Liver fibrosis is not an independent disease but
rather a histological change caused by liver
inflammation. Liver damage causes liver stellate
cells to become overactive and triggers increase of
extra cellular matrix (ECM) synthesis. When above
normal amounts of collagen fiber deposits in the
extra-cellular spaces of the liver cells, this
causes liver cells to lose blood infusion and
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
separations (or bridging) between the portal areas,
the center vein, and the formation of pseudo-lobule,
fibrosis enters the cirrhosis.
Histological (biopsy) diagnosis classifies the
severity of fibrosis into five general stages.
S-0 to S-4. Stage S-0 denotes no distinguishable
fibrosis activity. S4 is considered cirrhosis.
In between, S1 is a mild fibrosis seen at the portal
area. S2 is a moderate stage of fibrosis, between
portal areas, but without the destruction of the
liver lobular structure. S3 is severe fibrosis. At
this stage, there is fibrostic bridging between
portal areas and center veins. At S4, in addition to
S3's changes, there are pseudo-lobules formed. S4 is
the cirrhosis stage and approximately 15 to 20% of
HCV patients may progress to stage 4.
fibrosis is the net result of the imbalance between
the collagen fiber synthesis and decomposition. When
fiber synthesis is very active and the decomposition
process is suppressed, fibrosis will progress. Vise
versa, fibrosis can be reversed if the causal
factor, liver inflammation, can be 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. These cannot be decomposed by
water or weak acids and only collagen enzymes can
decompose them. With anti-fibrosis treatment, there
it is possible to enhance the activities of collagen
enzymes and to promote the decomposition of the
fibers, reducing ECM.