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Actos Bladder Cancer Lawsuits Notice

By admin | Published January 27, 2012

Actos Bladder Cancer Lawsuits : The incidence of bladder cancer has risen over the past 20 years. Currently, around 54 500 new cases of bladder cancer are diagnosed in the USA each year, and 15 000 cases in the UK. Bladder cancer is the fourth most common cancer in men in the USA and the tenth most common in women. It is one of the most frequent causes of cancer death, accounting for about 10 000 deaths annually in the USA and 5000 in the UK.

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The incidence of bladder cancer varies among different patient groups. For example, there is a 3:1 male-to-female ratio, though the prevalence among women appears to be rising.

The incidence is higher in elderly populations, with a median age at presentation of 60-65 years. No evidence exists for a familial or inherited pattern among any patient group, although occasional family clusters have been recorded. In black people the incidence is lower than in white people; in Asian races it appears to be intermediate. The lifetime risk of developing bladder cancer is:

  • 2.8% for white men
  • 0.9% for black men
  • 1.0% for white women
  • 0.6% for black women.

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Five-year survival for both black and white people during the period 1986-92 (60% and 82%, respectively) was significantly better than the equivalent rates for 1974-76 (47% and 74%, respectively; p < 0.05). It is not really known why there are substantial ethnic differences in incidence and prognosis, although putative factors include differences in diet and nutritional status, differences in gene expression (especially of enzymes that may metabolize carcinogens) and differential access to healthcare.

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

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Actos Side Effects Scoop

By admin | Published January 25, 2012

Actos Side Effects :

WHAT IS THE FUNCTION OF THE BLADDER?

A bladder stores urine and expels it at a convenient time. The bladder is a very useful organ, (tissues working together to accomplish a function), but an individual can live a normal life without one, if required, by surgical creation of a substitute.

 

ARE THERE DIFFERENT TYPES OF BLADDER CANCER?

More than 90% of bladder cancers arise from the lining bladder cells called transitional cells. Bladder cancer is almost always transitional cell cancer. These cells are also present in the urethra (the body tube which drains the bladder), as well as the renal pelvis (inner lining of the kidneys), and the ureters (the body tube draining the kidneys).

Bladder cancer can vary from the non serious, low grade superficial type (approximately 70%), to the invasive, aggressive type that can spread and prove to be fatal (approximately 30%).

5% of bladder cancer is accounted for by squamous cell carcinoma. This cancer is usually secondary to long term inflammation or infection of the bladder. Even rarer is adenocarcinoma, which accounts for less than 2% of all bladder cancers.

HOW COMMON IS BLADDER CANCER?

The American Cancer Society estimates that in 2006,61,420 new cases of bladder cancer were diagnosed in the United States with approximately 73% of those occurring in men. In the same year, this cancer caused approximately 13,060 deaths with approximately two out of three of those being in men. The disease is more common in whites than blacks. The incidence of bladder cancer increases with age in both sexes. When bladder cancer occurs in young people, it tends to grow slower and not be as serious. In men, it is the fourth most common cancer. However, because of the rate of recurrences and long term survival, it is the second most prevalent cancer in middle aged and elderly men. In women, it is the eighth most common cancer. The average age at diagnosis is 65. Over the past decade, there has been both an increased incidence, but also an increased rate of survival for bladder cancer [1]

WHAT CAUSED MY CANCER?

A mutation is a disruption in the DNA of a cell, leading to a loss of regulated cell growth. Mutations can occur spontaneously as we age. It is truly amazing that all of us don’t develop cancer as we are composed of trillions of cells dividing regularly over decades. Fortunately, our cells have repair mechanisms which can often fix damaged cells before cancer arises. In addition, the immune system can destroy cancer cells before they have a chance to grow into tumors.

Mutations and cancer can also be triggered by environmental factors. Certain chemicals have been identified to be particularly effective at inducing mutations in our DNA and subsequent cancer. These chemicals are called carcinogens. Smoking is the most common culprit! Cigarette smoking has a strong link with bladder cancer. Studies have shown approximately 50% of bladder cancer is secondary to tobacco smoke. Smoking releases dozens of carcinogens into the lungs and then into the blood stream. Many of these carcinogens are excreted by the kidneys.

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IT IS TOO DIFFICULT TO QUIT SMOKING; IS THERE ANY SURE FIRE WAY TO QUIT?

Tobacco smoke contains nicotine, an extremely addictive chemical. Men overall find it easier to quit smoking than women. When facing the prospects of losing your bladder to cancer or possibly your life, most individuals will become convinced and many simply stop smoking “cold turkey.” Unfortunately, many choose not to quit until their cancer repeatedly recurs or becomes invasive, needlessly placing their health at risk. For those who need assistance in quitting, nicotine patches, gum, and lozenges are all available over the counter. These products allow the smoker to quit without experiencing the discomfort of withdrawal from nicotine. Many smokers also find hypnosis or support groups useful. In addition, prescription medication is available.

ARE THERE ANY OTHER KNOWN CAUSES?

Occupational exposure may account for up to 20% of bladder cancers. Those exposed to aniline dyes (used to color fabrics), aldehydes (used in chemical dyes and in the rubber and textile industries) and those using organic chemicals (used in a wide range of occupations) are all at increased risk. Individuals previously treated with radiation to the pelvis or having received cyclophosphamide (a type of chemotherapy) are at markedly increased risk for developing bladder cancer. If your well water is high in arsenic, your risk may also be increased. Studies have also correlated obesity and a high fat diet, especially with increased cholesterol, as a possible contributing factor.

CAN I HELP TO PREVENT BLADDER CANCER BY DRINKING MORE FLUIDS?

Surprisingly, the answer may be yes. In a recent study, the relationship of diet to cancer was analyzed in a group of47,000 health professionals.[1] In the case of bladder cancer, those who drank the most fluid (greater than 10 cups/day) had half the risk as those who drank the least (less than 5 cups/day). The type of nonalcoholic beverage was less important than the total amount.

WILL MY CHILDREN BE AT HIGHER RISK OF DEVELOPING BLADDER CANCER?

Although there have been clusters of bladder cancer reported, most researchers believe these may be secondary to risk factors such as smoking and exposure to carcinogens. At this time, there is no convincing evidence bladder cancer risk is hereditary. If an environmental factor caused your cancer and your children are exposed as well, their risk of cancer may be increased.

WHAT IS CANCER?

The basic building block of the body is the cell. Cells are specialized to perform a particular function. Skin cells are distinctly different from liver cells which are different from bladder cells. An organ is composed of various cells working in unison to carry out a body function. Cells eventually get old and die. New cells are created by cell division. When cells are behaving normally, they only generate enough new cells to replace the old dying ones. Occasionally, cell growth becomes unchecked. As the cells continue to divide, a tumor (abnormal growth of cells) may form. Such tumors may be benign (no ability to spread beyond their organ of origin) or cancerous (a malignant tumor with the ability to spread beyond their organ of origin and cause harm and possibly death).

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HOW CAN I TELL IF MY BLADDER CANCER IS LIKELY TO SPREAD?

Larger tumors are more likely to spread than smaller tumors. Another critical concern is the grade of the tumor. Normal cells are specialized, differentiated to perform specific function, and have a typical structural arrangement with surrounding cells. As cancers worsen, the cells become less specialized, less differentiated, and lose their normal structural arrangement, resulting in a higher pathologic grade.

In the case of bladder cancer, pathologists classify them into 3 grades based on a number of criteria:

Grade 1: low grade, well differentiated Grade 2: intermediate grade, moderately differentiated Grade 3: high grade, poorly differentiated The higher grade tumors have a greater propensity to metastasize- spread throughout the body.

For bladder cancer, another key indicator for likelihood to spread is the depth of penetration into the bladder wall. The bladder wall is composed of an inner lining called the urothelium (made up of transitional cells) which rests on a membrane layer called the basement membrane, below which is the connective tissue layer (support tissues) called the lamina propria. Within the lamina propria lies a small amount of muscle called the muscularis mucosa. Deep to the lamina propria is the deep muscle of the bladder arranged in three layers. This layer is called the muscularis propria. Tumors located in the inside, superficial layers of the bladder wall are unlikely to spread. Tumors that grow into the deeper layers (down into the muscle of the bladder wall) are much more likely to spread. Furthermore, there is a definite link between the grade of the tumor and its likelihood of invasion. Low grade tumors are almost always noninvasive, while high grade tumors are usually invasive. In general, papillary tumors, which are delicate and frond like in appearance are usually low grade and superficial. This is to be contrasted to sessile tumors which appear solid, are often high grade and invasive. Depth of invasion is critical in establishing prognosis. The tumor which invades into the lamina propria is a far more serious tumor than the superficial tumor which demonstrates no invasion. It has a much higher propensity to progress to the muscle invasive tumor, a much more dangerous cancer, with a high risk for spreading beyond the bladder. For further information see Chapter 6.

 

 

Our use of the term or terms Actos Side Effects 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 Scoop

By admin | Published January 25, 2012

Actos and Bladder Cancer: For the practicing urologist it is often difficult to inform the patient on muscle invasive bladder cancer and the often need for radical surgery and some kind of urinary diversion to follow; however, it is even more elaborate to do so in case of a nonmuscle invasive tumor where the evidence calls for radical treatment. In Chap. 15, Waalkes, Merseburger, and Kuczyk present pathologies where a radical treat­ment is strongly advised.In Chapters 16-18 focus various aspects of cystectomy. In Chap. 16, radical surgery of the bladder is discussed by Dr. Gschwend. The improvement in surgical techniques had led this formerly challenging procedure into a more standardized one. Chapter 17 includes urinary diversion by Drs. Richard and Stefan Hautmann. The ileal neobladder has become one of the worldwide chosen procedures for con­tinent orthotopic urinary diversion. Chapter 18, laparoscopic cystectomy by Dr. John, is the latest evolvement in bladder surgery and covers innovative tech­niques as well as the well-established surgical routines in radical treatment of invasive bladder cancer.

 

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In 2010, only 5% of all urologists are performing neoadjuvant chemotherapy in patients with muscle invasive bladder cancer, hence the 5% survival benefit in5 years and possible down staging of the tumor. Dr. Sherif guides us along the current literature and discusses the pros and cons of the neoadjuvant chemotherapy. Diagnosis and treatment of upper tract tumors is challenging and Chap. 20 by Dr. Remzi discusses the basics as well as recent advances in this field. In Chap. 21, De Santis and Bachner focus on the development and optimal use of new regimens for systemic agents as well as standard treatment options for the treatment of meta­static urinary carcinoma in the areas of targeted drugs. Options for “unfit” patients and elderly as well as in second-line setting are discussed. In Chap. 22 non-TCC tumors: Diagnosis and treatment is discussed by Dr. Abol-Enein. He focuses mainly on the squamous cell and adenocarcinoma of the bladder.

We hope that this brief synopsis of the topics covered in each chapter will encourage the readers to use this book for a general read on bladder cancer and as a reference guide for specific molecular and clinical aspects of bladder cancer. We again thank the authors for contributing to this project. We thank our Mr. Michael Koy, production editor at Springer and Spi Editorial Department, India for helping us in the publication of this book. We would like to thank Brian Halm of Springer for helping us with the publication of this book.

 

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Abstract Bladder cancer (BC) is a worldwide health problem. In 2006 in Europe, there were an estimated 104,400 incident cases of BC diagnosed (82,800 in men and 21,600 in women) that represent a 6.6% of the total cancers in men and 2.1% in women.Tobacco use is a major preventable cause of death, and especially involved with BC carcinogenesis. Tobacco smoking is the most well-established risk factor for BC, causing around 50%-65% of male cases and 20%-30% of female cases.

Occupational exposure has been considered the second most important risk factor for BC. Work related cases account for a 20%-25% of all BC cases in several series.

In addition, chronic urinary tract infection had been related to BC, particularly, with invasive squamous cell carcinoma. Bladder schistosomiasis has particularly- been considered by the international agency for research on cancer (IARC) as a definitive cause or urinary BC with an associated fivefold risk.

 

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 Warning News Flash

By admin | Published January 25, 2012

Actos Warning : Recently, a metaanalysis of observational studies on cigarette smoking and cancer from 1961 to 2003 has been published. The authors extracted data from 254 reports published during that period of time and included them in the 2004 IARC Monograph on Tobacco Smoke and Involuntary Smoking. The analyses were arried out on 216 studies with reported estimates for current and/or former smokers. The pooled risk estimates for BC demonstrated significant association for both current and former smokers. In an analysis of 21 studies, the overall rela­tive risk calculated for current smokers was 2.77 [95% confidence interval (CI) 2.17, 3.54]; while from the analyses of 15 studies, the overall relative risk calcu­lated for former smokers was 1.72 (95% CI 1.46, 2.04) (Gandini et al. 2008).

 

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In a pooled analysis of 11 case-control studies regarding cigarette smoking and BC, the following three variables were analyzed: duration of smoking, average number of cigarettes smoked per day, and time since quitting smoking. The popula­tion consisted of 2600 cases and 5524 controls. An increasing risk of BC was observed with increasing duration of smoking, which appeared to be linear. The relative increase was approximately 100% after 20 years smoking and reaches to 400% after 50 years smoking. In addition, a relationship was observed between the number of cigarettes smoked per day and BC.

The OR increased to nearly threefold for those who smoked between 15 and 20 cigarettes per day, after which a plateau in the risk graph was observed. They concluded that the duration of smoking habit and not the amount of cigarettes smoked per day was the main determining factor for BC. An immediate decrease in risk of BC was observed for those who quit smoking. This reduction was about 40% within 1-4 years of quitting smoking and reaches 60% after 25 years of cessation. However, the risk does not reach the level of nonsmokers even after 25 years. This suggests that tobacco has a late effect in the carcinogenesis of BC, but the fact that this risk does not reach the levels of nonsmokers until 25 years after quitting smoking suggests that tobacco may also be involved in an early irreversible stage in the carcinogenesis process (Brennan et al. 2000).

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Other issues as type of tobacco could be taken into account. Six studies have published a significant higher risk of BC for the blacks who are cigarette smokers compared to smokers of otherraces. Also, case-control studies suggest a strong evidence of a carcinogenic effect of cigars and pipe, which is comparable to that of cigarettes (Boffetta 2008). The mode of inhalation of tobacco smoke has been related to BC risk, as well. In a case-control study of smoking and BC from Spain that included 1219 cases and 1271 controls, they concluded that the former and current smokers experienced risks of BC three to seven times higher than nonsmok­ers, respectively.

In addition, they found that the risk was higher for subjects who inhaled into the throat or chest [OR 4.8 (95% CI 2.3-9.9)] compared with those who inhaled only into the mouth [OR 10.0 (95% CI 6.7-15.0)], at each level of duration (Samanic et al. 2006).

Taking into account that current smokers have higher risk of BC than nonsmokers, and that this risk decreases by 40% after 1-4 years of quitting smoking, the promotion of cessation of smoking would allow reducing the incidence of BC in men and women.

Internationally, there is a general agreement on the broad strategy needed to successfully combat the tobacco epidemic.

 

Our use of the term or terms Actos 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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Actos Bladder Cancer News Flash

By admin | Published January 25, 2012

Actos Bladder Cancer : Bladder tumor “seeding” may occur during the procedure. As the tumors are resected, cancer cells are released into the irrigant which fills the bladder. These cells may implant in other areas of the bladder traumatized during the procedure. It should be understood that the bladder is generally filled with urine, and tumor cells can naturally implant at other locations even without surgery. Implantation can be lessened during surgery by avoiding injury to other bladder areas and by the use of adjuvant intravesical chemotherapy. There have been numerous studies over the past decade showing a number of chemotherapy agents can be effective in decreasing initial tumor recurrence, possibly by preventing seeding. Reduction in recurrence may however be short lived.

Previously, it was common practice to obtain multiple random bladder biopsies at the time of initial tumor resection. This was recommended to rule out the possibility of hidden CIS. Understanding these biopsy sites may increase the possibilities of tumor recurrence by tumor seeding, biopsies are now often limited to areas adjacent to the tumors removed and suspicious appearing areas only. CIS can be ruled out by using cytology, or by obtaining biopsies during future cystoscopy after the tumor has already been removed. When dealing with low grade tumors, random biopsies of the bladder will rarely show cancer.

After your procedure, depending on the level of anesthesia and the extent of surgery, you will be brought either to the recovery room or back to the area where you were first prepared for your procedure. You will be released to home only when you have fully recovered from you anesthetic and are doing well. The recurrence rate for superficial bladder cancer can be as high as 60-90%. Recurrences can cause bleeding and other difficulties and are best handled sooner rather than later. In addition, depending on the initial tumor grade and stage, progression to a more serious form of bladder cancer is an ongoing concern. Surveillance cystoscopy is therefore recommended. Cystoscopy is still the best means to check for recurrent disease. It is however, an invasive procedure and should be accomplished only as often as required. For solitary, low grade, non invasive disease, follow up cystoscopy can be accomplished with the flexible cystoscope if available. If negative at three months, further cystoscopic exams can be done yearly and eventually lengthened even further. For those with multiple tumors, large tumors, high grade tumors or those who also have CIS, frequent cystoscopies, initially every three months are called for. As long as there are no recurrences, the time between cystoscopies can be lengthened. Cytology can also be utilized to reduce the number of cystoscopies. If recurrence or progression does occur, heightened scrutiny is again called for.

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Adverse reactions are side effects of treatment. Approximately 95% of individuals will tolerate treatments well. Adverse reactions may be mild. Common reactions include cystitis (inflammation of the bladder characterized by burning on urination), hematuria, mild fever, malaise, and nausea. These symptoms generally pass without any treatment. For bothersome symptoms, various medications may prove helpful. Your physician can prescribe medication for burning or urinary frequency. For those with persistent cystitis, antibiotics can be utilized. For individuals experiencing severe symptoms lasting more than 48 hours, isoniazid, an anti-tuberculous drug can be prescribed.

A short course of 3 days, starting the day before the next dose of BCG can be used to prevent severe side effects. Fortunately severe reactions resulting in sepsis, a life threatening condition characterized by high fever, chills and drop in blood pressure, is exceedingly rare. Sepsis would be treated in a hospital with triple anti-tuberculous drugs, steroids, and broad spectrum antibiotics. There are other serious adverse reactions which may require dose reduction or discontinuation. These are all rare and include: inflammation of the prostate, persistent hematuria, hepatitis, inflammation of the testicles and or epididymis, bladder contraction, ureteral obstruction, joint pain or inflammation of the lungs.

Recurrence of bladder cancer after the initial induction course, or relapse after complete response, would indicate failure of therapy. When two or more courses result in recurrence or when recurrence develops during the first six to twelve months after induction and maintenance therapy, patients generally are felt to have disease which is at higher risk for progression. A high percentage of patients who are complete responders remain tumor free for up to five years. However, with the passage of more time, additional patients will have late recurrences. For those with late recurrences (two to three years after therapy), most will respond to repeat BCG therapy.

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Invasive bladder cancer is often recognizable to the urologist by its appearance during cystoscopy. These cancers are generally large, sometimes multi-focal, and solid in appearance as compared to the fine papillary appearance of superficial bladder cancers. During the transurethral resection of the tumor, the urologist can generally tell the tumor is invading into the deeper portions of the bladder wall.

The pathologist’s report will then indicate the grade of the cancer and the depth of invasion. If the tumor invades into muscle, it is an invasive tumor. Further staging would then include a CT Scan or MRI to assess local contiguous spread, lymph node spread, or more distant spread of the cancer. A chest X ray is also routine. If there are any suspicious areas, a CT Scan of the chest is ordered. A bone scan is generally not required unless the individual has had a new onset of bony pain that is not explained by injury or arthritis.

Our use of the term or terms Actos 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 Warning Advice

By admin | Published January 25, 2012

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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Actos Warning News Bulletin

By admin | Published January 25, 2012

Actos Warning : Chronic urinary tract infection had been related to BC, particularly with invasive squamous cell carcinoma. , Bladder schistosomiasis has particularly been consid­ered by the international agency for research on cancer (IARC) as a definitive cause or urinary BC with an associated fivefold risk. Schistosomiasis is the second most common parasitic infection after malaria and about 600 million people are exposed to infection in Africa, Asia, South America, and Caribbean (Khurana et al. 2005).The first to report on bilharziasis association with BC was Ferguson in 1911 and later on reports of the NCI registry stated that frequency of BC in Egypt was elevated, being 27.6% of all cancers (Gouda et al. 2007).

 

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Although the relationship between squamous cell carcinoma of bladder and schistosoma infection is well established, currently the trends of BC in endemic zones, as Egypt, are changing. In fact, data from the largest tertiary cancer hospital in Egypt, NCI Cairo, were analyzed to verify the incidence of squamous cell carci­noma in the area. Data from 1980 to 2005 were obtained and data from 2778cases were available for analyses. The authors demonstrated a statically significant asso­ciation between period of diagnoses and histopathological type. In this way, patients diagnosed in 2005 had a sixfold higher odds associated to transitional cell carcinoma compared to those patients diagnosed in 1980 (Felix et al. 2008). Bilharzias associa­tion dropped from 82.4% to 55.3% and there was a significant increase of transi­tional cell carcinoma from 16% to 65%, while squamous cell carcinoma was less frequent, from 76% to 28%. Intimately related to this, there was an increase in the median age of patients from 47 to 60 years. The decline in the frequency of BC is related to a decline in bilharzias egg positivity in the specimen and this suggests a better control of the endemic disease in rural population (Gouda et al. 2007).

 

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Even though association between inflammation in schistosoma infection and squamous BC is well established, the role of inflammation due to other infections in the origin of BC, even transitional cell carcinoma, is less clear.Of the epidemiologic studies regarding urinary tract infection (UTIs) and BC, including transitional cell carcinoma, with one exception (Kjaer et al.1989), all the retrospective observational studies have demonstrated a positive association between BC and UTIs. Relative risk in these studies range between 1.4 and 16 for any history of urinary infection versus none, and similar associations have been found in men and women. To date no prospective study has been conducted to clearly establish the role of infection in bladder carcinogenesis.

Therefore, it could be possible that those positive associations result from detec­tion bias or differential recall between cases and controls. Prospective studies with large number of patients and controls are warranted to determine the role of inflam­mation in BC (Michaud 2007).

 

Our use of the term or terms Actos 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 Liver Failure Action

By admin | Published January 25, 2012

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 Reports

By admin | Published January 25, 2012

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 FDA Breaking News

By admin | Published January 25, 2012

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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