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A cholesterol
stone is usually solitary (the cholesterol 'solitaire').
It is oval or
rounded in shape, and vary from 1 to 4 cm in diameter, or larger.
It is light in
weight as well as in color.
In its
absolutely pure state it is very pale yellow in colour and feebly translucent.
More often
bile pigments are deposited within it.
On section
it has a radiating crystalline interior.
Cholesterol
stones, which make up some 6% of all gallstones, are believed to
be formed primarily in aseptic static bile (in a "stasis" gallbladder). They tend to
reside in Hartmann’s pouch.
The stone is
composed of 50 to 100% cholesterol, the rest consists of calcium
salts and mucin.
Cholesterol
stones are often detected at autopsy. During their
reproductive period, women are three times more likely to develop
cholesterol gallstones than men.
The incidence is higher in users of
oral contraceptives and in women with several pregnancies.
Cholesterol
gallstones are common in certain ethnic group. This may
be due to the genetic factors.
Blacks in
the US have a lower incidence of gallstones than whites, but a
higher incidence than blacks in Africa. This difference probably
reflects environmental influence, although a role of genetic
admixtures is also possible.
It has been
suggested by some authors that gram-positive cocci are associated
with the formation of pure cholesterol stones.
Mixed (secondary or
inflammatory) gallstones may be formed later, or a mixed covering of
pigment and cholesterol may form around the primary cholesterol
stone. This is known as combination stone.
Pathogenesis:
Pathogenesis of
cholesterol stones relates mainly to the composition of the bile.
Normally,
cholesterol, a compound highly insoluble in water, is secreted by
the hepatocytes into the bile, where it is held in solution by the
combined action of the bile acids and lecithin and carried in the form of
mixed lipid micelles.
If the bile contains
excess cholesterol or is deficient in bile acids, the bile becomes
supersaturated, and under some circumstances the cholesterol
precipitates as solid crystals.
The bile of
persons with cholesterol gallstones has more cholesterol
as it leaves the liver than that of normal individuals, pointing to the liver, rather than gallbladder as the culprit in the genesis of
cholesterol stones.
The hepatocytes
of patients with cholesterol gallstones are deficient in cholesterol
7 alpha-hydroxylase, the enzyme involved in the rate-limiting step
by which bile salts are formed from cholesterol.
As a result,
the total size of the bile salt pool is reduced.
The resulting
decrease in bile salt secretion contributes to the stone-forming (lithogenic)
properties of the bile.
In
obese patients, cholesterol secretion by the liver is increased, adding to the supersaturation of the bile with cholesterol.
Although
cholesterol supersaturation of the bile is required for
gallstone formation , additional factors are also required.
Cholesterol
does not precipitate from saturated bile obtained from patients
without gallstones.
Bile from patients without gallstones, but with properties
similar to those in the bile of patients with gallstones,
crystallizes without difficulty.
It is
thought that the mucinous glycoproteins secreted by the gallbladder
epithelium provide the necessary nidus for crystallization.
Risk
factors:
The higher
prevalence of gallstones in premenopausal women has been attributed
to the fact that estrogens stimulate the formation of lithogenic bile by the liver.
Estrogens
increase the hepatic secretion of cholesterol and may decrease
the secretion of bile acids.
These effects
are augmented during pregnancy, because the gallbladder empties more
slowly in the last trimester, thereby causing stasis and increasing
the opportunity for precipitation of cholesterol crystals.
Progesterone has been
shows to inhibit discharge of bile from the gallbladder.
These mechanisms are
also invoked to explain the increased incidence of gallstones in
users of oral contraceptives.
Other risk
factors for the development of cholesterol gallstones can be divided
into those that relate to increased biliary cholesterol secretion,
those that relate to decreased secretion of bile salts and lecithin,
and those that relate to combination of the two.
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Risk factors associated with increased biliary cholesterol secretion
include the following:
- Age ;
- Food - i) high calory
diet and
ii) High intake of Cholesterol
- Obese patients ;
- Certain ethnic groups
- Familial predisposition ;
- Metabolic
abnormalities- Example: Diabetes ; Genetic hyperlipoproteinemias, Primary biliary cirrhosis.
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Decreased
secretion of bile salts and lecithin may occur in nonobese patients
who develop gallstones.
Gastrointestinal absorptive disorders that interfere with the enterohepatic circulation of bile acids, for instance pancreatic
insufficiency secondary to cystic fibrosis and Crohn's disease also decrease secretion of bile acids and favour gallstone formation.
Visit:
Pigment stones (calcium bilirubinate) ;
"Mixed" stones
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