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Hepatitis - Treatment

HEPATITIS B TREATMENT

Acute hepatitis B: it is not usually necessary to treat a new hepatitis B infection in the first six months. Nine out of ten new infections in adults clear up on their own, with or without treatment. In this early stage of disease, treatment makes very little difference to the chances of a cure. Antiviral drugs may only be necessary and helpful in rare cases, if the acute infection causes very aggressive liver inflammation.

Chronic (long-lasting) hepatitis B: consult with your doctor about your situation. Some people need treatment, while others should wait. Treatment does not usually cure you of hepatitis B, but it can turn an ‘aggressive’ hepatitis B infection into a mild infection. This can stop the liver from being damaged. If the infection is considered mild, it might be better to monitor it and wait until later for treatment. You can treat chronic hepatitis B with pegylated interferon alpha or with pills called nucleoside or nucleotide analogues.

Pegylated interferon alfa comes in a syringe and stimulates the immune system against the virus. This treatment may have side effects, such as fatigue, flu-like symptoms, depression, skin and hair problems and changes in blood chemistry, amongst others. Treatment continues for 24 to 48 weeks and while not all hepatitis B patients respond well to interferon, certain types of hepatitis B infection do.  For example, patients with genotype A, HBeAg positive, with elevated liver enzymes but NO cirrhosis can often successfully reduce their viral infection to a milder state. Your doctor needs to monitor your interferon treatment closely. Interferon treatment should not be used if you already have cirrhosis of the liver. 

Nucleoside and nucleotide analogues come in pills. They stop the virus from replicating. The pills have very few side effects, and even patients with cirrhosis can take them. However, patients need to take their pills every day, for several years and sometimes a lifetime. If the virus becomes resistant to one type of pill, it might stop working, and another, different drug will need to be added to the treatment to get the virus back under control. Your doctor should monitor your viral load (hepatitis B DNA) to make sure that your treatment works. Do not forget to take your pills, even if you feel well. If you miss many doses or stop treatment too early, the disease might become worse than it was before. If possible, make sure that you will have access to medication for several years before you start treatment with pills.

The World Health Organization has launched Guidelines for the prevention, care and treatment of persons with chronic hepatitis B infection which set out who should be treated and with what drugs. Since the guidelines are aimed at resource limited settings, they do not consider interferon which is more complicated to manage than the nucleoside and nucleotide analogue drugs

 

HEPATITIS C TREATMENT

There has been a huge amount of drug development in hepatitis C with many new drugs launched in the last two years. Whereas hepatitis C treatment used to consist of ribavirin and interferon, generally in the pegylated, longer-lasting form, which boosts the body’s own immune system, most of the new drugs work differently, attacking the virus itself. They primarily target one of three distinct parts of the virus called the protease, the polymerase and the NS5A area and are therefore known respectively as protease inhibitors, polymerase inhibitors and NS5A inhibitors. Collectively they are known as Direct Acting Antivirals (DAAs). Initially used with interferon, they are now being increasingly used in combination with each other and without interferon. This is allowing much shorter courses of treatment, 12 weeks or less, with fewer, more tolerable side effects.

The aim of treatment for hepatitis C is achieve a Sustained Virological Response (SVR), meaning that the virus is not detectable in blood originally 24 weeks, now more frequently 12 weeks, after treatment has stopped. This is the equivalent of a cure because the virus does not return, unless the person is newly infected. The new drugs are showing SVR rates of approaching 100% in trials. However this depends on which combination is used, how much liver damage the patient has, with those with cirrhosis generally doing less well, and also on genotype. Whereas genotype 1 was considered the hardest to treat successfully with interferon, genotype 3 seems to be the hardest with the new drugs and we have very little data on genotypes 5 and 6. However, new drugs that will work equally across all genotypes are in trials.

One of the most exciting aspects of the new drugs is that in the absence of interferon they appear to be safe enough to use on people who have decompensated cirrhosis, offering them the chance both of a cure and an improvement in their condition, perhaps no longer needing a transplant.

The new drugs are expensive in the developed world and in some countries this is limiting their use. Many governments are currently in discussions with the manufacturers to secure lower prices. In the developing world, some manufacturers have already announced ‘access programmes’ and the others will undoubtedly follow. These programmes generally involve significantly lower prices and sometimes licensing agreements with generic manufacturers. So far Gilead and BMS have announced access programmes. You can view the Gilead access programme here. Aside from the discussions over price, access to the drugs is slowed by the time it takes to license and/or register them. What is available and at what price is therefore currently different and changing in each country.

The World Health Organization has launched Guidelines for the screening, care and treatment of persons with hepatitis C infection, which set out who should be treated and with what drugs. This will be regularly updated as new drugs become available.

Examples of the DAAs currently available in at least some countries are:

Protease inhibitors (names end in –previr)

  • First generation: 
  • Boceprevir
  • Telaprevir, 

Second generation (better and with fewer side effects):

  • Asunaprevir
  • Paritaprevir
  • Simeprevir

Polymerase inhibitors (names end in –buvir)

  • Dasabuvir
  • Sofosbuvir

NS5A inhibitors (names end in –asvir)

  • Daclatasvir
  • Ledipasvir
  • Ombitasvir

Common Combinations marketed by a single manufacturer

  • Harvoni – Sofosbuvir and Ledipasvir
  • ‘3D’ – Paritaprevir, Dasabuvir and Ombitasvir

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