Reviewed By: Pramod Kerkar, MD, FFARCSI

Is Liver Fibrosis Cancer?

Fibrosis is a vital constituent of chronic liver diseases, which ultimately can cause complications such as cirrhosis.

Chronic liver diseases, regardless of their cause (chronic B or C virus infection, alcohol abuse, metabolic disorders such as hemochromatosis, congenital alpha-1 antitrypsin deficiency, autoimmunity, drugs, etc.) with an inflammatory process for a certain time produce a progressive increase of collagen fibers in the hepatic parenchyma called fibrosis, whose final stage is hepatic cirrhosis.

Is Liver Fibrosis Cancer?

The progression of hepatic fibrosis alters the normal structure of the liver, which involve disorders in its circulation with augmented portal pressure, which is the pressure of the blood in the portal territory (abdominal veins). When this increase reaches an important level it leads to the advent of esophageal varices, water retention, with edema in the lower limbs and ascites (accumulation of fluid in the abdomen).

Liver fibrosis is the result of gathering of fibrous and rigid scars in the liver. In order to reach hepatic fibrosis, a succession of events with the inflammatory process of the hepatic cell is necessary due to the aforementioned. This inflammatory process result in hepatocytes (functional cells of the liver) to suffer damage or die; then the immune system is activated by doing the repair process. The injury or death (necrosis) of hepatocytes stimulates the deliverance of cytokines, growth factors and other chemicals by immune cells.

These chemical messengers stimulate the functioning of a type of cells in the sinusoids (intrahepatic vessels where the blood circulates) called stellate hepatocytes, support cells located in the liver, which along with other cell types, begin to produce collagen, glycoproteins (such as fibronectin), proteoglycans, etc. All of these substances tend to restaurate the damaged sectors by the death of the affected liver cells.

All these elements are stored in the liver, causing buildup of extracellular matrix (non-functional connective tissue). At the same time, the process of dissolution of collagen is altered.

In a healthy tissue, there exists a balance between the synthesis (fibrogenesis) and the degradation (fibrolysis) of the matrix tissue. Fibrosis occurs when balance is disturbed, that is, when tissue accumulates at a faster rate than it can be degraded and eliminated by the liver.

As time passes by the inflammatory process continue, the accumulation of the collagen material inside the liver arises, which causes fibrosis. In some diseases this is very slow and has stopped many years to reach the final stage of cirrhosis.

Liver fibrosis does not establish at the same velocity in all patients and in fact in some people with hepatitis C or B, it prevails very stable. There are many factors that influence the progression of fibrosis: for example, the process advances faster in men than in women, and also in older people, mostly after 50 years.

In addition, it has been demonstrated that depression of the immune system - for instance, due to co-infection with HIV or consumption of immunosuppressive drugs after a liver transplant - also exacerbates fibrosis. Alcohol abuse is beyond doubt related to an aggravation of fibrosis and cirrhosis. Several studies indicate that steatosis (fatty liver) and insulin resistance are linked to a faster progression and a more advanced degree of fibrosis.

In the first stages, the liver works to some extent well and few people have symptoms. But as the inflammation continues and the lesions spread, the scar tissue begins to accumulate that connects with the existing scars, which leads to an alteration of the liver metabolic functions.

If the disease advances, it becomes in cirrhosis, in which the liver is full of scars that restrict the blood flow and impede the adequate functioning of the liver.

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Pramod Kerkar

Written, Edited or Reviewed By:


Pain Assist Inc.

Last Modified On: August 28, 2018

This article does not provide medical advice. See disclaimer

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