Multaq Liver Failure Legal Update

Multaq Liver Failure : Collectively called statins, this class of medications is used to treat elevated cholesterol and triglycerides. All statins work in similar ways, but the individual varieties may have differing degrees of potency. These medications have received extensive attention because they are widely used and have a propensity to cause elevations in liver enzymes (AST/ALT). It is estimated that 1 to 3 percent of patients taking statins will develop signifi­cantly elevated enzymes (greater than three times the upper limit of normal).

As the treatment guidelines for lowering cholesterol have become more aggressive over the past decade, the number of people taking these medications has increased substantially, leav­ing many clinicians (usually primary care providers) unclear about whether these medications should be used in patients with underlying liver disease and when to stop if liver enzymes become abnormal. These questions have not been fully answered, but statins seem extremely safe and should not be avoided by patients with underlying liver diseases if the statins are indicated for the treatment of high cholesterol or triglycerides. This is a clear case of the benefits outweighing the risks.

Most patients who develop an increase in liver enzymes during therapy with statins will have only transient and mild elevation, which will resolve if the medication is stopped.

Ezetimibe (Zetia). This is another cholesterol-lowering medica­tion, but it is not in the statin class of drugs. This medication inhibits the intestinal uptake of cholesterol and is often used with a statin when cholesterol cannot be lowered by a statin alone. In extremely rare cases, reports have connected it with drug-induced liver injury, but it is regarded as having an excellent safety profile. However, it is currently undergoing réévaluation of its effectiveness in preventing heart disease and stroke.

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More than two dozen different blood tests are in current use to monitor specific liver functions and indicate dis­orders. That number does not include popular imaging studies, such as sonograms, CT scans, and MRIs. For patients, the landscape of liver testing resembles a confusing maze of high-tech jargon and initial-talk.

The liver is an unusually complex organ, responsible for filter­ing nearly every substance that comes into the body. As a result, it is vulnerable to a long list of potential hazards, from overloads of copper or iron to the hepatitis alphabet.

Many liver tests, such as the liver function tests sometimes referred to as a hepatic function panel (HFP), cannot accurately diagnose diseases because the disorders themselves have so many shared features. What liver function tests can do is to narrow the possibilities, advance the diagnostic procedures a step toward con­firming the doctor s suspicions, and indicate which specialized tests the doctor and patient should undertake next. Imaging tests, too, can point the diagnostic team in the right direction. For some dis­orders, a more detailed scan, such as an MRI, can give a more definitive answer.

Liver function tests indicate how well the liver is performing par­ticular functions and the levels of certain measurements associated with inflammation. Dozens of different LFTs are performed in hospitals, but they all measure the levels of liver proteins, liver enzymes (called trans­aminases and cholestatic liver enzymes), and bilirubin.

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Liver function tests that check the levels of aspartate transaminase (AST) and alanine transaminase (ALT) are looking for inflamma­tion or injury to liver cells-—-in technical terms, hepatocellular liver injur)’’. When the liver is damaged, AST and ALT often leak into the bloodstream, so a blood test result that detected transamines would be a possible indicator of liver damage. However, AST is also found in the heart, kidneys, and muscles, so an elevated amount of AST doesn’t always mean a liver problem. When it is coupled with elevated ALT, which exists only in the liver, a higher AST level indicates that liver damage is more probable.

The extent of liver damage cannot be determined by high transaminase levels alone. If a patient drinks alcohol a few hours before the blood test or works out in the gym the morning his or her blood is drawn, the transaminase levels may be mildly elevated. On the other hand, if alcohol abuse damaged the liver five years ago, the transaminase level may be normal, but still there could be residual liver damage.

Moreover, men tend to have higher transaminase levels than women, and African American men usually show higher AST and ALT levels than Caucasian men. Almost everyone’s transaminase levels are higher in the morning than they are later in the day.

High, levels of AST and ALT serve as the first clues along a path of diagnostic testing to pinpoint what is wrong. Elevated transami­nase levels might indicate strenuous exercise or recent alcohol use, but they could also be caused by a fatty liver, alcoholic liver dis­ease, viral hepatitis, autoimmune hepatitis, a genetic liver disease, a tumor, heart or lung failure, or some toxic injury to the liver.

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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Propecia Lawsuit Information

Propecia Lawsuit: Even when erectile function is reduced following surgery, sen­sation in the penis remains, as does the ability to have an orgasm—although without a prostate gland and seminal vesicles, orgasms will be “dry,” with no discharge of semen. And because surgical removal of the prostate removes a section of the urethra, some men experience a slight reduction in penile length following surgery. Both changes may take some getting used to, but they aren’t enough to ruin the experience for men who really want to have a satisfying sex life after surgery.

Besides, research shows that improvements in both continence and potency can occur even 2 or more years following surgery. It may be a slow road back for some men, but positive changes can happen even when they don’t happen in the first year. Sexual func­tion may continue to improve for up to 4 years after prostate removal surgery.

Once removed, the prostate gland is thoroughly examined by a pathologist. Should the results of that examination reveal new information, you’ll discuss that with your medical team and decide whether additional treatments might be called for.

The pathology report is a detailed analysis that describes mar­gin status, final Gleason score, extent of the cancer, and the pres­ence or absence of any disease outside of the prostate capsule. These results are very important and can determine the need for additional therapy (aside from surgery) as well as the likelihood that prostate cancer will not come back. When there is no evidence of any cancer outside of the prostate (so-called organ-confined cancer), the man is said to have a surgical cure. This man has a greater than 90 percent chance of having undetectable PSA at 6 weeks postsurgery and of having that PSA will remain undetect­able for 5 3 years.

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Following any prostate removal surgery, you will need to have a urinary catheter for anywhere from 3 days to over a week. All pros­tatectomies involve cutting the urethra from where it enters the prostate gland and then reattaching it to the bladder. Time is required for this reattachment to heal. A surgical drain is also left in place following all three types of prostate surgery; the drain is stitched in place and can usually be removed the following day if there is no significant drainage in the tubing.

Urinary continence may take some time to return after surgery—1 to 3 months is not abnormal—and nocturnal (nighttime) continence may take longer to return than daytime continence. After catheter removal, retrain the urinary muscles by urinating whenever you feel the urge.

Do Kegel exercises every day: Contract and release the sphinc­ter muscles as though you were going to urinate, then stop the flow of urine. If you can do 300 or so repetitions a day, your continence is likely to return more quickly. I suggest doing Kegels in the weeks before surgery as well.

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Following prostate surgery, I encourage men to take an active role in restoring sexual function. Much of this is about maintaining ade­quate blood flow and oxygen to the penis with erectile dysfunction medications (Viagra, Levitra, Cialis) or other methods. Some men are not good candidates for oral ED drugs owing to heart problems or the use of certain medications that can create harmful interac­tions. Other methods like vacuum pumps or intracavernosal injec­tions of a drug called alprostadil are better options for these men. Rather than using ED-reversing methods just for intercourse, men are advised to use them on a regular schedule during the recovery period. This helps keep erectile tissues healthy while nerves that control erection recover from the trauma of prostate removal.

During my residency training, we used to tell patients they’d have to wait a year after prostate surgery for their erections to return to normal. This is no longer the case. Many leading author­ities in the field agree that early restoration of blood flow strongly supports long-term satisfaction with erections. The blood that enters the penis is rich in oxygen, which prevents or delays the onset of anj’ fibrosis or scarring within the tissues necessary for a normal erection. Now I think that a penile rehab program can start as early,as a few weeks after the catheter is removed, espe­cially once the man regains full urinary control (which will help him feel more confident in the bedroom and perform better sexu­ally). Other methods like acupuncture may also be helpful; at this writing, studies on this are ongoing at our center.

So far, small studies show that penile rehabilitation improves a man’s chances of restoring normal erectile function after surgery (as long as he has had nerve-sparing surgery and had normal erec­tile function before surgery). Speak with your doctor about penile rehabilitation if it’s something you wish to pursue. Remember, if you don’t use it, you could lose it!

Our use of the term or terms Propecia 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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Reclast Side Effect Announcement

Reclast Side Effect:Blood pressure is not just influenced by physiological factors like varying heart rates and the muscular tone of blood vessels. Genetic susceptibility may also influence a person’s blood pressure. Just as in diabetes research, determining which specific genes are responsi­ble for blood pressure and their relative contribution to hypertension has been very difficult. Researchers do not expect that a mutation in a single gene is responsible for hypertension. Most likely, the in­terplay of many genes promotes hypertension. Environment and lifestyle can also contribute to hypertension through a complex gene-environment interaction. One example of this type of inter­action is excessive salt (sodium) intake and retention.

Excess salt intake can lead to hypertension. However, each person responds to salt differently. At the extremes, some people are very sensitive to salt, whereas some are insensitive. These differences suggest that salt sensitivity has a genetic component. The renin-angiotensin system evolved to combat dehy­dration by retaining sodium and maintaining blood pressure when the body loses sodium. In this system alone, it is possible that many genes could be altered in a way that promotes hypertension.

Research on genes underlying hypertension is still in its infancy and will require many more studies to identify the specific genes responsible. Future research may also yield new medications to reduce hypertension. Because hypertension plays such an impor­tant role in kidney disease, these new medications may give physi­cians better tools to prevent kidney failure.

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Obesity contributes to hypertension as well as kidney damage induced by other diseases discussed in this chapter. Kidney dis­eases themselves are associated with increased blood pressure by a variety of mechanisms. Obese people often take in an excessive amount of salt, which can lead to hypertension. The high pressure on the glomerulus can slowly degrade its filtering capacity and pre­cipitate reactions similar to those that occur in diabetes-induced kidney failure. In addition, accumulating fat can contribute to hy­pertension. Considering that obesity, hypertension, and diabetes often accompany one another, it is hard to know which problem came first. However, obesity is often the primary cause of hyper­tension and diabetes.

We know that hypertension slowly destroys the kidneys’ ability to filter the blood, but how does hypertension lead to kidney fail­ure? With prolonged hypertension, the excess pressure can injure small blood vessels in the kidney and can destroy the filtering abil­ity of the glomerulus, leading to kidney failure. Using the hose metaphor, if you attach cheesecloth tightly over the end of the hose, water will flow through the cheesecloth without harming it. But if you pinch the hose, increasing the flow pressure, the cheesecloth will begin to degrade and eventually rupture.

Glomerular diseases are a complex set of disorders and are the third leading cause of kidney failure in the United States, accounting for 5 percent of cases. Glomerular disease often results in inflamma­tion of the glomerulus, which can eventually cause the formation of scar tissue. As a result, protein leaks into the urine instead of being absorbed back into circulation. Like diabetes and hypertension, glomerular diseases slowly destroy the filtering ability of the glom­erulus. Excess pressure on the sensitive glomerulus can lead to kidney failure. The three main causes of glomerular diseases are autoim­mune diseases, hereditary nephritis, and infections.

The bodys immune system provides the first line of defense against infections by generating antibodies and immunoglobulins. However, there are times when antibodies and immunoglobulins cause harm to the body which can lead to a number of medical problems. One of these complications is the deposit of antibodies in the glomeruli, causing inflammation.

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Lupus erythematosus, another autoimmune disease, primarily involves inflammation of the skin and joints. This disease affects more women than men. When lupus erythematosus attacks the kidney, autoantibodies form or are deposited in the glomeruli and cause scarring. Drugs that suppress the immune system are gener­ally used to treat the inflammation in the kidney.

One inherited form of glomerular diseases is Alport syndrome. Alport syndrome not only affects the kidney but may also impair vision and hearing. More men have difficulty with this disease than women, experiencing a decline in kidney function in their twenties and reaching total kidney failure by age 40.

Glomerular diseases are also caused by infections in other parts of the body. Similar to what happens in autoimmune diseases, the high number of antibodies produced to combat these infections can deposit in the kidneys and reduce kidney function. Although infections usually do not cause permanent damage, people with chronic infectious diseases like HIV/AIDS and hepatitis C have a risk of developing chronic kidney failure.

Focal segmental glomerulosclerosis is another glomerular dis­ease that disproportionately affects African Americans. It results in scarring of the glomerulus or clustering of glomeruli in a spe­cific segment of the kidney. Focal segmental glomerulosclerosis can be difficult to diagnose and treat. Biopsies to search for scar­ring in kidney tissue are the best means of a diagnosis. (A biopsy is a procedure in which a small amount of tissue is removed from the body for investigation and testing.) Flowever, if the biopsy sample is from an unaffected area of the kidney, scarring will not be evident. Thus, repeated biopsies in different segments of the kidney are needed to confirm a diagnosis of focal segmental glomerulosclerosis.

Our use of the term or terms Reclast Side Effect 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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Reclast Lawyer Information

Reclast Lawyer: The incubation period—the time between the entrance of the virus into the body and the initial appearance of symptoms and signs of the disease—of acute HCV is about six to eight weeks; however, it may be as short as two weeks or as long as about five months.

When symptoms of acute hepatitis C do occur, they are usually similar to those that characterize acute hepatitis in general. However, most people with acute hepatitis C experience no symptoms. Only about 25 to 35 per­cent of individuals with hepatitis C manifest any symptoms at all. Usually, these symptoms are nonspecific and may easily be mistaken as stemming from some­thing unconnected to hepatitis C, such as the flu. Symptoms, if they do occur, may include fatigue, decreased appetite, and weakness. Occasionally, a person may experience a skin rash and/or muscle and joint aches. People with acute hep­atitis C become jaundiced approximately 25 percent of the time. It has been shown that people with another liver disease, such as hepatitis B, who become additionally infected with acute hepatitis C, are particularly likely to experience a severe course of acute hepatitis C. Usually, the physical exam of a person with acute hepatitis C appears normal. Occasionally, a physical exam will reveal an enlarged and tender liver, jaundice, and/or a rash.

As mentioned previously, approximately 35,000 new acute hepatitis C infections are estimated to occur each year. However, it is also estimated that only 25 to 30 percent of these newly acquired infections are actually diagnosed. The most likely explanation for this low percentage is that most people with acute hepati­tis C are either asymptomatic or have very vague symptoms. Therefore, evalua­tion by a doctor during the acute stage of this disease is not common. As such, the majority of people with hepatitis C do not discover that they harbor this virus until years or, often, decades later. Therefore, there are probably millions of peo-pie who currently have hepatitis C and have no idea that they are infected. How­ever, if a person sees her doctor for an evaluation of symptoms, acute hepatitis C is usually detected from abnormal blood test results.

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Transaminases (AST and ALT) are often quite elevated initially. Levels of approximately 200 to 600 IU/1 can occur. (The normal range is approximately 0 to 45 IU/1.) Elevations in transaminases usually occur approximately six to eight weeks after infection with HCV (or within a range of two to twenty-six weeks). As the disease progresses, transaminases typically decrease. Transaminase levels often fluctuate between normal (or near normal) and elevated before perma­nently returning to normal. This fluctuation is a typical characteristic of hepati­tis C. Persistent normalization of transaminases by six months usually indicates that acute hepatitis C has resolved. This occurs 15 to 25 percent of the time. If transaminases remain elevated (usually around two to three times normal) after this period or if the ALT levels elevate after a period of normalization, it usually indicates progression to chronic hepatitis C, which occurs approxi­mately 60 to 85 percent of the time. Progression to chronic disease is always ac­companied by an elevated HCV viral load.

Cholestatic liver enzymes (AP and GGTP) are usually only mildly elevated during acute hepatitis C—around two to three times normal—and bilirubin levels are usually normal. Around one-fourth of all people with acute hepatitis C become jaundiced. Even among these people, bilirubin levels usually normalize rapidly, usually within about one month.

Hepatitis C is limited to acute infection in around 15 to 40 percent of people. Typically, those people who suffered from the most symptoms (such as those who were jaundiced) are the ones most likely to clear the virus. These fortunate people have a complete resolution of symptoms, physical signs, and any LFT ab­normalities due to infection with HCV. Also, their HCV RNA will permanently return to normal. These people do not develop chronic infection and. therefore, are not at risk for the long-term consequences of hepatitis C. Nor can they trans­mit HCV to others. However, eradicating one particular “strain” of HCV does not protect a person from becoming infected with other “strains” of HCV, or from other hepatitis viruses such as hepatitis A and B (see page 131 for a dis­cussion of the different strains of HCV, also referred to as genotypes). Also, these people will never be allowed to donate blood, as they will always have the anti­body for hepatitis C present in their blood.

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HCV is a virus that is very difficult to clear from the body. Thus, most people who become infected with HCV (acute hepatitis C) develop chronic disease (chronic hepatitis C). In fact, approximately 60 to 85 percent of infected people develop chronic hepatitis C. This is in stark contrast to the incidence of progres­sion from acute to chronic in other forms of viral hepatitis. For example, hepati­tis B progresses to chronic disease only about 5 percent of the time when the infection is acquired as an adult. And hepatitis A never leads to chronic disease. It appears that the immune system is not very efficient in clearing HCV. So, what makes HCV so formidable?

The genes that make up HCV can vary slightly from one strain to another. These different genetic variations of HCV are known as hepatitis C mutants, or quasispecies. The entire hepatitis C viral population that is present in a person in­fected with HCV is made up of a conglomerate of related, yet slightly different, HCV species. This virus population usually consists of one HCV mutant group that is strongest and dominant and numerous other HCV mutants that are weaker. These mutants are all similar in structure but differ slightly from one another. These slight variations in structure account for the fact that some HCV mutants are stronger and thus better equipped to tight the immune system than other HCV mu­tants. This is analogous to Darwin’s theory of evolution: the survival of the fittest.

The fact that HCV is such a resourceful and cunning virus probably accounts for why most people progress to chronic disease. When HCV is being attacked by the immune system during the acute infection, it can mutate into a stronger quasispecies variant. In this manner, HCV is able to outwit the body’s immune system and thwart its attempts to eradicate it. Thus, HCV tricks the body’s im­mune surveillance and escapes eradication, allowing for progression to chronic disease. This partly explains why long-term response rates to therapy with inter­feron, although getting much better, are still not 100 percent suc­cessful. It also may explain why it is so difficult to create a vaccination against HCV.

Certain factors have been identified as being predictive of which people are most likely to progress to chronic disease (that is, least likely to clear acute HCV).

Our use of the term or terms Reclast 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 Warnings Announcement

Multaq Warnings : Many infants are born with mild elevations in their blood unconju- gared bilirubin concentrations. In most cases, this is due to neonatal jaundice or neonatal hyperbilirubinemia. Neonatal jaundice occurs because enzymes and other cellular factors involved in bilirubin metabolism in the liver are not yet mature. The activity of UDP- glucuronosyltransferase, the enzyme that conjugates bilirubin, is decreased in newborn babies, especially those bom premature. In addition, newborns usually have increased destruction of red blood cells leading to increased production of bilirubin.

In most cases, there are no untoward consequences of neonatal jaundice. The condition usually resolves soon after birth. Infants with neonatal jaundice, usually those born premature, are at risk for ker- nicterus if the blood unconjugated bilirubin concentrations are very high. These babies may be treated with phototherapy until they mature to the point when their livers can adequately conjugate bilirubin and secrete it into bile.

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Biliary atresia is defined as the lack of a lumen in part or all of the bile ducts outside of the liver, causing complete obstruction of bile flow. In reality, there may be some bile flow, but it is severely decreased. New­born babies with biliary atresia present with jaundice, and the chal­lenge for the pediatrician is to differentiate this condition from other, less serious causes of jaundice.

Biliary atresia occurs in about one in ten to fifteen thousand live births. In some cases, it is associated with other congenita! malforma­tions. Alagille syndrome is an inherited condition characterized by bil­iary atresia and decreased numbers of smaller bile ducts within the liver. Children with Alagille syndrome suffer from associated conditions that include abnormal pigmentation in the eyes, heart valve problems, bone problems, and neurological changes. They also have characteristic phys­ical features such as a broad forehead, pointed jaw, and bulbous tip of the nose. There are also cases of biliary atresia with decreased bile ducts in the liver without these syndromatic malformations.

Without treatment, the prognosis of babies with biliary atresia is extremely poor. Most die within one year of diagnosis. Some surgical procedures have been shown to prolong survival, such as the commonly performed Kasai procedure. These surgical procedures attempt to restore the flow of bile from the liver to the intestine. They are usually of temporary benefit; in the long term, most children do not do well. Liver transplantation provides the best overall option for children with biliary atresia, even for those who have had previous Kasai operations. Liver transplantation not only reestablishes bile flow but also replaces an organ that may be damaged as a result of bile duct obstruction. The long-term prognosis for most children who receive liver transplanta­tion for biliary atresia is excellent.

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Should a woman with a chronic liver disease, who is able, become preg­nant? This question goes beyond science and medicine, and I cannot tell all such women what to do in this regard. Some facts, however, should be considered when a woman with chronic liver disease decides to, or becomes, pregnant.

In advanced cirrhosis, pregnancy can be life-threatening to the mother and fetus. Most women with very advanced cirrhosis are infer­tile, so pregnancy is not an issue. But elective abortion should be con­sidered as an option in cases where the lives of the mother and fetus are at high risk.

Most questions about pregnancy arise in women who have either chronic hepatitis B or chronic hepatitis C without cirrhosis or early cir­rhosis. In chronic hepatitis B and C, the mother should realize that there is a small risk of passing on the disease to her children. This consider­ation aside, pregnancy is probably not high risk in patients with hepati­tis B and hepatitis C who do not have cirrhosis. The risk increases in women with cirrhosis, even if they do not have clinical complications.

Autoimmune hepatitis generally affects young women of child­bearing potential. In autoimmune hepatitis, the drugs used to treat the disease are one issue. Prednisone and prednisolone are probably rela­tively safe in pregnancy, but the effects of azathioprine (Imuran) on the unborn baby are not known. If a woman with autoimmune hepatitis desires to become pregnant, azathioprine should be stopped and only prednisone or prednisolone should be used to manage the disease. If a woman with autoimmune hepatitis becomes pregnant while taking aza­thioprine, elective abortion should be considered as an option. If the woman wants to carry the pregnancy to term, all attempts should be made to stop the azathioprine as soon as possible and manage the dis­ease with only prednisone or prednisolone for the remainder of the pregnancy. Finally, a woman with autoimmune hepatitis must realize that if a flare-up in disease activity occurs during pregnancy, her con­dition could become quite complicated.

Other important issues related to pregnancy are the inherited liver diseases such as Wilson disease, hemochromatosis, and alpha-1- antitrypsin deficiency. These disorders can be passed on to the baby. Professional genetic counseling should be obtained in cases where the prospective parents have questions, including situa­tions where the disease runs in the mother’s and father’s families but the parents are not affected. Hemochromatosis, Wilson disease, and alpha-l-antitrypsin deficiency can theoretically be detected in the fetus prior to birth, but fetal testing for these diseases is not routinely per­formed. If testing is performed, elective abortion is an option if a fetus is found to be affected.

A few women have become pregnant and delivered healthy babies after liver transplantation. Pregnancy in a liver transplant recipient is a very special case. Such patients require complex medical care by sev­eral different specialists.

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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Actos and Bladder Cancer

Actos and Bladder Cancer : The urinary system (Figure i-i) is very important and has a pretty tough job to do in everyone’s body. It filters your blood and produces waste products in the form of urine. More importantly, it allows you to store urine until it is convenient to urinate. Just think, if we couldn’t store urine, then we would constantly leak waste products. This would make life very difficult and get in the way of things we do during the course of a normal day. The human urinary system is made up of the kidneys, ureters, bladder, and urethra. Men have a prostate gland in addition to the previously mentioned components.

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Your kidneys are two bean-shaped organs that reside in the rear of your abdomen, just under the diaphragm on the left and below the liver on your right side. The kidneys filter blood and produce urine. They are extremely important to life and work extremely hard to filter waste from your bloodstream. Just imagine, the kidneys filter approximately 20 percent of your blood each minute. Although most people have two kidneys, some individuals have one and do just fine. The kidneys function independently, and when one is not working as well, the other compensates and filters more blood. In addition to filtering blood and producing urine, your kidneys help to regulate your blood pressure. They produce special hormones and control the salt and water balance in your body. Normally, the kidneys do not release blood cells into urine. This is why it’s important to be evaluated by a doctor if you have blood in your urine.

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URETERS

After urine is formed by the kidneys, special nerves and muscles in the renal pelvis propel urine downward into the ureters. The ureters are small tubes, very much like the renal pelvis, that allow passage of urine from die kidneys down to the bladder. They function as drainage pipes for the kidney. The ureters have nerves and layers of muscle that propel urine to the bladder. There is so much that your body does that you may not realize. Like the renal pelvis, the ureters are also lined with transitional cells serving as a continuation of die uxothelium.

 

Our use of the term or terms Actos and Bladder Cancer 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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Actos and Bladder Cancer

Actos and Bladder Cancer :

BLADDER

The ureters connect to the bladder, which is a muscular, balloon-lilce structure in the pelvis. The bladder functions as the storage unit of the urinary system. It can hold upward of 500-600 mL (2 cups) of urine. Hie bladder is very thick and elastic with multiple layers .

An inner layer made up of transitional cells forming the urothelium; under this lies a thin layer (the lamina propria), with blood vessels supplying the bladder; and finally a thick muscular layer that contracts to empty your bladder. There is a layer of fat surrounding the muscular layer.

The bladder expands in relation to the amount of fluid inside of it Bladder contraction is under complex control by your central nervous system. When your bladder contracts during urination, urine passes though the urethra before leaving your body. The inner cells, closest to the bladder, are transitional cells, whereas the cells closest to the outside of the body are squamous cells resembling skin. Although the urethra has different lengths in men and women, it functions the same. In men, the urethra passes through the prostate gland near the bladder.

 

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PROSTATE

The prostate, a walnut-sized organ that lies at the base of the bladder in men, plays a role in male fertility. Along with the seminal vesicles, the prostate gland produces fluid that helps sperm after ejaculation. Although the urethra passes through the prostate, the gland itself does not add much, if anything, to the volume of urine that reaches the bladder. As the urethra passes through the prostate, it is lined by transitional cells comprising the urothelium. Therefore, tilings that affect the urothelium can affect the prostate as well. This is very important when it comes to staging bladder cancer.

 

The urethra is a hollow tube lined with transitional cells at its beginning that connects the bladder to the outside world. The structure of the urethra is different in men and women. The urethra is short in women and is much longer in men due to the presence of the penis. The cells lining the

urethra change along its length. The inner cells, closest to the

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Our use of the term or terms Actos and Bladder Cancer 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

Multaq Attorneys :

Is Primary Sclerosing Cholangitis Linked to Cancer?

Two possible malignancies are linked to primary sclerosing cholangitis. One is cholangiocarcinoma, or cancer of the bile ducts, and the second is colon cancer. Primary sclerosing cholangitis patients have a 10 to 15 percent lifetime chance of developing cancer in the bile ducts, most often when they have inflammatory bowel disease or cirrhosis. With a higher risk of colon cancer as well (especially patients with both PSC and ulcerative colitis), PSC patients are strongly advised to have annual colonoscopies.

Can Primary Sclerosing Cholangitis Be Cured?

Primary sclerosing cholangitis is an incurable disease, but its symptoms can be treated and its progression slowed. To resolve itching, patients should sample the range of available medications, including prescription medications such as cholestyramine (Questran), which binds bile salts in the intestine and allows them to be eliminated with stool, thereby reducing their accumulation in the liver and skin.

More serious complications of primary sclerosing cholangitis are osteoporosis and osteomalacia (bone-calcium deficiency). Patients are advised to increase their intake of calcium with vitamin D to boost absorption and to consider bone-density medications if these conditions are noted on a bone-density scan.

Gallstones, another complication frequently seen in primary sclerosing cholangitis patients, can be treated as they are in patients who do not have PSC.

If infections occur in the bile ducts, they should be treated with antibiotics. Restricted salt intake as well as use of diuretics can help reduce swelling of the abdomen and feet, once PSC becomes cirrhosis. Patients who are deficient in vitamins A, D, and K can supplement their diets.

 

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So How Do You Treat Primary Sclerosing Cholangitis?

One of the most successful treatments for primary sclerosing cholangitis is balloon dilation, or stenting, a procedure used to open narrowed bile ducts. During stenting, the physician places a small balloon-tipped tube into the constricted duct; once it is in place, the balloon is inflated to open up the duct and permit bile flow. Success rates of up to 85 percent have been reported with the initial dilation. Stents, or plastic tubes, are often inserted into the ducts to keep them open. In spite of this, renarrowing occurs in up to half of patients, so the procedure usually must be repeated and the stents need to be changed.

Only one drug, ursodeoxycholic acid (marketed as Ursodiol and Actigall), is used to treat PSC patients. However, it has not been definitively shown to improve survival or to delay the need for transplantation.

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The most worrisome symptom connected with PSC is liver failure, and if failure occurs, the only treatment option is a liver transplant. Fortunately, liver transplantation has advanced to the point where it is a proven mainstream treatment for severe,


chronic liver disease. The survival rate for liver-transplant patients is now well over 90 percent, and transplant patients can expect a high quality of life after their recovery. Patients like Ben, whose symptoms can be managed for years with medications and supplements, can have every expectation of maintaining their normal life expectancies.

 

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 Warning

Multaq Warning :Organ transplants strike most people as exotic procedures, but the fact is that liver transplants have been around for about 40 years. The first successful transplant was performed in 1968, and since then this surgery has become almost routine. Even better, the success rate of this transplant has become increasingly predictable, with transplant patients surviving two decades or more after their surgeries. In the vast majority of cases, the patients lead normal lives, with no restriction on vigorous work and play.

About 5,000 liver transplants are performed in the United States each year, at more than 125 transplant centers. When a doctor estimates that the patient cannot live more than two years without a new liver, he or she will enter the patient’s name on the waiting list for a new organ. Indications of liver failure (such as worsening jaundice) or of advanced cirrhosis (such as ascites or encephalophathy) justify a referral, and patients whose chronic liver disease has progressed to liver cancer should also be evaluated for a transplant. Physicians may even order evaluations when the patients symptoms, such as pruritus or fatigue, are dramatically affecting the patient’s quality of life, even if the disease itself may not have progressed to the transplant stage.

Some patients, unfortunately, will not qualify for a transplant because they exhibit certain conditions, known as absolute contraindications, that would prevent the transplants success. Among the absolute contraindications are serious heart or lung disease, active uncontrolled infection, active alcohol or drug abuse, AIDS (but not HIV), metastatic liver cancer (liver cancer that has spread to other parts of the body), and cancer elsewhere that did not originate in the liver.

Borderline candidates for successful transplants are patients who display relative contraindications. These patients are not necessarily denied referrals for a new liver, but they are evaluated very carefully and may or may not be granted a transplant if they exhibit morbid obesity, failed kidneys, advanced age (older than 70 years, with disease of other organs), previous cancer in any organ, malnutrition, HIV, extensive portal vein thrombosis (a blood clot in the portal vein), or a failure thus far to adhere to physicians’ medication or wellness regimens.

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The doctors approval is a patient’s first step toward obtaining a new liver. The patients next step is a meeting with the transplant team-—-liver specialists (hepatologists), a transplant surgeon, an anesthesiologist, a social worker, a psychiatrist, and possibly other doctors, such as heart or lung specialists, depending on the patient’s condition—and an evaluation by the team. Additional MRIs and diagnostic tests such as a colonoscopy, blood tests, and upper endoscopy (to check for esophageal varices) are ordered, and if the medical team concludes that the patient is a suitable candidate for a transplant, he or she is added to a waiting list.

In 2002, the system for distributing new livers was revised. The old system had been widely criticized because of the public’s perception of inequalities based on fame and or financial status. The new system, the Model for End-Stage Liver Disease (MELD), is a mathematical score that does not recognize celebrity or favoritism. Instead, the MELD score calculates the severity of the patient’s liver disease on the basis of the mathematical probability (derived from the results of three blood tests) of the patients dying within three months without a transplant. Patients with liver cancer receive a different MELD score, which measures the status of the cancer. Simply put, the sickest patient gets the new liver.

During the waiting period, patients should be as active as possible because their strength and stamina will be a tremendous help to them in their recovery from the surgery.

Patients who are not hospitalized while waiting for a liver are asked to carry a beeper or a cellular phone so the transplant team can notify them immediately when a liver is located. The transplant center performing the surgery must accept the liver within one hour of it being offered, and if the hospital staff cannot contact the patient, they will call (or beep) the next patient on the list. If the transplant recipient is feeling well when the call comes, with no fever or signs of a developing illness, then he or she should proceed to the transplant center immediately. Considerations such as babysitters, pet care, transportation to the hospital, and a packed suitcase should be arranged in advance so the patient can leave at a moment’s notice.

In the case of complete transplants-—-that is, when the donor’s entire liver is transplanted into the recipient-—-the donor will be a newly deceased or a brain-dead person with a healthy heart and circulatory system. A family member of the donor will have signed a consent form for the donation. However, even if the donor had, in life, indicated a wish to donate his or her liver, several factors can prevent the donation: If the prospective donor has been diagnosed with cancer, AIDS, or active hepatitis B, or tests positive for HIV, then that person’s liver cannot be used. In addition, the donor’s liver function tests should typically be in the normal range, and the liver shouldn’t contain more than 30 percent fat, as fatty livers typically are rejected by the recipients body shortly after the transplant. The donor should be relatively young (under 60, if possible), and the body size and blood type should be similar to the recipient’s. Livers from donors up to age 70 have been successfully transplanted, as have those from donors who have been diagnosed with hepatitis C, if the recipient is also a hepatitis C patient.

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Liver transplantation cures the liver failure that led to the need for the transplant. However, some diseases, such as hepatitis C or fatty liver, may recur in the new liver and, in rare cases, may lead to failure of the new liver. If failure happens, it typically occurs 10 to 20 years after transplantation. Recurrence of liver disease is a particularly strong possibility for patients whose transplants were necessitated by chronic hepatitis C. This problem is receiving a great deal of research attention in transplant centers around the world. Recurrence of a few other diseases, including PSC and PBC, have been reported infrequently.

For most patients, life and a return to normal health can be expected after a transplant. Women of childbearing age can become pregnant a year after receiving their new livers, and most patients can return to their previous occupations. Quality of life can be high, especially for patients who commit to managing their health with diet and exercise and careful adherence to their prescribed medications. Regular follow-up by the transplant team also assures a life-preserving and -enhancing outcome.

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 Warnings Information

Multaq Warnings : Insulin, the substance that keeps our glucose (blood sugar) levels from becoming too elevated, guides glucose from our bloodstream into the body’s muscle, fat, and liver cells. The cells convert the glucose into energy, but if the glucose isn’t metabolized correctly (i.e., if the cells resist the insulin and won’t allow it to do its job), then we produce less energy and feel fatigued.

People who are insulin-resistant can’t use insulin efficiently, and glucose builds in the blood, prompting the pancreas to produce even more insulin in an attempt to rid the body of the excess glucose. The result is an abundance of fatty acids that are converted to fat, which is stored in the liver, creating nonalcoholic fatty liver disease. Almost all people with NAFLD are insulin-resistant. Although overweight people are more likely to exhibit insulin resistance than people of normal weight, a sedentary lifestyle and a high-fat, high-sugar diet triggers insulin resistance regardless of body weight or body mass index.

The combination of factors and related disorders of metabolism (obesity, insulin resistance, diabetes, hypertriglyceridemia, and hypertension) comprises the group of findings known as the metabolic syndrome. People with the metabolic syndrome generally also have NAFLD, which in some cases will have progressed to NASH.

An easy way to distinguish between nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) is to put them into alphabetical order: NAFLD, or fatty liver disease, comes before NASH, or nonalcoholic steatohepatitis. This mnemonic is helpful because it reflects the order in which the two diseases occur: fatty liver disease arises first and can progress to nonalcoholic steatohepatitis.

Here are some facts at a glance:

•       Simple fatty liver (which is, just as its name describes, an accumulation of fat in the liver) is the beginning stage of nonalcoholic fatty liver disease. It is caused by insulin resistance, meaning that the insulin produced in the body is less effective than it should be. The primary factor in the development of insulin resistance is obesity, especially central obesity, or the accumulation of a disproportionate amount of weight in the abdomen. Simple fatty liver is relatively harmless and often disappears with weight loss.

•       The next stage of nonalcoholic fatty liver disease is nonalcoholic steatohepatitis. When NASH occurs, the liver is still fatty, but it also becomes inflamed (hepatitis) and liver cells can be destroyed. It can progress to scarring of the liver (fibrosis) and development of severe liver diseases, including cirrhosis, which is the last stage of NAFLD.

The Centers for Disease Control estimates that an astonishing 90 percent of people who are obese or have been diagnosed with type 2 diabetes also have simple fatty liver. About 20 percent of them have NASH, and 10 percent have cirrhosis.

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A high-fat diet, obesity, and insulin resistance are the most common causes of nonalcoholic fatty liver disease, but there are other, less common causes. One is drug-induced steatohepatitis, or more precisely drug-induced fatty liver, which is caused by medications such as prednisone (a steroid), tamoxifen (used in treating breast cancer), estrogen (a female hormone), methotrexate (used to treat

cancer and autoimmune conditions), amiodarone (used to treat heart conditions), or Arimidex (used to treat breast cancer).

Early symptoms of fatty liver disease are vague and nonspecific and include fatigue, malaise, and/or an ache in the upper right abdomen (where the liver is located).

Symptoms that appear in the advanced stages of nonalcoholic steatohepatitis mimic those of cirrhosis and include fluid in the abdominal cavity (ascites), severe itching, swelling (edema) of the legs and feet, weakness, nausea, easy bruising, yellowing of the skin and eyes (jaundice), dark (cola-colored) urine, and mental confusion.

To diagnose the problem, a physician may prescribe blood tests to rule out other liver-damaging conditions, including hepatitis B and C. Because excessive alcohol consumption can can cause fatty liver and alcoholic steatohepatitis (ASH), you may be asked about how much alcohol you consume. Excessive quantities are defined as three or more drinks a day for men and two or more drinks for women.

If fatty liver is suspected, the doctor will probably order further tests, including a liver-function blood test to measure whether enzymes are elevated (signaling possible liver damage), an ultrasound or a CT scan, and possibly a liver biopsy.

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One of the great health-care myths in our society is that iron supplements will pep you up and harmlessly make you a more energetic person. Most adults remember television commercials for breakfast cereals, tonics, and pills packed with iron that promised to cure our iron-poor blood. But few people realize that for anyone whose blood is already rich in iron, the addition of ferrous sulfate or iron supplements can do severe, irreparable damage to the liver and heart.

It is true that iron is essential to good health. Iron helps to form oxygen-carrying hemoglobin in our red blood cells, boosting brain function, producing energy, and giving us strong muscles and immune systems. For people who suffer from iron deficiency, anemia, or whose iron stores become diminished during pregnancy, iron supplementation is essential.

Normally, our bodies absorb only about 10 percent of the iron that we consume in food. Most iron circulates in the body in the form of hemoglobin, but some is also stored in the liver, bone marrow, and spleen. People with hemochromatosis, though, can absorb up to 20 percent or more of the iron they take in—twice as much as they need to replace iron lost from the body.

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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