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How You Can Stop HCV from Leading to Gallstones

February 26, 2007

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Recent research has shown how Hepatitis C patients have a greater tendency to develop gallstones. Learn how to prevent your diagnosis from leading to one of the 1 million new cases of gallstones reported each year.

by Nicole Culter, L.Ac.

Gallstone disease is the most common disorder affecting the body's biliary system, the network of organs and ducts responsible for creating, transporting, storing and releasing bile. Responsible for the digestion of fat, bile is a fluid produced by the liver and stored in the gallbladder. Bile primarily consists of water, cholesterol, fats, bile salts, proteins and bilirubin. If the chemical balance of bile contains too much of any of these components, particularly cholesterol, crystals form and harden into gallstones.

Gallstones can be as small as a grain of sand or as large as a golf ball. The gallbladder can develop just one large stone, hundreds of tiny stones, or anywhere in between. When gallstones lodge in bile ducts, they can prevent the flow of bile or digestive enzymes or lead to severe abdominal pain, vomiting, inflammation and possible infection.

Symptoms
Symptoms of gallstones are often called a gallstone "attack" because they occur suddenly. A typical attack can cause:

· Steady pain in the upper abdomen that increases rapidly and lasts from 30 minutes to several hours
· Pain in the back between the shoulder blades
· Pain under the right shoulder
· Nausea or vomiting

Gallstone attacks often follow fatty meals, and they may occur during the night. Other gallstone symptoms include:

1. Abdominal bloating
2. Recurring intolerance of fatty foods
3. Belching
4. Gas
5. Indigestion

The Link Between Hepatitis C and Gallstones
Over the years, the medical community has suspected a connection between liver disease and gallbladder disease. Researchers looking to prove this suspicion have shown how people with Hepatitis C have a greater tendency to develop gallstones.

· An Italian study published in the Archives of Internal Medicine in 1999 suggested that cirrhosis represents a major risk factor for gallstones.

· A New York study published in the May 2005 issue of Hepatology concluded that chronic Hepatitis C infection demonstrated a strong association with gallbladder disease and that gallbladder disease was more common in adults with severe liver disease.

· Published in the September 2005 issue of Journal of Gastroenterology and Hepatology, a Taiwanese study involving nearly 30,000 people confirmed that infection with Hepatitis C contributes to gallstone formation.

How This Impacts People with Hepatitis C
Considering the clinical proof that people with chronic Hepatitis C are at a greater risk for developing gallbladder disease, those harboring this virus are strongly encouraged to practice gallstone prevention.

Diet modification is the primary method to prevent gallstones from developing. Increasing consumption of both soluble and insoluble fiber may prevent gallstones. Fiber reduces the absorption of deoxycholic acid by producing a favorable shift in the triad of factors controlling cholesterol's solubility in bile. Soluble fibers that are effective include guar gum and pectin, as well as oat bran, wheat bran, and soy fiber, all of which are found in many fruits and vegetables.

Additionally, regular, vigorous, exercise may decrease gallstone risk. One study, reported by WebMD, found that men who performed endurance activities for 30 minutes, five times a week, experienced a 34 percent reduction in gallbladder disease risk. The benefits derived from exercise were more dependent on intensity than type of exercise. Researchers theorize that exercise helps to normalize blood sugar and insulin levels which may contribute to gallstones when abnormal.

Evidence gathered on gallstone formation clearly points to an increased risk for individuals with the Hepatitis C virus. While people with chronic Hepatitis C likely have plenty of other health concerns, practicing gallstone prevention is easy due to its similarity to liver supportive lifestyle changes. Now there is one more reason for those with liver disease to incorporate healthful habits by increasing the fiber in their diet and getting started on a regular exercise routine.

References:

Bini EJ, McGready J, Prevalence of gallbladder disease among persons with hepatitis C virus infection in the United States, Hepatology, May 2005.

Conte D, et al., Close relation between cirrhosis and gallstones: cross-sectional and longitudinal study, Archives of Internal Medicine, July 1999.

T S Chang, et al., Hepatitis C virus infection facilitates gallstone formation, Journal of Gastroenterology and Hepatology, September 20, 2005.

www.digestive.niddk.nih.gov, Gallstones, National Digestive Diseases Information Clearinghouse, November 2004.

www.womenshealth.about.com, Preventing Gallstones, Tracee Cornforth, About, Inc., 2006.

Posted by Editors at 04:29 PM --- Printer-friendly version | Comments (0)

Genetics May Determine Hepatitis C Treatment Success

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New research looks at gene expression as a possible explanation for the significant number of HCV interferon/ribavirin non-responders. In light of the difference in gene expression between responders and non-responders, genetics may play a role in predicting antiviral medication success.

Changes in Gene Expression during Hepatitis C Treatment Distinguish Responders from Non-Responders
www.hivandhepatitis.com
By Liz Highleyman

While treatment of chronic hepatitis C using pegylated interferon plus ribavirin leads to sustained HCV clearance and clinical improvement in approximately half of all patients, response rates are lower in certain "difficult to treat" groups, including patients with genotype 1 HCV and African-Americans.

It is unclear why treatment response rates vary by race/ethnicity, but genetic factors may play a role.

As reported in the January 31, 2007 electronic edition of the Journal of Virology, researchers used DNA micro-arrays to assess gene expression in a group of 33 African-American and 36 Caucasian-American patients with genotype 1 chronic HCV infection during the first 28 days of treatment with pegylated interferon/ribavirin.

Results

• Patients showed a response to treatment at the gene expression level in RNA isolated from peripheral blood mononuclear cells (PBMCs) regardless of degree of decrease in HCV RNA levels.

• Gene expression responses were relatively blunted in patients with poor virological response (< 1.5 log10 IU/mL decrease in HCV RNA at 28 days) compared to those with a marked (> 3.5 log10 decrease) or intermediate (1.5-3.5 log10 decrease) response.

• The number of genes that were up-regulated or down-regulated by pegylated interferon/ribavirin was fewer in patients with a poor virological response compared to those with a marked or intermediate response.

• Induced levels of known interferon-stimulated genes such as OAS, MX1, IRF-7, and the toll-like receptor TLR-7 were lower in poor responders compared to patients with marked or intermediate responses.

• However, African-Americans had stronger interferon responses than Caucasian patients overall.

Conclusion

The authors concluded that, "the relative lack of viral response to interferon therapy of hepatitis C is associated with blunted interferon cell signaling. No specific regulatory gene could be identified as responsible for this global blunting or racial differences."
It remains unclear why African-Americans tend to respond more poorly to interferon-based therapy, given their overall stronger gene expression response to interferon.

Posted by Editors at 03:01 PM --- Printer-friendly version | Comments (0)

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