Hepatitis C and Liver Cirrhosis – Its Treatment with Zinc Supplementation

Hepatitis C and Liver Cirrhosis – Its Treatment with Zinc Supplementation

Hepatitis C is one of the five known hepatitis Viruses: A, B, C, D and E. it is an infectious disease affecting the liver, caused by the hepatitis C virus (HCV). The infection is often asymptomatic, but when once established, chronic infection can progress to scarring of the liver (fibrosis) , and advance scarring (cirrhosis) which is generally apparent after many years.

Cirrhosis which is a medical term describing the formation of scar tissue on the liver is caused by one or more factors including genetic predisposition and chronic alcohol abuse, as well as hepatitis types B,C, and D, all of which have the potential to cause damage to the liver.

On the other hand, zinc is an essential trace element in the human body, with approximately two grams in healthy adults. The daily amount required by an adult is 10-15 mg and this is absorbed primarily from the upper gastrointestinal tract especially the small intestine. Zinc is involved in the activation of approximately 300 different metallic-enzymes and metal- activated enzymes in vivo and is regarded as essential for the metabolism of nucleic acids and proteins.

Therefore, it has been determined that zinc deficiency causes various pathological conditions in humans. Among these, it is known that in patients with C-viral chronic liver disease, the blood zinc concentration decreases with progression of the disease from chronic hepatitis (CH) to compensated cirrhosis (LC), to hepatocellular carcinoma (HCC), yoshida et al 2001. It is also known that patient with liver failure or HCC are in an especially severe state of zinc deficiency and the liver damage is found to improve with zinc supplementation. Recently, it was reported that the hepatitis C virus (HCV) NSSA protein is a zinc metalloproteinase and that zinc is closely involved in the activation of the NSSA protein. Also, it has been reported that the rate of HCV eradication is higher when interferon (IFN) therapy for C-viral CH is combined with zinc supplementation, compared to IFN therapy alone. Thus, it would appear that zinc supplementation has a clear influence on the clinical profiles of C-viral CH or LC.

However, there has been no report as to what influence zinc supplementation has on the long-term outcome of C-viral CH or LC till after the work of Matsuoka et al, 2001. They gave polaprezinc (orally administered, 150 mg/dm) to patients with C-viral CH or LC and studied prospectively the influence of zinc supplementation on the long-term outcome.

Hepatitis C, Liver Cirrhosis and Zinc

• Hepatitis C:

This is an infectious disease affecting the liver, caused by the hepatitis C virus (HCV). The infection is often asymptomatic, but when once established, chronic infection can progress to scarring of the liver (fibrosis). The existence of hepatitis C (originally “non –A, non-B hepatitis”) was postulated in the 1970s and proven conclusively in 1989. It is one of the five known hepatitis viruses. A, B, C, D and E. The hepatitis C virus is spread by blood contact. A distinct and major characteristics of hepatitis C is its tendency to cause chronic live disease, in which the liver injury persist for a long period of time. Most people have few of the symptoms (if any) after the initial infection, yet the virus persist in the liver in about 85% of those infected. Persistent infection can be treated with medication, peginteriferon and ribavirin being the standard of care therapy. Grongeriff 2005. About fifty-one percent of those who came down with CH can be cured overall. Those who develop cirrhosis or liver cancer may require a liver transplant, and the virus universally recurs after transplantation.

The common risk factors for acquiring hepatitis include:

• Hemodialysis for kidney failure,
• Birth to a HCV-infected mother
• Suffering a needle stick accident from a person with hepatitis C,
• Infecting drugs, including having used infection drugs.

Only once many years ago, sexual transmission etc. many people with chronic hepatitis C have no symptoms of liver disease. If symptoms are present, they are usually mild, nonspecific, and intermittently, they may include: fatigue, nausea, poor appetite, muscle and joint pains, mild right-upper-quadrant discomfort or tenderness (“Liver pain”) etc.

Liver Cirrhosis:

This is a medical term used to describe the formation of scar tissue on the liver (a process called fibrosis), this condition may be caused by any or more of the following: chronic alcohol abuse, genetic predisposition as well as hepatitis types B,C and D, all of these have the potential to cause liver damage. In some cases, those with liver cirrhosis will go on to develop liver failure or other complications of cirrhosis, including, liver cancer or life threatening esophageal varices and gastric varices.

The problem of liver cirrhosis arises when; the fibrosis scar tissue prevents blood flow through the liver, hindering the ability of the remaining tissue to continue to metabolize toxins, drugs and other chemicals in the blood. Alcohol is a notable example. In some cases, the cause of LC is unknown (“or cryptotogenic”) causes exist as well. One condition called non alcoholic steatohepatitis (NASH) is currently under study as a potential cause for many previously cryptogenic cases of cirrhosis. It involves excessive fat storage in the liver, and may be the genetic or environmental conditions. Some autoimmune conditions can produce what is called autoimmune hepatitis, which is the result of the body’s immune system attacking its own cells, specifically those of the liver, thereby producing scar tissue.

The risk factors include: liver damage, portal hypertension, enlargement of portal veins and others leading to them, life-threatening complications, liver cancer and esophageal varices. The clinical features include: enlarged liver, enlarged spleen, Jaundice, muscle wasting and excoriations (scaratehes or abrasions on the skin).

Zinc:

Zinc is an essential trace element in the human body, with approximately two grams in healthy adults the essentiality of zinc for humans was first documented by Prasad in the 1960s. During the past 42 years, zinc deficiency in humans as a result of nutritional factors and several diseases state has been recognized. Many of the clinical features of liver cirrhosis have been linked to zinc deficiency, including loss of body hair, testicular atrophy, poor appetite, immune dysfunction, altered Tasl and small, reduced vitamin A and thyroid hormone metabolism, altered protein metabolism, delayed sound healing, and diminished drug elimination capacity. One of the most interesting novel aspects concerning the presumable role of zinc deficiency in producing clinical features of liver cirrhosis is the possibility of the relationship between zinc and hepatic encephalopathy (HE).

Long term zinc supplementation in patients with hepatic encephalopathy improves neurological symptoms and metabolic parameters. In Wilson’s disease, an inherited defect of copper, zinc is used for maintenance as well as treating presymptomatic, pregnant and pediatric patients.

Polaprezinc Administration  

A total of 70 Japanese patients with CH or LC, who were examined by Matsouka at Nihon University Itabash Hospital from September 1999 through January 2001, gave informed consent to their participation in this study. All of the patients were positive for serum HCV RNA (Aplicor HCV monitor, ROCHE diagnostic K.K., Tokyo, Japan) and were observed for more than three years. All were negative for serum hepatitis B surface antigen (HBSAg, Enzyme-linked immunosorbent assay, EIA, Dinabot, Tokyo, Japan) LE cells, and anti-Mitochondria antibody. No heavy drinkers (More than 30g ethanol ( intake per day) were included in the study. Patients whose blood ALT levels remained persistently in the abnormal range (> 40 international units, IU/L) for more than 6 months were enrolled in the study.

The criteria for diagnosing patients as having ALT levels for more than 6 months, platelete courts below 100,000/mm³, the presence of esophageal varices and the presence of LC pattern and spleenomegally on abdominal diagnostic imaging. Blood samples were obtained only from patients who gave informed consent, and were stored frozon at – 80c A precise diagnosis was made by abdominal angiography, and when this could not be made, tumor biopsy was carried out and precise diagnosis was made on the basis of the pathological findings.

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This article was extracted from a Project Research Work/Material Topic “ZINC SUPPLEMENTATION IMPROVES THE OUTCOME OF CHRONIC HEPATITIS C AND LIVER CIRRHOSIS.”