What is Liver Fibrosis and How is It Different
Liver fibrosis is not an
independent disease but rather a histological change caused by liver
inflammation. Liver damage causes liver stellate cells to be over active
and triggers the extra cellular matrix (ECM) synthesis to increase. More
than normal amounts of collagen fiber deposits in the extra-cellular
spaces of the liver cells and causes the liver cells to lose blood
infusion and to be hardened.
Chronic viral hepatitis B
and C are the most common causes of liver fibrosis. During the chronic
hepatitis course, fibrosis is a part of the inflammation activities. In
the fibrosis stage, there is no lobular regeneration and this
distinguishes it from cirrhosis. When
fibrosis advances to cause fibrostic separations (or bridging) between the
portal areas or between the portal area, the center vein, and the
formation of pseudo-lobule, fibrosis enters the final stage, which is
diagnosis classifies the severity of fibrosis into five stages, S0 to S4.
S0 means no fibrosis. S4
is cirrhosis. In between, S1 is a mild fibrosis only seen at the portal
area. S2 is a moderate stage of fibrosis, between portal areas, but
without the destruction of the lobular structure. S3 is severe fibrosis.
At this stage, there is fibrostic bridging between portal areas and
between portal areas and center veins. At S4, in addition to S3's changes,
there are pseudo-lobules formed and this stage is the final stage,
Liver fibrosis is the net
result of the imbalance between the collagen fiber synthesis and
decomposition. When fiber synthesis is very active and the decomposition
is suppressed, fibrosis will progress. Vise versa, fibrosis can be
reversed if the driver, inflammation, is controlled. When fibers form, at
the early stage, it can be decomposed with water or weak acid. These are
soluble fibers. Older fibers deposited for long time, becomes thicker and
harder and cannot be decomposed by water or weak acids. Only collagen
enzymes can decompose it. With
anti-fibrosis herbal treatment, there is possibility to suppress the HSC,
enhance the activities of collagen enzymes and to promote the
decomposition of the fibers, reducing ECM.
Cirrhosis is always
developed from fibrosis. Although, fibrosis and cirrhosis are different,
they are closely related. They are two distinguished pathological
conditions. At the fibrosis stages, the amount of collagen increases and
the ratio of fibro-connective tissue verses liver cellular tissue
increases. But at this stage, the liver lobular structures are intact.
There is no pseudo-lobule formation. Cirrhosis consists of two
pathological features: fibro-connective tissue hypertrophy and
pseudo-lobule formation. At the cirrhosis stage, the liver's fundamental
structure is deformed, and the framework of the liver begins collapse.
Thus, reversal is more difficult at this stage.
Right now a liver biopsy
is the most accurate way to diagnose the fibrostic stages. Some blood
chemical measurements can also provide a referential diagnostic marker of
fibrosis. The chemical markers that can be used to assess the fibrostic
activities are: HA (hyaluronic acid), LN (Laminin), CIV(collagen IV),
PCIII (procollagen type III) etc. They can show the activities of
fibrosis, but can't classify stages of fibrosis.
Patients should also know
that most chronic Hepatitis cases will not lead to Cirrhosis. Only a very
small percentage does and it happens usually without proper treatment,
allowing fibrosis to go on for years.
The body has amazing
healing capabilities of its own and the liver is one of the most
“re-generable” organs in the body. Because fibrosis is the result of
the inflammation, halting or reversing fibrosis by controlling
inflammation is the key. Special anti-fibrosis treatments have been
developed in modern Chinese medicine and we will discuss these in next two