How do I get Hepatitis C | How do I keep it Myself

What is Hepatitis?
Hepatitis is an inflammation of the liver. The different types of hepatitis are caused by different things, but they all produce inflammation of the liver. Viral hepatitis refers to several common contagious diseases caused by viruses that attack the liver. The most important types of viral hepatitis are hepatitis A, hepatitis B, and hepatitis C. Newly discovered forms of viral hepatitis also include hepatitis D, hepatitis E, and hepatitis G. Non-viral forms of hepatitis can be caused by toxic agents (drugs or chemicals), alcohol, or autoimmune processes. Another form of hepatitis is toxic hepatitis. Toxic hepatitis can be caused by viruses or by liver damage due to toxic substances. Toxic hepatitis is a deterioration of the liver cells caused by chemicals, alcohol, drugs, and industrial compounds. Alcohol abuse is a common cause of toxic liver damage.

Hepatitis C is a viral infection of the liver. Some patients have amild, acute infection that disappears without treatment. When the infection continues for six or more months, it is known as chronic hepatitis C, which can be marked by fatigue and liver function impairment. Those with chronic hepatitis C have an increased risk of later developing cirrhosis or liver cancer.

HEPATITIS C (HCV)
Hepatitis C (HCV) is a form of hepatitis caused by an RNA virus. HCV accounts for the majority of the hepatitis cases previously referred to as non-A, non-B hepatitis. The hepatitis C virus was first identified and described in 1987, and in 1990 a hepatitis C antibody test (anti-HCV) became commercially available to help identify individuals exposed to HCV. In mid-1995 the hepatitis C virus was seen for the first time ever by scientists with the aid of an electron microscope. It is a linear single-strand RNA (ribonucleic acid) virus 40-50 nanometers in size. It is covered with a lipid envelope and is encased with glycoprotein peplomers or "spikes".

Patient Information - What is Hepatitis C?
Hepatitis C is a disease of the liver caused by a virus that was first discovered in 1989. Unlike hepatitis A which is caused by fecal contamination of food and water; or hepatitis B which is spread through contact with infected blood or other body fluids; hepatitis C is spread by direct contact with the blood of an infected person. Prior to the discovery of the virus, it was known that some agent caused hepatitis or inflammation of the liver in people who had been given blood, and it was known that the agent could be transmitted to patients and to experimental animals in blood. Before the virus was identified, this form of hepatitis was called non A non B hepatitis because the viruses causing hepatitis A and hepatitis B were already identified and could be tested for. Patients with hepatitis following exposure to blood who had negative tests for hepatitis A and for hepatitis B were said to have non A non B hepatitis. It is now known that the majority of these patients were infected with the virus identified and named hepatitis C virus or HCV for short. As tests for this virus have improved over the years since 1989, more and more people who have hepatitis which could not be diagnosed with accuracy are now being correctly diagnosed as infected with the hepatitis C.

Is the new hepatitis A vaccine effective and who needs it?
Yes, the new hepatitis A vaccine (Havrix) is very effective. It induces protective titres of anti-bodies in greater than 95%, and 99% of people after the first and second doses, respectively. If time does not permit two doses six months apart, then a single Havrix-1440 (double strength) dose may be given. The first dose of the vaccine probably requires at least three weeks to induce significant antibodies, so those travellers who did not have the foresight to have the first dose administered at least three weeks before departure to a high-endemic area should also have standard gammaglobulin to assure protection. Protective antibody titres to the vaccine last at least three years. At this time the need for booster doses is unclear, but it's likely that, similar to hepatitis B, they will be unnecessary. The vaccine should be administered as an IM injection into the deltoid. Children can be given half-strength (0.5 mL) doses.

Although the manufacturer has suggested a very broad range of people to be targeted for vaccination, the National Advisory Committee on Immunization (NACI) only recommends vaccinating:

1) long-term or frequent travellers to endemic regions (which means basically everywhere except Canada, USA, Western Europe, Japan, Australia, and New Zealand).
2) residents of communities with high endemic rates of recurrent outbreaks of hepatitis A, and
3) residents and staff of institutions for the mentally handicapped.

Who Should Receive Hepatitis A Vaccination?
Long-term or frequent travellers to endemic regions. Residents of communities with high endemic rates of hepatitis A. Residents and staff of institutions for the mentally handicapped

Is there any role for standard gammaglobulin in viral hepatitis prophylaxis?
Basically no. (See the answer above for one last small indication.) Development of highly effective hepatitis A vaccines has obviated the need for gammaglobulin. Note that standard gammaglobulin is useless for immunoprophylaxis against hepatitis B and hepatitis C.

What is universal hepatitis B vaccination?
This refers to vaccination of the entire population, usually at the neonatal or childhood level. The rationale for this is that targeted vaccination of high-risk groups has failed to achieve its aims, because most people in these risk groups are unaware or unwilling to be vaccinated. Moreover, 30% to 40% of hepatitis B virus (HBV) infections occur in people who deny any known risk factor.

What are the immunoprophylaxis recommendations for household contacts if an individual is found to be positive for HBsAg or develops acute hepatitis B?
All household contacts should be screened for HBsAg and anti-HBs. If the spouse or sexual partner is negative for both, then he or she should be given 5 mL of HBIG and a course of vaccine, if the index case has acute hepatitis B, whereas vaccine alone should suffice for partners of chronic HBsAg carriers. Other household contacts, if serologically negative, require only a course of vaccination. In Canada, almost all public health units will carry out the above or slightly variant programs when notified of a positive HBsAg result.

I have a general practice with very little ER work; why should I be vaccinated for HBV?
If your practice involves no work in emergency rooms, hospital wards, institutions for the handicapped and no administration of needles or minor surgery, and you never have hangnails, minor cuts and abrasions on your hands, then it is likely that you would not be susceptible to occupationally-acquired hepatitis B. There are very few practices that fit this description, and all other physicians would benefit from this safe and effective vaccine. Or, put another way, there has been several cases of unvaccinated physicians who died from occupationally-acquired acute hepatitis B; isn't your life worth the $150.00 cost of a course of vaccine?

I had a standard course of three deltoid injections of full-dose hepatitis B vaccination, but failed to make protective antibody titres.

What does this mean and what should I do now?
Lesser response rates to HBV vaccination are associated with age, increased body mass and smoking. For example, only 60% to 80% of those aged over 60 years make protective antibody titres. No one can reverse aging, but it you are overweight and smoke, losing weight and quitting smoking, followed by revaccination, might be effective. Even in healthy immunocompetent adults, about 5% will not develop protective antibodies after a course of vaccination. Recent work has discovered that the immune response to hepatitis B surface epitopes is genetically determined. For your interest, you probably have HLA haplotypes B8, DR3, SCO1; or B44, DR7, FC31. If a second complete course of vaccinations fails to induce protective titres, you will have to sadly accept that you are not protected against hepatitis B. You can blame your parents for giving you these bad genes.

Is a booster dose needed after five or ten years for recipients of hepatitis B vaccination?
No. If you originally demonstrated an adequate antibody response, even though anti-HBs titres may gradually fall below the critical 10 IU/L level, the immune system will mount a sufficiently protective anamnestic response if rechallenged with hepatitis B.

Is there anything on the horizon for a vaccine against hepatitis C?
No. Effects to develop an effective HCV vaccine have been frustrated by:

• initial difficulties in actually identifying the virus responsible for hepatitis C (although we knew its molecular structure in 1989, it was not until 1996 that a putative HCV was identified),
• difficulties in establishing stable cultures of the virus in a cell line, and
• high mutability of the HCV, which like HIV, mutates at a high rate.

What should be done in case of a needlestick injury?
Management will slightly differ depending on whether the recipient (usually a health care worker) has previously been vaccinated for HBV. If vaccinated, then the recipient (as a baseline) and the source patient, should be tested for anti-HCV and anti HIV. If not vaccinated, then HBsAg should be added to the tests for the source patient, and both HBsAg and anti-HBs added to the recipient's bloodwork. Since this article is focussed on hepatitis, we will only deal with the HBV and HCV-positive scenarios.

1) Source is HBsAg-positive, recipient unvaccinated (and negative for both HBsAg and HBs): give recipient HBIG, 5 mL, i.m., and first dose of hepatitis B vaccine. Complete the standard dosing protocol of vaccine at zero, one, and six months. Without intervention, there is about a 20% chance of the recipient contracting acute hepatitis B, and this figure is a composite of approximately a 50% to 80% chance if the source is HBeAg-positive (replicating, with high viral load), and a 10% to 15% chance if the source is HBeAg-negative. 2) Source is anti-HCV-positive, recipient anti-HCV-negative: test the recipient for ALT at baseline (as soon as possible after needlestick), and HCV-RNA by polymerase chain reaction and ALT at six to eight weeks after exposure. If HCV RNA is negative at this time, the chance of contracting acute hepatitis C is essentially zero. If the HCV-RNA test is not available locally, then the ALT should be repeated at three and six months, and the anti-HCV at six months. If they remain normal or negative at six months, the likelihood of developing HCV will be nil. If HCV-RNA turns positive at six to eight weeks, this heralds the onset of acute hepatitis C, and these patients should be treated with a- interferon at a dose of three million units s.c. thrice weekly for 24 weeks. In centres where HCV-RNA is not available, the diagnosis of acute HCV can be made using a combination of the ALT and anti-HCV serology, realizing that the development of anti-HCV-positivity, even with third generation enzyme immunoassays, sometimes lags behind the acute hepatitis by a month or more. Therefore, before embarking on interferon therapy with its cost and side effects, I would recommend confirming the diagnosis by HCV-RNA which can be sent out to a lab in a larger centre.

Fortunately, acute HCV developing after needlestick injury is uncommon. Several series have indicated that the risk of this occurring is approximately 5% to 10%.

What is the treatment of Acute Alcoholic Hepatitis?
General measures for treatment of acute alcoholic hepatitis include abstinence from alcohol, nutritive support, relief of vitamin deficiencies and dietary adjustments if ascites or hepatic encephalopathy are present. Gastrointestinal bleeding and infections, particularly spontaneous bacterial peritonitis, are potential complications that can be specifically treated. Patients with mild alcoholic hepatitis may have marked improvement with abstinence and supportive care while those with deep jaundice, hepatic encephalopathy and marked abnormality in prothrombin have a 30-50% mortality and will almost certainly develop severe hepatic fibrosis or cirrhosis if they survive. A discriminant function developed by Maddrey and Colleagues (4.6 x prothrombin time-control prothrombin time + serum bilirubin in mg/dl) of >32 indicates a poor prognosis.

Since we have lacked knowledge of the pathogenesis of alcoholic liver injury, specific treatment of acute alcoholic hepatitis has been necessarily empirical. Potential objectives of treatment in severe cases have been suppression of hepatic inflammation, reduction of collagen formation, stimulation of hepatocyte regeneration and interruption of possible immunologically mediated or cytokine-induced hepatocyte damage.

A large number of randomized controlled trials (RCT) of a number of different treatments have been published. These include propylthiouracil, insulin and glucagon, anabolic-androgenic steroids, colchicine, penicillamine, and parenteral nutrition. None have shown unequivocal benefit. Much attention has been directed toward corticosteroid therapy, with 14 published RCTs. Most have shown no benefit, including three from our USC Liver Unit ( 2 published, 1 unpublished). However, in 3 of 14 trials there was a significantly better survival in a subgroup of patients with the most severe illness as indicated by the presence of spontaneous hepatic encephalopathy or a high Maddrey discriminant function. Three meta-analyses of these trials have been published. Two concluded that there was modest benefit from corticosteroid treatment in a subgroup of patients with spontaneous hepatic encephalopathy. The third and most recent meta-analysis concluded that there was no statistically significant benefit from corticosteroid, including the subgroup with encephalopathy.

In our Liver Unit we have recently completed a 4-year RCT of pentoxiphylline treatment designed to inhibit synthesis of tumor necrosis factor, a potentially harmful cytokine. This trial, not yet published, showed significant benefit from the treatment with short-term death rate of 23/52 in control patients vs. 12/49 in those treated with pentoxifylline. Currently we are considering a trial of monoclonal antibody to tumor necrosis factor.