Sunday, October 16, 2011

Sunday Hepatitis News Ticker; ANA-598 Non-Nuke Phase 2b study preliminary data

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Anadys laid the foundation for the current Phase IIb clinical trial with prior clinical and preclinical work. In a Phase IIa combination trial in HCV patients, we reported data that showed that setrobuvir added to pegylated interferon and ribavirin accelerated the rate of viral clearance, with comparable response at setrobuvir doses of 200 mg bid and 400 mg bid. A single patient out of more than 60 exhibited viral breakthrough while receiving setrobuvir plus standard of care, corresponding to a low breakthrough rate of < 2%. Setrobuvir also showed an excellent safety profile in the study through the 12 weeks of dosing, with reported adverse events being typical for patients treated with interferon and ribavirin alone, although conclusions regarding safety cannot be made until results in more patients over longer duration are known.
See Full Data Here
Last updated at 6:22 PM on 16th October 2011
Up to 40 per cent of all cancers including brain tumors, cancer of the skin and prostate and leukaemia may be caused by viral infections, according to scientists. If proved, the information could lead to a preventative vaccine and therapies to cure many forms of the disease. While it was already known that some viruses can lead to cancers, the research study suggests that many more viruses are responsible for the condition.

Scientists had discovered hepatitis B and C viruses can cause liver cancer and human papilloma virus (HPV) which can cause cervical cancer. But the new research study using DNA analysis has shown that viruses could be implicated as the cause in 40 per cent of the 200 forms of cancer. German virologist Harold Zur Hausen, who jointly discovered the link between cervical cancer and HPV, said in the paper the discovery could be ground-breaking.
He said: 'Although we know that currently slightly more than 20 per cent of the global cancer incidence is linked to infectious events, some epidemiological observations suggest that this this percentage may increase'. He also said that virus could be involved in skin, breast, guts and lung cancer. An important result of the study was the discovery that an aggressive form of skin cancer, Merkel cell carcinoma, often follows infection by polyomavirus. The virus, which is common in birds and mammals may also be the cause of other types of skin cancer.

Researchers also found that anti-viral therapies slowed down the growth of brain tumours in animals by up to 70 per cent - suggesting evidence of viral involvement in the disease. The discovery is welcomed by sufferers of childhood brain tumours thought to be caused by medulloblastoma, Kerry Edwards was a gymnast tipped to have a promising career before being struck down with the disease. The operation to remove the tumor affected her balance and she still struggles to walk. She told the Sunday Times: 'Anything that can save people from what I have endured has to be a good thing.' It is unknown why viruses cause infection as in most cases they invade a cell before altering it to produce more viruses - ultimately killing it.

However in cancer-causing viruses, it is thought, yet unproven, that they remain hidden in the cells for years, before subverting their hosts so that they cannot repair mutations. Professor Luiz Gissmann a senior scientist at the German Cancer Research Centre told the newspaper: 'Over the years such mutations can build up to the point where cells turn cancerous.' The discovery could be life-changing with the possibilities of vaccinations against the key viruses, cutting the number of cancer sufferers - however the cost of development and trials will be enormous. In Britain 310,000 people are diagnosed with the disease every year, of which 156,000 will die
Alan Rickinson, professor of cancer studies in Birmingham is overseeing trials of a vaccine against the Epstein-Barr virus, identified as causing a rare blood cancer. He said: 'If we can understand how these viruses work we could prevent people from contracting them and even create therapies that use the patient's own immune system to destroy infected or cancerous cells.'

Zania Stamataki1,2*, Samantha Tilakaratne1, David H. Adams1,2, Jane A. McKeating1
1 Medical Research Council Centre for Immune Regulation, University of Birmingham, Birmingham, United Kingdom, 2 National Institute for Health Research Biomedical Research Unit and Centre for Liver Research, University of Birmingham, Birmingham, United Kingdom

Abstract Only Full Data Available Here
Hepatitis C virus (HCV) infected patients with vasculitis are often treated with the B-cell-depleting anti-CD20 antibody rituximab. Treatment reduces the cryoglobulins that cause vasculitis, yet it also leads to a transient increase in liver enzymes and HCV genomic RNA in the periphery. The mechanism underlying the increased viral load is unclear and both direct and indirect roles have been proposed for B cells in HCV infection. We previously reported that HCV can associate with B cells and can trans-infect hepatocytes. We established an in vitro assay to study the effect(s) of rituximab on B cell-associated HCV infectivity. Rituximab-mediated lysis of B cells in vitro increases the level of infectious HCV released from B cells. Our results, using a model where virus does not replicate in B cells, recapitulate observations seen in patients and may explain in part the rapid increase in blood HCV RNA observed after rituximab treatment.

Noëlla Arnaud1, Stéphanie Dabo1, Daisuke Akazawa2, Masayoshi Fukasawa3, Fumiko Shinkai-Ouchi3, Jacques Hugon4, Takaji Wakita2, Eliane F. Meurs1*
1 Institut Pasteur, Hepacivirus and Innate Immunity, Paris, France, 2 National Institute of Infectious Diseases, Department of Virology II, Tokyo, Japan, 3 National Institute of Infectious Diseases, Department of Biochemistry and Cell Biology, Tokyo, Japan, 4 Institut du Fer à Moulin, INSERM UMRS 839, Paris, France

Abstract Only Full Text Available Here
Recognition of viral RNA structures by the intracytosolic RNA helicase RIG-I triggers induction of innate immunity. Efficient induction requires RIG-I ubiquitination by the E3 ligase TRIM25, its interaction with the mitochondria-bound MAVS protein, recruitment of TRAF3, IRF3- and NF-κB-kinases and transcription of Interferon (IFN). In addition, IRF3 alone induces some of the Interferon-Stimulated Genes (ISGs), referred to as early ISGs. Infection of hepatocytes with Hepatitis C virus (HCV) results in poor production of IFN despite recognition of the viral RNA by RIG-I but can lead to induction of early ISGs. HCV was shown to inhibit IFN production by cleaving MAVS through its NS3/4A protease and by controlling cellular translation through activation of PKR, an eIF2α-kinase containing dsRNA-binding domains (DRBD). Here, we have identified a third mode of control of IFN induction by HCV. Using HCVcc and the Huh7.25.CD81 cells, we found that HCV controls RIG-I ubiquitination through the di-ubiquitine-like protein ISG15, one of the early ISGs. A transcriptome analysis performed on Huh7.25.CD81 cells silenced or not for PKR and infected with JFH1 revealed that HCV infection leads to induction of 49 PKR-dependent genes, including ISG15 and several early ISGs. Silencing experiments revealed that this novel PKR-dependent pathway involves MAVS, TRAF3 and IRF3 but not RIG-I, and that it does not induce IFN. Use of PKR inhibitors showed that this pathway requires the DRBD but not the kinase activity of PKR. We then demonstrated that PKR interacts with HCV RNA and MAVS prior to RIG-I. In conclusion, HCV recruits PKR early in infection as a sensor to trigger induction of several IRF3-dependent genes. Among those, ISG15 acts to negatively control the RIG-I/MAVS pathway, at the level of RIG-I ubiquitination.These data give novel insights in the machinery involved in the early events of innate immune response.

Thousands possibly exposed to infection at Ottawa clinicFull story: CTV
Letters will be sent to nearly 7,000 people after a three-month investigation into the possible exposure of HIV, Hepatitis B and Hepatitis C at a non-hospital Ottawa clinic.

By Genevra PittmanNEW YORK Fri Oct 14, 2011 4:24pm EDT
NEW YORK (Reuters Health) - People who have had a kidney stone seem to have a heightened risk of gallstones -- and vice versa, according to a new study.
Researchers already know that obesity, diabetes and having a generally unhealthy diet put people at risk for both types of stones. But even when those common risks were taken into account, the link remained.

The report "raises our antenna to this shared relationship between these two disorders," said Dr. Brian Matlaga, a urologist at the Johns Hopkins University School of Medicine in Baltimore."From an anecdotal standpoint, certainly it's not an uncommon scenario that a patient would have had both," Matlaga, who wasn't involved in the new research, told Reuters Health. But, he continued, "I'm a little bit at a loss trying to define what that relationship would be."That's because stones in the kidney and gallbladder form differently, he said, and are made of two different things -- kidney stones of calcium and gallstones of cholesterol, most of the time.Data for the current analysis came from three different long-term studies of nurses and doctors who completed a health and lifestyle questionnaire, then reported any new medical conditions every two years afterward. In total, more than 240,000 people were followed for between 14 and 24 years.
Over that time, there were about 5,100 new kidney stones diagnosed and close to 18,500 new cases of gallstones.

Depending on the population -- male or female, older or younger -- people with a history of gallstones were between 26 and 32 percent more likely to get a kidney stone than people who hadn't ever had gallstones.

And the link also went in the opposite direction. A past history of kidney stones meant study participants were between 17 and 51 percent more likely to report a new gallstone.That was after factoring in the impact of age, diabetes, high blood pressure, weight and certain aspects of diet on the risk of both kinds of stones.

Researchers led by Eric Taylor from the Maine Medical Center in Portland said it's possible that a shift in the type of bacteria in the intestines might somehow predispose people to both kidney stones and gallstones. But, Taylor said, "the fairest thing is that we just don't know" why the two would be linked.

In their report in the Journal of Urology the researchers echoed Matlaga's call for more detailed research into any explanations for a common cause -- which might help doctors prevent or treat both kidney stones and gallstones, they added.
"They are really two different kinds of stones, so the relationship is not going to be simple between the two conditions," Taylor told Reuters Health.Matlaga said that for now, there are steps people can take to reduce their risk of both gallstones and kidney stones, even if they've already had one condition."You'd like to try to minimize those common risk factors and work on things like weight loss and cholesterol control," he said.Taylor agreed that the findings "emphasize the importance of healthy diet and healthy weight."
SOURCE: Journal of Urology, online September 23, 2011.

Wash your hands before dinner; rinse your vegetables; keep the milk refrigerated–all important habits to keep yourself healthy. But what about the things you can’t control—and usually don’t even consider? What happens when the regulators you assume are inspecting your food aren’t doing their job?

The Food and Drug Administration (FDA) oversees much of the U.S. food system, but according to recent reports by the Government Accountability Office (GAO) and an investigation by News21, the FDA is failing to keep U.S. food safe.
The U.S. only inspects 2 percent of all imported food, according to News21. Of particular risk to Americans is imported seafood because 80 percent of seafood consumed in the U.S. is imported, according to a GAO study.

The tilapia at Whole Foods may look pristine in those giant beds of ice, and bouncing shrimp in fast food commercials might make your mouth water, but chances are they came from an overseas farm or facility far outside the eyes of the FDA.

Of the 13,459 foreign seafood facilities that export seafood to the U.S., only 128 were inspected by the FDA in 2010, according to a GAO report. And 2010 was the best year mentioned in the report. Only 503 facilities in total have been inspected since 2005.

The U.S. has stricter rules about what chemicals and antibiotics can be used to grow fish in factory farms than many other countries, specifically China and countries in Southeast Asia, which are the main seafood exporters to the U.S. The FDA doesn’t have the manpower to inspect all of the seafood imported to the U.S., and has been criticized by the GAO for not putting more emphasis on testing for these drugs.

Brett C. Hall, the deputy commissioner for the Alabama Department of Agriculture and Industries, told News21, “In Vietnam and other foreign countries, there are extreme limitations regarding a desirable water supply.” He added, “In order to grow fish in contaminated water, they would use antibiotics to keep the fish alive.”

Even if you are a proud buyer of good ol’ American seafood, that doesn’t mean you are out of the seaweed. The FDA is failing to address raw Gulf Coast oysters with a potentially deadly, according to the GAO.

The bacteria, Vibrio vulnificus (V. vulnificus), only causes 32 illnesses a year, but half of those people die from their illness. The V. vulnificus bacteria is “the most common cause of death from seafood consumption in the United States,” according to the GAO report.
The bacteria only come from raw oysters, and can be greatly reduced through a variety of post-harvest procedures. The problem is thatthe FDA and the Interstate Shellfish Sanitation Conference (ISSC), a voluntary organization of 22 state officials who promote shellfish safety policies, are at odds over the best way to keep consumers safe.
The GAO concluded that without FDA and ISSC collaboration, “it is unlikely that the states’ efforts to significantly reduce the number of consumption-related V. vulnificus illnesses will be effective.”

It’s just one example of the disconnect often found between federal and state officials when it comes to enforcing food safety rules.

But if you think the lack of inspections of imported food and the poor coordination between state and federal regulators was enough to worry about, there’s also the fact that our farmers are under growing pressure to increase profit margins, often at the expense of safety.
It’s enough to make you swear off seafood. But the better alternative might be to become a more educated consumer.

Check out the FDA’s tips on buying and preparing seafood and Food and Water Watch’s Smart Seafood Guide.

Ultimately, the News21 investigation found the solutions are far from simple:
Food safety advocates like Food & Water Watch say consumers are better off avoiding imported seafood altogether and sticking to locally raised fish or fish caught in the wild.
But Lorenzo Juarez of the National Oceanic and Atmospheric Administration’s Aquaculture Program said that’s not practical.

“There is no more fish from the wild,” he said, and a better approach would be to encourage more domestic aquaculture, which is subject to U.S. standards.
Corrigan’s Food & Water Watch says that’s not good enough.
“We need to find a way to protect people in the United States from seafood and that means more inspections on what’s coming in from our borders,” he said.
Andre Francisco is a POGO Communications Associate.
Cirrhosis is scarring of the liver.

Widespread nodules in the liver combined with fibrosis characterize cirrhosis anatomically. The fibrosis and nodule formation causes distortion of the normal liver architecture, which interferes with blood flow through the liver. Cirrhosis can also lead to an inability of the liver to perform its biochemical functions. To understand the pathophysiology of cirrhosis, the normal anatomy and physiology of the liver must first be briefly reviewed.

Liver Blood Flow
Oxygenated blood that has returned from the lungs to the left ventricle of the heart is pumped to all of the tissues of the body. This is called the systemic circulation.

After reaching the tissues, blood is returned to the right side of the heart, from where it is pumped to the lungs and then returned to the left side of the heart after taking up oxygen and giving off carbon dioxide. This is called the pulmonary circulation.

Systemic and Pulmonary Circulation

Portal Circulation
Blood from the large and small intestines and spleen flow to and through the liver before returning to the right side of the heart. This is called the portal circulation and the large vein through which blood is brought to the liver is called the portal vein. After passing through the liver, blood flows into the hepatic vein, which leads into the inferior vena cava to the right side of the heart. The liver also receives some blood directly from the heart via the hepatic artery. In the esophagus, stomach, small intestine and rectum, the portal circulation and veins of the systemic circulation are connected. Under normal conditions, there is little to no back flow from the portal circulation into the systemic circulation.

Bilirubin Secretion
The liver is the site of bile formation. Bile contains bile salts, fatty acids, cholesterol, bilirubin and other compounds. The components of bile are synthesized and modified in hepatocytes (the predominant cell type in the liver) and secreted into small bile ducts within the liver itself. These small bile ducts form a branching network of progressively larger ducts that ultimately become the common bile duct that takes bile to the small intestine. Bilirubin is a yellow pigment that derives primarily from old red blood cells. Bilirubin is taken up by hepatocytes from the blood, modified in the hepatocytes to a water-soluble form and secreted into the bile.

1. Bile ducts: 2. Intrahepatic bile ducts, 3. Left and right hepatic ducts, 4. Common hepatic duct, 5. Cystic duct, 6. Common bile duct, 7. Ampulla of Vater, 8. Major duodenal papilla
9. Gallbladder, 10-11. Right and left lobes of liver. 12. Spleen.
13. Esophagus. 14. Stomach.
Small intestine: 15. Duodenum, 16. Jejunum 17. Pancreas: 18: Accessory pancreatic duct, 19: Pancreatic duct. 20-21: Right and left kidneys (silhouette). The anterior border of the liver is lifted upwards (brown arrow). Gallbladder with Longitudinal section, pancreas and duodenum with frontal one. Intrahepatic ducts and stomach in transparency.

Biochemical Functions
The liver performs many biochemical functions-over 200 in all. Blood clotting factors are synthesized in the liver. Albumin, the major protein in the blood, is also synthesized in and secreted from the liver. The modification and/or synthesis of bile components also take place in the liver. Many of the body's metabolic functions occur primarily in the liver including the metabolism of cholesterol and the conversion of proteins and fats into glucose. The liver is also where most drugs and toxins, including alcohol, are metabolized.

What Goes Wrong in the Liver with Cirrhosis?
Cirrhosis results from damage to liver cells from toxins, inflammation, metabolic derangements and other causes. Damaged and dead liver cells are replaced by fibrous tissue, which leads to fibrosis (scarring). Liver cells regenerate in an abnormal pattern primarily forming nodules that are surrounded by fibrous tissue. Grossly abnormal liver architecture eventually ensues that can lead to decreased blood flow to and through the liver.

Decreased blood flow to the liver and blood back up in the portal vein and portal circulation leads to some of the serious complications of cirrhosis. Blood can back up in the spleen causing it to enlarge and sequester blood cells. Most often, the platelet count falls because of splenic sequestration. The low platelet count seen in cirrhosis is due to trapping in the spleen, not due to a primary problem with production in the bone marrow. If the pressure in the portal circulation increases because of cirrhosis and blood back up (note: this can also sometimes occur in severe cases of acute hepatitis and liver damage), blood can flow backwards from the portal circulation to the systemic circulation where they are connected. This can lead to varicose veins in the stomach and esophagus (gastric and esophageal varices) and rectum hemorrhoids or rectal varicies). Gastric and esophageal varices can rupture, bleed massively and even cause death. Hypertension in the portal circulation, along with other hormonal, metabolic and kidney abnormalities in cirrhosis, can also lead to fluid accumulation the abdomen (ascites) and the peripheral tissue (peripheral edema).

Decreased bilirubin secretion from hepatocytes in cirrhosis leads to the back up of bilirubin in the blood. This leads to jaundice, the yellow discoloration of the skin and eyes. As the water-soluble form of bilirubin also backs up in the blood, bilirubin can also spill into the urine giving it a bright yellow to dark brown color.

Abnormal biochemical function of the liver in cirrhosis can lead to several complications. The serum albumin concentration falls, which can lead to aggravation of ascites and edema. The metabolism of drugs can change requiring dose adjustments. In men, breast enlargement (gynecomastia) sometimes occurs because metabolism of estrogen in the liver is decreased. Sexual function in men will also become abnormal. Decreased production of blood clotting factors can lead to bleeding complications. Derangements in the metabolism of triglycerides, cholesterol and sugar can occur. In earlier stages, cirrhosis frequently can cause insulin resistance and diabetes mellitus. In later stages or in severe liver failure, blood glucose may be low because it cannot be synthesized from fats or proteins. Cirrhosis, especially in advanced cases, can cause profound abnormalities in the brain. In cirrhosis, some blood leaving the gut bypasses the liver as blood flow through the liver is decreased. Metabolism of components absorbed in the gut can also be decreased as liver cell function deteriorates. Both of these derangements can lead to hepatic encephalopathy as toxic metabolites, normally removed from the blood by the liver, can reach the brain. In its early stages, subtle mental changes such as poor concentration or the inability to construct simple objects occurs. In severe cases, hepatic encephalopathy can lead to stupor, coma, brain swelling and death.
Cirrhosis of the liver can also cause abnormalities in other organ systems. Cirrhosis can lead to immune system dysfunction causing an increased risk of infection. Ascites fluid in the abdomen often becomes infected with bacteria normally present in the gut (spontaneous bacterial peritonitis). Cirrhosis can also lead to kidney dysfunction and failure. In end-stage cirrhosis, a type of kidney dysfunction called hepatorenal syndrome can occur. Hepatorenal syndrome is almost always fatal unless liver transplantation is performed.

Clinical Symptoms and Diagnosis of Cirrhosis
Cirrhosis is usually an easy diagnosis to make when any or all of the above abnormalities and complications are present. This is especially true when the underlying liver disease can be identified. The underlying liver disease is identified in most patients, however, sometimes it will not be discovered. Such cases are called "cryptogenic" cirrhosis. Sometimes, other conditions such as metastatic cancer, hepatic or portal vein thrombosis, severe acute hepatitis or acute bile duct obstruction can cause some of the abnormalities seen in cirrhosis. A careful history combined with special diagnostic tests will usually identify these conditions. I rare cases, despite having cirrhosis of the liver, patients may still have very few, vague complaints. Some patients, especially early in the course of the disease, will have no overt clinical signs or symptoms. Some may have only subtle physical changes such as red palms, red spots that blanch on their upper body (spider angiomata), enlargement of the parotid glands in the face, gynecomastia, or fibrosis of tendons in the palms. Some patients may only have subtle abnormalities on blood tests, and in some cases, all blood tests may be normal. Radiological tests may give clues as to the presence of cirrhosis, but the diagnosis of cirrhosis must often be made by liver biopsy.

Causes of Cirrhosis
There is a general misunderstanding that alcohol is the sole cause of cirrhosis. Alcohol accounts for approximately 50% of the cases of cirrhosis. Almost any chronic liver disease can lead to cirrhosis. This list gives some of the many causes:
  • Alcoholic liver disease - most common cause in the U. S. A.

  • Chronic viral hepatitis B, C and D

  • Chronic autoimmune hepatitis

  • Inherited metabolic diseases (e. g. hemochromatosis, Wilson disease)

  • Chronic bile duct diseases (e. g. primary biliary cirrhosis)

  • Chronic congestive heart failure

  • Parasitic infections (e. g. schistosomiasis)

  • Nonalcoholic steatohepatitis (liver inflammation that can be caused by fatty liver)

  • Long term exposure to toxins or drugs

Cirrhosis of the liver is irreversible but treatment of the underlying liver disease may slow or stop the progression. Such treatment depends upon the underlying etiology. Termination of alcohol intake will stop the progression in alcoholic cirrhosis and for this reason, it is important to make the diagnosis early in a chronic alcohol abuser. Similarly, discontinuation of a hepatotoxic drug or removal of an environmental toxin will stop progression. Treatments of metabolic diseases, such as treatment of iron overload in hemochromatosis or copper overload in Wilson disease, are also effective therapies.
Chronic viral hepatitis B and C may respond to treatment with interferon or recently approved (Boceprevir and telaprevir, 2 NS3 protease inhibitors for the treatment of hepatitis C), and autoimmune hepatitis may improve with prednisone and azathioprine (Imuran). Drugs such as ursodiol (Actigall) may slow the progression of primary biliary cirrhosis and possibly sclerosing cholangitis.

In patients with cirrhosis of the liver, treatment must also be directed at the complications. Bleeding esophageal varices can be treated with endoscopic sclerotherapy or rubber band ligation (banding). Ascites and edema are often responsive to a low sodium diet and such a diet must be emphasized in patients with these symptoms. More advanced ascites and edema can respond to diuretic therapy. A low protein diet and agents such as lactulose may help hepatic encephalopathy. Infections such as spontaneous bacterial peritonitis must be rapidly treated with appropriate antibiotics. Drugs metabolized in the liver must be given with caution. Coagulation/clotting disorders will sometimes respond to vitamin K.

Liver transplantation is an effective for the treatment of end-stage cirrhosis in the proper setting. Transplantation is usually needed when complications such as encephalopathy, ascites or bleeding varices are uncontrollable or when biochemical function is severely depressed. In patients with primary biliary cirrhosis, a rising bilirubin indicates a poor prognosis and such patients should be considered for transplantation as the serum bilirubin concentration begins to rise. Active drug or alcohol abuses are contraindications to liver transplantation. However, alcoholics who have abstained from drinking for an extended period of time (usually more than six months), and have participated in rehabilitation programs and support groups such as Alcoholics Anonymous, can be considered as candidates and will often have a good prognosis. Liver cancer needs to be evaluated on a case-by-case basis. In many cases, it is a contraindication to transplantation. Liver transplantation is usually not performed in patients more than 70 years old.

How are complications of cirrhosis treated?
The abnormal accumulation of fluid may cause swelling of the ankles (edema) and abdomen (ascites). Therefore, patients should reduce the amount of fluid and salt in their diet or use drugs call diuretics that mobilize and excrete the excess fluid through the kidneys. Usually, you’ll be instructed to limit you daily sodium (salt) intake to 2,000 mg of sodium/day or less.
Occasionally, the ascites may become infected, a condition known as Spontaneous Bacterial Peritonitis, and require treatment with antibiotics. This complication is associated with increased complications, and an increased risk of premature death. Liver transplantation needs to be considered at this time should peritonitis develop.When the liver does not efficiently function to cleanse the body of toxins and drugs, the mental state of patients may change dramatically and lead to coma, called Hepatic Encephalopathy. Treatment is directed at reducing the protein in the diet, avoiding sedatives and pain medications, and using laxatives and/or antibiotics to decrease absorption of toxins from the intestines.

Sometimes, bleeding from the esophagus or stomach caused by abnormal veins (varices) may occur and is a life-threatening emergency requiring hospitalization. Variceal bleeding can usually be controlled with the use of a flexible tube (endoscope) that is inserted through the mouth into the esophagus and stomach and used to inject clotting agents into the veins or to rubber band ligate the varices.

Liver failure refers to end stage of liver disease and cirrhosis when the liver stops working and cannot support life. Liver failure is difficult to treat and survival is limited. Therefore, patients with any complication of cirrhosis are considered to be at risk of developing liver failure.
When complications develop, it may be possible to manage them, though more complications are likely to develop. At this time, liver transplantation should be considered

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