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December 29, 2004
New Early Liver Disease Test
This article from the BBC speaks of a new test to detect fibrosis/cirrhosis markers. It represents just one more advance in the diagnosis and treatment of liver disease.
It is especially valuable to note that this test is non-invasive.
Test to spot early liver disease.
Technique could lead to a blood test.
A technique for identifying early liver damage could help improve detection of the deadly condition cirrhosis.
Essex University scientists teamed up with a German team to pinpoint a group of biochemical markers that indicate the disease is in its early stages.
The markers are made up of debris from damage to proteins, a well-known early sign of cirrhosis.
The Journal of Hepatology study could lead to a blood test to detect damage earlier, and stop progression.
Lead researcher Professor Paul Thornalley, who led the research, said: "It is likely that debris from this damage, leaking into the blood, will prove a novel biochemical test for early liver damage."
Cirrhosis kills an estimated 4,000 people in the UK each year. Over the last 20 years, there has been a massive increase in the numbers killed by liver damage, with fatalities among men up 121% since the early 1980s and among women by around 68%.
The disease is most commonly associated with alcohol but it can also affect anyone infected with hepatitis C.
Up to 15% of chronic alcoholics develop alcoholic cirrhosis, of whom 75% will eventually die through liver damage.
Scarred tissue
It begins with the formation of scarring, known as fibrous tissue.
Left unchecked, this can gradually develop into full-blown cirrhosis, for which the only treatment is a transplant. However, there is a national shortage of donor organs.
A test that could pick up early liver damage could help identify hepatitis C sufferers and also be used to monitor whether patients are following doctors' instructions to abstain from alcohol.
The new marker is a by-product of the destruction of proteins in the liver. This destruction takes place as disease sets in.
Tests showed a 15-fold increase in the level of this marker in cases where scarring of the liver was underway.
Although the test does not differentiate between alcohol damage and other causes, it could still be used to check progress of drink-related disease.
Abstinence test
Professor Thornalley said: "Alcohol represents 50% of cirrhotic livers in the UK.
"This test could be an indication of whether people are sticking to their abstinence programmes.
"People have been looking for such a marker for many years. We've not seen one that changes so dramatically as this."
Charles Gore, of the Hepatitis C Trust, said if the test showed liver damage then patients could be given drugs to rid the body of the hepatitis virus.
But he said he doubted it would make a huge difference, because liver disease progressed so slowly treatment may not be immediately necessary.
"Damage from hepatitis C is very slow. The disease may be setting in but it could be 10 years before something happens."
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December 21, 2004
Experimental Stem Cell Therapy for Cirrhosis
Cirrhosis is still officially considered an irreversible condition. Some experiments have shown natural substances like milk thistle (especially Maximum Milk Thistle) can slow or possibly even reverse fibrosis (the process that leads to cirrhosis).
Now, scientists are utilizing stem cells to repair damaged livers. This appears to be regardless of the cause of cirrhosis (alcoholic induced hepatitis or viral hepatitis).
These are the kinds of experiments that offer real hope to people with serious liver concerns.
Reading between the lines in the report from the medical journal "Hepatology" gives us some interesting data. One fact that stands out is that 25 million Americans (one in ten) have liver related diseases---making this the seventh leading cause of death.
Another fact stated is that 10,000 Hepatitis C patients die due to cirrhosis each year, and another 5,000 from chronic Hepatitis B.
Clearly, it is important to protect and support your liver. While a small minority of Hepatitis C patients will progress to end stage liver disease (just 20 to 30% according to the Centers for Disease Control), this is a very serious life-threatening condition for those most negatively affected.
A pioneering stem cell therapy designed to heal otherwise irreversible liver damage has started trials in Japan. A similar trial on people with cirrhosis is about to start in London, UK.
The need for new treatments is urgent. Cirrhosis kills 27,000 Americans each year, and one in 10 of the population - 25 million Americans - have liver-related diseases making it the seventh most common cause of death. For now, the only real hope for patients who suffer severe liver damage through heavy drinking or viral infections is a liver transplant from a matched donor. But waiting lists for livers are growing.
In the U.S., 18,500 patients await transplants. In the UK, the waiting list has more than doubled between 1994 and 2003, from 101 to 239, although around 600 people a year receive a transplant.
Antiviral drugs tackle viral-related cirrhosis if given in time, but sometimes the damage is too advanced, resulting in up to 10,000 cirrhosis deaths from hepatitis C in the US, and 5000 deaths from hepatitis B.
Younger drinkers
The situation is just as dire in the UK, where cirrhosis cases are increasing, according to Alison Rogers, chief executive of the British Liver Trust. Alcohol-related cirrhosis accounts for around half of cases.
"People are drinking more, and younger than they used to, and women are drinking more," says Rogers. Extrapolating from a recent, unpublished study of hepatitis C prevalence in Southampton, Rogers says that as many as 750,000 drug users in the UK could be harbouring the virus.
The pioneering Japanese trial builds on successful experiments with mice. "Our results showed that even if chronic liver injury exists, transplantation of bone marrow stem cells can reverse this," says Isao Sakaida of Yamaguchi University in western Japan, head of the team that developed the new procedure. He says it is too soon to know if people in the trial are responding to the treatment.
For their mouse experiments, Sakaida and his team damaged the livers of the animals by injecting carbon tetrachloride, to produce a condition called liver fibrosis in which interconnected strands and patches of damaged and dead tissue criss-cross the organ. Fibrosis eventually develops into cirrhosis when nodules of cells form at the junctions of the fibrous strands.
After four weeks, Sakaida took bone marrow cells from donor mice that had a jellyfish gene inserted to make their cells glow green. He then injected the cells into the tail veins of half the mice with damaged livers. Sakaida was able to track where the glowing cells ended up in the liver-damaged mice. In the fifth and eighth weeks of the experiment he found the cells had migrated en masse to the liver.
"Ready to go"
Following the infusion of bone marrow cells, the proportion of fibrous tissue in the liver shrank from an average of nearly 5.4% in the fifth week to less than 4.2% three weeks later. Mice in a control group given only saline solution showed no such change.
The team were able to show that bone marrow cells reaching the liver changed into liver cells and made large amounts of an enzyme called matrix-metalloproteinase-9 (MMP-9), which may play a role in dissolving fibrotic tissue.
For the trials on people, Sakaida's team favours injecting bone marrow stem cells extracted from the patients themselves to avoid problems of rejection of donor cells. At Hammersmith Hospital in London, a team headed by Nagy Habib claims to be "ready to go" with a similar trial. The London team plans to concentrate stem cells obtained from the patients' bone marrow and inject them into the liver through the hepatic portal vein.
Both techniques risk quite serious side effects. Some bone marrow cells, for example, might form scar tissue, making the cirrhosis worse. But Habib says the Japanese work in mice indicates that this is unlikely.
Further question marks arise from an almost identical study published last year in Proceedings of the National Academy of Sciences (vol 100, p 11850) by Inder Verma and Yoshiyuki Kanazawa of the Salk Institute for Biological Studies in La Jolla, California, US. They found hardly any evidence of healed liver tissue after they infused bone marrow cells, and concluded that "bone-marrow derived cells cannot generally lead to a cure for liver damage".
Journal reference: Hepatology (vol 40, p 1304)
Posted by Ralph at 02:20 PM --- Printer-friendly version | Comments (2)
December 16, 2004
The "Other" Hepatitis and Hepatitis C
The following article is from the Conway Daily Sun. It is quite instructive for all hepatitis patients.
If high fat and alcohol can cause the sorts of liver problems mentioned in otherwise healthy people, then how much more important is it for chronic viral hepatitis people to keep these factors under control.
The bottom line is what I have been recommending for years. Regardless of what other approach you take to dealing with your condition, eat a whole foods balanced diet and do not drink alcohol.
Incidentally, milk thistle in general (and Maximum Milk Thistle in particular) has been shown to help maintain, protect and support a healthier liver, regardless of the condition. It has even been shown in laboratory testing to help regenerate healthy liver cells. Read more...
The Other Hepatitis
Dr. Brian Irwin
— Hepatitis literally means "inflammation of the liver." There are many causes of hepatitis. Quite often when they hear the term, most people immediately think of hepatitis caused by a series of viruses. Over time, an increasing number of viruses that cause liver inflammation have been identified and have been named accordingly. Hepatitis A. Hepatitis B. Hepatitis C, which, until fairly recently, was named "Hepatitis non-A, non-B." Delta hepatitis. The list goes on.
However as well known as these famous viruses are, they cause a proportionally small number of hepatitis cases in the Western Hemisphere. What is responsible for much more liver disease and subsequently death in the western world, and particularly in the United States, is fat.
By fat, I'm referring to accumulation of fat in the liver cells themselves. Triglycerides can, due to a number of causes, accumulate in the liver cells and ultimately cause inflammation, liver congestion and even liver failure. By far the most common cause of excess fat accumulation in liver cells is alcohol abuse. Excessive alcohol intake can damage the liver in a number of ways, but one of the known mechanisms is by excess fatty acid production that is a result of ethanol metabolism, and subsequent deposition of these acids in the liver.
Malnutrition alone can also cause this to occur, but unfortunately many heavy drinkers do not eat properly. Subsequently, these people suffer damage from their poor nutrition AND from their alcohol intake.
There are other causes for fat deposition in the liver. Other than alcohol, the most common cause in this country is a high-fat diet. The liver performs the function of "detoxifying" the bloodstream. The liver produces the enzymes and a material (called bilirubin) that is required to "dissolve" fat, help metabolize it and store or excrete it.
A tremendously high concentration of triglycerides can easily overwhelm the system, back up and regurgitate into the liver cells proper. The result is slow, but steady liver damage that can, eventually, become irreversible.
The recent documentary "Supersize ME" showed the effects of a fat- and sugar-rich diet on a previously healthy person. One of the major changes in this previously healthy subject's condition was his liver function. The subject of the film experienced an increase in his "Liver Function Tests," which are a series of tests that measure enzyme production by liver cells. These "LFT?s" are increased in almost all cases of inflammation; quite literally the subject of the film, by diet alone, gave himself hepatitis.
So what happens if you ignore hepatitis, fatty or alcoholic? Hepatitis can be with or without symptoms and, quite often, is a diagnosis that health-care providers "stumble" upon by finding incidentally elevated LFTs. Symptoms can range from painless jaundice (yellowing of the skin that occurs as bilirubin, one of the products of the liver, "spills over" into the bloodstream and deposits in the skin), to nausea, vomiting, atrophy of the testicles, hair loss or a whole host of other symptoms.
More concerning, perhaps, than the health ramifications of hepatitis are the health ramifications of chronic hepatitis....cirrhosis. Cirrhosis is the end-stage result of hepatitis. A liver with chronic inflammation will eventually scar, shrink up and eventually stop working. At this point severe fluid accumulation, severe mental status changes (confusion, seizures or coma), infection, bleeding tendencies and cancer can all present.
As ominous as all this sounds, there is good news. Not all cases of hepatitis progress to cirrhosis. Although not all kinds of hepatitis are reversible, most cases of fatty liver caused by increased fat intake or excess alcohol will revert to normal or near-normal liver function...IF the offending agent is removed! While health-care providers can't promise all cases will totally revert to normal, we can promise that if a patient has fatty liver disease and hepatitis, if lifestyle changes aren't instituted, that patient's liver will progress to failure.
Of course, there is a genetic component to liver disease. Some people can eat a very high fat diet and never develop fatty hepatitis. Some people drink eight drinks every day and never have a problem. However, others can develop fatty liver disease from a relatively small amount of dietary fat and triglycerides or only a modest alcohol intake history.
This doesn't mean everyone should be on a no-fat diet or that no one should ever have a glass of wine. What it does mean is that at this time there's no way to tell who will luck out and who won't. Some of us are more susceptible to liver disease than others, so to be safe, eat right, take everything, not just alcohol and fat, in moderation and if you ever have any questions ask your health-care provider for
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December 13, 2004
Weight-based treatment dosing for Hepatitis C
The following article is from hepatitisneighborhood.com, a website of priorityhealthcare.com.
While the basic information in this article is very enlightening, I also like to read between the lines.
What is most relevant here? First of all, that the study focused on genotype 1 (the most common in North America, with approximately 70% of patients). The study verified that genotype 1 is hardest to treat with current conventional (read, interferon) therapy.
Next, I find it very telling that the response was TWICE AS GOOD with weight based dosing. That begs the question---why isn't everyone with genotype 1 treated based on weight?
Then, I found it very telling that even at the best-possible response they did no better than 29 percent of patients with SVR (with only a measily 16% at standard dosing).
Then, they talk about relapses. So, as I understand it, 29% responded but then 22% of them relapsed. So, isn't that a success rate that is closer to just 20% of patients, even with the superior weight dosing?
Finally we have the side-effects information. Wow! Discontinuation for adverse events were nearly neck and neck at 18% vs 17%. So, if that were the only criteria, I'd certainly choose weight based dosing (whether African American or not). However, If 29% responded, but 22% of them relapsed and 18% dropped out due to adverse effects, how many were actually helped?
Food for thought, don't you agree?
African-Americans with Hepatitis May Benefit More from Weight-Based Ribavirin
by John C. Martin
Article Date: 12-08-04
A new, large study finds that African-Americans diagnosed with hepatitis C (HCV) respond better to treatment when the antiviral drug, ribavirin, is dosed based on weight rather than standardized.1
Lower SVR Found
Previous studies have found that African-Americans with HCV have lower response rates to treatment compared to other ethnic groups for unknown reasons.2,3 In hepatitis C, there are several genotypes, or species, of virus that can infect any one person. Studies have found that genotype 1, which also happens to be the most common, is the most difficult to treat.4,5
But "the high prevalence of HCV genotype 1 is insufficient to explain the low SVR [sustained virologic response] rates in this population," write Ira Jacobsen, MD, in the department of Gastroenterology & Hepatology at Cornell University, and his colleagues.
How Does Ribavirin Impact SVR Rates?
So, Jacobson and his team set out to determine African-Americans' response to combination therapy using peginterferon alfa-2b (PEG-Intron/Schering-Plough) with ribavirin, as well as to determine the optimal dose of ribavirin in this group. Of 5000 patients who were selected at random to receive peginterferon alfa-2b with either weight-based doses or fixed doses of ribavirin, 387 African-Americans with genotype 1 HCV were analyzed for this study. All the patients were taking part in an unrelated clinical study.
Three hundred sixty-two patients who weighed more than 65 kg (143 lbs) received 1.5 micrograms (mcg) of peginterferon alfa-2b per kilogram of body weight (1.5 µg/kg) once per week combined with either a standard dose of 800 milligrams (mg) of ribavirin, or a weight-based dose of 800 to 1400 mg. The criteria were as follows:
• Those weighing less than 143 lbs (less than 65 kg) received 800 mg
• Those weighing between 143 lbs and 187 lbs (65-85 kg) received 1000 mg
• Those weighing between 189 lbs and 229 lbs (86-104 kg) received 1,200 mg
• Those weighing between 231 lbs and 273 lbs (105-124 kg) received 1,400 mg
Therapy lasted for a total of 48 weeks, with 6 months of post-treatment follow-up. Patients who remain virus-free for a minimum of 6 months following the end of therapy are considered to have achieved a sustained virologic response (SVR) to the treatment.6
After the follow-up period, it was found that twice as many African-American patients who received weight-based ribavirin doses responded to therapy compared to those who were given the standard dose. Of 174 patients who received weight-based doses, 29 percent responded. That compares to only 16 percent of those who received the standard 800 mg dose, Jacobson and his associates reported, a difference they considered significant. Further, relapses occurred in 22 percent of patients receiving weight-based ribavirin versus nearly a third of those who received standard doses, they wrote.
Dealing with Ribavirin Side Effects
Anemia—a common side effect of ribavirin—was more common in those who received weight-based dosing, they noted (47 percent of those taking weight-based doses had anemia compared to 29 percent of those on the fixed dose). As a result, "dose reductions of ribavirin (12% v 8%) and erythropoietin use were more common with weight-based dosing, but overall safety for the two groups was similar," the researchers wrote. "Discontinuations for adverse events were 18% in weight-based dosing and 17% for standard dosing, with 25 severe adverse events in each group."
Erythropoietin is a hormone that helps regulate red blood cell production in the body. It is also used as an anemia treatment.
"Weight-based dosing of ribavirin offers a significant advantage in the treatment of African-American patients infected with HCV genotype 1," the study investigators concluded.
1. Jacobson I, Brown R Jr., McCone J et al. Weight based ribavirin dosing improves virologic response in HCV-infected genotype 1 African-Americans (AA) compared to flat dose ribavirin with peginterferon alfa-2b combination therapy. 55th Annual Meeting of the American Association for the Study of Liver Diseases. 2004 Oct 29-Nov 2. Boston, MA.
2. Muir AJ, Bornstein JD, Killenberg PG; Atlantic Coast Hepatitis Treatment Group. Peginterferon alfa-2b and ribavirin for the treatment of chronic hepatitis C in blacks and non-Hispanic whites. N Engl J Med 2004 May 27;350(22):2265-71.
3. McHutchinson JG, Poynard T, Pianko S et al. The impact of interferon plus ribavirin on response to therapy in black patients with chronic hepatitis C. The International Hepatitis Interventional Therapy Group. Gastroenterology 2000 Nov;119(5):1317-23.
4. Trepo C. Genotype and viral load as prognostic indicators in the treatment of hepatitis C. J Viral Hepat 2000 Jul;7(4):250-7.
5. Fried MW. Viral factors affecting the outcome of therapy for chronic hepatitis C. Rev Gastroenterol Disord 2004;4 Suppl 1:S8-S13.
6. Berg T, Kronenberger B, Hinrichsen H et al. Triple therapy with amantadine in treatment-naïve patients with chronic hepatitis C: a placebo-controlled trial. Hepatology 2003 Jun;37(6):1359-67.
John Martin is a long-time health journalist and an editor for Priority Healthcare. His credits include coverage of health news for the website of Fox Television's The Health Network, and articles for the New York Post and other consumer and trade publications.
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December 11, 2004
Share Your Personal Hepatitis C Story
Would you please share your Hepatitis C survival story?
This is a chance for you to tell all about your personal experience with this disease---and possibly have your words seen by thousands of other patients who could be helped by your insights.
We are putting together a collection of patient stories in a book as part of our patient education and advocacy mission. The purpose is to provide a realistic frame of reference for all Hepatitis C patients. A frame of reference gained directly from others in similar circumstances, with shared experiences.
We believe this book could help all Hepatitis C patients better cope with the fear, confusion and adjustment that inevitably come after a Hepatitis C diagnosis.
Your own personal experience might be extremely valuable for others to learn from, especially as part of a collection of Hepatitis C survival stories from a wide variety of patients. This is true whether you you believe your experience to be extraordinary or commonplace.
Please consider that your own story could be just what someone else needs to hear to get them through---even if you don't think there is anything particularly special about it. Even if you've never really told it to another patient before.
I've heard that a burden shared is a burden halved. Just knowing others have gone through, or are going through, similar circumstances can do a lot to help one deal better with any reality that confronts them. Your sharing could help others who are very much like you. And, you may find the simple act of sharing your story to be therapeutic for you, as well.
As a Hepatitis C patient, you can probably understand how it might help others immensely if they have the opportunity to learn from your experiences (both good and bad).
Wouldn't you like to know how others have dealt with (or are dealing with) Hepatitis C in their lives? In the same way, other patients might very well appreciate knowing about your experiences.
If you have chronic Hepatitis C and you are reading this email, then you are a Hepatitis C survivor. If you are here today, then one way or another, you are surviving. You have probably survived decades with this chronic, potentially deadly disease (although you were most likely unaware you even had it for most of this time). Since your diagnosis, you have dealt with this disease in your own way. The disease has affected your life uniquely.
Each and every survivor's story is unique. We want to consider yours for inclusion in this collection. Think of it as a potential contribution to the entire Hepatitis C community.
Incidentally, once the book is published you will be able to get a copy for yourself at Amazon.com, or your local bookstore, to see how other patient's stories are similar and different from your own.
To make your submission most informative and relevant, you might look at sharing the following aspects of your experience:
How did you discover you have HCV?
What genotype do you have?
How elevated were/are your liver enzymes?
How do you believe you contracted it?
Do you suffer physical symptoms from the disease? If so, what are they?
How were you affected emotionally when you found out?
How did your family react? Your friends? Your lovers?
What did your doctor say? What was their recommendation?
What did you do to learn more? Where did you find the most helpful information (recommended resources)?
Did you get a biopsy? If so, what was it like? What did it show? If not, why not? And what did you do instead?
What stage and grade is your inflammation/fibrosis?
Did you choose interferon therapy? Why (or why not)? If yes, what was your experience with it?
Did you make lifestyle changes? If so, which? If not, why?
Did you choose nutritional supplementation and/or other natural remedies? If so, which and why?
Did you join a support group or online bulletin board?
Do you have health insurance? Is it covering your treatment choices?
What about Social Security or disability insurance?
If you are veteran, what has your experience with the VA been like?
Has the disease affected your job?
Are you secretive about having the disease because of concerns about what people might think or how it might affect your work or social relationships?
If you've cleared the virus, how long have you been undetectable?
If you are on a transplant list, what is that like?
If you've had a transplant, what would you most like to share about that experience?
These are just suggestions. You can be detailed or brief. You might consider elaborating on just one or two of these topics. You may choose to address them all, and more. The fundamental question is, "what do you think is most important for others to know about your experience with Hepatitis C?" The choice is yours. We simply ask that you keep your submission to no more than 1,000 words. And we reserve the right to edit appropriately.
You can participate anonymously with your first name and last initial (along with your state of residence) or you can give your full name and state (or country if not in the USA).
If you choose anonymity, with first name and last name initial only, your anonymity will be respected and protected.
Send submissions to Ralph@hepatitis-central.com
We will let you know whether or not your story is chosen for the book. This is not a writing contest. Stories will be included in the book based on their appropriateness as part of the entire project. They will not be judged on grammer, punctuation or writing style. Even those not chosen for the book will be posted directly on an associated website for public access. That way, even if not included in the book, your story will be told.
Thank you, in advance, for sharing your story.
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December 07, 2004
BILN 2061 For Hepatitis C Revisited
We have reported on BILN 2061 before because of its exciting promise as a Hepatitis C therapy. Unfortunately, testing has been suspended because of animal studies that indicated possible cardiac toxicity with the substance.
The November issue of the medical journal, Gastroenterology, further reported on the promising results and also mentioned the subsequent suspension of human studies.
We will keep you posted on any change or progress we hear of regarding BILN 2061.
Further Human Trials of BILN 2061 on Hold Pending Resolution of Animal Toxicity Issues
Novel, potent, and well-tolerated hepatitis C virus (HCV) drugs are needed. BILN 2061 is a potent and specific inhibitor of HCV serine protease in vitro. Preclinical toxicology data and studies in healthy volunteers supported the administration of BILN 2061 to patients with HCV infection.
The antiviral efficacy, pharmacokinetics, and tolerability of 25, 200, and 500 mg BILN 2061 twice daily given as monotherapy for 2 days in 31 patients infected with chronic genotype 1 HCV infection and with minimal liver fibrosis (Ishak score of 0–2) were assessed in a placebo-controlled, double-blind pilot study.
In 2 subsequent placebo-controlled studies of similar design, 200 mg BILN 2061 twice daily was administered for 2 days to 10 patients with advanced liver fibrosis (Ishak score of 3 or 4) and to 10 patients with compensated cirrhosis (Ishak score of 5 or 6).
Results
Viral RNA reductions of 2–3 log10 copies/mL were achieved in most of the patients. There was a trend toward a higher number of patients receiving 500 mg BILN 2061 achieving a viral RNA reduction ≥3 log10 copies/mL as compared with patients receiving 25 mg BILN 2061.
Advanced fibrosis or compensated cirrhosis did not affect the antiviral efficacy of BILN 2061. BILN 2061 was well tolerated in all studies.
Conclusions
The authors conclude, “BILN 2061 is a well-tolerated and very active compound that reduced serum viral RNA concentrations after 2 days of treatment in patients infected with genotype 1 HCV independent of the degree of fibrosis. Nevertheless, further clinical trials are on hold pending resolution of animal toxicity issues.”
12/01/04
Reference
H Hinrichsen and others. Short-term antiviral efficacy of BILN 2061, a hepatitis C virus serine protease inhibitor, in hepatitis C genotype 1 patients. Gastroenterology 127(5): 1347-1355. November 2004.
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December 03, 2004
Blood Tests vs. Biopsy For Fibrosis Assessment
This reference is from an article in the latest issue of the medical journal, Gastroenterology.
What we found most interesting is the reference to the fact that biopsy can be painful and dangerous and that assessment of biopsies is subjective and prone to sampling error. So much for accuracy in the gold standard test for gauging liver condition.
More and more progress is being made with blood and serum tests to determine fibrosis progression and liver condition. This bodes very well for keeping an eye on liver disease progress without invasive and potentially dangerous or faulty biopsies.
Our only question is why the authors concluded this could or should be used in conjunction with biopsy. We feel "instead of" may be a better choice.
Serum Markers Detect the Presence of Liver Fibrosis
Histologic examination of a liver biopsy specimen is regarded as the reference standard for detecting liver fibrosis. Biopsy can be painful and hazardous, and assessment is subjective and prone to sampling error.
Researchers developed a panel of sensitive automated immunoassays to detect matrix constituents and mediators of matrix remodeling in serum to evaluate their performance in the detection of liver fibrosis.
In an international multicenter cohort study, serum levels of 9 surrogate markers of liver fibrosis were compared with fibrosis stage in liver biopsy specimens obtained from 1021 subjects with chronic liver disease.
Discriminant analysis of a test set of samples was used to identify an algorithm combining age, hyaluronic acid, amino-terminal propeptide of type III collagen, and tissue inhibitor of matrix metalloproteinase 1 that was subsequently evaluated using a validation set of biopsy specimens and serum samples.
Results
The algorithm detected fibrosis (sensitivity, 90%) and accurately detected the absence of fibrosis (negative predictive value for significant fibrosis, 92%);
Performance was excellent for alcoholic liver disease and nonalcoholic fatty liver disease.
The algorithm performed equally well in comparison with each of the pathologists.
In contrast, pathologists’ agreement over histologic scores ranged from very good to moderate.
Conclusions
The authors conclude, “Assessment of liver fibrosis with multiple serum markers used in combination is sensitive, specific, and reproducible, suggesting they may be used in conjunction with liver biopsy to assess a range of chronic liver diseases.”
12/03/04
Reference
W M C Rosenberg and others. Serum markers detect the presence of liver fibrosis: A cohort study. Gastroenterology 127(6): 1704-1713. December 2004.
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