Multaq Warning Advice
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.
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