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July 31, 2008
Diabetes Prevention a Priority with Hep C
Diet and exercise are often quoted as the solution to most of our modern health problems. For reducing the risk of developing liver cancer, new research shows that these lifestyle changes are crucial to people with chronic Hepatitis C.
by Nicole Cutler, L.Ac.
Approximately 50 percent of the millions of people living with Hepatitis C are lucky enough to defeat the virus with interferon combination therapy. For the other half of people infected, the therapeutic goal remains to prevent their liver disease from progressing to cirrhosis or liver cancer. While stopping the worsening of liver disease constitutes approaches ranging from lifestyle changes to herbal supplements to unproven drug therapies, diabetes prevention appears to be more important than ever.
According to the American Diabetes Association, there are 20.8 million Americans living with diabetes. While an estimated 14.6 million have been diagnosed, experts estimate that about 6.2 million people are currently unaware that they have the disease. Although nobody wishes this increasingly common problem upon themselves new research points to another reason for practicing diabetes prevention. According to a recently published study from the Netherlands, having diabetes increases the risk of liver cancer for those with chronic Hepatitis C with advanced fibrosis or cirrhosis.
Study Details
Researchers at the Erasmus MC University Medical Center in Rotterdam analyzed data on 541 European and Canadian patients with advanced, chronic Hepatitis C. The researchers discovered that patients with more severe liver fibrosis were more likely to have diabetes. In addition, they concluded that individuals with advanced Hepatitis C and diabetes were at increased risk of developing liver cancer.
The severity of fibrosis was assessed by an Ishak fibrosis score, a system that measures the degree of scarring (fibrosis) of the liver:
· Stage 0 represents no fibrosis
· Stage 1 and 2 indicate degrees of fibrosis where there is minimal scarring around liver blood vessels
· Stage 3 indicates scarring extended out from liver blood vessels
· Stage 4 means that the scarring has formed bridges between blood vessels
· Stage 5 indicates nodular formation in the liver
· Stage 6 represents cirrhosis
According to researchers, the higher a person with Hepatitis C’s Ishak score, the more likely they were to have diabetes:
· Of those with an Ishak score of four, 10.5 percent had diabetes mellitus
· Of those with an Ishak score of five, 12.5 percent had diabetes mellitus
· Of those with an Ishak score of six, 19.1 percent had diabetes mellitus
Among the participants with diabetes, the study found an increased occurrence of liver cancer. As the primary test warning of diabetes (fasting glucose test) showed increased amounts of sugar in the blood, the risk of developing liver cancer also increased. The authors of the study postulated that hyperinsulinemia might explain the increased liver cancer risk among diabetic patients.
What is Hyperinsulinemia?
Although it does not necessarily equate to diabetes, hyperinsulinemia means having too much insulin in the blood. Unfortunately, hyperinsulinemia often leads to adult onset diabetes. Insulin is produced by the pancreas to help regulate blood sugar. The most common cause of hyperinsulinemia is insulin resistance, a condition where the body is resistant to insulin’s effects causing the pancreas to compensate by making more insulin.
Prevention
There is great hope for those who have hyperinsulinemia to prevent diabetes. The American Diabetes Association’s Diabetes Prevention Program (DPP) study conclusively showed that people with pre-diabetes can prevent the development of type 2 diabetes by making changes in their diet and increasing their level of physical activity. They may even be able to return their blood glucose levels to within normal range. Despite the DPP showing that some medications may delay the development of diabetes, diet and exercise had the most dramatic results. Just 30 minutes a day of moderate physical activity, coupled with a 5-10 percent reduction in body weight, produced a 58 percent reduction in diabetes.
Although the authors of this Dutch study do not explain why excessive amounts of insulin predispose someone to developing liver cancer, future studies are sure to investigate this established connection. In the meantime, this research warns people with chronic liver disease to take diabetes prevention seriously. It is now clearer than ever that those with Hepatitis C who don’t want liver cancer to be a part of their future must make diet and exercise their immediate priority.
References:
www.caringmedical.com, Condition: Hyperinsulinemia, Caring Medical & Rehabilitation Services, 2008.
www.diabetes.org, Diabetes Statistics, American Diabetes Association, 2008.
www.diabetes.org, How to Prevent or Delay Diabetes, American Diabetes Association, 2008.
www.idenix.com, Glossary of Terms, Idenix Pharmaceuticals, 2008.
www.mayoclinic.com, Hyperinsulinemia: Is it Diabetes?, Maria Collazo-Clavell, MD, Mayo Foundation for Medical Education and Research, 2008.
www.nlm.nih.gov, Diabetes Boosts Liver Cancer Risk in Hepatitis, Cirrhosis Cases, Robert Preidt, June 2008.
www.phoenixcme.org, Liver Fibrosis, phoenixcme.org, 2008.
Posted by Editors at 03:33 PM --- Printer-friendly version
July 29, 2008
Two Promising Ways to Quit Alcohol
In addition to cutting the risk for fatty liver disease, research presented at the Research Society on Alcoholism conference confirmed two distinct approaches that can help those battling alcoholism.
Two new medications may help alcoholics kick the bottle
http://www.thaindian.com/newsportal/entertainment/two-new-medications-
may-help-alcoholics-kick-the-bottle_10073049.html
Washington, July 18 (ANI): Researchers at the Medical University of South Carolina (MUSC) have identified two new medications that may help heavy drinkers modify their consumption, reduce alcohol withdrawal symptoms, and prevent relapse.
In the first study, MUSC researchers along with a team from the University of Virginia Health System have found that topiramate, an effective therapeutic medication, not only decreases heavy drinking, but also cuts risk factors associated with heavy drinking.
The medication effectively lowers all liver enzymes, plasma cholesterol, body mass index (BMI), and systolic and diastolic blood pressure, thus reducing heart disease risk.
“These findings add growing data indicating that heavy drinkers who modify their drinking with the help of medication and supportive counseling may see an improvement in health and well-being, as well as a potential reduction of risk for the development of heart and liver diseases, said Raymond Anton, M.D., distinguished university professor.
This shows that treatment of alcoholism has potential health benefits beyond the immediate behavioural and emotional improvement caused by a reduction in drinking," he added.
In addition to decreasing liver enzymes and cholesterol levels, topiramate can also cut fatty liver disease risk, which leads to cirrhosis - a common consequence to end-stage liver disease leading to death in some alcoholics.
Topiramate significantly contributed to a decline in obsessive thoughts and compulsions, components of alcohol craving, and also had a greater improvement in their overall quality of life.
Another study by Anton showed that PROMETA alcoholism treatment program, a combination of generic medications, led to significant reductions in cravings and alcohol withdrawal symptoms.
It promoted abstinence, and improved mood and sleep only in those who had symptoms of alcohol withdrawal.
The results were presented at Research Society on Alcoholism (RSA) conference in Washington D.C. (ANI)
Posted by Editors at 04:07 PM --- Printer-friendly version
Liver Donor Pool Expands For Hepatitis C Patients
Learn about the discovery made by St. Louis researchers that will expand the liver donor pool for HCV patients, and find out if Hepatitis C serology affects post-liver transplant survival rate.
Donor's Age Not Linked to Poor Outcomes in Liver Transplants
http://www.washingtonpost.com/wp-dyn/content/article/2008/07/22/
AR2008072201552.html
TUESDAY, July 22 (HealthDay News) -- Patients with hepatitis C who receive a liver from a donor over age 60 aren't at an increased risk for transplant failure, death or recurrent disease within five years after transplantation, say researchers at the Washington University School of Medicine, in St. Louis.
They analyzed data from 489 adults who had liver transplants at the school between 1997 and 2006. Of those patients, 187 (38.2 percent) had hepatitis C and 302 (61.8 percent) had other indications for liver transplant.
Of the patients with hepatitis C, 88.1 percent were still alive after one year, 78.3 percent survived three years, and 69.2 percent survived five years. Donor livers were still functioning in 85.6 percent of hepatitis C virus-positive recipients after one year, 75.6 percent after three years, and 65.6 percent after five years.
When they compared patients with hepatitis C and those without hepatitis C, the researchers found no differences in rates of patient survival and transplanted liver survival at one, three and five years.
"However, similar to other long-term transplant centers, we observed a negative effect from recurrent hepatitis C virus with a trend toward worsened long-term survival between years five and 10," the researchers wrote.
Among the patients in the study, 24 (12.8 percent) of those with hepatitis C and 48 (15.9 percent) of those without the virus received livers from donors age 60 and older. These recipients and those who received livers from younger donors had similar one-, three-, and five-year survival rates.
The findings were published in the July issue of theArchives of Surgery.
"In conclusion, overall patient and graft (organ) survival in hepatitis C virus-positive recipients is comparable with that in hepatitis C virus-negative patients, and there seems to be little, if any, adverse effect on short- and medium-term follow-up with the use of carefully selected older donor grafts in recipients with hepatitis C virus," the researchers concluded. "Data from this series suggest that the continued use of selected older donors is a safe method of expanding the liver donor pool, even for hepatitis C-positive recipients."
More information
The U.S. Centers for Disease Control and Prevention has more about hepatitis C.
SOURCE:JAMA/Archivesjournals, news release, July 21, 2008
Posted by Editors at 03:48 PM --- Printer-friendly version
July 21, 2008
Natalie Cole Optimistic About Her Battle with Hepatitis C
Although currently recovering from combination therapy's side effects, the well-respected vocalist Natalie Cole may have conquered the Hepatitis C virus.
Natalie Cole says she has hepatitis C
The Associated Press
Published: July 16, 2008
http://www.iht.com/articles/ap/2008/07/16/arts/People-Natalie-Cole.php
NEW YORK: Grammy-winning singer Natalie Cole has been diagnosed with hepatitis C, her publicist said in a statement Wednesday.
Hepatitis C is a liver disease spread through contact with infected blood. The statement said the disease was revealed during a routine examination and was likely caused by her drug use years ago.
"I've been so fortunate to have learned so much from my past experiences," said Cole. "I am embraced by the love and support of my family and friends; I am committed to my belief in myself and in my abiding faith to meet this challenge with a heartfelt optimism and determination. This is how I intend to deal with this current challenge in my life."
Her physician at Cedars-Sinai Medical Center in Los Angeles, Dr. Graham Woolf, said Cole has had a "terrific response to her medication and is now virus negative."
"This gives her an increased chance of cure," he said. Woolf said Cole is recovering from side effects of the medicine she's taking, including fatigue, muscle aches and dehydration.
Cole, 58, the daughter of jazz legend Nat King Cole, has sold millions of records over her long career. She is due to release "Still Unforgettable," the follow-up to 1991's Grammy-winning, multi-platinum CD "Unforgettable ... With Love," on which she remade some of her father's classics, in September.
Posted by Editors at 10:06 AM --- Printer-friendly version
July 09, 2008
Hep C and Fatty Liver Disease Linked
Pittsburgh researchers have found an enzyme known to participate in fat production is elevated in those with Hepatitis C. Further exploration of this enzyme could help physicians better predict which HCV patients are at risk of developing fatty liver disease.
Hepatitis C Virus May Need Enzyme's Help To Cause Liver Disease
http://www.sciencedaily.com/releases/2008/07/080709091717.htm
ScienceDaily (July 9, 2008) — A key enzyme may explain how hepatitis C infection causes fatty liver -- a buildup of excess fat in the liver, which can lead to life-threatening diseases such as cirrhosis and liver cancer, report University of Pittsburgh Graduate School of Public Health and School of Medicine researchers.
The study shows that an enzyme known to play a major role in lipid production, fatty acid synthase (FAS), was highly elevated in human liver cells exposed to the hepatitis C virus. While preliminary, the research suggests that testing for elevated levels of FAS could help determine which patients with hepatitis C virus may go on to develop more serious, long-lasting health consequences brought on by fatty liver.
Nearly 200 million people worldwide are infected by hepatitis C, including 4 million Americans. Seventy percent of people with hepatitis C develop chronic liver disease, and the infection is the leading reason for liver transplantation in the United States.
Unlike hepatitis A and B, there is no vaccine to prevent hepatitis C infection. Since hepatitis C typically has no symptoms, many people do not know they have the infection until they develop signs of liver failure or fatty liver, sometimes decades after infection. The virus replicates and mutates quickly, helping it to evade discovery and attack by the immune system and allowing it to slowly wreak damage on the liver.
"Our study has provided new insight into how hepatitis C causes fatty liver. This has important implications for future studies and efforts to understand how the virus causes an increase in fatty acid levels that can lead to serious liver conditions," said Tianyi Wang, Ph.D., assistant professor, Department of Infectious Diseases and Microbiology, University of Pittsburgh Graduate School of Public Health, and the study's lead author.
To identify possible proteins in the hepatitis C virus linked to an increase in fatty acids, Dr. Wang worked with Thomas Conrads, Ph.D., co-director of clinical proteomics at the University of Pittsburgh Cancer Institute, and colleagues on a mass spectrometry-based proteomics approach in which they measured protein expression from liver cell cultures exposed to the hepatitis C virus. The approach sorted proteins based on their weight and electrical charge, looking for divergent patterns linked to the virus. Of the 175 proteins they identified, only FAS was highly elevated in cell cultures. Furthermore, when they blocked the expression of FAS, they noted a three to four times decrease in the level of the virus, indicating that FAS is directly linked to the virus's expression.
"Viruses are very complex, so it is challenging to determine what proteins may be at play in their survival and growth," said Dr. Wang. "The proteomic approach we used revealed many proteins linked to hepatitis C that may be worthy of further study, but FAS appears to be the protein most strongly associated with the production of fatty acids that can cause liver disease."
"Our next step in this research is to see how high the level of FAS is in tissue samples from hepatitis C patients and determine whether elevated FAS levels directly result in overproduction of fat in livers. If we learn that FAS is highly present in tissue, testing for it may be a way to predict those at risk for liver disease."
The study was published in the July 9 online issue of Hepatology. In addition to Drs. Wang and Conrads, other authors include Wei Yang, Ph.D., Sara Chadwick, B.S., and Shufeng Liu, Ph.D., University of Pittsburgh Graduate School of Public Health; Brian Hood, Ph.D., University of Pittsburgh Cancer Institute; Simon Watkins, Ph.D., University of Pittsburgh School of Medicine; and Guangxiang Luo, Ph.D., University of Kentucky College of Medicine.
The research was supported by a grant from the National Institutes of Health and University of Pittsburgh Central Research Development Funds.
Adapted from materials provided by University of Pittsburgh Schools of the Health Sciences, via EurekAlert!, a service of AAAS.
Posted by Editors at 03:29 PM --- Printer-friendly version
Anadys' ANA773 Hepatitis C Phase I Trials in Netherlands
Reducing the dosing schedule in half, Anadys Pharmaceuticals continues its investigation of ANA773, a Toll-Like Receptor-7 agonist prodrug. Approaching the Hepatitis C virus differently from most other contenders, Phase I clinical trials evaluating the safety, tolerability and viral-load decline associated with ANA773 are about to begin in the Netherlands.
Anadys Pharmaceuticals Resumes Clinical Investigation of TLR7 Mechanism in HCV
http://money.cnn.com/news/newsfeeds/articles/prnewswire/200807071605PR_NEWS_USPR_____LAM070.htm
SAN DIEGO, July 7 /PRNewswire-FirstCall/ -- Anadys Pharmaceuticals, Inc. (Nasdaq: ANDS) announced today that it is resuming clinical investigation of the Toll-Like Receptor-7 (TLR7) mechanism for the treatment of chronic hepatitis C. Based on preclinical pharmacology testing and the results of completed 13-week GLP animal toxicology studies, Anadys has received clearance to initiate a clinical trial of ANA773, the Company’s oral TLR7 agonist prodrug, under a clinical trial application (CTA) in the Netherlands. Following initial dosing in healthy volunteers, this trial will explore every-other-day dosing over 28 days in HCV patients. Anadys also continues to enroll patients in a separate Phase I clinical trial of ANA773 in oncology that is ongoing under an IND in the United States.
"In an extensive preclinical program conducted with ANA773, we have previously shown that the profile of immune stimulation resulting from TLR7 activation can be dramatically modulated by altering the schedule of administration," said James Freddo, M.D., Anadys’ Chief Medical Officer. "Now, results of toxicology studies employing every-other-day dosing of ANA773 have shown that we can achieve desired levels of immune stimulation sustained over 13 weeks without adverse toxicology findings. The favorable toxicology profile seen to date, coupled with the stable induction of interferon-alpha dependent responses when ANA773 is dosed every other day over 13 weeks, have convinced us that ANA773 has the potential to demonstrate benefit in patients infected with HCV."
Steve Worland, Ph.D., Anadys’ President and CEO, commented, "The decision to take ANA773 into HCV, which will be our third clinical development program to commence dosing this year, reflects an expansion of Anadys’ development efforts in HCV. As an approach to treat hepatitis C, the TLR7 mechanism is independent from, and potentially complementary to, ANA598, Anadys’ non-nucleoside HCV polymerase inhibitor currently in Phase I clinical development." Commenting on the expected impact this expansion will have on the Company’s cash outlook for 2008, Dr. Worland added, "Because the ANA773 hepatitis C program is highly leveraged off our oncology program, we expect to carry forward all three clinical development programs this year within our previous 2008 cash utilization projection of $29 to $31 million."
ANA773 Phase I Clinical Trial in HCV
The Phase I clinical trial of ANA773 in HCV will be conducted under a two-part protocol. Part A of the study will include both single and multiple doses of ANA773 in healthy volunteers. Successive cohorts of volunteers will receive ascending dose levels of ANA773. The primary objectives of Part A of the study are to assess safety and tolerability. In Part B of the study, HCV patients will receive ANA773 every other day for 28 days. The primary objectives of Part B are to assess safety, tolerability and viral load decline. The starting dose level in HCV patients will be selected based on safety, tolerability and immune responses seen in healthy volunteers in Part A. It is expected that this study design will allow initial dosing in HCV patients at a dose that will have demonstrated a desired magnitude of immune stimulation in the healthy subjects, and that dosing in patients will initiate prior to completion of dose escalation in Part A of the study. Approximately 40 healthy volunteers and 24 patients are anticipated to be enrolled in this study. Dosing is expected to begin in healthy volunteers within the next few weeks and in HCV patients early in the fourth quarter of 2008.
About ANA773 and TLR Pharmacology
ANA773 is an orally administered prodrug of a novel TLR7-specific agonist. Results from pre-clinical pharmacology studies have shown that ANA773 can elicit desired immune responses and that the profile of response can be modulated by both dose and schedule of administration. Results of recently completed 13-week GLP toxicology studies have shown that with every-other-day dosing of ANA773, immune stimulation of a magnitude believed to confer therapeutic potential can be achieved without adverse toxicology findings. The immune stimulation observed with every-other-day dosing of ANA773 in monkeys included induction of interferon-alpha and interferon dependent responses at levels that are sustained over 13 weeks of dosing.
The recently obtained results with every-other-day dosing of ANA773 over 13 weeks contrast with results from prior 13-week animal toxicology studies that utilized daily dosing of ANA975, a TLR7 agonist prodrug previously in development by the Company for the treatment of chronic hepatitis C. In initial 13-week animal toxicology studies of ANA975 dosed daily, unexpected findings associated with intense immune stimulation were observed. When lower daily doses of ANA975 were then explored in a subsequent 13-week animal toxicology study, it was determined that adverse findings were present even at dose levels where desired immunostimulatory effects were not measurable, following which the decision was made in 2007 to discontinue development of ANA975.
Webcast of Conference Call
Anadys will host a conference call today, July 7, 2008 at 2:00 p.m. Pacific Daylight Time to discuss Anadys’ plans to resume clinical investigation of the TLR7 mechanism in HCV. A live webcast of the call will be available online at http://www.anadyspharma.com. A telephone replay will also be available approximately one hour after completion of the call. To access the telephone replay, dial 888-286-8010 (domestic) or 617-801-6888 (international), passcode 84526379. The webcast and telephone replay will be available through July 21, 2008.
About Anadys
Anadys Pharmaceuticals, Inc. is a clinical-stage biopharmaceutical company dedicated to improving patient care by developing novel medicines in the areas of hepatitis C and oncology. For the treatment of chronic hepatitis C, the Company is developing ANA598, a non-nucleoside polymerase inhibitor, and ANA773, an oral TLR7 agonist prodrug. The Company is also developing ANA773 for the treatment of cancer.
Safe Harbor Statement
Statements in this press release that are not strictly historical in nature constitute "forward-looking statements". Such statements include, but are not limited to, references to (i) the expected timing and planned development activities for ANA773, including the timing for commencing dosing in the planned ANA773 HCV clinical trial; (ii) the belief that ANA773 has the potential to demonstrate benefit in patients infected with HCV; (iii) the belief that the TLR7 mechanism will potentially be complementary to ANA598; (iv) expectations regarding Anadys’ cash utilization for 2008; (v) the planned study design of the two-part protocol of the ANA773 clinical trial in HCV; (vi) Anadys’ expectation to begin dosing HCV-infected patients with ANA773 prior to the completion of the healthy volunteer portion of the study at a dose that will have demonstrated a desired magnitude of immune stimulation in the healthy subjects; and (vii) the belief that ANA773 can elicit immune stimulation of a magnitude sufficient to confer therapeutic potential without adverse safety issues. Such forward-looking statements involve known and unknown risks, uncertainties and other factors, which may cause Anadys’ actual results to be materially different from historical results or from any results expressed or implied by such forward-looking statements. For example, the results of preclinical studies, including the toxicology studies described in this press release, may not be predictive of future results, and Anadys cannot provide any assurances that ANA773 or ANA598 will not have unforeseen safety issues in future toxicology studies, will have favorable results in future clinical trials or will receive regulatory approval. In addition, Anadys’ results may be affected by risks related to competition from other biotechnology and pharmaceutical companies, its effectiveness at managing its financial resources, its ability to successfully develop and market products, difficulties or delays in its preclinical studies or clinical trials, difficulties or delays in manufacturing its clinical trials materials, the scope and validity of patent protection for its products, regulatory developments involving future products and its ability to obtain additional funding to support its operations. Risk factors that may cause actual results to differ are more fully discussed in Anadys’ SEC filings, including Anadys’ Form 10-K for the year ended December 31, 2007 and Anadys’ Form 10-Q for the quarter ended March 31, 2008. All forward-looking statements are qualified in their entirety by this cautionary statement. Anadys is providing this information as of this date and does not undertake any obligation to update any forward-looking statements contained in this document as a result of new information, future events or otherwise.
SOURCE Anadys Pharmaceuticals, Inc.
Posted by Editors at 03:23 PM --- Printer-friendly version
July 07, 2008
Popular Illegal Drug Extra Harmful with HCV
Scientists have found a popular street drug worsens Hepatitis C infection in two worrisome ways.
by Nicole Cutler, L.Ac.
Since an estimated 4.1 million Americans are infected with Hepatitis C, more people are concerned with which factors increase the damage this virus can cause. Considered to be a drug by healthcare professionals, alcohol is well-known to worsen Hepatitis C infection. As more research is conducted on the impact other types of drugs have on the Hepatitis C virus (HCV), it seems that an increasing number of controlled substances also encourage this virus to gain strength. In addition to causing neurological decline in people with HCV, methamphetamine has recently been charged with encouraging this virus to replicate.
About Methamphetamine
According to the 2005 National Survey on Drug Use and Health, 10.4 million Americans age 12 and older had tried methamphetamine at least once in their lifetimes. In many Western and Midwestern states, methamphetamine is second only to alcohol and marijuana as the drug most frequently used. A highly addictive central nervous system stimulant, methamphetamine’s low cost, ease to manufacture and variety of ways to take it make this substance a popular choice among those looking for a high.
In contrast to many other illicit drugs, methamphetamine can be made in small, homemade, illegal laboratories. Street methamphetamine is referred to by many names, such as “speed,” “meth” and “chalk.” Also referred to as “ice,” “crystal,” “glass” and “tina,” methamphetamine hydrochloride appears as clear chunky crystals resembling ice. Methamphetamine can be taken as a pill, injected, snorted, smoked or administered anally. Abusers may become addicted quickly, needing higher doses more often to feel its effects.
Meth’s Impact on the Body
While it is chemically related to amphetamine, methamphetamine’s effects are much more potent, longer lasting, and more harmful to the central nervous system. Methamphetamine increases the release of very high levels of the neurotransmitter dopamine, which stimulates brain cells, enhancing mood and body movement. Chronic methamphetamine abuse significantly changes how the brain functions. Taking even small amounts can result in:
· increased wakefulness
· increased physical activity
· decreased appetite
· increased respiration
· rapid heart rate
· irregular heartbeat
· increased blood pressure
· hyperthermia
Other effects of methamphetamine abuse may include irritability, anxiety, insomnia, confusion, tremors, convulsions, cardiovascular collapse and death. Long-term effects may include paranoia, aggressiveness, extreme anorexia, memory loss, visual and auditory hallucinations, delusions and severe dental problems.
Meth and Hepatitis C
Besides the possibility of acquiring Hepatitis C by using this drug, methamphetamine has been shown to wreck havoc on the body of a person already infected with the virus. Separate trials have shown that methamphetamine interacts with Hepatitis C in two damaging ways: cognition dysfunction and proliferation promotion.
1. Cognition Dysfunction – In a University of California at San Diego study, researchers examined how the Hepatitis C virus contributes to neurocognitive dysfunction in individuals with methamphetamine dependence. Investigators discovered that people with the Hepatitis C virus who had a dependence on methamphetamine had a higher likelihood of cognition issues, including overall neurocognitive performance deficits and problems in the specific areas of learning, abstraction, motor skills, speeded information processing and delayed recall.
2. Proliferation Promotion – In the April 2008 issue of Journal of Viral Hepatitis, researchers from the University Of Pennsylvania School Of Medicine reported on a laboratory study looking at whether methamphetamine lowered immunity in host cells, thus facilitating Hepatitis C replication in human liver cells. The researchers found that methamphetamine use affected the immune system in the following ways:
1. Methamphetamine inhibited natural intracellular interferon alpha expression.
2. Methamphetamine compromised the effect of recombinant interferon alpha as used for Hepatitis C treatment.
3. Methamphetamine inhibited expression of the signal transducer and activator of transcription 1 (STAT-1), a key modulator of interferon-mediated biological responses.
4. Methamphetamine also down-regulated expression of interferon regulatory factor 5 (IRF-5), a transcriptional factor that activates the interferon pathway.
Based on these findings, the investigators concluded that the manner in which methamphetamine compromises a person’s immune system encourages HCV viral load to rise.
As Hepatitis C infection rates climb, so does the effort to minimize the damage this virus inflicts. With its documented ability to favor central nervous system deterioration in people with HCV, methamphetamine use has an effect opposite of what many initially use this drug for – alertness. Additionally, new research presents evidence that methamphetamine’s effect on the immune system provides an ideal environment for Hepatitis C to replicate. Based on these two injurious effects of methamphetamine specific to HCV, people with the virus are hereby advised to avoid this illicit drug.
References:
L Ye, JS Peng, Z Wang, et al., Methamphetamine enhances Hepatitis C virus replication in human hepatocytes, Journal of Viral Hepatitis, April 2008.
www.hivandhepatitis.com, Methamphetamine Promotes Hepatitis C Virus Replication in Human Liver Cells, Liz Highleyman, hivandhepatitis.com, 2008.
www.neurology.org, Hepatitis C augments cognitive deficits associated with HIV infection and methamphetamine, M. Cherner, PhD, Neurology, April 2005.
www.nida.nih.gov, NIDA InfoFacts: Methamphetamine, National Institute on Drug Abuse, 2008.
www.usdoj.gov, Methamphetamine, United States Drug Enforcement Administration, 2008.
Posted by Editors at 12:19 PM --- Printer-friendly version
Hep C Long-Term Management Strategies
Since only about half of those on combination therapy beat Hepatitis C, the remaining people must strive to prevent their liver disease from progressing. Thus far, a liver wellness approach is a safer, more effective way to remain healthy compared to long-term interferon therapy.
by Nicole Cutler, L.Ac.
Over the past decade, clinical trials worldwide have been evaluating the effectiveness of Hepatitis C’s current standard of treatment, pegylated interferon and ribavirin. Most study results concur that approximately 50 percent of infected individuals are able to successfully clear the virus with the combination of these medicines. While this is good news for those who have been able to beat Hepatitis C, it leaves about half of those infected with a need for long-term management.
Sustained Viral Response
Successful Hepatitis C treatment is determined by the achievement of a sustained viral response (SVR). Considered to be the absence of detectable virus six months after the completion of treatment, SVR may even be a cure for those lucky enough to reach it. Although pegylated interferon and ribavirin have the potential to permanently get rid of Hepatitis C, it is a common occurrence for viral loads to rebound shortly after completing the medicine.
In the past, people with Hepatitis C who fail to achieve SVR have had few drug options for the continued battle against their liver disease. In general, Western medicine offers two choices for individuals in this position. They can:
1. repeat the pegylated interferon and ribavirin treatment with all of their side effects.
2. wait by the sidelines to see if new drugs are approved for Hepatitis C.
In lieu of curing the disease, those aiming to manage Hepatitis C share the goal of minimizing liver inflammation, thus reducing liver damage. Managing Hepatitis C has two distinct approaches – supporting liver wellness and using medications to slow down liver damage.
Liver Wellness for Hepatitis C Management
An increasing number of physicians and patients are recognizing the value of practicing liver wellness to delay disease advancement and enhance quality of life. Liver wellness is an approach that incorporates many daily aspects of living such as:
· Good nutrition
· Restful sleep
· Toxin avoidance
· Supplementing with milk thistle
· Alcohol abstinence
· Regular exercise
· Other liver supportive action
Despite being infected with Hepatitis C, combining the different facets of liver wellness has helped thousands of people live long, healthy lives.
Medications for Hepatitis C Management
In addition to practicing liver wellness, pharmaceutical companies also appreciate the value of keeping Hepatitis C viral loads to a minimum. Two U.S. studies have been conducted to determine if liver fibrosis progression caused by Hepatitis C can be stopped or significantly slowed with long-term, low-dose interferon treatment. The two studies, known as Hepatitis C Antiviral Long-term Treatment against Cirrhosis (HALT-C) and Colchecine versus Peg-Intron Long-term (COPILOT), evaluated approximately 1,600 people with Hepatitis C.
· HALT-C – The 517 patients randomized to the treatment arm in the HALT-C study received 90 micrograms of pegylated interferon in weekly injections for 3.5 years. Preliminary results from HALT-C looked promising, since pegylated interferon maintenance therapy led to improvements in liver enzymes, viral load and liver inflammation – markers typically assumed to predict liver disease progression. However, while these markers remained true, they ultimately did not translate into a lower likelihood of fibrosis progression, liver cancer, liver failure or death. Based on the HALT-C trial, maintenance doses of pegylated interferon are not an effective means of managing Hepatitis C.
· COPILOT – In this trial, patients are given a weekly injection of Peg-Intron or a twice-daily dosage of colchecine, an anti-inflammatory drug that has been found to help stave off the instance of liver cancer in cirrhotic patients. Differing from HALT-C, the COPILOT trial administers low dose Peg-Intron based on the patient’s weight. Given the side effects associated with standard doses of pegylated interferon, it was unclear whether lower-dose maintenance therapy would improve or impair quality of life. Thus far, the researchers have determined that treatment with weight-based, low-dose pegylated interferon does not adversely affect quality of life over a two-year period. Although it is too soon to determine the outcome of COPILOT, these preliminary results suggest that the weight-based low dosages of pegylated interferon may be tolerable by previous non-responders as maintenance therapy.
Major progress has been made in treating chronic Hepatitis C infection since the virus was isolated nearly 20 years ago. Since the current standard of therapy successfully eliminates the virus in approximately 50 percent of those affected, strategies to help people manage their illness is crucial for the remaining half of Hepatitis C infections.
At this time, no therapy is approved by the U.S. Food and Drug Administration for treatment failures of pegylated interferon and ribavirin. So far, the studies investigating low-dosage interferon as a maintenance therapy are inconclusive. However, preliminary results give us hope that a pharmaceutical concoction could delay liver disease advancement. Until an official approval for Hepatitis C maintenance therapy surfaces, liver wellness programs are an infected person’s best option for preserving their liver’s health. Often referred to as healthful lifestyle choices, investigating the many components of supporting the liver may help maintain hepatic health until a sustained viral response can be attained.
References:
Kelleher, T. Barry, et al., Maintenance Therapy for chronic hepatitis C, Current Gastroenterology Reports, June 2007.
www.hivandhepatitis.com, HALT-C Trial Shows Minimal Long-term Benefit of Pegylated Interferon Alfa-2a (Pegasys) Maintenance Therapy in Patients with Chronic Hepatitis C, Liz Highleyman, hivandhepatitis.com, November 2007.
www.hivandhepatitis.com, Treatment with Low-dose Pegylated Interferon Alfa-2b (PegIntron) Did Not Adversely Affect Quality of Life over a 2-year Period in Patients Staying on Therapy: The COPILOT Trial, hivandhepatitis.com, November 2007.
www.liverhealthtoday.com, Stalling Hepatitis C, Marc S. Botts, Liver Health Today, 2007.
www.nih.gov, Hepatitis C Treatment Reduces the Virus but Serious Liver Problems May Progress, US Department of Health and Human Services, November 2007.
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