Gluten and Your Liver

  • Thursday, September 30, 2010
  • Posted by HCV New Drugs
  • File Under

Gluten and Your Liver

Description:
Celiac hepatitis can go undetected until it's too late

By Doug Childress, M.D.


Emily had been seeing her regular physician for years and years for an annual checkup.

And every year he would say, “Emily, you have got to stop drinking.” “But I have never had a drink in my life, doctor,” she would reply. Emily's liver function enzymes were always slightly elevated, which can be a side effect of alcohol use. But in Emily's situation, this was not the cause.


By the time she was 85, she had only 4 percent of her liver function left and was diagnosed with cirrhosis.
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Did Emily have alcoholic cirrhosis?
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No. She had what is now known as celiac hepatitis. In order to understand celiac hepatitis, it is necessary to understand the broader category of celiac disease and gluten sensitivity.

If you have not heard of these conditions, don't fret – many physicians haven't, either.

What is celiac disease?

Although it has been described in the medical literature for centuries, the term “celiac disease” was not assigned to the disorder until the late 19th century. Classically, celiac disease is an intolerance to a protein called gluten that is found in wheat, rye and barley. In susceptible people, the body's immune system reacts against this protein and its subcomponents, causing damage to various parts of the body.
In celiac disease, most of the damage occurs to the intestinal lining, but substantial evidence now shows that gluten can cause health effects in other parts of the body without significant intestinal involvement.

This specific fact accounts for an underappreciation of glutenrelated health effects with many clinicians who require intestinal findings to support the diagnosis of celiac disease. The current estimate of celiac disease in the U.S. and Europe is approximately 1 percent of the population. Celiac disease is defined by evidence of intestinal damage related to an immune reaction to gluten, and physicians often require an intestinal biopsy to make the diagnosis.


Once defined, the only effective treatment is to avoid gluten completely in the diet. Thomas O'Bryan, D.C., is a diplomate of both the National Board of Chiropractic Examiners and of the Clinical Nutrition Board of the American Chiropractic Association. He counsels patients on functional health and nutrition in his private practice in the Chicago area. As a certified clinical nutritionist and one of the world's most dedicated speakers on gluten-related health disorders, he has dedicated his current career to educating the public and clinicians on the effects of gluten on health.
Accordingly, he feels the biggest challenge currently is to clarify the difference between celiac disease and nonceliac gluten sensitivity (NCGS).

The lack of distinction is causing a great deal of confusion and significant numbers of missed diagnoses among patients.
A problem arises because in many circumstances gluten causes immune reactions and other health issues without involving the intestinal lining, and therefore a diagnosis of celiac disease is never made.

These patients have NCGS, and by O'Bryan's conservative estimates,
NCGS is 10 times more common than celiac disease. Other body systems that can be affected by gluten include the brain, the skin, the thyroid, the musculoskeletal system and, yes, the liver. Gluten and the liver The most common clinical effect of gluten on the liver is elevated levels of the liver enzymes alanine aminotransferase (ALT) and aspartate aminotransferase (AST). When liver tissue is damaged, it releases these enzymes into the bloodstream. Alcohol is the most common cause of liver enzyme elevation, but gluten sensitivity is a major cause as well.
According to a recent Harvard study, one-third of the population has nonalcoholic fatty liver disease .

Based on O'Bryan's experience and research, he estimates that 4 percent of these patients have gluten sensitivity as a cause of their liver condition. Gluten damages the liver through two main mechanisms.
First, in people with gluten intolerance, gluten causes the intestinal lining to become inflamed and leaky. Because the lining is more permeable, larger molecules of digested food that normally would not do so “sneak” across the intestinal lining into the bloodstream.

Once across, the immune system sees the larger molecules as foreign material and launches an attack against them. This immune response not only targets these molecules but also spills over into normal tissues. As normal liver tissue is attacked, liver enzymes are released into the bloodstream. If this inflammation goes on chronically, scarring and even cirrhosis can occur.


The other mechanism involves an increased toxic load on the liver. Gluten's irritation of the intestinal lining allows food toxins that would normally be eliminated as waste to escape into the body.

The liver is one of the major organs responsible for ridding the body of toxins, so overloading the liver with toxins can also result in elevated liver enzymes. In both instances, the primary event is an intolerance of gluten and the resultant inflammation of the intestinal lining.
But if the intestine is involved, why isn't this celiac disease? By medical definition, celiac disease requires two key features of intestinal pathology. One is villous atrophy, and the other is infiltration of lymphocytes into the intestinal walls. The small intestine normally has small, finger-like projections called villi on the surface that assist in absorption of nutrients and fluid. When gluten causes inflammation, over time the villi become damaged and flattened, which is termed villous atrophy.
Likewise, as chronic inflammation against gluten occurs, immune cells called lymphocytes lodge themselves within the intestinal wall.

If neither of these pathologies exists, then a diagnosis of celiac disease is not made. “Gluten sensitivity is a spectrum of ongoing pathology,” says O'Bryan. “At the severe end, you have villous atrophy and lymphocytes in the intestinal walls, but at the other, the degree of intestinal damage is not enough to cause these features. As a result, only the people on the severe end of the spectrum are labeled as celiac disease, and many others go undiagnosed.”
Rick and Vikki Petersen both are chiropractors as well as certified clinical nutritionists.

Based on their 20 years in private practice in Sunnyvale, Calif., they agree with O'Bryan's opinions about the number of people unaware of their intolerance to gluten. “From our clinical experience, of patients that have lab elevations in liver function enzymes, approximately 20 percent have gluten sensitivity,” says Rick Petersen.
Because of this frequency, they routinely screen most of their patients for gluten sensitivity.

The Petersens say they are amazed at the number of patients with gluten sensitivity they have diagnosed since making functional health a focus of their practice.

The symptoms are incredibly vast – headaches, memory loss, osteoporosis, thyroid dysfunction, sleep difficulty and abdominal discomfort are just a few of the common complaints. Later this year, the Petersens are releasing a comprehensive book on the health effects of gluten sensitivity. The book describes the varied effects of gluten on our bodies and gluten's history in our diets.

An entire chapter is dedicated to celiac hepatitis. Making the diagnosis One of the world's renowned researchers on celiac hepatitis is Joseph Murray, M.D., of Mayo Clinic Rochester.
His research published in the medical journal Hepatology in 2007 acknowledges that elevated liver enzymes are the most common liver manifestation of gluten intolerance.

In addition, other liver disorders including primary biliary cirrhosis, autoimmune hepatitis and primary sclerosing cholangitis are frequently associated with gluten sensitivity.
The recommendation from his review was that celiac disease and gluten sensitivity should be evaluated in anyone with these liver conditions.

Given the limitations of intestinal biopsies in diagnosing gluten intolerance, the question arises as to how a diagnosis can actually be made. Fortunately, blood tests now enable accurate diagnosis in many people.
Antibodies against gluten and gluten-related enzymes in the body are quite sensitive and specific at detecting gluten intolerance. Many researchers no longer feel that an intestinal biopsy is needed for making the diagnosis of celiac disease or NCGS if antibody tests are positive.

Blame your parents Gluten intolerance is primarily a genetic disorder. In people with celiac disease and NCGS, the HLA genes, which encode the development of immune system proteins, are aberrant. Specifically, people who have HLA DQ2 and HLA DQ8 genes are most susceptible to gluten intolerance.

However, while screening for these genes through blood work is possible, antibody tests are more effective in making the diagnosis.
Because of the underlying genetic cause, those known to be at risk include anyone with a first degree relative with celiac disease or gluten sensitivity. Anyone with any autoimmune disorder should be screened for gluten-related disorders as well.

These screenings should occur even if symptoms are absent. Identifying gluten-related antibodies and invoking treatment can prevent progressive health disorders later in life.
Delaying a diagnosis of gluten intolerance can have significant effects on long-term health. For example, in Emily's case, the failure to recognize gluten sensitivity as the cause of liver enzyme elevation eventually led to cirrhosis from chronic inflammation.
She was eventually diagnosed and is now on a gluten-free diet, but much of the liver damage is now irreversible. Just as detecting viral hepatitis can help prevent cirrhosis by allowing earlier treatment, the same applies for early detection of gluten intolerance.
The good news In O'Bryan's clinical experience, all of his patients with elevated liver enzyme tests who were gluten sensitive reverted to normal within a few months of proper diet. However, the medical literature indicates that this recovery will not occur in 100 percent of patients.

Early detection and elimination of gluten from the diet allows the liver to fully recover from the inflammatory damage, but the chance of permanent injury increases the longer gluten-induced immune reactions exist.
As greater awareness of gluten's effects on health becomes evident, these missed opportunities for early diagnosis will diminish. For now, you can do your part by discussing the potential presence of gluten intolerance with your own physician – especially if you have a liver-related condition. Addressing a concurrent condition of celiac hepatitis with proper treatment will help your overall health and allow your liver to recover.
Gluten freedom If it turns out you are gluten intolerant, avoiding gluten is not the end of the world. In all honesty, gluten-free diets can be incredibly healthy – with fruits, vegetables and many legumes being completely void of gluten. Also, there are many alternatives to wheat, barley and rye in bread-type products made from rice, corn, soy and others.


An explosion of gluten-free foods has now surfaced in the market, and these continue to grow every day. As we as a country move toward evidenced-based health care and preventive health, we are looking more closely at diet and lifestyle. Gluten is one of the most common dietary factors that contribute to poor health, and learning to detect gluten sensitivity and to change dietary habits will pave the way for other preventive health care measures.

Celiac hepatitis is an example where both prevention and early detection are important. If this had been available for Emily, her cirrhosis would have never developed.


There is indeed still much to learn about how our diet affects our health.


We are what we eat.


http://www.liverhealthtoday.org/viewarticle.cfm?aid=379



Doctors explore link between liver disease and gluten intolerance
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Every year we are introduced to a new way of eating or an exciting new diet plan that promises to solve all of our health problems. In years past, we have seen a raw food revolution, no carb diets, and various types of cleanses, among others. Although some of these eating recommendations border on being fad diets, there are some nutritional changes that may in fact benefit everyone, whether they need to lose weight or not. In recent years, more and more people are being diagnosed with Celiac Disease, which requires them to eat a diet free of gluten, which is a protein found in wheat, rye, barley, oats, and spelt. Although this gluten-free diet is geared toward people who suffer with Celiac Disease, more and more nutritionists and doctors are finding that gluten hastens the development of liver disease in certain individuals and should be avoided.

According to a report on the website Liver Support, more and more physicians are finding a connection between liver disease and gluten intolerance. The article notes that although full blown Celiac Disease may be rare, many people suffer from a form of gluten intolerance. Gluten may harm individuals with liver disease by causing the intestinal lining to become inflamed and eventually weakening, allowing food particles to the bloodstream. When the body’s immune system attempts to attack these molecules, it may also attack the liver’s tissues, thereby causing inflammation and possible scarring. Furthermore, the food in the bloodstream may also lead to a higher instance of toxic substances further weakening the liver, which attempts to get rid of the waste. If it cannot discard these toxins, it is again subject to inflammation and further scarring. In fact, researchers in Finland found that individuals who suffered from Celiac Disease and liver damage prevented further damage to the liver by refraining from ingesting gluten.

It may be beneficial for you to experiment with a gluten free diet to see if your body responds well to consuming less of the particular protein. There are so many products on the market today that act as great substitutions for the food you are used to. After discussing it with your doctor, see if you can gradually introduce gluten free items into your diet and after a couple of months have some blood work done to see if your liver enzymes have improved. There is nothing harmful about gluten free products, and you may just be able to thwart the progression of your liver disease.

A Practical Guide to Abnormal Liver Tests

A Practical Guide to Abnormal Liver Tests
David A. Johnson, MD
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Authors and Disclosures
Posted: 09/21/2010
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Interesting Folks : Case Study.
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Enjoy !
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Support: Hep C Chat And Message Boards

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Support
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Do you need support and someone to talk too ?
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The Liver an amazing degree of diversity




Cell division typically associated with cancer may also protect the liver from injury Science Centric

23 September 2010 09:57 GMT


Researchers at Oregon Health and Science University have discovered that a form of cell division typically associated with cancer called multipolar mitosis can yield diverse, viable cells capable of protecting the liver from injury and poisonous substances, such as pesticides, carcinogens or drugs. Their findings are published online in the journal Nature.

'Our findings show that the liver, which is known to have a tremendous capacity for regeneration, also has an amazing degree of diversity. A better understanding of this process may reveal why some individuals are more susceptible to different forms of liver injury than others, which could lead to new therapies for the treatment of liver disease,' said Andrew Duncan, Ph.D., principal investigator and postdoctoral researcher in the lab of Markus Grompe, M.D., Pape Family Pediatric Institute, OHSU Doernbecher Children's Hospital; and the Oregon Stem Cell Centre at OHSU.

The liver comprises a pool of genetically distinct hepatocytes, the primary functional cell type in the liver. Duncan and colleagues' work suggests that in response to liver injury that is toxic to most hepatocytes, a subset of select hepatocytes may respond favourably, thereby preventing liver failure and ensuring survival of the organism.

Unique among other cells in the body, hepatocytes in humans and rodents contain either a single nucleus with one set of DNA, called diploid hepatocytes, or one-two nuclei with multiple sets of DNA, called polyploid hepatocytes, explained Duncan. The functional significance of hepatic polyploidy is unknown.

Duncan and colleagues endeavoured to study the function of mouse polyploid hepatocytes using multiple approaches, including therapeutic liver repopulation, live cell imaging and cytogenetic analysis. While most polyploid hepatocytes underwent normal cell division to generate two identical daughter cells, approximately 4 percent of polyploid hepatocytes underwent specialised cell divisions, or multipolar mitosis, generating genetically distinct daughter cells. These unique daughter hepatocytes contained either chromosomal gains/losses, known as aneuploidy, or one-half DNA content of the parental polyploid hepatocyte.

The research team characterised the extent of hepatocyte aneuploidy in livers from healthy adult mice and found chromosomal gains and/or losses in more than 60 percent of hepatocytes. Together, the data show that hepatocyte proliferation involves a cycle of polyploidisation, 'ploidy reversal' - the opposite of polyploidisation - and aneuploidy. The researchers call this dynamic process the 'ploidy conveyor.'

'Aneuploidy is most often associated with cancer, therefore our finding of pervasive aneuploidy in the liver is very surprising. Despite the high prevalence of numerical chromosome abnormalities, spontaneous liver cancer is rare in wild-type mice. We believe aneuploidy is a normal characteristic of hepatocytes. Furthermore, we speculate aneuploidy may be common in many different tissues. Studies are currently under way to characterise aneuploidy in human hepatocytes and other normal tissues in rodents and humans,' said Duncan.

Although it is well known that hepatocytes become polyploid, the function of polyploid hepatocytes has been unknown. Andrew and colleagues suggest that proliferating hepatocytes polyploidise and undergo ploidy reversal, that is the ploidy conveyor, to specifically generate unique hepatocytes with different mixtures of chromosomes. This genetic diversity may operate as an adaptive mechanism, serving as a substrate for selection of those hepatocytes most resistant to foreign compounds, Duncan explained. In response to liver injury that is toxic to most hepatocytes, a subset of select hepatocytes may respond favourably, thereby preventing liver failure and ensuring survival of the organism.



Source: Oregon Health and Science University

HCV Faces A New Weapon

Hepatitis C Virus Faces New Weapon From Florida State Scientists
Main Category: Liver Disease / Hepatitis

In recent human trials for a promising new class of drug designed to target the hepatitis C virus (HCV) without shutting down the immune system, some of the HCV strains being treated exhibited signs of drug resistance.

In response, an interdisciplinary team of Florida State University biologists, chemists and biomedical researchers devised a novel genetic screening method that can identify the drug-resistant HCV strains and the molecular-level mechanisms that make them that way -- helping drug developers to tailor specific therapies to circumvent them.

The potentially life-saving technology also works when screening other viruses with drug-resistance issues, notably human immunodeficiency virus (HIV) and influenza.

More than 170 million people worldwide are infected with HCV, which leads to both acute and chronic liver diseases.

"In collaboration with pharmaceutical firm Gilead Sciences and researchers from the University of Heidelberg (Germany), what our research team discovered was how the latest drug for HCV works and what changes in the virus that makes it resistant to this unique therapy," said Hengli Tang, a Florida State University molecular biologist.

"This is knowledge that is essential to drug developers focused on HCV," said Tang, "but equally important is that our method, which we call 'CoFIM' (Cofactor-independent mutant) screening, can also be applied to other drug targets and other viruses.

"And, since we now understand how this latest class of drug works and what causes resistance to it, we can better select other classes of drugs with distinct mechanisms -- in other words, those that target other parts of the virus -- in order to craft a combination therapy, which is the future of HCV therapy and the key to overcoming drug resistance."

The groundbreaking research is described in a paper published online in the September 2010 issue of the journal PLoS Pathogens.

Florida State biology doctoral student Feng Yang led the research team. The award-winning scholar earned her Ph.D. in August 2010 and is now a postdoctoral associate at Yale University. Yang designed the CoFIM screening methodology with fellow FSU graduate students, postdoctoral associates and distinguished faculty colleagues -- including Associate Professor Tang; chemistry/biochemistry Professor Timothy M. Logan, director of FSU's Institute of Molecular Biophysics; and Research Assistant Professor Ewa A. Bienkiewicz, of the FSU College of Medicine, where she directs the Biomedical Proteomics Laboratory.

Driving the team's development of CoFIM screening was the need to identify key "cellular cofactors" and their mechanisms of action -- a fundamental aspect of virus-host interaction research.

'Cellular cofactors' are proteins that normally exist in host cells that have been hijacked by viruses to facilitate viral replication." Tang said. "They became accomplices to the invading viruses.

"Our research team was the first to show that 'cyclophilin A' (CyPA) is an essential cellular cofactor for hepatitis C virus infection and the direct target of a new class of clinical anti-HCV compounds, which include cyclosporine A (CsA)-based drugs that are devoid of immunosuppressive function," Tang said.

"In addition, we went a step further than other research teams by employing our newly developed CoFIM screening method, which we used to demonstrate not only HCV's dependence on cellular cofactor cyclophilin A and susceptibility to cyclosporine A drugs but also to uncover the molecular-level regulators that determine those two traits in the virus."

Those molecular-level regulators are known as "small interfering RNA libraries" -- collections of molecules so named for their size and ability to suppress gene expression. They act to individually suppress every gene in the cell, resulting in different consequences depending upon which gene is suppressed by a given member in the library.

The CoFIM screening method involves inducing or "coaxing" the HCV virus to mutate by itself, in vitro, absent the replication assistance it normally receives from a particular cellular cofactor. Then, CoFIM tracks the changes in the virus's response both to CsA-based drugs and any other drug designed to inhibit the cofactor.

Funding for the research conducted at Florida State University came in largest part from a $1.4 million grant awarded by the National Institutes of Health (NIH). And, because chronic liver disease caused by HCV can lead to liver cancer, a grant from the American Cancer Society provided additional support.

In addition to now-doctoral alumna Feng Yang and faculty members Hengli Tang, Timothy M. Logan and Ewa A. Bienkiewicz, the Florida State University co-authors of the PLoS Pathogen paper ("A Major Determinant of Cyclophilin Dependence and Cyclosporine Susceptibility of Hepatitis C Virus Identified by a Genetic Approach") are current biology doctoral students Henry Grise and Stephen Frausto and postdoctoral associates Anita Nag and Jason M. Robotham. Co-authors from the University of Heidelberg Department of Infectious Diseases are Vanesa Madan, Margarita Zayas and Ralf Bartenschlager, and from Gilead Sciences (Foster City, Calif.), Andrew E. Greenstein and Margaret Robinson.

Source:
Florida State University
http://www.medicalnewstoday.com/articles/202939.php

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Hepatitis C Chat Room and Message Boards

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Support


Do you need support and someone to talk too ?

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Talk to people who are on treatment and understand
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There are also members at the forum who are unable to treat and living daily with HCV.

If you're new, introduce yourself and ask questions. If you're having problems with registering - post that here also, as this is the only forum that does not require you to register.


Hepatitis C Newly Diagnosed, What Now?

In the United States

Hepatitis C infection is the most common chronic blood borne infection in the U.S. Approximately 4.1 million persons, or 1.6% of the total U.S. population, are infected with hepatitis C

..

Of persons infected with hepatitis C 85% will remain infected for life; of those: 60 - 70% will develop chronic liver disease 10 – 20% will develop cirrhosis (scarring of the liver) 1 – 5% will develop liver cancer Liver failure from chronic hepatitis C is one of the most common reasons for liver transplants.
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In 2005, about 6,500 liver transplants were performed in the U.S. The number of liver transplants performed per year has been increasing steadily for more than 15 years. Chronic liver disease is the tenth leading cause of death among adults in the U.S., causing approximately 25,000 deaths annually. 40% of deaths from chronic liver disease can be attributed to hepatitis C. The Centers for Disease Control and Prevention predicts that deaths due to hepatitis C will double or triple in the next 15 to 20 years.
From year 2010 through 2019, direct medical costs of HCV-related liver disease are projected to reach $10.7 billion.
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The first thing anyone diagnosed with Hepatitis C wants to know is how quickly, if at all, will the disease progress.
],

Here is an article from HCV Advocate to answer that question
],

Disease progression of hepatitis C
Alan Franciscus, Editor-in-Chief
(HCV) is highly variable, which means that it is difficult to tell
who will and who will not have severe HCV disease progression.In general about 80% of people with chronic hepatitis C will have a slow rate ofdisease progression that may not lead to serious complication.

The other 20% of people with chronic hepatitis C will have
severe disease progression that could lead to complications such
as severe fibrosis, cirrhosis, liver failure, liver cancer and death.
The question that has vexed us all is why some people with HCV
have serious disease progression while others only have mild progression.
Although we are far from completely understanding and
answering this important question there is information available about
some of the factors that will likely increase the risk for serious HCV
disease progression. This article will discuss the various factors that
increase the likelihood of disease progression and steps we can all
take to minimize these effects – at least for those factors over which
we have some control.

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ALT Levels
Alanine aminotransferase or ALT (previously called SGPT) is
a chemical produced in the liver.
ALT levels are elevated when liver cells are inflamed, damaged, or
destroyed by HCV, HBV, alcohol and certain drugs.Persistently elevated ALT levels are more of a sign that there is ongoing damage to the liver,and, if elevated over a long period of time, indicate ongoing fibrosis progression. But it is important to know that people with
persistently normal ALT levels can also have fibrosis progression, although
the risk is much lower.
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Inflammation
The amount or degree of inflammation in the liver roughly
correlates with the development of fibrosis and cirrhosis. The amount
of inflammation can be reduced by taking HCV medical treatment
and avoiding any substance that causes harm to the liver, such as
alcohol, etc.

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Fibrosis/Cirrhosis

Light, moderate, or severe scarring of the liver (fibrosis) can eventually
lead to even more severe scarring of the liver called cirrhosis.
The damage caused by hepatitis C is not linear – this means that once
fibrosis and cirrhosis start to develop, the progression of liver disease
speeds up. In other words, it may take 10 years to progress
from one degree or stage of liver damage to another, but the next
increase in the amount of damage may take less time – say 7 years.
Progression to the next stage may only take 5 years and so forth.
HCV treatment can help to reduce, slow down or stop the disease
progression progress especially if HCV treatment is successful.
Lifestyle changes can also help the liver to stay healthy by maintaining
a healthy weight, eating a healthy diet, avoiding alcohol and drugs,
moderate exercise, stress reduction, etc.

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AGE
Age plays a critical role in HCV disease progression. The age at
the time that someone acquired HCV plays an important role in
disease progression – so the older you are when you acquire HCV
the faster the disease progression.
This is because the body’s immune system doesn’t work
as well to minimize the damage HCV causes. On the other hand,
if someone acquires HCV at an early age, as they get older the
greater the chances of more severe disease progression due to the accumulation
of damage over time.
For instance, some studies have found that people over 60 years old
have a quicker disease progression and other studies have found that
having HCV for 25 years or longer increases the chances of disease
progression.
,

Steatosis
Fatty liver or steatosis can contribute to lower HCV treatment
response and a faster rate of HCV disease progression. The cause
of steatosis in most people with HCV is a synergistic effect of thevirus,
poor diet and lack of exercise. If you are HCV genotype 3,
however, steatosis is most likely caused by the hepatitis C virus.
For example, in people with genotype 3 who are successfully treated
with HCV medications steatosis has been found to be decreased
or eliminated. This is not true of steatosis in people with HCV non-3
genotype.

For most people, steatosis can be prevented and even reversed by
the simple, but not so easy, methods that we all struggle with – a
healthy diet and exercise program.
We recommend that anyone who undertakes a diet and exercise
program consult with a medical provider and experts in the field of
diet and exercise.
Unfortunately,these tools are not available to
everyone; but there are still many avenues and resources open to
become even healthier. On the internet there is a wealth of diet
and exercise sites to help.

,

Marijuana
There have been some studies that have found that regular daily
use of marijuana can significantly increase the risk of fibrosis progression.
There is a caveat, however, about the data that has surfaced.
The studies have been self-disclosure studies that are typically extremely
difficult to gauge as to how truthful people may answer questions
about how much they smoke.
But the most important factor is that it is impossible to measure the
concentrations of THC (the active ingredient in marijuana) that the
participants were smoking. Interestingly,
the studies that report that daily marijuana causes significant
fibrosis progression also report that non-daily use of marijuana did not
accelerate fibrosis progression. The bottom line – more is not better
when it comes to many issues including using marijuana.
.

Cigarettes
I don’t think anyone these days would be surprised to learn that
smoking cigarettes causes many health-related problems including
increasing the chances of fibrosis progression and liver cancer.
.


ALCOHOL
Another no-brainer is that alcohol consumption can increase
fibrosis and cirrhosis progression.
Excessive alcohol consumption – in and of itself – can lead to cirrhosis,
liver failure and liver cancer. If both of the negative effects, alcohol and
HCV, were combined I think it’s easy to see why people with HCV
should avoid alcohol. If someone has trouble stopping, they should
cut back on the amount of alcohol they drink and get help to stop.
There are many effective programs to help people stop drinking.
Metabolic Syndrome
In the last decade the relationship between metabolic disorders
and fibrosis progression has been well-documented. Metabolic disorders
are a group of conditions that increase the likelihood for
cardiovascular disease and other health problems.Components of
metabolic syndrome include:
• Abdominal obesity
• High blood cholesterol and
high triglycerides
• High blood pressure
• Insulin resistance
• State of inflammation caused
by obesity, insulin resistance,
etc.
• Prothrombotic state – increased
platelets
Although there are different components that define metabolic
syndrome they are also interconnected interconnected
especially with obesity.
Obesity and insulin resistance are the two factors that stand out as
factors that increase fibrosis progression.
A simple tool to measure insulin resistance is the HOMA-IR
– the higher the score, the higher the degree of insulin resistance.
The higher the HOMA-IR score, the more rapid fibrosis progression
is.

.
Many of the factors of metabolic syndrome can be treated with
lifestyle changes (diet, exercise, stress reduction) and medications
to control diabetes, high blood pressure, cholesterol, etc.


How is hepatitis C spread? Who's at risk?

Hepatitis C virus (HCV) is transmitted through contact with an infected person's blood.


The following list outlines sources of hepatitis C transmittal:

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-Blood and blood product transfusions;
-Sharing needles and syringes (IV drug abuse);
-Other possible risk behaviors: tattoos, body piercing, living and medical care in a developing country, folk medicine, intranasal cocaine;
-Extensive surgical procedures
-Unknown--up to 5% of patients have no identifiable risk factors;
-Sexual transmission is rare; the risk of sexual transmission to an individual is probably less than 3% when a person is in a stable monogamous relationship;
-Vertical transmission from mother to baby;
-Reused needles in a medical or health care setting.

Is hepatitis C transmitted sexually?


According to studies in the Journal of the American Medical Association, a low sexual transmission rate of hepatitis C was suggested. Of the 62 patients studied, none of the monogamous heterosexual partners had developed the hepatitis C antibody. In general, the probable risk of heterosexual transmission of hepatitis C is less than 3%.
It is recommend that all patients in a non-monogamous relationship use a condom or spermicide and patients in a monogamous relationship use a barrier method only if they are anxious or concerned about transmission.


All non-monogamous individuals should use safe sex practices.
For patients with hepatitis C, testing of spouses, babies and significant others is recommended by Centers for Disease Control(CDC). Please discuss these issues with your physician.

Is hepatitis C transmitted by breast milk to infants?


There is no substantial evidence that hepatitis C is transmitted through breast milk, however, a few studies have been performed that tested breast milk and very rarely is hepatitis C found in the breast milk--even using the most sensitive tests such as PCR. The CDC has issued a statement explaining that mothers who have HCV can breast feed, but should avoid it if there are sores around the nipple.


Can hepatitis C be transmitted to other members of my family (household contacts)?


There is a slight risk of hepatitis C transmission among household contacts, so family members should not share items such as razors or toothbrushes that may transmit blood or secretions. Women who have hepatitis C and are menstruating as well as men or women with hepatitis C and sores in the genital area should avoid sexual contact. The CDC recommends that spouses or partners of a hepatitis C patient be tested for hepatitis C.


Can a pregnant woman give hepatitis C to her baby?


A report in New England Journal of Medicine suggested a 7% transmission rate of hepatitis C from mother to child at birth. Though this is a high estimate, the possibility of transmission must be considered when a woman with hepatitis C is deciding whether to have children.
For infants who have received the hepatitis C virus from their mother, brief elevations of liver enzymes may occur, but no chronic liver disease has been reported. There have been no reports of cirrhosis in newborns, infants or child due to mother-to-child hepatitis C infection. It is recommended that all babies born to mothers with HCV be tested annually until age three with antibody tests.


Women with AIDS and hepatitis C are at high risk for transmitting the virus to their babies, and research has shown that these women consistently transmit the virus to their babies at birth.

Is hepatitis C transmitted by insects?


There is no documented transmission of hepatitis C through insects. The virus, however, is related to a group of viruses including yellow fever and Dengue, and those are known to have been spread by insects.


Exams and Tests »


The following tests are done to help diagnose hepatitis C:


ELISA assay to detect hepatitis C antibody
Hepatitis C genotype. Six genotypes exist. Most Americans have genotype 1 infection, which is the most difficult to treat.



Hepatitis C RNA assays to determine virus levels (called viral load)


Viral Load Test


Unlike antibody tests, HCV RNA tests directly measure for the presence of the hepatitis C virus. HCV RNA tests may be qualitative or quantitative.

Qualitative HCV RNA tests are used to diagnose hepatitis C. Your doctor might choose to perform an HCV RNA test instead of the ELISA, especially if you are at high-risk for hepatitis C. The HCV RNA test will be positive in as little as 1 to 2 weeks after exposure.


A positive HCV RNA test means a person has hepatitis C infection.Quantitative HCV RNA tests allow your doctor to determine exactly how much virus is in the blood. This is referred to as the viral load.


The viral load is usually expressed as units per milliliter or copies per milliliter. In patients with chronic hepatitis C infection, viral loads vary widely from 50,000 to 5 million copies per milliliter. A higher viral load may not necessarily be a sign of more severe or more advanced disease but it does correlate with likelihood to respond to treatment. HCV RNA tests can also be used to monitor response to hepatitis C treatment. For example, if the viral load decreases during treatment, this suggests that treatment is working and should be continued. Conversely, if the viral load remains the same, it suggests that the patient is not responding to treatment.


The following tests are done to identify and monitor liver damage from hepatitis C:
Liver function tests
Albumin level
Prothrombin time



Can you have a "false positive" anti-HCV test result?


Yes. A false positive test means the test looks as if it is positive, but it is really negative. This happens more often in persons who have a low risk for the disease for which they are being tested. For example, false positive anti-HCV tests happen more often in persons such as blood donors who are at low risk for hepatitis C. Therefore, it is important to confirm a positive anti-HCV test with a supplemental test as most false positive anti-HCV tests are reported as negative on supplemental testing.


Can you have a "false negative" anti-HCV test result?


Yes. Persons with early infection may not as yet have developed antibody levels high enough that the test can measure. In addition, some persons may lack the (immune) response necessary for the test to work well. In these persons, research-based tests such as PCR may be considered.
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How long after exposure to HCV does it take to test positive for anti-HCV?
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Anti-HCV can be found in 7 out of 10 persons when symptoms begin and in about 9 out of 10 persons within 3 months after symptoms begin. However, it is important to note that many persons who have hepatitis C have no symptoms..

How long after exposure to HCV does it take to test positive with PCR?


It is possible to find HCV within 1 to 2 weeks after being infected with the virus
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Will I need a Liver Biopsy ?


According to your genotype some doctors may want you to have a liver biopsy.




A good reason for having a liver biopsy is that it can show just how much damage has been done to the liver
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Understanding Your Liver Biopsy Results
When you receive the results of your liver biopsy, you will hear the terms inflammatory grade and fibrotic stage. Health care providers use these terms to indicate the amount of injury to the liver.There are three different methods used for scoring liver biopsies. This can cause confusion for both patients and health care providers. Be aware that the scoring systems are also subject to interpretation by the pathologist who examines your biopsy.
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Grading and Staging
There are a variety of ways to interpret a liver biopsy. The most common scoring methods include Metavir and the histologic activity index (HAI) also called the Knodell. There are important things to know about how biopsies are scored in order to understand what your score means.
A score for a given biopsy characteristic in one system does not mean the same thing in the other systems.
The scores for all of the characteristics of the tissue sample are added together for a final score, except as specified in the notes under the table for that systemA final score from one biopsy may have the same score as that of a follow-up biopsy, but the scores for individual characteristics may have changed.
This means your situation could actually be better or worse depending on the individual characteristic scores.Until there is a single biopsy scoring system, there are things you need to know and track regarding your liver biopsy results.
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What system did the pathologist use to grade each of your biopsies?
If you have had more than one biopsy, you need to look at changes in both the individual characteristics and the overall score.Make sure your health care provider completely explains the results of your biopsy to you. Ask for an explanation of the individual scores as well as the overall score. You should be given a description of the inflammatory grade and fibrotic stage. Ask to speak with the pathologist who evaluated your biopsy if your health care provider is unable to provide this information.
Biopsies are invasive and therefore, you are not likely to have one done often. For this reason, it is very important that you understand the results of your liver biopsy so you can use this information to help you make decisions about your health care.
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Metavir
The Metavir scoring system was specially designed to evaluate the liver in people with HCV. The scoring consists of using a grading and a staging system. The grade gives an indication of the activity or amount of inflammation and the stage represents the amount of fibrosis or scarring.


The grade is assigned a number based on the degree of inflammation, which is usually scored from 0-4 with 0 being no activity and 3 or 4 considered severe activity.
The amount of inflammation is important because inflammation somewhat correlates with the development of fibrosis.
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The fibrosis score is also assigned a number from 0-4:
• 0 = no scarring
• 1 = minimal scarring
• 2 = scarring has occurred and extends outsidethe areas in the liver that contains blood vessels
• 3=bridging fibrosis is spreading andconnecting to other areas that contain fibrosis
• 4=cirrhosis or advanced scarring of the liverKnodellThe Knodell score or histologic activity index (HAI) is also commonly used to stage liver disease.


It is somewhat of a more complex process, but some experts believe that it is a better tool for defining the extent of liver inflammation and damage because it provides more information about various aspects of inflammation and scarring. It is composed of four individually assigned numbers that make up a single score.
The first component (periportal and/or bridging necrosis) is scored 0-10. The next two components (intralobular degeneration and portal inflammation) are scored 0-4.
The combination of these three markers indicates the amount of inflammation in the liver:• 0 = no inflammation
• 1-4 = minimal inflammation
• 5-8 = mild inflammation
• 9-12 = moderate inflammation
• 13-18 = marked inflammation
The fourth component indicates the amount of scarring in the liver and is scored from 0 (no scarring) to 4 (extensive scarring or cirrhosis).
Information about the grade and stage of liver disease is helpful for the healthcare provider and the patient in guiding medical management

HEPATITIS C SYMPTOMS
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When you are first exposed to the hepatitis C virus and become infected, you are said to have "acute hepatitis C". Most people have no symptoms of infection during this time.
In 70 to 80 percent of people, the infection becomes chronic. The word "chronic" implies that the infection will be prolonged, or even lifelong, unless you get treatment that cures the infection.
Many people with chronic hepatitis C have no symptoms, even if there is serious liver damage. Of those who do develop symptoms, the most common symptom is fatigue; other less common symptoms include nausea, lack of appetite, muscle or joint aches, weakness, and weight loss.


Also See :Symptoms
.

Treatment for Hepatitis C

Treating HCV

New Drug Update/Sept 2010

HCV Advocate Video Update Top Line Phase III Data:

Telaprevir -- REALIZE

___________________

DONT MISS

Below : Link To HCV Advocates Video/Phase III Results :Boceprevir

Top Line Phase III Results: Boceprevir

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Video/Treating With Standard Of Care



Talking To Your Doctor

,
.The first thought on treating HCV is you may wish to discuss the new HCV therapies ready tobe FDA approved with your physician. With that said the links below will give you the information you need to know before you start treatment, or even if you should treat this disease.The new drugs are Telaprevir or Boceprevir , Telaprevir should be FDA approved by the end of the year.

This drug is giving genotype 1 a 70 percent or higher success rate.Your chances of an effective response to FDA current treatment SOC= (Pegylated+Ribavirin) can be up to 40% in the more difficult-to-treat type of the virus, genotype 1, and nearly 70% in the easier-to-treat type of the virus.

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Read Study Results: Boceprevir & Telaprevir
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Merck/Schering and Vertex released exciting news about their top-line results from phase III studies in August 2010.
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Merck’s top-line data included the use of their HCV protease inhibitor, boceprevir, in combination with pegylated interferon and ribavirin in HCV Genotype 1 patients who have never been treated (treatment-naïve) and people who have ‘failed’ a previous course of pegylated interferon plus ribavirin therapy.
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Vertex’s data included a study with their HCV protease inhibitor, telaprevir, used in combination with pegylated interferon and ribavirin for treatment of HCV Genotype 1 treatment-naïve patients. This is the data that we have all been waiting to hear about – with one exception—we are still waiting to hear the results of the phase III study of telaprevir triple therapy (pegylated interferon plus ribavirin) for people who have not achieved an SVR with a previous course of pegylated interferon and ribavirin combination therapy. Unfortunately, the three studies only include top-line results so we will have to wait until AASLD to hear more in-depth information.
These results, however, give hope that the new triple combinations of HCV protease inhibitors, pegylated interferon and ribavirin will increase the efficacy for people who have never been treated and for those who have been treated, but didn’t achieve an SVR.
Continue Reading...........

..
Clinical Trials and Medical Research.

A clinical trial is a rigorously controlled test of a new drug or a new invasive medical device on human subjects. In the United States, it is conducted under the direction of the FDA before being made available for general clinical use.

If you're looking for up-to-date information about federally and privately supported Hepatitis C clinical research studies, ClinicalTrials.gov helps link patients living with Hepatitis C to medical research.

.

From http://www.hepcbc.ca/faqsenglish.htm
The FAQ List WILL answer evey question
you may have about Hepatiitis C.
FAQ English (PDF) 881 KB


Questions for a specialist.

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It's important to keep an open dialogue with your doctor, especially when it comes to understanding your treatment options, and how your body is responding to the therapy.

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The following list of questions may be helpful to print and take to your appointment:
What is my genotype and how does it impact my therapy?
What is my viral load and how does it impact my therapy?
What are my expected outcomes with treatment?
What are my expected outcomes without treatment?
Do I have any other conditions that will complicate treatment?
What changes should I make in my everyday life?
What is the most important information I need to know before starting treatment?
What should I do next?

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A specialist can help determine whether treatment is right for you. Ask your doctor to recommend one today; your chances for recovery may be better than you think.

HCV Treatment and Neutropenia(low white count)

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White blood counts: What is to low ?

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Combination therapy with interferon and ribavirin commonly drives down the white count and especially a certain type of white cell called neutrophils that are important in fighting bacterial infections. It is important for people to appreciate that it is the interferon part of the treatment that really drives down the white count. It is possible that the (ribavirin) part contributes, but studies show that when they use interferon alone, they see the same problem. As a result, if the white count or the neutrophil count gets to be very low, doctors might typically adjust down the interferon dose and not the Ribavarin dose.

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With time and experience, studies have showed that people treating hepatitis C can tolerate a lower white count on treatment than originally thought. If they are able to keep the neutrophil count (ANC) above 750, people do not typically develop infections.

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Also, doctors sometimes use a second drug called GM-CSF or Neupogen to keep up the white count. Neupogen is a drug that is used primarily for cancer patients receiving chemotherapy. It is effective in getting the bone marrow to make more white cells. Like interferon, it has to be injected.

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How To Figure Out If Your Neutrophil Count

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Neutrophil% x White Blood Cell = Absolute Neutrophil Count
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For example, if a person's white blood cell count were 6,000 cells, and neutrophils made up 50% of those, that person's absolute neutrophil count would be 3,000.

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A normal range for neutrophil% is between 33% and 72%. This makes the normal range for the ANC between 1500 and 7200. Since every individual is unique, you should consult your physician or nurse if you have questions concerning your white blood cell count and ANC.
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If you’re total white count is 1.0 (1000) or below then your neutrophils would be around 500… to low to continue therapy. Although treatment is not always discontinued (in some cases) the dose is cut back until the white count increases.

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Here Is The Latest Abstract

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Hepatology. 2010 Oct;52(4):1225-31.

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Risk factors for infection during treatment with peginterferon alfa and ribavirin for chronic hepatitis C.

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Roomer R, Hansen BE, Janssen HL, de Knegt RJ.
Departments of Gastroenterology and Hepatology, University Medical Center Rotterdam, Rotterdam, The Netherlands.
Abstract

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Neutropenia During HCV Treatment

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Neutropenia during treatment with peginterferon alfa and ribavirin for chronic hepatitis C virus (HCV) infection is a common cause of dose reductions of peginterferon alfa. These reductions are performed to prevent bacterial and fungal infections, which are common during HCV treatment and can be attributed to neutropenia.

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What Are The Aims Of This Study ?

The aims of this study were to investigate the occurrence of infections and their relation to neutropenia and to identify potential risk factors for infections during HCV treatment.


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How Many People In The Study ?

In this single-center cohort study, 2,876 visits of 321 patients treated with peginterferon alfa and ribavirin were evaluated for neutropenia, infections, dose reductions, and potential risk factors for infection during HCV treatment.


The baseline mean absolute neutrophil count (ANC) was 3,420 cells/μL, and 16 patients had a baseline ANC of less then1,500>

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How Many People Had Infections ?


Ninety-six infections were observed in 70 patients (21.8%).

Thirteen infections (13.5%) were defined as severe.

Infections were not correlated with neutropenia during treatment.

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Did Dose Reductions Decrease Rate Of Infection?

Dose reductions did not lead to a decrease in infection rate. Multivariate logistic regression analysis revealed that age >55 years (odds ratio [OR] 2.06, 95% confidence interval [CI] 1.19-3.56, P = 0.01) and baseline hyperglycemia (OR 2.17, 95% CI 1.15-4.10, P = 0.016) were associated with an increased risk of infection during HCV treatment.

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Did Cirrhosis and COPD Have Risk Factors ?

Cirrhosis and chronic obstructive pulmonary disease were not risk factors for infection.

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Was Infection Associated With Treatment and Low White Count ?

Conclusion:

Bacterial infections during treatment with peginterferon alfa and ribavirin are not associated with neutropenia. Older patients and patients with poorly controlled diabetes mellitus have a greater risk of developing infections during HCV treatment. (HEPATOLOGY 2010).
PMID: 20830784 [PubMed - in process]
LinkOut - more resourcesk


Bacterial Infections and Low White Count During Treatment
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White blood cell:

One of the cells the body makes to help fight infections. There are several types of white blood cells (leukocytes). The two most common types are the lymphocytes and neutrophils (also called polymorphonuclear leukocytes, PMNs, or "polys").

Lymphocytes are made in lymphoid tissue in the spleen, lymph nodes, and thymus gland. There are different kinds of lymphocytes. Lymphocytes identify foreign substances from germs (bacteria or viruses) in the body and produce antibodies and cells that specifically target them. It takes from several days to weeks for lymphocytes to recognize and attack a new foreign substance.

Neutrophils are also major players in the body's defense against bacterial infections. Neutrophils are made in the bone marrow and circulate in the bloodstream. Neutrophils move out of the blood vessels into the infected tissue to attack the bacteria. The pus in a boil (an abscess) is made up largely of neutrophils. Normally a serious bacterial infection causes the body to produce an increased number of neutrophils, resulting in a higher than normal white blood cell count (WBC). When the WBC is low, there may not be enough neutrophils to defend against bacterial infections.

The white blood cell count is done by counting the number of white blood cells in a sample of blood. A normal WBC is in the range of 4,000 to 11,000 cells per microliter. A low WBC is called leukopenia. A high WBC is termed leukocytosis.

A normal absolute neutrophil count (ANC) is in the range of 1,500 to 8,000 cells per microliter. If the ANC is below 500 for an extended period of time, the risk of serious bacterial infection may increase significantly. A low neutrophil count is called neutropenia.



Sep 17, 2009 —
SOURCE: Digestive Diseases and SciencesReduction in Neutrophil Count During Hepatitis C Treatment:


Drug Toxicity or Predictor of Good Response?


BACKGROUND:
Bone marrow suppression is a well-recognized toxicity of the treatment of hepatitis C virus (HCV). Reduction of the peginterferon dose because of neutropenia is common in clinical practice. However, reduction of peginterferon dose during the first weeks of HCV treatment is associated with failure to achieve sustained virological response. AIMS: The objective of this study is to investigate whether the fall of neutrophil count during hepatitis C treatment is associated with achieving sustained virological response.


METHODS:
We performed an observational study of patients who completed peginterferon and ribavirin treatment in an Infectious Diseases Department in Manchester, UK.


RESULTS:
Of the 74 patients included in the analysis, 78% had genotype 2 or 3 hepatitis C and 15% had liver cirrhosis. Sustained virological response was achieved in 78% of patients. On univariate analysis, factors related to achieving sustained virological response were younger age, genotype 2 or 3, baseline neutrophil count, and fall of neutrophil count during treatment. Multivariate analysis showed baseline neutrophil count>3.5 x 10(3) cells/mm(3) [odds ratio (OR) 5.7; 95% confidence interval (CI) 1.24-26.3] and a reduction of neutrophil count>60% (OR 4.5; 95% CI 1.03-19.9) to be independently associated with achieving sustained virological response. Neutropenia was not associated with an increased risk of infections.


CONCLUSIONS:
In this observational study, higher baseline neutrophil count and fall of neutrophil count during the treatment of
was associated with achieving sustained virological response. These findings could have important implications for the monitoring and management of HCV treatment with peginterferon if they are confirmed in other studies.


NAMENEUTS (Neutrophils)NORMAL RANGE2.2-8.6 K/µl
DEFINITIONThese are WBC that play a key role in inflammation, allergic reactions, pus formation, and in destroying bacteria and parasites.


EXPLANATION OF TESTRESULT
Low neutrophil can mean infection or inflammation. Interferon treatment is associated with low neutrophil levels. Therefore, you must have normal levels of neutrophils to start interferon.

Source



Low weight predicts neutropenia and peginterferon alfa-2a dose reductions during treatment for chronic hepatitis C


Y. Rotman1,2,4, L. Katz3, M. Cohen1,2,4, O. Cohen-Ezra1, V. Manhaim1, M. Braun1,4, Z. Ben-Ari1,4, R. Tur-Kaspa1,3,4
Article first published online: 11 FEB 2009DOI: 10.1111/j.1365-2893.2009.01079.x


Keywords:bone marrow depression;chronic hepatitis C;neutropenia;pegylated interferon alfa-2a;side-effects;weightSummary.


Treatment-induced neutropenia frequently complicates the treatment course of patients treated with pegylated interferon alfa and ribavirin for chronic hepatitis C.


We investigated the effect of weight on the risk for dose reductions caused by neutropenia in patients treated with a weight-independent dose of peginterferon alfa-2a.


We retrospectively analysed single centre data for 172 patients enrolled in a multi-centre, open-label trial of peginterferon alfa-2a and ribavirin for chronic hepatitis C.


Low body weight was significantly associated with dose reductions due to neutropenia.


Patients weighing less than 62 kg had a 35% risk for significant neutropenia as opposed to a 12% risk for heavier patients (P = 0.001), and this side-effect occurred earlier during treatment. Low weight was an independent risk factor by multivariate analysis (hazard ratio 0.956/kg).


The risk for treatment-induced neutropenia was associated with body surface area more than with the body mass index. In conclusion, a low pre-treatment weight strongly predicts the need for peginterferon alfa-2a dose reductions. This apparently reflects overall body size more than body fat content. It is prudent to frequently monitor blood counts for smaller-sized patients, especially during the first weeks of treatment.

Source




Diagnosing Neutropenia During Chemo (Not HCV Treatment)

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Neutropenia can be a serious side effect of treatment, so your doctor will carefully monitor your blood cell counts during treatment. A complete blood count (CBC) is a blood test that measures the levels of these cells in your blood. To diagnose neutropenia, your doctor will evaluate the absolute neutrophil count (ANC) portion of the CBC. The result of the ANC dictates your risk of infection and what treatment may be necessary to prevent or treat existing infection.
When discussing your CBC results, your doctor may talk about specific numbers in relation to your results. Of course, he or she will explain them in detail, but the summary below will help you get see the "bigger picture" in relation to ANC values:

Normal ANC Values: Normal ANC values range from 2,500 to 6,000 neutrophils per cubic millimeter. Ranges vary on a number of factors, from someone just getting over being sick; the presence of infection, diseases and other conditions that may influence count; and even race.

Mild Neutropenia:


Once ANC counts drop to 1,000-1,500, this is considered to be mild neutropenia. If you have mild neutropenia, you aren't at a great risk of developing an infection, but your doctor will probably instruct you to look for any signs of infections and report back any changes.

Moderate Neutropenia:


Moderate Neutropenia occurs when ANC levels are between 500-1,000. If you have moderate neutropenia, then your risk of developing infection is moderate. If you develop symptoms of infection, like fever, you may still be able to monitor them at home, but some people may require hospitalization depending on other factors and test results.

Severe Neutropenia:


If you have a "neutropenic fever" (a fever as well as an ANC count below 500), hospitalization is usually required. People with severely low ANC counts often do not show any signs of infection when it is present. This is due to the lack of neutrophils to elicit a biological response.

Treating Neutropenia


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If your ANC reveals a low neutrophil count, treatment may be necessary to prevent infection. Mild cases of neutropenia may only require monitoring at home for signs of infection while more severe cases may need hospitalization.
In some cases, your doctor may recommend a course of antibiotics to prevent infection before it develops. This is called prophylactic antibiotic therapy.

Other medications, called growth factors or granulocyte-colony stimulating factors (G-CSF), are often used to increase white blood cell production in the bone marrow. Commonly used growth factors include:


Leukine (sargramostim)
Neulasta (pegfilgrastim)
Neupogen (filgrastim)


Your doctor may also want to halt or delay treatment until your neutrophil count is stable. A lowered dosage of chemotherapy may also be necessary.


Source


Neutropenia and HCV Treatment


Neutropenia - Interferon Therapy of Hepatitis C - HCV Advocate -
In conclusion, neutropenia is frequent during treatment of hepatitis C with .... The changes in neutrophil and lymphocyte counts during treatment are shown in Fig. 1. .... Among the exclusion criteria for therapy, low white blood cell and ... Bacterial infections did not occur in neutropenic patients, and the only ...



Side Effect Management: Neutropenia


Maintaining the maximum dose of interferon and ribavirin
is important for achieving a sustained virological response
(SVR) so some medical providers will prescribe an injectable
growth factor, granulocyte colony-stimulating factor (G-CSFfilgrastim),
brand name Neupogen
Hepatitis C Support Project •
www.hcvadvocate.org ...


,What About Neutropenia and Telaprevir ?


Excerpt From : 2008 Telaprevir, peginterferon alfa-2a, and ribavirin for 28 days in chronic hepatitis C patients


EDITORIAL


Decreases in hemoglobin, total white blood cell count, neutrophils, and platelets occurred during the study drug dosing period; median changes from baseline to day 28 were _2.8g/dL for hemoglobin (range: _6.2 to _0.8), _3.75_109/L for white blood cell count (range: _6.45 to _1.26), _2.39_109/L for absolute neutrophil count (range: _3.94 to _0.17), and _86_109/L for platelet count (range: _125 to 21). The only clinically significant hematology abnormalities were anemia in four patients and mild neutropenia in one patient.

Chronic parkinsonism associated with liver cirrhosis

Liver Transplantation Improves Symptoms in Patients With Cirrhosis-Related Parkinsonism: Presented at EFNS
By Jenny Powers

GENEVA -- September 28, 2010 -- Patients with cirrhosis-related parkinsonism have improved overall symptoms after liver transplantation, according to preliminary data from a study presented here at the 14th Congress of the European Federation of Neurological Societies (EFNS).

A form of chronic parkinsonism associated with liver cirrhosis is rapidly evolving and involves symmetrical akinetic-rigid syndrome, gait and postural impairment, and focal dystonia. Unlike classic Parkinson's disease, resting tremor is notably minimal or absent in this form of parkinsonism, but postural tremor is prominent.

Diana Apetauerova, MD, Lahey Clinic, Burlington, Massachusetts, presented the findings on September 26. The researchers are conducting an ongoing trial to determine the relationship between the neuroradiological and biological aspects of parkinsonism and liver cirrhosis severity.

Cirrhosis-related parkinsonism is seen in acquired hepatocerebral degeneration, but its prevalence and post-transplant natural history have not been determined. This prospective study will enrol up to 120 patients with liver cirrhosis who were treated at the Lahey Clinic liver-transplant facility.

Parkinsonism is being evaluated by use of the United Parkinson's Disease Rating Scale (UPDRS), brain magnetic resonance imaging, Mini-Mental State Examination, and videotaping. Patients are also undergoing standard liver transplant evaluation and repeat testing at 6 weeks and 3 and 12 months after transplantation.

The researchers examined the possible correlations between the severity of liver disease, determined by the Model for End-Stage Liver Disease (MELD) scale, and the stage of parkinsonism, determined by the motor part of UPDRS.

Of the patients with cirrhotic liver disease, 46% (38 of 81) exhibited parkinsonism. No association was seen between the severity of MELD and motor UPDRS (P = .74) or increased copper, ammonia, manganese, or iron levels. Abnormal signal in the basal ganglia was seen in all of the patients with parkinsonism.

Seven parkinsonian patients underwent liver transplantation. At 3 months after surgery, statistically significant improvement was seen in several aspects of parkinsonism, specifically gait (P = .02), total motor UPDRS (P = .03), and activities of daily living (P = .06).

Dr. Apetauerova concluded that this study identified a high incidence of parkinsonism in patients with liver cirrhosis. Although no correlations were found between the severity of liver cirrhosis and the severity of symptoms, a statistically significant improvement was observed in symptoms after liver transplantation.

The ongoing study has accumulated substantial data that have yet to be analysed, Dr. Apetauerova said. One aspect that will be retrospectively investigated is the effect of portal systemic shunting.

[Presentation title: Chronic Parkinsonism Associated With Liver Cirrhosis. Abstract P1671]

http://www.docguide.com/news/content.nsf/news/852576140048867C852577AC007702A1

What sort of problems can I have if I have cirrhosis?

  • Posted by HCV New Drugs
  • File Under


Damaged livers, ruined lives

By Dr Y.L.M.

MY father had a hepatitis B infection once. Recently, he had an ultrasound done as part of a routine check-up, and the report came out that his liver had cirrhosis. What is cirrhosis?

Cirrhosis of the liver is what happens to your liver as a complication of many diseases. It is how your liver looks anatomically - with a lot of scar tissue manifested in nodules and fibrous tissue that is hard.

This is what happens to your liver: