 43-year-old man with hepatitis C virus cirrhosis who underwent orthotopic liver transplantation from a cadaveric donor was treated with cyclosporine, mycophenolate, and steroids and was discharged from hospital at 35 days. Two months later he was readmitted with a febrile syndrome. Abdominal computed tomography showed necrosis of hepatic segments IV, V, and VI. Magnetic resonance imaging and angiography revealed partial thrombosis of the hepatic artery and stenosis of the portal anastomosis secondary to an aneurysm of the hepatic artery. A few hours after the radiological diagnosis, the patient suffered a bout of upper gastrointestinal bleeding and shock. Emergency surgery revealed a mycotic pseudoaneurysm of the common hepatic artery, which had ruptured into the bile tract with hemobilia. The liver graft was removed because of severe necrosis of the right liver. The patient died awaiting a new liver transplantation.
 ...
PMID:Mycotic pseudoaneurysms after liver transplantation. 1586 59

Clinical, radiographic, and pathological features of 18 patients with biliary necrosis in their explanted liver allografts were reviewed. Twelve patients were men and ages ranged from 27 to 72 years. Indications for initial liver transplant (LT) were viral hepatitis (n = 7), steatohepatitic cirrhosis (n = 3), cryptogenic cirrhosis (n = 3), secondary sclerosing cholangitis (n = 2), primary sclerosing cholangitis (n = 1), biliary atresia (n = 1), and nodular regenerative hyperplasia (n = 1). Donor age ranged from 16 to 75 years. Duct-to-duct biliary anastomoses were fashioned in 13 cases; warm and cold ischemia times were not significantly different from general LT population. Seventeen allograft biopsies after recirculation had no significant findings. Post-LT, clinical and radiographic evaluation indicated biliary strictures (n = 7), bile leak (n = 7), intrahepatic abscess (n = 1), and duodenal perforation (n = 1). Radiographic vascular studies suggested hepatic arterial thrombosis or stenosis in 11 cases. Biopsies prior to retransplantation were performed on 17 patients and showed acute rejection (n = 10), biliary outflow impairment (n = 4), normal histology (n = 2), and centrilobular necrosis (n = 1). Retransplantation was performed 14 to 334 days after initial LT. Pathological examination of explants revealed perihilar duct necrosis in all cases, with bacterial colonies (n = 10) and fungal organisms (n = 2). Arterial thrombi were seen in 10 cases, and two had prominent arteriosclerosis. Infarction and centrilobular necrosis were seen in 9 and 13 cases, respectively. Four explants showed features of biliary outflow impairment. Twelve patients were alive 6 to 18 months following retransplantation. We conclude that post-LT biliary necrosis is associated with ischemia, and such a complication is rarely evident in allograft biopsies. Biliary and vascular imaging studies are essential in evaluating patients for this complication.
 ...
PMID:Clinicopathological review of 18 cases of liver allografts lost due to bile duct necrosis. 1596 83

Non Alcoholic Fatty Liver Disease (NAFLD), with prevalence of 10-51% in general population involving all ages, is the major cause of elevation of ALT and a common finding by ultrasound screening and may range from simple steatosis, to Non Alcoholic Steatohepatitis (NASH) and its clinical consequences as cirrhosis and hepatocellular carcinoma. In this review will be analyse factors influencing the onset of the disease. NAFLD, primarly associated with insulin resistance, is in fact considered the hepatic manifestation of the metabolic syndrome: a cluster of disorder that includes obesity, diabetes mellitus, dyslipidaemia, arteriosclerosis and hypertension. The increased incidence and prevalence of obesity and diabetes may explain growing interest in NAFLD. Racial, ethnic, enviromental and behaviour models are also reviewed.
 ...
PMID:Nonalcoholic fatty liver disease: defining a common problem. 1623 86

Primary sclerosing cholangitis (PSC) is a chronic inflammatory disease of unknown aetiology affecting the large bile ducts and characterized by periductal fibrosis and stricture formation, which ultimately result in biliary cirrhosis and liver failure. Arteriosclerosis involves the accumulation of altered lipids and lipoproteins in large arteries; this drives inflammation and fibrosis and ultimately leads to narrowing of the arteries and hypoperfusion of dependent organs and tissues. Knowledge of the causative factors is crucial to the understanding of disease mechanisms and the development of specific treatment. Based on pathogenetic similarities between PSC and arteriosclerosis, we hypothesize that PSC represents "arteriosclerosis of the bile duct" initiated by toxic biliary lipids. This hypothesis is based on common molecular, cellular, and morphological features providing the conceptual framework for a deeper understanding of their pathogenesis. This hypothesis should stimulate translational research to facilitate the search for novel treatment strategies for both diseases.
 ...
PMID:Primary sclerosing cholangitis--the arteriosclerosis of the bile duct? 1725 34


<< Previous 1 2 3 4 Next >>