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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In patients with cirrhosis and hepatocellular carcinoma (HCC), orthotopic liver transplantation (OLT) offers hope for cure of both the complicating HCC and the underlying chronic liver disease. Excellent 5 year survival has been reported when the restrictive Milan criteria are used to select transplant candidates. Alternative recommendations have recently been proposed by groups at University of California San Francisco, University of Pittsburgh and Mount Sinai. We review current and evolving concepts regarding selection criteria for OLT in patients with HCC, along with strategies to reduce waiting times, such as the impact of the implementation of the model for end-stage liver disease (MELD) scoring system on organ distribution and the role of living donor OLT for this indication. The possible efficacy of adjuvant anti-tumour therapies in limiting HCC growth while waiting for OLT, along with factors influencing the risk of HCC recurrence post-OLT, the major cause of death in this setting, are also discussed.
Best Pract Res Clin Gastroenterol 2005 Feb
PMID:Liver transplantation for hepatocellular carcinoma. 1575 10

This chapter will focus on studies within the last 5 years of nutrition in end stage liver disease, but earlier studies illustrating the present state of affairs will also be mentioned. The first part will focus on descriptive epidemiological studies that help to set the scene for the intervention studies, which will be described in the second part. Each part will discuss liver cirrhosis, acute liver failure and liver transplantation separately. The aim is to provide the reader with sufficient background for the decision in clinical practice about when to see nutrition support as an important part of treatment of the patient.
Best Pract Res Clin Gastroenterol 2006
PMID:Nutrition in end stage liver disease. 1678 28

Gallstone disease is common: >700,000 cholecystectomies and costs of approximately 6.5 billion dollars annually in the U.S. The burden of disease is epidemic in American Indians (60-70%); a corresponding decrease occurs in Hispanics of mixed Indian origin. Ten to fifteen per cent of white adults in developed countries harbour gallstones. Frequency is further reduced in Black Americans, East Asia and sub-Saharan Africa. In developed countries, cholesterol gallstones predominate; 15% are black pigment. East Asians develop brown pigment stones in bile ducts, associated with biliary infection or parasites, or in intrahepatic ducts (hepatolithiasis). Certain risk factors for gallstones are immutable: female gender, increasing age and ethnicity/family (genetic traits). Others are modifiable: obesity, the metabolic syndrome, rapid weight loss, certain diseases (cirrhosis, Crohn's disease) and gallbladder stasis (from spinal cord injury or drugs like somatostatin). The only established dietary risk is a high caloric intake. Protective factors include diets containing fibre, vegetable protein, nuts, calcium, vitamin C, coffee and alcohol, plus physical activity.
Best Pract Res Clin Gastroenterol 2006
PMID:Gallstone disease: Epidemiology of gallbladder stone disease. 1712 83

Hepatolithiasis (oriental cholangiohepatitis) has reportedly been endemic only in East Asia. The disease is now occasionally recognized in Western societies, especially in people who have lived in the Orient. Hepatolithiasis is characterized by its intractable nature and frequent recurrence, requiring multiple operative interventions, which is in distinct contrast to gallbladder stones. In addition to frequent cholangitis and chronic sepsis, it is widely known that longstanding intrahepatic stones lead to intrahepatic cholangiocarcinoma. Symptoms of hepatolithiasis include abdominal pain, jaundice and cholangitis. Pyogenic cholangitis due to strictures and hepatolithiasis tends to recur, and sometimes patients may present with liver abscesses. Radiological studies and percutaneous procedures are keys in the diagnosis and treatment of hepatolithiasis. Non-invasive imaging modalities such as ultrasonography (US), computed tomography (CT), and magnetic resonance imaging (MRI) accurately depict the normal anatomy and presence of intrahepatic stones. It should be stressed that each modality has its pros and cons, and imaging studies should be performed on the basis of understanding the pathophysiology. As the diagnostic role of magnetic resonance cholangiopancreatography (MRCP) evolves, the roles of both endoscopic retrograde cholangiopancreatography (ERCP) and percutaneous transhepatic cholangiography (PTC), and their most significant advantage, is primarily therapeutic with their ability to extract stones, biopsy intraductal lesions, and place stents easily. The primary goals of treatment are to eliminate attacks of cholangitis and to stop the progression of the disease (which leads to biliary cirrhosis). Surgery has a primary role in hepatolithiasis because hepatolithiasis tends to recur, so that multiple sessions of the endoscopic approach (i.e. two or three times a year) are often required. PTC is an alternative when surgical resection of the affected lobe is difficult. Techniques for lithotripsy, including shockwave and laser, can be applied in endoscopic sessions, offering a better chance of clearing the stones.
Best Pract Res Clin Gastroenterol 2006
PMID:Gallstone disease: Management of intrahepatic stones. 1712 92

Several methods have been studied in the attempt to reach a diagnosis of cirrhosis by non-invasive means. Although abdominal ultrasound can detect the hepatic and extra-hepatic changes consistent with cirrhosis, its ability to distinguish chronic hepatitis from compensated cirrhosis is limited. Serum markers can rule in or rule out fibrosis in up to 35% of patients but, in individual patients, cannot differentiate the stages of fibrosis reliably. Transient elastography (Fibroscan) might be of value for the non-invasive diagnosis of cirrhosis; however, its reproducibility needs to be further validated. Cirrhosis can be divided into 4 stages: stage 1, no varices, no ascites; stage 2, varices without ascites and without bleeding; stage 3, ascites+/-varices; stage 4, bleeding+/-ascites. Yearly mortality ranges from 1% in stage 1 to 57% in stage 4. The yearly incidence of oesophageal varices is 5-7%; their rate of enlargement is 10-12% per year. The incidence of variceal bleeding is about 25% at 2 years. Bleeding stops spontaneously in about 50% of cases but early rebleeding occurs in 30-40% of patients. Bleeding-related mortality has declined over time and is now around 20% at 6 weeks.
Best Pract Res Clin Gastroenterol 2007
PMID:Non-invasive diagnosis of cirrhosis and the natural history of its complications. 1722 93

Variceal bleeding is a serious complication in patients with cirrhosis. Although bleeding related mortality rates have fallen recently, it continues to be amongst the leading causes of death. Cirrhotics should be screened for varices at diagnosis. Data on preventing formation/growth of oesophageal varices (pre-primary prophylaxis) are conflicting, with insufficient evidence to use beta-blockers. In order to prevent first bleeding, there is strong evidence in patients with medium/large size oesophageal varices that either non-selective beta-blockers or banding ligation can be used. Banding is superior with respect to bleeding but mortality is similar. Non-selective beta-blockers should remain first line treatment being effective, cheap and without serious complications. In contrast banding ligation is more expensive, requires specialised staff, cannot prevent bleeding from portal hypertensive gastropathy and can cause iatrogenic bleeding. Patients with small varices, particularly if they have progressive liver disease also benefit from beta-blockers, but fewer studies confirm this therapeutic approach.
Best Pract Res Clin Gastroenterol 2007
PMID:Prevention of the development of varices and first portal hypertensive bleeding episode. 1722 95

The natural course of patients with cirrhosis is frequently complicated by the accumulation of fluid in the peritoneal or pleural cavities and interstitial tissue. Functional renal abnormalities that occur as a consequence of decreased effective arterial blood volume are responsible for fluid accumulation in the form of ascites and hepatic hydrothorax. Ascites is the most common complication of cirrhosis and poses an increased risk for infections, renal failure and mortality. Patients have a poor prognosis and it is estimated that nearly half will die in approximately 2 years without liver transplantation. Hepatic hydrothorax is defined as a pleural effusion greater than 500 mL (mostly right-sided) in patients with cirrhosis without cardiopulmonary disease; the estimated prevalence is approximately 5-10%. Liver transplantation is the most definitive cure for both conditions in those patients that are suitable candidates. However, the mainstay of therapy for minimizing fluid accumulation in both conditions includes sodium restriction and administration of diuretics. This article reviews the most current concepts of pathogenesis, clinical findings, diagnosis, and treatment of these complications of cirrhosis.
Best Pract Res Clin Gastroenterol 2007
PMID:Management of ascites and hepatic hydrothorax. 1722 97

Patients with cirrhosis have altered immune defenses and are considered immunocompromised individuals. Changes in gut motility, mucosal defense and microflora allow for translocation of enteric bacteria into mesenteric lymph nodes and the blood stream. Additionally, the cirrhotic liver is ineffective at clearing bacteria and associated endotoxins from the blood thus allowing for seeding of the sterile peritoneal fluid. Thus, hospitalised cirrhotic patients, particularly those with gastrointestinal hemorrhage, are at high risk of developing bacterial infections, the most common being spontaneous bacterial peritonitis. Given the significant morbidity and mortality associated with spontaneous bacterial peritonitis and the fact that half of the cases are community acquired, all hospitalised cirrhotic patients should have a diagnostic paracentesis to exclude infection. Those admitted with gastrointestinal bleed and a negative paracentesis require short-term prophylaxis with norfloxacin. A third generation cephalosporin is the treatment of choice for spontaneous bacterial peritonitis and, once the acute infection is resolved, secondary prophylaxis with oral norfloxacin is warranted. Patients who develop renal dysfunction at the time of active infection have the highest mortality and require adjunctive albumin therapy. This article reviews the pathogenesis of SBP, the evidence behind the antibiotics used, the rationale for adjunctive albumin therapy in the setting of acute renal failure, and the role of prophylactic antibiotics in specific high-risk populations.
Best Pract Res Clin Gastroenterol 2007
PMID:Prevention and treatment of infections in patients with cirrhosis. 1722 98

The term hepatic encephalopathy encompasses a spectrum of neuropsychiatric abnormalities seen in patients with liver dysfunction. Distinct syndromes are identified in acute liver failure and cirrhosis. Rapid deterioration in consciousness level and increased intracranial pressure that may result in brain herniation and death are a feature of acute liver failure whereas manifestations of hepatic encephalopathy in cirrhosis include psychomotor dysfunction, impaired memory, increased reaction time, sensory abnormalities, poor concentration and in severe forms, coma. In patients with acute-on-chronic liver failure the pathophysiology remains undefined. Ammonia has been considered central to its pathogenesis. In the brain, the astrocyte is the main site for ammonia detoxification, during the conversion of glutamate to glutamine. An increased ammonia level raises the amount of glutamine within astrocytes, causing an osmotic imbalance resulting in cell swelling and ultimately brain oedema. Recent studies suggest that inflammation and it modulators may play a synergistic role with ammonia in the pathogenesis of hepatic encephalopathy. Therapy of hepatic encephalopathy is directed primarily at reducing ammonia generation and increasing its detoxification. The currently accepted regimens to treat hepatic encephalopathy such as lactulose and protein restricted diets need further clinical trials and therefore placebo controlled clinical trials in hepatic encephalopathy are justified. In liver failure, ammonia metabolism involves multiple organs and therefore ammonia reduction will require simultaneous targeting of these organs. The present review describes the pathophysiological basis of hepatic encephalopathy and evaluates the available therapies.
Best Pract Res Clin Gastroenterol 2007
PMID:Management of hepatic encephalopathy in patients with cirrhosis. 1722 99

In patients with cirrhosis, acute renal failure is due to prerenal failure (a result of decreased renal perfusion) and tubular necrosis. There are 3 main causes of prerenal failure: 'true hypovolemia' (which complicates hemorrhage, gastrointestinal or renal fluid losses), sepsis, and type 1 hepatorenal syndrome (HRS). Prerenal failure may also be due to the administration of non-steroidal antiinflammatory drugs, or intravascular radiocontrast agents. Prerenal failure is reversible after restoration of renal blood flow. Treatments target the cause of hypoperfusion, and fluid replacement is used to treat 'non-HRS' prerenal failure. In patients with type 1 HRS with very low short-term survival rate, liver transplantation is the ideal treatment. Systemic vasoconstrictor therapy with terlipressin (combined with intravenous human albumin), noradrenaline (combined with albumin and furosemide) or midodrine (combined with octreotide and albumin) may improve renal function in patients with type 1 HRS waiting for liver transplantation. MARS (for Molecular Adsorbent Recirculating System) and the transjugular intrahepatic portosystemic shunt may also improve renal function in these patients. In patients with cirrhosis, acute tubular necrosis is mainly due to an ischemic insult to the renal tubules. Studies are needed on the natural course and treatment (e.g., renal-replacement therapy) of acute tubular necrosis in patients with cirrhosis.
Best Pract Res Clin Gastroenterol 2007
PMID:Diagnosis and treatment of acute renal failure in patients with cirrhosis. 1722


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