Research & Treatment News
October 27, 2009
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Repeated studies prove that those with chronic hepatitis must be evaluated directly for fibrosis progression. Although your doctor or peers may single out a normal ALT from a liver panel as good news, discover why this measurement provides little information about liver fibrosis.
by Nicole Cutler, L.Ac.
Although chronic hepatitis causes relatively minor symptoms by itself, those with chronic Hepatitis B or C run the risk of developing fibrosis. As fibrosis worsens, it may lead to permanent scarring of the liver. Known as cirrhosis, this permanent liver injury is the tenth leading cause of death in the United States. As one of the markers of a person's liver health, measuring liver enzymes sparks some controversy. While elevated levels of the liver enzyme, alanine aminotransferase, is often measured as an indicator of liver injury, it may not accurately reflect fibrosis progression.
Chronic viral hepatitis is a relatively common problem; worldwide, an estimated 350 million individuals are chronically infected with Hepatitis B (HBV) and 170 million are chronically infected with Hepatitis C (HCV). To monitor the health of patients with chronic hepatitis, there are two primary components of the liver that attending physicians evaluate: necro-inflammatory activity and fibrosis:
1. Necro-inflammation - This refers to liver cell inflammation and cell death.
2. Fibrosis - This refers to the hardening of liver tissue.
Alanine Aminotransferase
The laboratory findings most correlated with necro-inflammation are measurements of the liver enzymes, aspartate and alanine aminotransferases. In particular, alanine aminotransferases (ALT) is released into the bloodstream when the liver incurs damage. Traditionally, a panel of liver blood tests including ALT is used to evaluate whether or not a person's liver function is deteriorating. Although this measurement is used ceremoniously by physicians, there appears to be little correlation between the aminotransferases and fibrosis. An increasing amount of evidence suggests that, while ALT is a standard sign of liver inflammation, it is not a good reflection of fibrosis progression.
Very high levels of ALT (more than 10 times the highest normal level) are usually due to acute viral hepatitis. In acute hepatitis, ALT levels typically stay high for about one to two months, but can take as long as three to six months to come back to normal. ALT levels are usually not as high in chronic hepatitis, often less than four times the highest normal level. In cases of chronic hepatitis, ALT levels often vary between normal and slightly increased, so doctors will typically order this test frequently to detect a pattern. In some liver diseases, especially when the bile ducts are blocked, a person has cirrhosis, and when other types of liver cancer are present, ALT may be close to normal levels.
Measuring Fibrosis
The feature that best correlates with the likelihood of developing cirrhosis is fibrosis. To evaluate the extent of fibrosis, physicians rely on the liver biopsy or more recently approved comparable methods:
· Liver Biopsy - Riddled with complications, liver biopsy is an expensive, invasive procedure with a considerable risk of complications (particularly bleeding) and a small chance of death. Since chronic hepatitis does not affect the liver uniformly, the extent of fibrosis may vary from one part of the liver to another. Also, because a liver biopsy samples only one small part of the liver, it can easily miss a fibrotic area. Even with adequate-sized samples, cirrhosis is estimated to be missed in 15 - 30 percent of liver biopsies. Even with these drawbacks, a liver biopsy is still considered to be the gold standard of measuring fibrosis.
· Transient Elastography - An alternative to a liver biopsy, transient elastography (FibroScan) is a non-invasive method of evaluating liver tissue. By measuring a low-frequency sound wave as it moves along the liver, this test records the speed with which the sound wave moves and correlates it with the degree of liver fibrosis. The stiffer (more fibrotic) the tissue, the faster the sound wave moves. Using ultrasound technology, this test is quick and painless. The primary drawbacks for using transient elastography are that, at this time, it cannot be used with patients who have ascites or who are obese.
· Serum Markers - The other leading alternative to liver biopsy is using serum markers to test the degree of liver fibrosis. Currently licensed in the United States and several European countries, FibroTest measures the levels of five components in the blood: bilirubin, gamma-glutamyltranspeptidase (GGT), haptoglobin, alpha 2-macroglobulin and apoliprotein A1. By computing these five components, a mathematical formula produces a score, which correlates with the degree of fibrosis in the liver. Another liver serum marker test used specifically for those with HCV is Fibrosure. By carefully combining the measurements of six liver-related chemicals in the blood with age and sex, a Fibrosure test determines the degree of inflammation and fibrosis in the liver.
ALT and Liver Injury
While measuring ALT may accurately reflect liver inflammation, more and more evidence is showing it to be unreliable for determining liver fibrosis.
1. As reported in the December 2000 Journal of Hepatology, researchers aimed to determine whether normal ALT is associated with liver injury in patients with chronic HBV who were undergoing biopsy. After tabulating the results, the authors of this study concluded that "there is significant fibrosis and inflammation in 37 percent of patients with persistently normal ALT levels."
2. In another 2000 study, Pennsylvania researchers evaluated the advisability of utilizing ALT elevation as the basis for recommending liver biopsy in adults co-infected with HIV and HCV. The authors of this study reported that, while biopsy-proven fibrosis was evident in all patients with abnormal ALTs, 80 percent of those with normal ALTs also had fibrosis. These findings showed that 80 percent of co-infected patients for whom biopsy may have been deemed inappropriate based on normal ALT levels, had significant liver pathology consistent with chronic HCV infection.
3. Presented at the 2007 American Association for the Study of Liver Diseases, H. Gui and colleagues announced their aim to identify predictors of significant histological findings in chronic HBV with normal ALT and low viral load. The researchers found that 23.7 percent of HBV patients with significant liver inflammation and fibrosis had persistently normal ALT levels - regardless of HBeAg status or viral load levels. Based on their findings, the researchers advised that, "Liver biopsy be considered in chronic Hepatitis B patients with persistently normal ALT and detectable viral load, even low viral load, especially in those older than age 40 years and [with] higher ALT within 0.75-1 x ULN."
Although ALT levels are repeatedly measured during a person with chronic hepatitis's doctor visits, these numbers should not be cause for alarm or relief. Although elevated levels of this enzyme usually correlate with hepatic inflammation, they don't appear to give much information about the progression of fibrosis. At this point in time, it appears that the only way to measure fibrosis is by using one of the tests designed directly for that purpose: a biopsy, transient electrography or serum marker fibrosis tests.
References:
Dufour, Robert, D., Assessment of Liver Fibrosis: Can Serum Become the Sample of Choice?, Clinical Chemistry, January 2005.
Hoffman-Terry, M., Reed J., Correlation of ALT with Degree of Liver Damage by Biopsy in HIV/HCV Coinfected Adults, Intersci. Conference of Antimicrobial Agents and Chemotherapy, September 2000.
www.hivandhepatitis.com, Chronic Hepatitis B Patients May Have Significant Liver Disease Despite Normal ALT, Liz Highleyman, hivandhepatitis.com, December 2007.
www.hivandhepatitis.com, Clinical Significance of Persistently Normal ALT in Chronic Hepatitis B Patients, hivandhepatitis.com, 2008.
www.labtestsonline.org, ALT: The Test, American Association for Clinical Chemistry, 2008.
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October 23, 2009
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SciClone begins a Phase II trial to evaluate how a new drug designed to stimulate the immune system fares against Hepatitis C.
SciClone starts hepatitis C drug trial
Wednesday, October 21, 2009
SciClone Pharmaceuticals Inc. enrolled the first patient in a mid-stage test of a hepatitis C treatment.
Foster City-based SciClone (NASDAQ: SCLN) signed up the patient in Atlanta to test SCV-07, a small molecule that stimulates the immune system. In this Phase II trial it's being tested alone or in combination with ribavirin, another drug.
Read the entire article:
http://sanfrancisco.bizjournals.com/sanfrancisco/stories/2009/10/19/daily47.html
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October 22, 2009
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By focusing in on HCV polymerase NS5B, two companies join forces to develop new and effective medications for inhibiting the Hepatitis C virus.
Medivir AB Broadens Its Hepatitis C Collaboration with Tibotec, Entering a Partnership in the Field of HCV Polymerase
Regulatory News:
Medivir AB (STO:MVIRB) announced today a new Research, Development and License agreement in the field of hepatitis C virus (HCV). Under the agreement, executed with Ortho Biotech Products L.P. of Bridgewater, NJ (a wholly owned subsidiary of Johnson & Johnson), Medivir will partner with Tibotec BVBA of Mechelen, Belgium.
The goal of the HCV partnership is to identify and develop orally active inhibitors of the HCV polymerase NS5B. Activities will centre on screening new and existing libraries of nucleoside analogues, developed by Medivir, that show anti-HCV activity in vitro.
Read the entire article:
http://www.chiroeco.com/chiropractic/news/4114/44/Medivir-AB-Broadens-Its-Hepatitis-C-Collaboration-with-TibotecEntering-a-Partnership-in-the-Field-of-HCV-Polymerase/
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October 20, 2009
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Mixed cryoglobulinemia is a common extrahepatic manifestation of Hepatitis C. Although not much is known about why this vascular disease frequently accompanies the Hepatitis C virus, researchers have uncovered some new information.
by Nicole Cutler, L.Ac.
As one of the most infectious viruses to affect the liver, Hepatitis C has been associated with a wide range of systemic problems. Called extrahepatic manifestations, the immune system is typically involved when the Hepatitis C virus (HCV) reveals itself in organs other than the liver. A vascular autoimmune disease that can become problematic, mixed cryoglobulinemia is an extrahepatic manifestation that has developed a close relationship with HCV.
What Is Mixed Cryoglobulinemia?
Literally meaning "cold antibody in the blood," cryoglobulinemia is defined by abnormal proteins in the blood that become thick or gel-like in cold temperatures. Scientists have yet to discover why the antibodies known as cryoglobulins solidify at low temperatures. When cryoglobulins congeal, they can block blood vessels throughout the body, a situation capable of causing many complications ranging from skin rashes to kidney failure.
One of the diseases causing vasculitis, cryoglobulinemia causes damage and inflammation to the blood vessels throughout the body. Depending on the type of antibody affected, cryoglobulinemia is categorized into Type I, II or III. While Type I cryoglobulinemia is most often related to cancer of the blood or immune systems, Types II and III are referred to as mixed cryoglobulinemia and are usually found in people who have chronic HCV.
Cryoglobulinemia can cause different problems depending on the antibody type and the organs affected. Potential symptoms include:
· Difficulty breathing or fatigue
· Enlargement of the liver and spleen
· Glomerulonephritis - a type of kidney disease that reduces the kidneys' ability to remove waste and excess fluids.
· Joint or muscle pain
· Purpura - the appearance of red or purple discolorations caused by bleeding underneath the skin.
· Raynaud's phenomenon - when the smallest arteries that bring blood to the fingers or toes constrict from cold temperatures or strong emotions.
· Skin ulceration or death
The Immune System and Cryoglobulinemia
Normally increasing in quantity to fight an illness, the immune system's B cells make antibodies to fight infection. As these B cells multiply, the antibodies they make are released into the blood where they latch onto the invading pathogens, marking them for destruction. In mixed cryoglobulinemia, the B cells continually multiply, sending the body into a spiral descent of pathological vascular conditions that increasingly cause damage.
Why HCV Is Connected to Cryoglobulinemia
As far back as 1990, researchers observed that most patients with Hepatitis C also developed mixed cryoglobulinemia. Worldwide, an estimated 100 to 170 million people have both HCV and mixed cryoglobulinemia. Ever since the association between these two conditions was realized, researchers have been perplexed about the origin of their relationship. Because HCV primarily infects the liver, scientists have been trying to understand why the B cells of someone with Hepatitis C replicate out of control to cause cryoglobulinemia.
A popular theory proposed that a protein scattered around the outer coat of the Hepatitis C virus binds to a certain receptor. Called CD81, this receptor is found on the surface of almost every cell in the body - including B cells. If the viral protein directly latches onto the surface of a B cell, it may elicit uncontrolled B cell proliferation resulting in cryoglobulinemia. Researchers from Rockefeller University say that this decade-old explanation of how one disease causes the other is likely wrong and instead offer a new theory: that the factor associated with HCV and cryoglobulinemia pursues a specific, as yet unidentified, cellular target.
In the immune system, billions of B cells are on guard. Each B cell can produce only one kind of antibody, which ordinarily can recognize and fight off only one specific pathogen. Rockefeller University clinicians isolated B cells from patients with both conditions and found they had remarkably similar antibodies. For those with Hepatitis C, their findings suggest that the CD81 receptor was not the vehicle for activating B cells. If this were the case, B cells with different antibody molecules and markers would have been activated.
Published in the February 2008 edition of the journal Blood, Rockefeller University researchers enrolled HCV-infected patients and looked at their antibody genes. They found the activated B cell genes to be identical in almost every mixed cryoglobulinemia participant. Although technical obstacles and the nature of the disease have prevented scientists from identifying the exact pathogen that triggers mixed cryoglobulinemia, they are hopeful that finding this elusive disease-causing factor will provide new insight into recovery, prevention and treatment of cryoglobulinemia.
Despite a clear understanding of why Hepatitis C often coexists with mixed cryoglobulinemia, there is an unmistakable association between these two diseases. Although the coexistence of these ailments is still poorly understood, the mechanism linking them together could end up providing us with a way to eliminate both diseases from future generations.
References:
http://clinicaltrials.gov, Rituximab to Treat Hepatitis C-Associated Cryoglobulinemic Vasculitis, National Institutes of Health, 2008.
Kayali Z, Labrecque DR, Schmidt WN, Treatment of hepatitis C cryoglobulinemia: mission and challenges, Current Treatment Options in Gastroenterology, December, 2006.
www.hcvadvocate.org, Extrahepatic Manifestations of Chronic Hepatitis C, Roderick Remoroza MD, Herbert Bonkovsky, MD, Hepatitis C Support Project, 2008.
www.medicinenet.com, Essential Mixed Cryoglobulinemia, William C. Shiel Jr., MD, FACP, FACR, MedicineNet, Inc., 2007.
www.millercenter.uchicago.edu, The University of Chicago, 2007.
www.nlm.nih.gov, Cryoglobulinemia, National Institutes of Health, 2008.
www.sciencedaily.com, New Theory Suggests How Hepatitis C May Cause Rare Immune Disease, ScienceDaily LLC, May 2008.
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October 14, 2009
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Find out the strengths and weaknesses of immune globulin for preventing viral hepatitis.
by Nicole Cutler, L.Ac.
A fascinating type of immunization therapy, immune globulins can help lessen disease severity or even prevent a disease from developing. Also known as IGs, immune globulins are collected from the purified blood of hundreds of people and contain various antibodies to a certain pathogen. While immune globulins can successfully avert some chronic diseases, (including two hepatitis viruses), they also have several limitations.
About Immune Globulin
Blood is a complex substance made up of red and white blood cells floating in a protein-rich fluid called plasma. Plasma contains antibodies, which are used by the immune system to identify and neutralize bacteria and viruses, thus protecting against disease. Immune globulins are particularly useful because they can protect someone before or after they have been exposed to a particular disease. However, complacency in disease education and prevention is a potential danger of relying too heavily on immune globulins.
Comparing IG to Vaccine
The main differences between immune globulins and vaccinations are:
· IG is composed of antibodies from people's plasma. IG is considered to be a passive solution, because the body of the person receiving it does not react to the IG, but simply circulates it.
· Vaccines are considered to be an active form of disease protection, because they are actual viral or bacterial components that stimulate the recipient's immune system to build its own antibodies.
· A dose of IG supplies the body with antibodies that are ready to immediately start defending against a pathogen.
· Although IGs begin working immediately, they only provide several months of protection.
· Since vaccines must wait for the immune system to produce antibodies, they take several weeks to become effective, but typically provide protection for decades.
IG for Hepatitis
Commonly administered to healthcare professionals who suffer from an accidental viral exposure from an infected patient, immune globulins are available for Hepatitis A and Hepatitis B.
· Hepatitis A - If given within two weeks of exposure to the virus, IG is more than 85 percent effective in preventing infection with the Hepatitis A virus (HAV). For those who don't have immunity, IG is advised for household and sexual contacts of people with HAV, as well as to travelers visiting foreign countries where Hepatitis A is a known problem or where sanitary conditions are questionable. In addition, those needing protection from HAV include those who are allergic to the vaccine or staff and residents of institutions where an HAV outbreak occurs. However, IG is only effective for approximately three months.
· Hepatitis B - Hepatitis B immune globulin is given to those who have been exposed to someone (or their blood or bodily fluids) with infectious Hepatitis B. Most commonly, this involves a needle stick or blood splashing accident. IG for Hepatitis B must be administered within two weeks of contact to be effective. Again, IG will only be effective for approximately three months.
· Hepatitis C - Unfortunately, there is no IG for Hepatitis C. Experts believe that IG with a high titer of Hepatitis C antibodies is ineffective because of this virus' rapid mutation rate. This unique characteristic of Hepatitis C allows the virus to escape protective antibodies and has made the quest to find a vaccine or cure much more challenging.
Immune globulins are ingenuous ways to prevent a person who has been exposed to certain hepatitis viruses from becoming sick. However, they are not a cure-all. IGs short-life span and inability to protect against Hepatitis C highlight the need to educate everyone about hepatitis and how to prevent viral transmission of chronic liver infection.
References:
http://hepatitis.about.com/od/treatment/a/ImmuneGlobulin.htm, What is Immune Globulin?, Charles Daniel, Retrieved May 17, 2009, About.com, 2009.
http://www.hcvadvocate.org/hcsp/articles/Jensen.html, Needlestick Exposure and Hepatitis C, Nancy Reau, MD, Donald M. Jensen, MD, Retrieved May 17, 2009, Hepatitis C Support Project, 2009.
http://www.liverdisease.com/vaccinations.html, Vaccinations for Liver Disease, Retrieved May 17, 2009, Melissa Palmer, MD, 2009.
http://www.mckinley.uiuc.edu/Handouts/immunoglobulin.html, Immunoglobulin (IG or Immune Globulin or Gamma Globulin), Retrieved May 17, 2009, The Board of Trustees of the University of Illinois, 2009.
http://www.webmd.com/hepatitis/immune-globulin-ig-for-hepatitis-a, Immune Globulin (IG) for Hepatitis A, Retrieved May 17, 2009, WebMD LLC, 2009.
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October 9, 2009
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Make sure you know the facts about how oral sex could transmit the three most common types of viral hepatitis. Please note: explicit descriptions of sexual activity are contained within this article.
by Nicole Cutler, L.Ac.
The education campaign following the AIDS epidemic of the 1980s has made most people aware that unprotected sex can lead to sexually transmitted diseases (STDs). However, stopping our understanding at that point leaves many questions unanswered, especially regarding oral sex. Since viral hepatitis is contagious and has the potential of being an STD, many people are unsure if any viral hepatitis strains can be transmitted through oral sex.
Illnesses like the common cold and flu are primarily spread through respiratory secretions. Thus, our wellness depends on people covering their noses and mouths then washing their hands after sneezing or coughing. However, preventing the spread of respiratory secretions is insufficient to protect against STDs. This is because the viral particles of most STDs are spread through other bodily fluids. This applies to the three most common strains of viral hepatitis:
1. Hepatitis A is transmitted when infected feces enters another person's digestive system. There is an effective vaccine to prevent against Hepatitis A infection.
2. Hepatitis B can be transmitted through contaminated blood, sweat, tears, saliva, semen, vaginal secretions, menstrual blood and breast milk. There is an effective vaccine to prevent against Hepatitis B infection.
3. Hepatitis C is transmitted through blood when infected blood of one person enters another person's bloodstream. There is currently no vaccine to prevent against Hepatitis C infection.
Oral sex refers to sexual activities that involve the stimulation of the genitals with the mouth, tongue, teeth or throat. For the purpose of discussing STDs, the three types of oral sex are:
1. Cunnilingus - this refers to oral stimulation of a female's outer genitalia.
2. Fellatio - this refers to oral stimulation of a male's outer genitalia.
3. Analingus - this refers to oral stimulation of the anus.
Oral stimulation of other parts of the body is generally not considered oral sex. Those in long-term monogamous relationships who do not have any contagious illnesses have virtually no risk of getting a sexually transmitted disease through oral sex. For everyone else, the risks of STDs are a major concern, and can only be avoided through education, protection and/or abstinence.
The risk of contracting viral hepatitis through oral sex is different for each viral strain:
· Hepatitis A Risk - The Hepatitis A virus is highly concentrated in the feces. Unfortunately, it will almost inevitably be present on apparently clean anal skin of infected individuals. Thus, there is a substantial risk in acquiring Hepatitis A from analingus. Several epidemic outbreaks have been reported among gay men, but heterosexual couples practicing analingus are just as likely to be at risk.
· Hepatitis B Risk - The Hepatitis B virus can cause chronic liver disease - and has the potential to be fatal. Considered to be 100 times more infectious than HIV, Hepatitis B viral particles are in semen, vaginal secretions, stool, tears, saliva, sweat and blood (including menstrual blood). There is clear evidence that Hepatitis B can be transmitted through vaginal and anal intercourse, but it is unproven whether it can be transmitted through oral sex. Since it is so contagious, there is a theoretical risk of transmitting Hepatitis B through cunnilingus, fellatio or analingus.
· Hepatitis C Risk - The Hepatitis C virus can also cause chronic liver disease with a potential for being fatal. Transmitted via blood-to-blood contact, this illness is harder to acquire from sexual contact. While there is little evidence proving Hepatitis C acquisition through oral sex, a theoretical risk exists if there is any blood present in the giver or receiver. Thus, a risk of transmitting Hepatitis C via cunnilingus, fellatio or analingus exists if there is any menstrual blood, bleeding gums, a throat infection, cold sores, canker sores, genital warts, hemorrhoids or any other breaks in the skin in any involved body structure - vagina, clitoris, labia, penis, testicles, anus, perineum, lips, tongue or anywhere else on the genitalia or inside the mouth.
Experts believe that viral hepatitis is more likely to be transmitted if either the positive or the negative partner has another STD, especially one that causes sores or lesions. Thus, suspicious symptoms should always be checked by a doctor before engaging in oral sex.
Besides being vaccinated against Hepatitis A and B, safer sex practices can help prevent the spread of viral hepatitis. Using condoms can prevent disease transmission during fellatio; latex or polyurethane condoms are best for disease prevention since natural skin condoms have small pores that can let viruses through. Latex dental dams, sheets of plastic wrap and latex sheets sold specifically for oral sex can help prevent disease transmission during cunnilingus or analingus.
Although the risk of transmitting viral hepatitis during oral sex is low, practitioners suggest abstaining if there are any cuts or sores on the mouth or genitalia areas. Additionally, some experts suggest avoiding brushing or flossing their teeth right before or after oral sex since these activities may create tiny abrasions or result in bleeding gums.
Vaccinations against Hepatitis A and B can protect you if you've been exposed to one of these viral particles during oral sex. However, these vaccines will not protect you from Hepatitis C or any other STD. Therefore, knowing what situations are riskiest, and being prepared to abstain or practice safe sex, is your best bet for engaging in disease-free oral sex.
References:
http://menshealth.about.com/cs/diseases/a/hepatitis_4.htm, How You Get Hepatitis, Jerry Kennard, Retrieved October 1, 2009, About.com, 2009.
http://www.hcvadvocate.org/hepatitis/factsheets_pdf/sextrans.pdf, Sexual Transmission of Hepatitis C, Retrieved September 30, 2009, Hepatitis C Support Project, 2009.
http://www.netdoctor.co.uk/infections/infectionoralsex.htm, Infection Risk and Oral Sex, Retrieved September 30, 2009, netdoctor.co.uk, 2009.
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October 7, 2009
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For some, not being able to get rid of Hepatitis C can leave them feeling helpless over the course of their illness. However, there are many everyday choices that can either fan the flames or reduce the impact of this virus. Sugar consumption is a prime example of how food selection can affect the progression of Hepatitis C.
by Nicole Cutler, L.Ac.
As one of the most common causes of chronic liver disease, Hepatitis C affects approximately four million Americans. Until modern medicine determines how to eliminate this contagious disease, infected individuals must focus their attention on minimizing the damage Hepatitis C causes in their liver. Unfortunate for those of us with a sweet tooth, sugar consumption has the capacity to worsen liver inflammation. Thus, sugar can encourage Hepatitis C's progression to more advanced stages of chronic liver disease.
Liver Disease Progression
One way to hinder the progression of Hepatitis C is by preventing the first step toward permanent liver damage - inflammation. In general, the stages of liver disease involve inflammation, fibrosis and cirrhosis:
1. Inflammation is the first stage of any liver disease. With the liver often being tender and enlarged, inflammation is the body's way of trying to fight infection or heal an injury. However, inflammation that is continual can cause permanent liver damage.
2. If permitted to persist, an inflamed liver will scar. Known as fibrosis, scar tissue can replace healthy liver tissue. By impeding blood from flowing freely through the liver, scar tissue inhibits healthy liver tissue function.
3. When fibrotic liver tissue continues to build, the scarring can no longer heal. At the point when the liver damage is irreversible, cirrhosis is diagnosed. Characterized by hardened and shrunken liver tissue, cirrhosis can lead to fatal complications, such as liver failure or liver cancer.
About Inflammation
A newly understood phenomenon, inflammation underlies many modern health problems, from heart disease to obesity to diabetes to liver fibrosis. According to Dave Grotto, RD, a spokesperson for the American Dietetic Association, "Sugar can play a role in inflammatory diseases. Poor regulation of glucose and insulin is a breeding ground for inflammation."
Whether from the Hepatitis C virus or some other cause of liver disease, liver inflammation is due to an immune response that helps this organ rebound from injury. However, researchers agree that there is a limit to inflammation's usefulness. Factors that create excessive amounts of inflammation, like sugar consumption, perpetuate a destructive continuation of inflammation.
Sugar and Inflammation
During the past 25 years, the average person's intake of sugar and other natural sweeteners has increased dramatically, from approximately 123 to 160 pounds a year. Many assume that an emphasis on low-fat diets has precipitated a rise of nearly two percent per year in Americans' sugar consumption. Because this health trend has led to the removal of oils from processed foods, sugar has replaced it to maintain the tastefulness of reduced-fat foods.
While sugar has never been considered a mainstay of a healthy diet, biologists now recognize a link between sugar and inflammation. Below are two reasons that high levels of sugar in the bloodstream contribute to inflammation:
1. Glycosylation - When blood sugar goes up rapidly, sugar can attach itself to collagen in a process called glycosylation. When collagen becomes glycosylated, it loses its flexibility and becomes inflamed.
2. Interleukin-6 - In addition, high blood sugar levels encourage the production of interleukin-6 (IL-6), a powerful inflammatory chemical.
Blood Sugar Levels
Some foods are obviously high in sugar, like candy, pastries, cookies and sodas. However, certain carbohydrates are another culprit of high blood sugar. Because they break down into glucose (sugar) molecules quickly, refined carbohydrates cause a quick jump in blood glucose levels. Thus, refined carbohydrates like white breads, white pasta and potato chips, can have similar deleterious effects as a sugary desert.
Americans typically consume loads of sugar each day without a thought as to how it affects their health. By simply reducing the amount of sugar and refined carbohydrates in the diet, the liver is protected from unnecessary inflammation through glycosylation and excess IL-6 production. Since rapid rises in blood sugar encourages inflammation throughout the body - including the liver - those with chronic Hepatitis C can slow down their progression of liver disease by being cautious with their sugar intake.
References:
Atkins, Robert C., Dr. Atkin's Age-Defying Diet, St. Martin's Press, New York, NY, 2001; 46.
http://articlesunlimited.holisticnetworkexchange.com/inflammation_sugar.html, Sugar and Inflammation, Retrieved September 26, 2009, Andrew Pacholyk, MS, LAc, 2006.
http://www.care2.com/greenliving/whats-causing-your-inflammation-2.html, What's Causing Your Inflammation?, Catherine Guthrie, Retrieved September 25, 2009, Experience Life Magazine, Care2.com, 2009.
http://www.diabetes.org/food-nutrition-lifestyle/nutrition/meal-planning/sweeteners-desserts.jsp, Sweets and Deserts, Retrieved September 26, 2009, American Diabetes Association, 2009.
http://www.dkfz.de/en/presse/pressemitteilungen/2009/dkfz_pm_09_37.php, Glowing Insight into the Liver: New Reporter System Detects Connection between Inflammation and Blood Sugar Level, Retrieved September 25, 2009, German Cancer Research Center, July 2009.
http://www.nanowerk.com/news/newsid=12071.php, New reporter system detects connection between liver inflammation and blood sugar level, Retrieved September 25, 2009, Nanowerk, LLC, August 2009.
http://www.procto-med.com/progression-of-liver-disease/, Progression of Liver Disease, Retrieved September 26, 2009, Procto-Med, 2009.
http://www3.interscience.wiley.com/journal/122537273/abstract?CRETRY=1&SRETRY=0, In vivo PEPCK promoter mapping identifies disrupted hormonal synergism as a target of inflammation during sepsis in mice, Evgeny Chichelnitskiy, et al, Retrieved September 25, 2009, Hepatology, August 2009.
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October 5, 2009
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An Italian study demonstrates that women co-infected with HIV and either Hepatitis B or Hepatitis C are likely to have lower bone densities than those only with HIV.
Bone Problems Among Women, But Not Men, With HIV and Hepatitis
September 28, 2009
HIV-positive women who are also infected with hepatitis B virus (HBV) or hepatitis C virus (HCV) have lower bone density than positive women not infected with HBV or HCV, according to a study published online September 23 in AIDS. Among men in the study, however, no connection between HIV, viral hepatitis and bone mineral loss was documented.
As increasing numbers of people with HIV are now living well into their 50s and 60s, diseases typically associated with aging have become a greater concern. Low bone mineral density can increase the risk of serious fractures, which in turn increase the risk of further illness and death.
Click link below for full article:
http://www.aidsmeds.com/articles/hiv_coinfection_bone_1667_17322.shtml
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