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)

A 60-year-old male with liver cirrhosis (Child-Pugh class B) underwent laparotomic radio frequency ablation for the treatment of a solitary hepatocellular carcinoma (-4.5 cm in diameter). Severe lactic acidosis (base excess < -12 mEq.l-1, lactate > 150 mg.dl-1) developed during the intraoperative period, when neither his hemodynamics nor arterial oxygenation was significantly impaired. The blood loss was small (-200 g), and the serum hemoglobin level was maintained -10 g.dl-1 during the procedure. There was no evidence for impairment of either peripheral perfusion or renal function. In addition, there was no evidence for development of either splanchnic ischemia or diabetic ketoacidosis. Thus, the acidosis appeared to be caused by significant impairment of liver function possibly resulting from the ablation (total ablation time = -60 min). The core temperature increased rapidly (-1.5 degrees C/60 hr) immediately after the ablation was started, suggesting that a large amount of heat was produced in the ablated area and/or that the vicinity of the ablated area was richly supplied by blood flow. As a result, intact liver cells in the vicinity of the tumor probably suffered from thermal injuries. In conclusion, depending on preoperative liver function, ablated area, and/or blood flow in the vicinity of ablated area, the ablation may become significantly invasive.
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PMID:[Development of severe lactic acidosis during radio frequency ablation conducted for the treatment of hepatocellular carcinomata in a patient with liver cirrhosis]. 1248 57

Phlebosclerosis of the mesenteric vein is a rare condition causing chronic intestinal ischemia, it has only been reported in Japan. A 56-year-old man with liver cirrhosis and hepatic tumor presented with phlebosclerosis of mesenteric vein without any abdominal symptoms. He was admitted for examination of suspected hepatic tumor. Abdominal plain x-ray films and computed tomography revealed calcification of the mesenteric vein. Barium enema revealed narrowing and thumbprinting from the cecum to transverse colon. On colonoscopic examination, blue-black vessels were visible in the terminal ileum, and hyperemic nodular mucosa with small irregular ulcers surrounded by dark purple mucosa was found from the cecum to transverse colon. The etiology of mesenteric vein phlebosclerosis is unknown, although a physical mechanism rather than inflammatory changes appear to be involved in this rare and usually progressive condition of chronic intestinal ischemia.
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PMID:Asymptomatic chronic intestinal ischemia caused by idiopathic phlebosclerosis of mesenteric vein. 1249 90

Severe congestive heart failure is associated with two distinct forms of liver dysfunction: jaundice that is related to passive congestion and acute hepatocellular necrosis that is caused by impaired perfusion. Cardiac cirrhosis (fibrosis) may result from prolonged recurrent congestive heart failure. Ischemic hepatitis (shock liver) usually manifests as asymptomatic elevation of the serum aminotransferase levels after an episode of hypotension, although the clinical presentation may mimic that of acute viral hepatitis. In most cases, ischemic hepatitis is of little clinical consequence and is self-limited. Acute liver failure may occur in patients with preexisting cirrhosis, severe chronic heart failure, or sustained hepatic ischemia.
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PMID:The liver in heart failure. 1251 1

The present paper summarizes the various themes of research which have been developed in the department of medical gastroenterology since it was created in 1977. These include: in pancreatology, the study of chronic pancreatitis pathogenesis, acute pancreatitis pathogenesis and immunomodulation, endoscopic treatment of chronic pancreatitis, the development of new imaging techniques of the bile ducts and the pancreas, as well as the treatment of pancreatic cancer and benign or malignant biliary diseases. in hepatology, the immunomodulation of liver cirrhosis, especially alcoholic liver disease, the modulation of experimental acute and chronic hepatitis, the study of liver ischemia-reperfusion. Clinical hepatology has focused on liver transplantation, prognosis factors of chronic liver disease and treatment of portal hypertension and viral hepatitis. in gut diseases, the treatment of gastro-oesophageal reflux and its complications, the therapeutic endoscopy of the upper and lower GI and the prevention, as well as the treatment, of colon cancer, the pathogenesis and the immunopharmacology of inflammatory bowel diseases and the clinical enteral and parenteral nutrition.
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PMID:[The medical gastroenterology department]. 1258 14

The offer of liver transplantation to many patients affected by liver failure is limited by organ shortage. Clinical application of human-based liver cell therapies, such as bioartificial liver and hepatocyte transplantation, might support liver transplantation, allowing more patients to be treated and decreasing mortality in the waiting list. The development of a standardized method of hepatocyte isolation is a mainstay for large-scale application of liver cell therapy. The aim of this study is to analyze retrospectively a 2-year experience of human hepatocyte isolation from livers rejected from transplantation at organ harvesting, performed on a national basis in Italy. All the livers judged unsuitable for transplantation were considered for hepatocyte isolation. Macrosteatosis greater than 60% was the most common reason of refusal, followed by nonviral cirrhosis. Fifty-four organs were used. Human hepatocyte isolation resulted in more that 7 million liver cells/g of tissue digested with 73% +/- 14% viability. Steatotic organs gave better results in terms of cell yield than cirrhotic livers. Isolated hepatocytes were able to perform specific liver functions, and evidence of factor IX and albumin messenger RNA (mRNA) production was reported when cells were plated in culture. Modifications of the traditional method of hepatocyte isolation, aimed at reducing ischemia-reperfusion damage and improving post-isolation cell conditions, showed improvements in post-isolation viability. In conclusion, we show that it is possible to use the vast majority of livers not suitable for transplantation on a national basis for human hepatocyte isolation, obtaining a large amount of viable functioning human hepatocytes that might be used for cell transplantation and therapy.
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PMID:Isolation of human hepatocytes from livers rejected for liver transplantation on a national basis: results of a 2-year experience. 1274 Jul 95

Advanced donor age has been considered a risk factor for the use of organs for transplantation. We report the case of an orthotopic liver transplant performed using a 93-year-old donor. The donor had been admitted to the intensive care unit 3 days before due to cerebral hemorrhage. History, viral serology, liver function tests and hemodynamics were normal. At laparotomy, the liver appeared macroscopically normal; histology showed mild parenchymal congestion and focal signs of steatosis (less than 10%). The liver was therefore procured and transplanted into a 52-year-old recipient with alcoholic, post-hepatitis C. cirrhosis. Cold and warm ischemia times were 8 hours 20 min and 67 min, respectively. Production of bile was observed after reperfusion. Six months post-transplantation there is clinical and histological evidence of hepatitis C virus recurrence. Nevertheless, the patient enjoys an acceptable quality of life. Even very old donor livers can be used for transplantation, although it is still debatable whether hepatitis C virus-positive patients are good recipients of such livers.
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PMID:Transplantation of a ninety-three-year-old donor liver. Case report. 1274 59

Primary sclerosing cholangitis (PSC) is an idiopathic inflammatory disorder of the biliary tract characterized by diffuse biliary tract stricture formation, progressive chronic cholestasis and the development of secondary biliary cirrhosis. Biliary tract ischemia can produce morphological changes identical to PSC. We propose the existence of a localized renin-angiotensin system within the liver and extend the hypothesis that aberrant production of angiotensin II within the portal tract is the critical event contributing to the pathogenesis of PSC. A chronic reparative and proliferative state caused by chronic ischemia may promote carcinogenesis. Proof of this hypothesis will have implications for future therapeutic approaches given that current treatments for PSC aimed at reducing inflammation or the effects of cholestasis have proven ineffective.
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PMID:Aberrant local renin-angiotensin II responses in the pathogenesis of primary sclerosing cholangitis. 1278 43

The cytoprotective effect of prostaglandin E(1) (PGE(1)) has been demonstrated experimentally and clinically against hepatic ischemia and reperfusion injury and against the effects of partial hepatectomy in both individual and combined models of noncirrhotic livers. Cirrhotic livers are more vulnerable to ischemia/reperfusion injury during hepatectomy than are noncirrhotic livers, and postoperative malfunctioning complicates life with multiple organ failure. Cirrhotic livers with tumors have mostly been treated conservatively because extended hepatectomy with induced ischemia during surgery is impossible. The purpose of our study was to document postoperative surgical adaptation in inoperable cases with improved survival after extended hepatectomy in a rat model of cirrhosis treated by PGE(1). Cirrhosis was induced by intraperitoneal injections of 1% dimethylnitrosamine. The liver was subjected to 15 minutes of total ischemia by occluding the hepatoduodenal ligament. Hepatectomy was performed during ischemia. Pretreatment with PGE(1) (0.4 microg/kg/min) (or without it in the controls) was given for 15 minutes by intravenous infusion prior to inducing ischemia and during reperfusion. Portal venous flow (PVF) and liver tissue blood flow (LTBF) were measured during reperfusion. At the end of 60 minutes of reperfusion, venous blood was collected for liver function tests. The animals were followed up regarding survival for 48 hours. The PVF and LTBF were significantly improved in the PGE(1) group. The blood chemical analysis indicated that PGE(1) significantly suppressed posthepatectomy liver dysfunction. Most importantly, PGE(1) treatment markedly improved the survival rate, from 42% in the controls to 75% in the test animals at 24 hours after hepatectomy and from 17% in the controls to 58% in the test animals at 48 hours. We concluded that short-term administration of PGE(1) makes extensive hepatectomy possible under ischemic conditions in cirrhotic livers.
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PMID:Effect of short-term administration of prostaglandin E1 on viability after ischemia/reperfusion injury with extended hepatectomy in cirrhotic rat liver. 1292 1

Biliary stricture and duodenal obstruction have been increasingly recognized as complications of chronic pancreatitis. The anatomical relationship of the distal common bile duct and the duodenum with the head of the pancreas is the main factor for their involvement in chronic pancreatitis. In hospitalized patients with pancreatitis, the incidence of biliary stricture and duodenal obstruction is reported to be about 6% and 1.2%, respectively. For patients requiring an operation for chronic pancreatitis the incidence increases to 35% for biliary stricture and 12% for duodenal obstruction. Fibrosis around the distal common bile duct can cause stenosis with obstruction of bile flow. Clinically, the presentation of these patients ranges from being asymptomatic with elevated alkaline phosphatase or bilirubin, or both, to being septic with cholangitis. Jaundice, cholangitis, hyperbilirubinemia, and persistent elevation of serum alkaline phosphatase occur more frequently in patients with pancreatitis with a biliary stricture. A twofold elevation of alkaline phosphatase is a marker of possible common duct stenosis in patients with chronic pancreatitis. The incidence of both biliary cirrhosis and cholangitis in these patients is about 10%. ERCP reveals a characteristic long, smoothly tapered stricture of the intrapancreatic common bile duct. In duodenal obstruction, the factors that convert self-limiting edema to chronic fibrosis and stricture formation are unknown, but ischemia superimposed on inflammation may be the major cause. These patients present with a prolonged history of nausea and vomiting. Barium studies typically show a long constricting lesion of the duodenum, and endoscopy reveals reactive inflammatory changes in a narrowed duodenum. Operation is indicated in patients with common bile duct strictures secondary to chronic pancreatitis when there is evidence of cholangitis, biliary cirrhosis, common duct stones, progression of stricture, elevation of alkaline phophatase and/or bilirubin for over a month, and an inability to rule out cancer. The operation of choice is either choledochoduodenostomy or choledochojejunostomy. A cholecystoenterostomy is less favored because of its higher failure rate (23%). Endoscopic stenting plays a role in patients who are unfit for surgery, but it is not recommended as definitive therapy. For duodenal obstruction, failure to resolve the obstruction with 1-2 weeks of conservative therapy is an indication for bypass. The operation of choice is a gastrojejunostomy. Not uncommonly, combined obstruction of the pancreatic duct, common bile duct, and duodenum will develop. Combined drainage procedures or resection are used to manage these problems.
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PMID:Management of biliary and duodenal complications of chronic pancreatitis. 1453 24

Fatty liver disease involves the accumulation of triglycerides in hepatocytes, necrosis of hepatocytes, inflammation, and often fibrosis with progression to cirrhosis. The two-hit model summarizes the important early metabolic events leading to hepatocellular necrosis in nonalcoholic steatohepatitis (NASH). In this article, we provide evidence of lipid release from hepatocytes in posttransplant fat necrosis and in NASH and quantify vascular obliteration in a series of biopsies with NASH. Obliteration of small hepatic veins (<30 microm) in small numbers is compensated by collateral flow. Obliteration of larger hepatic veins (>30 microm) is associated with fibrotic collapse lesions that are not easily resorbed. Based on these observations, we propose a new four-step model that includes the later events that lead to cirrhosis after necrosis has occurred. This model is applicable to nonalcoholic fatty liver disease (NAFLD), alcoholic disease, postjejunoileal bypass disease, and posttransplant fat necrosis. The first step is steatosis facilitated by insulin, and the second is necrosis induced by intracellular lipid toxicity or lipid peroxidation, or both, modified by alcohol, drugs, and ischemia. The third step is release of bulk lipid from hepatocytes into the interstitium leading to direct and inflammatory injury to hepatic veins. The fourth step is venous obstruction with secondary collapse and ultimately fibrous septation and cirrhosis.
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PMID:The pathogenesis of nonalcoholic steatohepatitis and other fatty liver diseases: a four-step model including the role of lipid release and hepatic venular obstruction in the progression to cirrhosis. 1508 90


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