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Multaq FDA Breaking News

By admin | Published January 23, 2012
Multaq FDA Contact Page
1-800-611-7080

 

Multaq FDA : Hepatitis B virus can be transmitted by sharing needles. Intra­venous drug users frequently share needles to inject heroin or cocaine, and blood is transmitted from one individual to the other via needle. In inner cities in the United States, intravenous drug use is a major risk factor for hepatitis B. Hepatitis B virus can also be transmitted by tat­tooing, acupuncture, ear piercing, and piercing of other body parts if unsterilized needles are used.

Sexual contact is another way to transmit the hepatitis B virus. Individuals with multiple sexual partners are at significantly increased risk for hepatitis B. Male homosexuals and female professional sex workers have much higher rates of hepatitis B virus infection than the genera! population. Patients at sexually transmitted disease clinics also have higher incidences of hepatitis B. Male prisoners are at increased risk for hepatitis B, most likely due to increased rates of unprotected homosexual activities among inmates and also because many are intra­venous drug users. In households with an infected individual, the sex­ual partner runs a higher risk of contracting hepatitis B than from other household contact. Sexual transmission of hepatitis B virus most often occurs by intercourse, either anal or vaginal, as hepatitis B virus can be isolated from seitien. The sexual transmission rate from infected women to men is probably less than that from men to women or men to men. Sexual transmission from women to men does occur, however.

Health care workers who are regularly exposed to blood are at increased risk for hepatitis B virus infection. The most likely route of infection is by accidental sticks with needles and other sharp equip­ment used on infected patients. The hepatitis B virus may also be trans­mitted by various other pieces of hospital equipment that can contain small quantities of blood, such as unsterilized endoscopes and mechan­ical ventilators. Hemodialysis is an important route of transmission. Patients with chronic kidney failure who receive hemodialysis are at significantly increased risk for hepatitis B virus infection. There have been sporadic case reports of hepatitis B virus transmission from health care workers to patients, but, fortunately, transmission by this route is rare. Most cases have been traced to persistently infected surgeons, dentists, or physicians who perform invasive procedures. Health care workers who transmit the hepatitis B virus to patients are almost always found to be HBeAg-positive upon blood testing.

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Antibodies of the IgG class against the hepatitis B core antigen (IgG anti-HBc) are present in the blood of almost all individuals who have been infected with, or possibly exposed to, the virus. These anti­bodies become detectable in the blood a few months after acute infec­tion, usually after the IgM class antibodies disappear. IgG anti-HBc persists in the blood after infection resolves, sometimes for the patient’s lifetime. It may be detected in someone with acute infection that is nearly resolved. IgG anti-HBc is not protective against subsequent hepatitis B virus infection.

Individuals with hepatitis B virus infection who clear the virus from their bodies develop antibodies against hepatitis B surface antigen (anti-HBs). If present, these antibodies indicate protection against rein­fection. Anti-HBs antibodies are virtually never present in chronically infected individuals who have HBsAg. They are also the type of anti­bodies induced by vaccination.

The significance of hepatitis Be antigen (HBeAg) has been dis­cussed previously in reference to states of high viral replication versus low viral replication. HBeAg is detectable in the blood of patients with high levels of viral replication. It is present in the blood of individuals with acute infection because, in acute infection, the virus replicates at a high level. Antibodies against HBeAg (IgG anti-HBe) are usually present in the blood of individuals with hepatitis B who do not have HBeAg, that is, those who have low-level viral replication.

In individuals with suspected acute hepatitis B virus infection, blood testing for HBsAg, IgM anti-HBc, and anti-HBs should be per­formed. Acute hepatitis B virus infection is usually suspected in the patient with new-onset jaundice and other symptoms including fatigue, right upper quadrant abdominal pain, fever, loss of appetite, nausea, and vomiting. A risk factor for infection may be elicited from the patient’s history, for example, intravenous drug use, an accidental nee­dle stick (in a health care worker), or exposure to an infected contact within the past several weeks or months. The presence of HBsAg in blood will indicate acute infection or the continued presence of the virus. The detection of IgM anti-HBc, in the absence of HBsAg, will suggest resolving infection. The presence of anti-HBs will indicate res­olution of the disease and that the patient is now immune to future infection. In rare cases, HBsAg and antibodies against it (anti-HBs) can be present at the same time. Such individuals can have complica­tions if these two types of antibodies react with each other in the bloodstream and deposit in the small blood vessels of various organs.

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Chronic hepatitis B is defined as infection with the hepatitis B virus for more than six months. Chronic hepatitis B infection should be sus­pected in individuals with known risk factors and individuals from parts of the world where the disease is endemic. Most patients from parts of the world where hepatitis B is endemic were infected as new­born babies or in childhood. A smaller percentage was infected as adults. Most chronically infected individuals in ‘Western countries acquired the disease as adults.

Individuals with chronic hepatitis B infection may have no symp­toms (chronic carriers) or have symptoms and clinical evidence of chronic hepatitis, cirrhosis, or even hepatocellular carcinoma. Some­times, the disease is suspected when elevated ALT and AST activities are detected on routine blood tests or testing for other purposes. The most important test to establish or exclude chronic hepatitis B is blood testing for HBsAg.

If HBsAg is detected in the blood, and presumably has been pres­ent for more than six months if no recent history of acute hepatitis can be ascertained, chronic hepatitis B virus infection is established. If HBsAg is not detected in the blood, the individual does not have chronic hepatitis B. It must be emphasized that, in the absence of HBsAg, the detection of IgG anti-HBc in the blood does not indicate a diagnosis of chronic hepatitis B. This is critical to realize and is a mis­take that I have seen many doctors make. HBsAg must be detected in the blood—or the individual does not have chronic hepatitis B. In indi­viduals who have clinical evidence of chronic hepatitis but do not have detectable blood HBsAg, a search for another cause of hepatitis (for example, hepatitis C, alcohol, drugs) should be initiated.

Our use of the term or terms Multaq FDA is for descriptive purposes only. There is no relationship between the owners of this website and the maker of the product discussed in this post. Our use of the words Recall, Class Action Lawsuit and other similar words related to an event do not necessarily mean that this event has occurred. Refer to the website of the United States Food and Drug Administration for information on drug or medical device recalls. If a Class Action Lawsuit is formed in relation to the product discussed in this post we will provide that information at the time the Class Action is formed. A Class Action Lawsuit is not required to exist for you to file a lawsuit if you have been injured by the product discussed in this post.
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Multaq Warning Advice

By admin | Published January 23, 2012
Multaq Warning Contact Page
1-800-611-7080

 

Multaq Warning : Individuals with chronic hepatitis B infection, especially those with cirrhosis, are at increased risk for development of hepatocellular carci­noma (primary liver cancer), as in Case 5. As noted previously, while relatively rare in the United States, hepatocellular carcinoma is the num­ber one or number two cause of cancer death in the world, especially in certain Asian and African countries. Individuals with hepatitis B and cirrhosis bear the greatest risk for development of hepatocellular carci­noma. Individuals with hepatitis and no cirrhosis are also at increased risk compared to the general population.

Chronic hepatitis B infection is separated into two distinguishable “states.” The best way to distinguish these two states of hepatitis B virus infection is by the presence or absence of hepatitis Be antigen (HBeAg) in blood. In instances where the hepatitis B virus is rapidly replicating, a short form of the hepatitis B core antigen, called HBeAg, is usually detected in the blood. HBeAg is detected in the blood dur­ing acute infection, when the virus rapidly replicates, and becomes undetectable as the acute infection resolves. In most cases of chronic infection, HBeAg is not detected because the virus enters a state of low replication and its genetic material integrates into the DNA of infected cells. In some cases of chronic infection, however, the virus maintains a highly replicative “lifestyle” (are viruses alive?) and, in most of these cases HBeAg will be detected in the blood. In individuals chronically infected with hepatitis B virus, the state of infection can switch from HBeAg-positive (high replication) to HBeAg-negative (low replication) at any time.

The distinction between HBeAg-positive and HBeAg-negative chronic hepatitis B is critical regarding disease severity, prognosis, con­tagiousness, and treatment. Patients who have HBeAg in their blood usually have more severe clinical disease with a greater amount of inflammation in the liver. They are usually sicker and have more symp­toms. The chances of progression to cirrhosis and hepatocellular car­cinoma are greater. In addition, individuals with detectable HBeAg in their blood are highly infectious as high viral replication is associated with the presence of more viral particles in the blood. A major goal of treatment for chronic hepatitis B is to convert a patient who has detectable HBeAg in the blood (a state of high virus replication) to one who does not have detectable HBeAg in the blood (a state of low-level virus replication). This change after treatment is associated with a bet­ter long-term prognosis.

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Individuals with chronic hepatitis B virus infection can sponta­neously convert from HBeAg-negative to HBeAg-positive. This is asso­ciated with worsening disease severity and prognosis. Paradoxically, conversion from HBeAg-positive to HBeAg-negative, which is associ­ated with a better long-term outlook, is associated with a transient worsening of hepatitis and higher elevations in blood ALT and AST activities. This probably occurs because the immune system attacks the hepatocytes in which the virus is rapidly replicating, causing increased liver inflammation and cell death as infected cells are killed. The “flare” in hepatitis associated with conversion from HBeAg-positive to HBeAg-negative usually resolves with improvement in condition.

An exception to the rule that HBeAg is detectable in the blood of individuals infected with the hepatitis B virus when the virus is rapidly replicating occurs when there is infection with mutant forms of hepati­tis B virus known as precore mutants. Precore mutants of the hepati­tis B virus have mutations in their core proteins. As a result, they do not make HBeAg, even when they are rapidly replicating. Therefore, in precore mutant infection, the presence or absence of HBeAg in the blood is not a determinant of prognosis. It may be suspected when patients do not have detectable HBeAg but do have high concentra­tions of hepatitis B virus DNA in the blood. Precore mutants are defin­itively identified only by isolating the virus irony the patient and exam­ining its DNA sequence.

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Approximately 350 million individuals throughout the world are chronically infected with the hepatitis B virus, making it the number one worldwide cause of liver disease. The geographic distribution of cases varies tremendously from one part of the world to another. Hepatitis B virus infection is relatively uncommon in the United States and other Western countries. In the United States, just over one mil­lion individuals are chronically infected with hepatitis B virus. On the other hand, hepatitis B virus infection is endemic in Southeast Asia and sub-Saharan Africa. In countries such as Senegal, Thailand, and parts of China, as many as 25 percent of the population may become infected with hepatitis B virus by early childhood.

Transmission of hepatitis B virus from mother to baby may occur either before delivery or by exposure to the mother’s blood at the time of delivery. The hepatitis B virus is also present in the breast milk of infected mothers, but a large study has shown that breast-feeding is not a major source of transmission of hepatitis B. Some babies of infected mothers who are not infected with the hepatitis B virus at birth become infected during the first few months or first year of life—prob­ably by household exposure to the mother’s blood or that of infected brothers or sisters.

A major route of transmission of hepatitis B in the West was trans­fusion of blood and blood products. Since the association of the Aus­tralia antigen with serum hepatitis in the 1960s, tremendous efforts have been taken to screen the blood supply and keep it free of hepati­tis B virus. In most industrialized countries, the risk of contracting hepatitis B from a blood transfusion is extremely low as donated blood is screened for the virus. In addition, intravenous drug users and other individuals at high risk for hepatitis B are excluded from donating blood if they are identified. Although the blood supply is remarkably safe, no screening test is perfect, and the risk of contracting hepatitis B from a transfusion of one unit of blood in the United States is approx­imately one in sixty thousand to one in one hundred thousand. The hepatitis B virus can also be transmitted by organ transplantation, but the organ donor’s blood is generally tested for hepatitis B virus infec­tion before an organ is used.

Our use of the term or terms Multaq Warning is for descriptive purposes only. There is no relationship between the owners of this website and the maker of the product discussed in this post. Our use of the words Recall, Class Action Lawsuit and other similar words related to an event do not necessarily mean that this event has occurred. Refer to the website of the United States Food and Drug Administration for information on drug or medical device recalls. If a Class Action Lawsuit is formed in relation to the product discussed in this post we will provide that information at the time the Class Action is formed. A Class Action Lawsuit is not required to exist for you to file a lawsuit if you have been injured by the product discussed in this post.
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Multaq Reports

By admin | Published January 23, 2012
Multaq Reports Contact Page
1-800-611-7080

 

Multaq  : A little background on the virus that causes hepatitis B is essential for understanding the disease, its symptoms, and especially its diagnosis. The existence of hepatitis B virus was discovered by accident in the 1960s. In 1965, Dr. Baruch Blumberg and collaborators discovered a protein of the hepatitis B virus in the blood of an Australian aborig­ine. This protein was called the Australia antigen. At the time of its discovery, the Australia antigen was not thought to be a viral protein. Over the next few years, however, Dr. Blumberg, his collaborators, and other groups proved that the Australia antigen was associated with hepatitis, specifically a form that was then known as serum hepatitis and was transmitted by blood. Dr. Blumberg was awarded the Nobel Prize in Physiology or Medicine in 1976 for this discovery.

In subsequent years, the hepatitis B virus was photographed under an electron microscope and was propagated in cell culture. Its genetic material was analyzed. A schematic diagram of hepatitis B virus. The hepatitis B virus is a member of the Hepad- naviridae family; other very similar viruses in this family cause liver disease in woodchucks, ground squirrels, and ducks. These animals have served as experimental models for research on hepatitis B.

The genetic material of hepatitis B virus is a circular strand of DNA. This circular DNA encodes four viral proteins, two of which are struc­tural proteins of the viral particle.  It is important to be familiar with these proteins, especially the hepatitis B surface and core proteins, because detection of these proteins in the blood, or detection of antibodies against them, plays a critical role in diagnosis.

Hepatitis B core antigen (HBcAg) is a protein that forms the nude- ocapsid, or core, of the viral particle and is associated with the viral DNA. Hepatitis B core antigen is not readily detectable in the blood of infected individuals but can be seen in the liver cells. If the virus is rapidly replicating in the liver, a smaller form of the hepatitis B core antigen can be detected in the infected patient’s blood. This form is known as hepatitis Be antigen (HBeAg). Detection of HBeAg in the blood has important clinical significance in the diagnosis of more seri­ous and more highly contagious disease.

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Acute infection with the hepatitis B virus can cause a wide range of initial conditions, from no symptoms to fulminant hepatic failure. In newborn babies, acute infection, usually transmitted from the mother at the time of delivery, generally does not cause clinical disease. In younger children, acute infection with hepatitis B virus also does not usually cause clinically apparent disease. In adults, most acutely infected individuals develop acute clinical hepatitis that varies in severity.

In most adult cases, acute infection with the hepatitis B virus causes moderate illness that spontaneously resolves, as in Case 1 above. Symp­toms of hepatitis typically occur within six to fifteen weeks after infec­tion. Symptoms include nausea, vomiting, fever, right upper quadrant abdominal pain, and jaundice. Blood ALT and AST activities are ele­vated roughly in proportion to the degree of acute inflammation and liver cell death. Elevations in blood bilirubin concentration and, in more severe cases, prolongation of PT may also occur. About 2 percent of acutely infected adults develop fulminant hepatic failure. This is what happened to the patient described in Case 2. Most of these individu­als either die or require emergency liver transplantation. The vast majority of acutely infected adults, as seen in Case 1, have spontaneous resolution of acute hepatitis. About 5 percent of individuals infected as adults go on to develop chronic hepatitis. B, as did the patient in Case 4.

Hepatitis B virus infection is the leading cause of chronic liver dis­ease in the world. Most chronically infected individuals are infected as infants or children. Chronic infection can cause various problems. Some chronically infected individuals are clinically classified as chronic carriers. Chronic carriers have no clinically apparent liver disease; how­ever, this may be an inaccurate term as some so-called chronic carri­ers exhibit evidence of hepatitis on liver biopsy. Other individuals chronically infected with hepatitis B virus have clinically apparent chronic hepatitis. Long-standing chronic hepatitis resuiting from hepatitis B can lead to cirrhosis. Long-standing hepatitis B infection is also a major risk factor for the development of hepatocellular carci­noma or primary liver cancer, which is the number one or two (along with lung cancer) cause of cancer death worldwide.

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Chronic carriers are considered to be individuals persistently infected with the hepatitis B virus who do not have clinical evidence of hepatitis. The woman described in Case 3 is an example of a chronic carrier. Chronic carriers have detectable HBsAg in their blood but no signs or symptoms of hepatitis or liver disease. The diagnosis is often made during routine screening of pregnant women, as in Case 3, or of blood donors. Typically, blood ALT and AST activities are normal and there is no laboratory evidence of liver damage or dysfunction. The term chronic carrier derives from the fact that these individuals have laboratory evidence of hepatitis B virus infection but no clinical or lab­oratory evidence of liver disease. About 75 percent of chronic carriers will have no evidence of inflammation on liver biopsy and can truly be called carriers who do not have evidence of chronic hepatitis. About 25 percent of chronic carriers, however, are not really only carriers and will have evidence of inflammation on liver biopsy. These individuals have chronic hepatitis despite normal laboratory tests and no exhibi­tion of symptoms. Some so-called chronic carriers may even have cir­rhosis if liver biopsy is performed. Therefore, although almost universally used to describe patients chronically infected with hepati­tis B virus and no evidence of liver disease, chronic carrier may not technically be a correct description of all such patients. Furthermore, individuals who are defined as chronic carriers can sometimes develop clinically apparent hepatitis at a later time.

Chronic hepatitis that is clinically apparent, as in the patient described in Case 4, occurs in many individuals chronically infected with the hepatitis B virus. These individuals have detectable serum HBsAg. They may have symptoms of chronic hepatitis including fatigue, depression, loss of appetite, and other nonspecific complaints. Sometimes, the disease is clinically silent and the patient will not have symptoms. Blood tests will usually reveal elevated ALT and AST activ­ities. Sometimes, chronic hepatitis will be diagnosed only by liver biopsy in an individual who is diagnosed clinically as a chronic carrier. •*– Individuals with chronic hepatitis B infection, especially those with evidence of ongoing liver inflammation, are at risk of developing cir rhosis over time. Signs and symptoms of cirrhosis may not be appar­ent, and the diagnosis may be made only on liver biopsy. Case 4 describes such an example. Some patients with long-standing chronic hepatitis B may not even seek medical attention until they are suffer­ing from complications of cirrhosis

Our use of the term or terms Multaq is for descriptive purposes only. There is no relationship between the owners of this website and the maker of the product discussed in this post. Our use of the words Recall, Class Action Lawsuit and other similar words related to an event do not necessarily mean that this event has occurred. Refer to the website of the United States Food and Drug Administration for information on drug or medical device recalls. If a Class Action Lawsuit is formed in relation to the product discussed in this post we will provide that information at the time the Class Action is formed. A Class Action Lawsuit is not required to exist for you to file a lawsuit if you have been injured by the product discussed in this post.
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Multaq Warnings Process

By admin | Published January 23, 2012
Multaq Warnings Contact Page
1-800-611-7080

 

Multaq Warnings : The large majority of patients with hepatitis A recover without complications. Hospitalization and supportive care may be necessary for very ill patients who are unable to eat or drink fluids. Occasionally, patients may suffer from fatigue and malaise for several months after the disease resolves. About 1 percent of individuals with hepatitis A, usually those over age fifty, develop serious liver failure, sometimes ful­minant. These patients require hospitalization and supportive care. In the United States, about one in three hundred cases of hepatitis A results in death or emergency liver transplantation.

Hepatitis A virus is spread primarily by the fecal-oral route. The virus is excreted in feces of infected people and infects susceptible individ­uals who consume contaminated water or foods. Water, shellfish, and salads are the most frequently implicated sources of transmission. Cold cuts, fruits, fruit juices, milk, and vegetables also have been implicated in various outbreaks. Hepatitis A is more common in underdeveloped parts of the world with poor sanitary conditions, and travelers to these regions are at an increased risk for infection. The time from infection with hepatitis A virus to onset of symptoms varies from ten to fifty days. Thirty days is the average. The greatest dan­ger of infecting others occurs during the middle of the incubation period and before presentation of symptoms. The patient remains potentially infectious up until a week or more after the onset of symptoms.

Although ingestion of contaminated food and water is the most common route of transmission, hepatitis A virus can be transmitted in other ways. Infected individuals can spread the virus to others who live in the same household or with whom they have sexual contact. In particular, hepatitis A virus may be spread by sexual practices in which the mouth comes in direct contact with the anal area of an infected indi­vidual. Homosexual men are at an increased risk for hepatitis A. Casual contact at work or in social settings usually does not spread the virus. Hepatitis A virus infection, however, can be spread among children and employees in child-care centers where a child or employee is infected. Residents and staff workers in institutions for developmentally disabled persons are at a particularly increased risk for being infected with hepatitis A virus. There also have been reports of transmission by shar­ing contaminated materials among intravenous drug users.

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The most important issue regarding hepatitis A is prevention. There are three primary ways to prevent hepatitis A—hygiene, passive immu­nity, and vaccination. Hygienic measures to prevent hepatitis A infection include pre­venting the contamination of food and water and avoiding contact with contaminated foods. In many developing countries, widespread sewage systems have not been constructed, especially in rural areas. Water from lakes and rivers into which people defecate may be used for drink­ing, washing, or preparing foods. Living conditions are often crowded. Only overall improvement in the socioeconomic structure can remedy these problems. Visitors to such areas should avoid drinking from the local water supply and eating fresh fruits or vegetables that may have been washed with water from local rivers, lakes, or reservoirs. Locally caught shellfish also should not be consumed. If local water must be consumed, it should be boiled first.

People living in the same household as an individual with hepati­tis A, or individuals working in situations where the disease is com­mon, should follow commonsense rules. Hand washing should be strictly observed, especially when using the bathroom and before preparing or eating food. People working in child-care centers or insti­tutions for developmentally disabled individuals should wash their hands after changing diapers or sheets, before eating, or after any close contact with residents.

Passive immunization with immune globulin is recommended for short-term protection against hepatitis A and for persons who have been exposed to the hepatitis A virus. Immune globulin is a concen­tration of antibodies pooled from the blood of individuals with IgG antibodies against the hepatitis A virus. Immune globulin should be administered to individuals who will be traveling to endemic areas chat have not received vaccination far enough in advance of departure (about four weeks) for it to be effective. The U.S. Centers for Disease Control and Prevention (cdc.gov) provides recommendations for trav­elers going to various parts of the world. Immune globulin should also be given to individuals who may have been exposed to hepatitis A virus within two weeks of suspected exposure.

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Hepatitis A vaccines provide long-term protection against hepati­tis A. Two shots administered in six- to twelve-month intervals are given. Vaccination is recommended for individuals who will travel to or work in areas where hepatitis A is endemic. Again, the U.S. Centers for Disease Control and Prevention provides recommendations for travelers to various parts of the world. The first dose of vaccine should be given at least four weeks before travel. This usually provides pro­tection for a short trip, but a booster is necessary six to twelve months later for long-term protection.

Children in communities with high rates of hepatitis A should also be vaccinated. These communities include Alaska Native villages, Native American reservations, and some religious communities, for example, the Kiryas Joel Hassidic community in New York. Homo­sexual men should also be vaccinated, as should people who use street drugs. Individuals with chronic liver diseases should be vaccinated as hepatitis A virus infection may be more severe in individuals with another underlying liver disease. This may be particularly true for indi­viduals with chronic hepatitis C. People with some other chronic dis­eases, such as inherited clotting factor deficiencies like hemophilia, should also be vaccinated. Hepatitis A vaccination is not recommended for all health care workers; however, those working in high-risk envi­ronments, such as institutions for the developmentally disabled, should receive the hepatitis A vaccine. Individuals who work with hepatitis A virus-infected animals or with the hepatitis A virus in a research lab­oratory should also be vaccinated.

Our use of the term or terms Multaq Warnings is for descriptive purposes only. There is no relationship between the owners of this website and the maker of the product discussed in this post. Our use of the words Recall, Class Action Lawsuit and other similar words related to an event do not necessarily mean that this event has occurred. Refer to the website of the United States Food and Drug Administration for information on drug or medical device recalls. If a Class Action Lawsuit is formed in relation to the product discussed in this post we will provide that information at the time the Class Action is formed. A Class Action Lawsuit is not required to exist for you to file a lawsuit if you have been injured by the product discussed in this post.
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Multaq Liver Petitions

By admin | Published January 23, 2012
Multaq Liver Contact Page
1-800-611-7080

 

Multaq Liver : Viruses are small and range in size from about 15 nanometers to 250 nanometers in their longest dimension. There are a billion nanome­ters in a meter, which is roughly equal to one yard. The human red blood cell, one of the smallest cells in the body, is about thirty times the size of the largest virus. Hepatocytes, the predominant liver cells, are much larger than the various hepatitis viruses. Particles as small as viruses cannot be observed under a light microscope. Electron micros­copy is necessary to see virus particles.

Viruses contain either ribonucleic acid (RNA) or deoxyribonucleic acid (DNA) as their genctic material (animals and plants have DNA as their genetic material). Viruses also contain proteins. Most viruses have core or capsid proteins that form a nucleocapsid around which the viral RNA or DNA winds. Some viruses are enveloped in that they contain a lipid (fat) outer layer that derives from the cells in which they repli­cate. The envelope usually contains specific viral proteins. In addition to the proteins that comprise the viral particle, most viruses also pro­duce proteins that perform essential biochemical functions necessary for their replication. These proteins may be expressed and function only within the cells that the virus infects and not be present in the mature viral particles.

An important property of viruses is cellular tropism. Tropism indi­cates a virus’s ability to infect a particular type of cell or cells. Viruses that cause hepatitis are referred to as primarily bepatotropic because they preferentially infect hepatocytes, the major cells of the liver. Pri­marily hepatotropic viruses may also infect cells other than hepato­cytes. Various viruses have different cellular tropisms. For example, the human immunodeficiency virus (HIV) primarily infects certain cells of the immune system.

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Another important property of viruses is their ability to mutate. Because the genomes of viruses are small and replicate rapidly, the mutation rates of viruses are usually high. This ability to mutate is of critical importance in the ability of viruses to cause disease. Constant mutation allows viruses to escape detection by the host’s immune sys­tem. For this reason, it is sometimes not possible for the body to clear a viral infection. Mutation may be an important way that hepatitis C virus escapes detection by the immune system. Mutation also makes it difficult to design drugs against viruses as they can cause changes in the viral proteins that are targets for drugs.

Latency is another property of viruses of major significance for treatment of human diseases. Viruses may stop replicating and inte­grate their DNA, or a DNA copy of their RNA, into the host cell DNA. The virus then can be propagated as the host cell divides. However, viral particles will not be made and the immune system will usually not kill the cells in which viral genetic material is integrated. A latent or integrated virus can later be activated for various reasons and begin to replicate and make infectious viral particles. This is an important property of the hepatitis B virus, which can either replicate in infected individuals at high levels or integrate into the cell’s DNA.

Viruses do not have their own independent metabolism, utilizing instead the energy, chemical compounds, and protein synthesis machin­ery of the cells they infect. For this reason, it has been an extremely difficult task to design antiviral drugs. Antibiotics that kill bacteria are often targeted against the bacterial proteins involved in protein syn­thesis or energy metabolism. Since viruses use host cell metabolites and protein synthesis machinery, drugs directed against these targets would not only inhibit viral replication but also kill host cells. Fortunately, some viruses make a few proteins that are uniquely essential for their own replication that can be targets for antiviral drugs. An example that has received a lot of attention in recent years is the protease of HIV, which is a viral protein essential for replication of the virus that is the target of drugs known as protease inhibitors.

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The illness caused by infection from the hepatitis A virus is called hepatitis A. In the past, several different terms were used to describe this illness, including infectious hepatitis, epidemic hepatitis, epidemic jaundice, catarrhal jaundice, and infectious icterus. These terms are generally no longer used. The hepatitis A virus causes only acute liver disease. This is criti­cal to understand as many patients, and even some doctors, consider hepatitis A as a possible cause of chronic liver disease. Individuals with other chronic liver diseases, as might any susceptible individual, can be infected with hepadds A virus and develop acute hepatitis. However, hepatitis A virus does not cause chronic liver disease. Hepatitis A always resolves itself or, in rare cases, kills the patient.

In most patients, hepatitis A is either a relatively mild disease or no apparent disease at all. Many children who get infected do not develop clinically apparent liver disease. There is a correlation between age and disease severity. Most cases of fulminant hepatic failure from hepatitis A virus infection occur in older individuals, usually over age fifty. Patients with a relatively mild form of the disease may suffer from nausea, vomiting, fever, fatigue, and loss of appetite. Blood tests usu­ally reveal elevations in aminotransferase activities and possible eleva­tions in bilirubin concentration. Patients with a more severe hepatitis A condition develop jaundice and laboratory examination reveals sig­nificant elevation in blood bilirubin concentration. In more severe cases, prothrombin time may be prolonged. In instances of massive hepato- cyte death, blood alanine aminotransferase (ALT) and aspartate amino­transferase (AST) activities can be very highly elevated.

Our use of the term or terms Multaq Liver is for descriptive purposes only. There is no relationship between the owners of this website and the maker of the product discussed in this post. Our use of the words Recall, Class Action Lawsuit and other similar words related to an event do not necessarily mean that this event has occurred. Refer to the website of the United States Food and Drug Administration for information on drug or medical device recalls. If a Class Action Lawsuit is formed in relation to the product discussed in this post we will provide that information at the time the Class Action is formed. A Class Action Lawsuit is not required to exist for you to file a lawsuit if you have been injured by the product discussed in this post.
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Multaq Liver Failure Action

By admin | Published January 23, 2012
Multaq Liver Failure Contact Page
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Multaq Liver Failure : Patients with ascites are at risk for SBP. This infection should be con­sidered in any patient with ascites who develops fever or abdominal pain. Sometimes, SBP will appear as a general deterioration in overall condition or worsening hepatic encephalopathy in the absence of fever. The diagnostic procedure for SBP is paracentesis. Usually, only a small volume of ascites fluid needs to be removed with a needle and syringe. The diagnosis of SBP is made if the white blood cell count in the ascites fluid is elevated. Treatment with antibiotics is essential and usually done intravenously in the hospital. Some studies have suggested that long­term oral antibiotics may be useful to prevent subsequent infections in individuals with recurrent episodes of SBP.

The first step in the treatment of hepatic encephalopathy is a low- protein diet. Proteins are high in nitrogen content. Ammonia and other nitrogen-containing compounds, which are toxic to the brain when not removed by the cirrhotic liver, are produced by the metabolism of pro­teins by bacteria in the colon. Therefore, meats, nuts, and other high­protein foods should be consumed only in very low quantities by individuals with hepatic encephalopathy. Vegetables, fruits, grains, and pastas should be substituted. This diet is in many aspects similar to the low-salt diet for ascites and edema.

The first-line drug treatment is usually lactulose, a sugar that is not absorbed from the gut. In part, it acts as a laxative to expel nitrogen- containing compounds from the colon before bacteria can metabolize them into substances toxic to an individual with a liver that cannot ade­quately clear them from the blood. Lactulose also causes the inside of the gut to be increasingly acidic, making it less favorable for nitrogen- containing toxins and ammonia to be absorbed. Another drug treat­ment for encephalopathy is neomycin, an antibiotic not absorbed from the gut, which kills bacteria in the colon that produce ammonia and other nitrogen-containing toxic compounds.

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Administration of vitamin K can sometimes help the decreased pro­duction of clotting factors in patients with cirrhosis. In emergency bleeding situations, or prior to invasive medical procedures that may be necessary, fresh frozen plasma can be transfused intravenously. Fresh frozen plasma is the component of blood from which red and white cells have been removed; it contains clotting factors and other proteins. Platelet transfusions may also be given to patients with low platelet counts to help stop or prevent bleeding.

In some patients, the complications of cirrhosis become refractory to all medical therapies. As the liver continues to fail, hepatic encepha­lopathy worsens, ascites continue to accumulate, and other complica­tions worsen. These complications may no longer be responsive to medical interventions. Cachexia and muscle wasting cannot be halted no matter how many nutrients the patient receives. Kidney function may gradually fail and hepatorenal syndrome may develop. In these advanced cases of cirrhosis—also known as end-stage liver disease— only a liver transplant can save the patient’s life. The general goal of liver transplantation is to replace the patient’s liver just before compli­cations of cirrhosis become refractory to medical treatment. In ideal cases, this can be estimated. In many cases, as previously mentioned however, there is considerable uncertainty as to how soon the compli­cations of cirrhosis and liver failure will become life-threatening. Patients with cirrhosis and one or more of its complications should probably be evaluated at a center for liver transplantation at least two years before the doctor anticipates that the condition will deteriorate and medical treatment will no longer suffice to control the complica­tions.

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HEPATITIS means “inflammation of the liver.” By now, it should be obvious that there are many causes of hepatitis, including drugs and alcohol. However, most people equate hepatitis with the liver disease caused by several different viruses. Hepatitis caused by a virus is more precisely called viral hepatitis. After alcohol, viral hepatitis is the leading cause of chronic liver disease in the United States. It is estimated that, at the present time, about one million Americans are chronically infected with the hepati­tis B vims and three to four million with the hepatitis C virus. World­wide, viral hepatitis surpasses alcohol as the number one cause of chronic liver disease. Approximately 350 million people, mostly in Southeast Asia and sub-Saharan Africa, are chronically infected with hepatitis B virus. The hepatitis C virus chronically infects about 170 million people worldwide. These numbers are staggering, especially since hepatitis B and hepatitis C are infectious diseases whose trans­mission can be prevented by avoiding certain behaviors and using some commonsense precautions. Hepatitis B can also be prevented by vaccination.

Because of advances in basic molecular biology and the large num­bers of affected individuals, diagnosis and treatment of viral hepatitis is currently the most active area of medicine related to diseases of the liver. The different forms of viral hepatitis are also the liver diseases most patients seem to have questions about. Our knowledge of viral hepatitis is still expanding, especially regarding hepatitis C, which was identified only about fifteen years ago. However, currently available information makes it possible to understand a good deal about the major hepatitis viruses and the diseases that each causes.

Before discussing the various types of viral hepatitis, it is important to have some understanding of what a virus is. This will hopefully pro­vide some insight as to why viral diseases are formidable problems. So sit tight and try to bear with a little basic biochemistry and cell biology. Some people define viruses as the simplest forms of life. It is really a matter of philosophical debate—and not science—to decide if viruses are “alive.” Like other life-forms, viruses reproduce and mutate (ran­domly change their genetic material). However, viruses do not have an independent metabolism and can replicate only within another organ­ism’s cells. You can decide for yourself if this constitutes life.

Our use of the term or terms Multaq Liver Failure is for descriptive purposes only. There is no relationship between the owners of this website and the maker of the product discussed in this post. Our use of the words Recall, Class Action Lawsuit and other similar words related to an event do not necessarily mean that this event has occurred. Refer to the website of the United States Food and Drug Administration for information on drug or medical device recalls. If a Class Action Lawsuit is formed in relation to the product discussed in this post we will provide that information at the time the Class Action is formed. A Class Action Lawsuit is not required to exist for you to file a lawsuit if you have been injured by the product discussed in this post.
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Multaq Lawyer Releases

By admin | Published January 19, 2012
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Multaq Lawyer :

When a doctor orders a liver biopsy, it is because he or she needs a definitive answer about the type of prob­lem affecting the liver and the extent of the damage the problem has caused. With that information, the medical team can plan a course of treatment, anticipate your body’s response to that treatment, and form a prognosis. The liver biopsy is the only diagnostic test that provides accurate and complete informa­tion. For many liver diseases, all the tests that have been made to that point—blood work, imaging tests, and others-—-have given supportive information but cannot accurately diagnose the extent of the problem.

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Do All Patients with Suspected Liver Disease Undergo Liver Biopsies?

A liver biopsy will not help doctors determine the best course of treat­ment in every instance. In the case of a patient with acute hepatitis A, for example, patients receive the same treatment regardless of the biopsy results, so the biopsy is usually not ordered. Another is when a patients liver disease is thought to have been caused by a medication;

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Liver Biopsy: What to Expect

Before the procedure:

  • Eat a light breakfast.
  • A doctor will explain the biopsy procedure in detail, includ­ing possible complications, and answer any questions you may have.

During the procedure:

■ You will wear a hospital gown.

  • You will lie on your back, with your right elbow out to the side and your right hand under your head. It is important that you remain as still as possible during the procedure.
  • An ultrasound may be used to mark the location of your liver.
  • You may receive a small dose of a sedative just prior to the procedure.
  • The doctor will clean and numb an area on your upper abdo­men with a local anesthetic (pain-relieving medication). The doctor will then make a small incision on your upper abdomen and insert a needle into this incision to take a small sample of liver tissue for analysis. You may feel like you’ve been punched, which is normal. A bandage will be placed over the biopsy site.
  • The procedure takes about five minutes.

Our use of the term or terms Multaq Lawyer is for descriptive purposes only. There is no relationship between the owners of this website and the maker of the product discussed in this post. Our use of the words Recall, Class Action Lawsuit and other similar words related to an event do not necessarily mean that this event has occurred. Refer to the website of the United States Food and Drug Administration for information on drug or medical device recalls. If a Class Action Lawsuit is formed in relation to the product discussed in this post we will provide that information at the time the Class Action is formed. A Class Action Lawsuit is not required to exist for you to file a lawsuit if you have been injured by the product discussed in this post.
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Multaq Lawsuit Petition

By admin | Published January 19, 2012
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Multaq Lawsuit:

Many people think of ultrasounds as the procedures that allow a pregnant woman to see her fetus, but sonograms are most frequently prescribed for liver patients. Unlike X-rays, sonograms use sound waves rather than radiation to produce the image.Typ­ically, the patient is directed to fast during the 12 hours before the scan so the gallbladder will be full of bile, making it easy for the radiologist to spot gallstones. Sonograms may also show tumors and allow doctors to estimate their size, though it is often impos­sible to tell with an imaging study whether the growth is benign or malignant..Sonograms are also often the first indication that a person has a fatty liver.


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Additionally, more detailed images of the liver may be ordered if a tumor is suspected. Using radiation that sends an X-ray beam into the liver, a CT scan can identify abnormal growths (benign or malignant), while MRIs, which use electromagnetic radiation, are helpful in identifying iron overload, hemangiomas (benign blood tumors), or sometimes a fatty liver.

After a series of liver function tests and imaging studies has been completed, doctors may decide to order a liver biopsy, the only test that can definitively diagnose certain serious but treatable liver diseases.

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To respond to the reluctance of some patients to undergo liver biopsy, and to offer a less invasive, less painful, and safer way to detect scarring or cirrhosis, liver specialists have been looking for an alternative to the traditional liver biopsy. The development of noninvasive blood markers for liver fibrosis (scarring of the liver) is a step toward achieving that goal. Once finalized, these blood tests will be able to identify the amount of fibrosis or scar tissue present in the liver. Unfortunately, thus far these tests have played only a limited role in clinical use because they can detect only the two extremes in the spectrum of liver fibrosis (i.e., very mild disease or very advanced disease). They are not very useful in identifying patients with liver fibrosis that falls between the two extremes.

Another new noninvasive evaluation of liver fibrosis is transient elastography. The commercial name for this technique, which is designed to measure liver stiffness, is Fibroscan. During this test, a machine measures the elasticity or stiffness of the liver and generates a report. The greater the degree of scarring, the less elastic the liver appears. Unfortunately, as with the blood markers mentioned above, this test is not yet accurate enough to replace the liver biopsy.

Our use of the term or terms Multaq Lawsuit is for descriptive purposes only. There is no relationship between the owners of this website and the maker of the product discussed in this post. Our use of the words Recall, Class Action Lawsuit and other similar words related to an event do not necessarily mean that this event has occurred. Refer to the website of the United States Food and Drug Administration for information on drug or medical device recalls. If a Class Action Lawsuit is formed in relation to the product discussed in this post we will provide that information at the time the Class Action is formed. A Class Action Lawsuit is not required to exist for you to file a lawsuit if you have been injured by the product discussed in this post.
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Multaq Attorneys Notice

By admin | Published January 19, 2012
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Multaq Attorneys :

Prothrombin is a protein that the liver produces as one of the clotting factors that stop bleeding. Prothrombin time (PT) is the time the body needs to begin clotting-—-normally between 9 and

10   seconds—and vitamin K must be present for clotting to hap­pen. When vitamin K is deficient (which is often the case with certain cholestatic liver diseases) or the liver has suffered exten­sive damage, the PT will be abnormally long, compromising the patients ability to stop bleeding. Injections of vitamin K or oral supplementation sometimes help; when an injection returns the PT to normal, doctors know that the liver is working. If clotting does not improve after the vitamin K injection, the coagulopathy (inability to stop bleeding) might indicate liver disease.

The immunoglobulins are another group of liver-related pro­teins connected with the immune system. They are produced partly by the liver itself, but mostly by the immune system outside the liver. Many patients with chronic liver diseases display high lev­els of immunoglobulins. Specific immunoglobulins, such as IgA, IgG, and IgM, are possible indicators of liver disease, particularly primary biliary cirrhosis and autoimmune hepatitis.

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Platelets

During the clotting process, platelets are the blood cells that form clots; they are stored in the spleen. In cirrhotic patients, the spleen becomes enlarged because of portal hypertension (the blood backs up behind the scarred liver) and causes a condition known as sple­nomegaly, which traps the platelets. Low platelet levels are known as thrombocytopenia. When the spleen is enlarged and platelets are low, cirrhosis is a likely diagnosis.

After a first round of liver function tests, doctors may order more blood tests (see the table on page 161) to confirm a specific diagnosis. Depending on the hospital, the laboratory, and the test itself, it take as little as wo days or as long as two weeks before the results of a given test are known.

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Imaging Studies and the Liver

After the medical team has collected the chemical information from various blood tests, it is helpful for the doctors to be able to view the entire liver. They will look at its size, noting whether it has shrunk with scarring or grown larger, its location, and any possible growths. They will also check for gallstones in the gallbladder.

The imaging studies performed on liver patients are sonograms (ultrasounds), computerized axial tomography scans (CT or CAT scans), and magnetic resonance imaging (MRIs). None of these procedures involves surgery, and all are performed while the patient is awake, often in a doctor’s office.

Our use of the term or terms Multaq Attorneys is for descriptive purposes only. There is no relationship between the owners of this website and the maker of the product discussed in this post. Our use of the words Recall, Class Action Lawsuit and other similar words related to an event do not necessarily mean that this event has occurred. Refer to the website of the United States Food and Drug Administration for information on drug or medical device recalls. If a Class Action Lawsuit is formed in relation to the product discussed in this post we will provide that information at the time the Class Action is formed. A Class Action Lawsuit is not required to exist for you to file a lawsuit if you have been injured by the product discussed in this post.
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Multaq Attorney Discovery

By admin | Published January 19, 2012
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A high bilirubin level, or jaundice, is a hallmark of liver dis­ease, but it can also be related to other conditions. When jaundice is present in a person with liver disease, it usually signals cho­lestasis (blockage or injury to the bile ducts) or progression of the disease. When elevated bilirubin is found alongside high levels of GGTP and AP, the patient is said to be cholestatic. In this case, the elevated levels of bilirubin, GGTP, and AP may indicate alcoholic hepatitis, primary biliary cirrhosis, primary sclerosing cholangitis, gallstones in the bile duct, liver failure, tumors, viral hepatitis, a flare of autoimmune hepatitis, or a destruction of the red blood cells called hemolysis.

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Elevated bilirubin levels can also indicate Gilbert’s disease, which is a common, benign, inherited condition that affects bili­rubin uptake and metabolism by the liver. It is estimated that 6 to

10   percent of adults have the syndrome, though most are unaware of its presence. Usually, doctors discover it while screening for unrelated problems. A bilirubin measurement will indicate that the level of unconjugated bilirubin is elevated. This is bilirubin before it has been metabolized by the liver. This completely harm­less condition has no clinical significance or complications, and no treatment is needed.

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Liver Proteins

The liver produces many proteins, including albumin, prothrom­bin, and ceruloplasmin (containing copper). Sometimes inflam­mation in the liver stimulates the production of gamma globulin in other organs as well as in the liver. Abnormal levels of these pro­teins are abnormal and may signal disease in the liver.

A severely damaged liver cannot make albumin efficiently, so an abnormally low level of this protein can point to liver damage such as cirrhosis and chronic liver diseases. However, a malnourished person or someone otherwise in ill health might also lose the ability to produce albumin without experiencing a specific liver disease, so further tests are indicated to sort this out.

Our use of the term or terms Multaq Attorney is for descriptive purposes only. There is no relationship between the owners of this website and the maker of the product discussed in this post. Our use of the words Recall, Class Action Lawsuit and other similar words related to an event do not necessarily mean that this event has occurred. Refer to the website of the United States Food and Drug Administration for information on drug or medical device recalls. If a Class Action Lawsuit is formed in relation to the product discussed in this post we will provide that information at the time the Class Action is formed. A Class Action Lawsuit is not required to exist for you to file a lawsuit if you have been injured by the product discussed in this post.
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