Focal nodular hyperplasia of the liver

by Jason Wasserman MD PhD FRCPC
October 2, 2023

What is focal nodular hyperplasia of the liver?

Focal nodular hyperplasia (FNH) is a noncancerous type of growth in the liver. It is much more common in young women and it rarely occurs in men or children.

What causes focal nodular hyperplasia of the liver?

At the present time, we do not completely understand what causes FNH. However, it is often associated with abnormal blood vessels in the liver which has led to the theory that the growth is a response to increased blood flow.

What are the symptoms of focal nodular hyperplasia of the liver?

Most patients with FNH of the liver will not experience any symptoms and the growth will be found incidentally when imaging of the abdomen is performed for other reasons. In rare cases, the growth will become large enough to cause symptoms such as abdominal pain

Can focal nodular hyperplasia of the liver turn into cancer over time?

No. FNH of the liver is a benign (noncancerous) condition that will not transform (change) into liver cancer over time.

How is this diagnosis made?

In most cases, the diagnosis can be made by imaging studies alone. However, the diagnosis can also be made after some or all of the growth is removed and the tissue is sent to a pathologist for examination under a microscope.

What does focal nodular hyperplasia of the liver look like under the microscope?

When examined under the microscope, FNH is made up of normal liver cells called hepatocytes. The hepatocytes are arranged in groups two cells thick called plates. The hepatocytes do not show any increased mitotic activity (cells dividing to create new cells) or cytologic atypia (abnormal cell shape, size, or colour). A scar is often seen in the center of the growth along with numerous abnormal-looking blood vessels. When a test called immunohistochemistry (IHC) is performed, the hepatocytes are often strongly positive for a protein called glutamine synthetase (GS). The hepatocytes in FNH express high levels of GS as a result of over-activation of the beta-catenin pathway.