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Viral Hepatitis

Acute viral hepatitis refers to liver inflammation caused by certain viruses, including the hepatitis A, B, C, D and E viruses. Other viruses that affect the liver include EBV, herpes simplex, yellow fever and cytomegalovirus, and are usually considered as separate disorders.

Hepatitis A virus (HAV)

Hepatitis A virus (HAV) is a single-stranded RNA picornavirus. Upon investigation the viral antigens may be found in the blood, stool, and liver but only during acute infection. A characteristic of the early, acute stage of the disease is a temporary elevation of IgM antibody followed by the development of protective IgG antibody that persists for the remainder of the patient's life.

The transmission of HAV depends on transmission from person to person via the oral-fecal route. Epidemics usually occur in unsanitary conditions although improperly cooked shellfish may also transmit the infection. The infection is particularly high among homosexuals via the oral-anal route. HAV is mostly benign, self-limiting disease that does not play a role in the pathogenesis of chronic hepatitis or cirrhosis. (Berkow 1992; Rubin and Farber 1990, 402-10)

Hepatitis B virus (HBV)

Hepatitis B virus (HBV) is a liver-specific DNA virus that causes both acute and chronic liver disease. The virus is comprised of an inner core and a surface coating. The HBV viral core contains a circular double-stranded DNA molecule and DNA polymerase that can only replicate within the nuclei of liver cells. The surface coating of the virus consists of a mixture of carbohydrates, lipids and proteins that is synthesized independently of the virus in the cytoplasm of an infected liver cell. Although not infectious this surface coating can be detected in the blood by laboratory methods as the hepatitis B surface antigen (HBsAg). The intact and infectious virus is also found in the serum as the Dane particle, consisting of both the inner core and the surface coating. (Berkow 1992; Rubin and Farber 1990, 402-10)

HBsAg usually appears during the viral incubation period, one to six weeks before clinical symptoms develop and then disappears as the patient recovers. The corresponding protective antibody (anti-HBsAg) appears weeks or months later after recovery, and usually persists for life, indicating past HBV infection and a relative immunity to the virus. The HBV viral core antigen (HBcAg) can be found in infected liver cells but is not detectable in serum except by specialized laboratory techniques. Antibody to HBcAg (anti-HBc) usually appears at the onset of illness, and only gradually diminishes over a period of years or for life. (Berkow 1992; Rubin and Farber 1990, 402-10)

It is estimated that 300 million people worldwide are chronic carriers of HBV, the carrier rates as low as 0.3% in industrialized nations and up to 20% in developing countries. Humans are the only significant reservoir for HBV, and unlike HVA which is spread via the oral-fecal route, HBV is not and nor does it contaminate water supplies. HBV has been found in secretions of the blood, saliva and semen and is through to be transmitted either through infected blood products, injection drug users, or through intimate contact (with a higher prevalence in homosexual communities). (Berkow 1992; Rubin and Farber 1990, 402-10)

Unlike HAV, HBV is associated with significant liver diseases, including acute self-limiting hepatitis, fulminant hepatitis, and chronic hepatitis. Acute self-limiting hepatitis is associated with the majority of infected persons, with complete recovery and lifelong immunity. Fulminant hepatitis is experienced much less of the time, characterized by hepatocytes necrosis, hepatic failure and a high mortality. In 5-10% of HBV infections patients do not develop anti-Hbs, and the infection persists leading to chronic hepatitis B. Chronic hepatitis is discussed later in this lesson. (Berkow 1992; Rubin and Farber 1990, 402-10)

Hepatitis D virus (HDV)

The hepatitis D virus (HDV) is a defective RNA virus that can only replicate only in the presence of either acute or chronic HBV infection, and usually increases the severity of existing chronic hepatitis. A combination HBV and HDV infection accounts for a large proportion of fulminant HBsAg-positive hepatitis. (Berkow 1992; Rubin and Farber 1990, 402-10)

Hepatitis C virus (HCV)

Although grouped along with HAV and HBV, the hepatitis C virus (HCV) is considered to be quite a different pathogen, from the family known as Flaviviridae, close cousin to the viruses that cause bovine diarrhea, hog cholera, and yellow fever. Researchers have identified more than 100 strains of the virus and grouped them into six major "genotypes," which tend to be in specific regions around the world. (Berkow 1992; Rubin and Farber 1990, 402-10)

The evolution of HCV began when clinicians observed a small fraction of transfusion recipients suffering from short-lived flu-like symptoms followed in some cases by liver disease years later. To distinguish the disease from HAV and HBV, they originally called it non-A, non-B hepatitis. Researchers from Chiron Corp. and the Centers for Disease Control and Prevention (CDC) finally determined the infectious agent in 1988, and published paper describing it and a method for testing for it in blood samples. (Berkow 1992; Rubin and Farber 1990, 402-10)

There is no evidence pointing to where or when HCV first infected humans, as no other species appears to serve as a natural host. Studies clearly have established that the main routes of transmission are by tainted blood transfusions and non-sterile needles. The development of a screening test in 1990 has virtually eliminated the spread of HCV through blood transfusions in industrial countries, and now sharing contaminated needles is the most common route of infection. Although the numbers of infected persons has dropped dramatically since testing began, the CDC estimates that perhaps 1.8% of the U.S. population harbors the virus, and as these patients age, HCV-related liver disease, accounting for 8000 to 10,000 annual deaths in the United States, is the single most common reason for liver transplants (Williams 1999, CDC 1998). Apart from direct blood contact HCV appears to be a very difficult agent to transmit, with only 4-7% maternal-to-fetal transmission is low (Roberts and Yeung 2002). Some have suggested that HCV can be transmitted sexually, the CDC officially stating that sex accounts for between 15% and 20% of the infection in the United States numbers (CDC 1998).

The severity of HCV varies enormously from person to person and there are few reliable indicators to predict who will do well or badly. It is estimated that 15% to 25% of people infected with HCV will effectively deal with the virus during initial infection, with the remaining proportion of patients developing a chronic infection (Berkow 1992). The prevalence of any significant clinical complication of the disease is estimated to be between 10-20% of chronically infected people, with an even smaller percentage developing hepatocellular carcinoma. Several studies show however that the majority of patients have none of these symptoms even 20 years after infection. In one seven year study of more than 400 patients who had tested positive for HCV, and whose infection could in most cases be traced to a transfusion or injection, only 13% of 81 patients who had undergone liver biopsy had evidence of severe hepatitis (8%) or cirrhosis (5%), despite a duration of infection that generally exceeded 15 years (Alter et al 1997). These results closely parallel other studies that have shown that HCV is generally not associated with any significant liver pathology. There is little correlation between the viral lode in the patients serum and the progression of the disease. More significant factors include alcohol consumption, cocaine and intravenous drug use, body piercing and tattoos, and in older patients, blood transfusion. Although HCV is stated to be a blood borne disease, researchers have identified a few alcoholics with HCV who do not have any other risk factors (Verbaan et al 1993). Even commonly relied upon indicators such as elevated serum alanine aminotransferase (ALT), an enzyme released by liver cells when they die, is not an indicator of the progression of HCV-related disease (Ghany et al 1996).

Signs and symptoms

In acute viral hepatitis the liver acini are affected by hepatocellular necrosis and mononuclear inflammation. The symptoms and signs can vary from a minor flu-like illness to a fulminant liver failure that can cause death, depending on the patient's immune response as well as a number of other factors that have yet to be fully elucidated. The initial onset of viral hepatitis usually begins quite suddenly, with poor appetite, fatigue, nausea and vomiting, and fever, with skin eruptions and joint pain (particularly in HBV). Between 3 and 10 days after the prodromal symptoms occur the urine darkens and signs of jaundice manifest, but the patient often feels somewhat better, with a decline in systemic symptoms. With jaundice there is hepatomegaly and liver tenderness upon palpation, with splenomegaly present in up to 20% of patients. Blood tests often reveal an elevation in the enzymes AST (aspartate amino transferase) and ALT (alanine amino transferase), which are released by damaged hepatocytes. WBC counts are usually low to normal, and with cholestasis tests may also reveal an elevation in alkaline phosphatase. (Berkow 1992; Rubin and Farber 1990, 402-10)

The prognosis for acute viral hepatitis is good, especially in HAV, and in most cases there is a spontaneous remission within four to eight weeks. With HBV however, elderly or hospitalized patients have an increased risk of mortality, and up to 10% of cases develop into a chronic hepatitis leading to cirrhosis or hepatocellular carcinoma. Infection with HCV is more likely to become chronic, appearing mild at the outset of the illness and for many years afterwards, with cirrhosis occurring only after several years if not decades. The vast majority of patients with HCV and who require a liver transplant have a significant history of chronic drug and alcohol use. (Berkow 1992; Rubin and Farber 1990, 402-10)

Medical treatment

There are no satisfactory treatments for viral hepatitis, and thus much of the focus is upon prophylaxis, including personal hygiene, blood-screening, drug and alcohol counseling, and safe injection sites for drug users. Medical prevention includes the use of globulin preparations or the newly developed vaccines for HAV and HBV. The development of a vaccine for HCV however has thus far eluded researchers. Current medical treatment for HCV consists of various anti-viral agents including interferon, serine protease inhibitors, inosine monophosphate dehydrogenase inhibitors, nuceloside analogues, protease inhibitors, RNS inhibitors and monoclonal antibodies, some of which are still in the early phases of clinical trials. Many patients will experience a sudden onset or worsening of symptoms with medical treatment, including fatigue, joint pain, memory loss, mental confusion, skin problems, depression, irritability, anxiety, nausea, sleep disturbances, chills, fever, eyesight changes, flu-like symptoms, headaches, weight loss, anorexia, hemolytic anemia, hair loss, dental problems, diarrhea, hearing problems, mouth sores, excessive bleeding, heat/cold sensitivity, shortness of breath, thoughts of suicide, social isolation, and RUQ pain.

Holistic treatment

The holistic treatment of viral hepatitis is to support liver function through the usage of nutrient trophorestoratives, hepatics and liver trophorestoratives and antiviral botanicals. Like many chronic illness and infections, the holistic orientation is that HCV is less an actual disease with a specific viral etiology, but rather a kind of non-specific liver injury that is directly related to the chronic exposure of various liver toxins, derived from industry, the environment, drugs and alcohol, along with lifestyle behaviours that weaken the immune response. The basic treatment consists of trophorestorative nutrients and botanicals, liver trophorestoratives, gentle cholagogues and hepatics, lifestyle counseling and harm reduction. Antiviral botanicals are used on the basis that HCV is caused by a virus, and that the disease progression can be correlated with viral load.

1. Dietary measures

Avoid protein-restricted diets, e.g. veganism
Avoid junk foods, fasts foods, transfats
Emphasize leafy greens and other vegetables in the diet
Emphasize whole grain, fiber-rich foods
Emphasize grass-fed and wild meats, poultry and fish to ensure adequate omega 3 fats
Emphasize live-culture foods, e.g. pickled vegetables

2. Trophorestorative nutrients:

Vitamin A, 25,000 IU daily
Vitamin B complex, 100 mg daily
Vitamin C, 2-3 g daily
Vitamin D3, 5000-20,000 IU daily
Vitamin E, 400 IU daily
Magnesium, 250 mg twice daily
Selenium, 200 mcg daily
Zinc, 30 mg daily
EFAs, EPA/DHA, 1000 mg each daily
NAC, 1 g daily
MSM, 2-3 g daily
Probiotics

3. Trophorestorative botanicals, e.g. Reishi (Ganoderma spp), Shiitake (Lentinus edodes), Maitake (Grifolia frondosa), Caterpillar fungus (Cordyceps), Huang Qi (Astragalus membranaceus), American Ginseng (Panax quinquefolium), Milky Oats (Avena sativa), Mandukaparni (Centella asiatica), Brahmi (Bacopa monniera), Ashvagandha (Withania somnifera), Bai Shao (Paeonia lactiflora), Shu Di Huang (Rehmannia glutinosa), He Shou Wu (Polygonum multiflorum), Gou Qi Zi (Lycium barbarum)

4. Liver trophorestoratives, e.g. Milk Thistle (Silybum marianum), Artichoke (Cynara scolymus), Amalaki (Emblica officinalis), Dandelion (Taraxacum officinale), Guduchi (Tinospora cordifolia), Chai Hu (Buplerum falcatum), Wu Wei Zi (Schizandra chinensis)

5. Antiviral botanicals, e.g. Garlic (Allium Sativum), Nu Zhen Zi (Ligusticum lucidum), Biscuit root (Lomatium spp), St. John's Wort (Hypericum perforatum), Purple Coneflower (Echinacea angustifolia), Bhunimba (Andrographis paniculata), Ban Lan Gen (Isatis tinctoria), Reishi (Ganoderma spp), Shiitake (Lentinus edodes), Maitake (Grifolia frondosa), Caterpillar fungus (Cordyceps)