Cirrhosis from Hepatitis C: Severity and Potential Complications

What is it about cirrhosis that can kill people and what to do about it?


There are many causes of cirrhosis (CIRRHOSIS)(LIVERFOUNDATION).  A partial list would include: hepatitis C, hepatitis B, alcohol, fatty liver disease, hemochromatosis, autoimmune hepatitis, primary biliary cirrhosis, primary sclerosing cholangitis, Wilson’s disease and alpha-1-antitrypsin deficiency, to name just a few.  Of these, the ones that cause most of the cases are fatty liver, hepatitis C and alcohol.

Let’s look at hepatitis C cirrhosis in a bit more detail.

Hepatitis C cirrhosis

Of the 2.7 million people in the United States with chronic hepatitis C (HEPATITIS C), about 20% will develop cirrhosis within 20 years and 30% within 30 years. Not everyone with hepatitis C will automatically develop cirrhosis – almost 30-40% will never develop cirrhosis.  This suggests that there may be additional factors involved for those developing cirrhosis, and this is correct.  We know that men are more likely than women to develop cirrhosis, and that individuals infected at an older age develop cirrhosis more commonly than those infected in childhood. Drinking alcohol is also a risk factor, with as little as 2 drinks per day being associated with a greater risk than in abstainers. Additional infections with hepatitis B or HIV also may be associated with a greater risk of cirrhosis. Finally, coffee consumption may actually prevent or lower the risk of cirrhosis (COFFEE).

How does cirrhosis form?

Any longstanding (chronic) inflammation in the liver can give rise to scar tissue formation as the body’s protective mechanism to wall off the inflammation. Just as an infected cut on your skin can lead to a scar, the same process occurs in the liver.  But unlike an infected cut, the inflammation in the liver proceeds for decades and is spotty throughout the liver, not in just one area.

  These mini-scars in the liver accompany death of liver cells from the infection.  However, healthy neighboring cells have the ability to regenerate to replace those which are dying. The increasing scar tissue (fibrosis) physically limits the space available for regeneration and leads to the formation of tiny nodules of apparently healthy liver cells surrounded by scar tissue. These are referred to as “cirrhotic nodules” and are the definition of cirrhosis.

What are the consequences of cirrhosis?

As the healthy liver is gradually replaced by this honeycomb appearance of multiple cirrhotic nodules, several things happen. The presence of these scarred nodules makes it more difficult for blood from the intestines and spleen (in the portal vein) to filter through the liver. This causes the blood to back up in the portal vein system and raise its pressure.  This is known as portal hypertension (PORTAL HYPERTENSION). Upstream from the liver, this backup of pressure causes the spleen to enlarge which subsequently removes more and more platelets, white blood cells and red blood cells from the circulation.

The pressure exerted by the portal blood flow in the liver gives rise to weepage of the fluid component of the blood across the liver membrane and into the abdominal cavity.  This is called ascites (ASCITES).  The blood also needs to find an alternate route around the liver and back to the heart, so new vessels are formed in many places, but along the lining of the esophagus is a major one.  These are called esophageal varices (ESOPHAGEAL VARICES) since they look like varicose veins in the legs.  These can sometimes reach a large size and rupture and bleed into the esophagus and stomach. This shunting of blood around the liver, rather than through it, has consequences for those necessary liver functions which process nutrients from the intestines. One of these intestinal chemicals that bypasses the liver is ammonia.  The liver is normally highly effective in clearing the portal blood of ammonia and turning into a harmless byproduct. But when too much ammonia bypasses the liver it can reach the brain and cause confusion, or even coma. This is called hepatic encephalopathy (HEPATIC ENCEPHALOPATHY). Finally, as the inflammation destroys more liver cells than can be replaced, the volume of the liver shrinks, sometimes quite dramatically. All of the above problems are then worsened. In addition, the liver can no longer supply the body energy and nutritional needs, so weakness, tiredness and loss of muscle occurs.  A liver with cirrhosis is also more likely to develop liver cancer (HEPATOCELLULAR CARCINOMA).  Eventually, bacterial infections and kidney failure may occur that may be resistant to typical therapy and a patient may expire.

Can this process be reversed?  What can be done to save someone?

We now know that successful therapy to eradicate the hepatitis C virus can stop the inflammation within the liver and halt the placement of new scar tissue (CURE).  We have also recently discovered that older scar tissue may be remodeled and eventually disappear in many successfully treated subjects, though this may take years. For those who already have significant portal hypertension, an endoscopy examination may disclose esophageal varices. Medications called beta blockers may be prescribed to reduce the risk that these would eventually rupture and bleed.  A low salt diet and the use of water pills (diuretics) may be prescribed to treat ascites, while lactulose or rifaximin may be used to treat the confusion of hepatic encephalopathy by lowering blood ammonia levels.  When all else fails (and hopefully before this point), liver transplantation may be considered. One can also contact the American Liver Foundation for additional information (LIVERFOUNDATION).

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