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Re: Stone pathogenesis
 
aznatural Views: 1,260
Published: 18 years ago
 
This is a reply to # 95,961

Re: Stone pathogenesis



This is an excerpt from a post by Spirit from forum #13 from last year. He/She excerpt it from some web sites that were linked there but I cannot copy over the links. Search on CureZone for Stone formations and you should find a reference that says 2 weeks, 2 months, 2 years...

Basically there is an imbalance in the chemistry of the bile that leads to cholesterol saturation. Some nucleator, which may be a protein, then accelerates the formation of cholesterol stones.

I am looking for a way to restore that balance. Because Lecithin
is the part of the mechanism that emulsifies and encapsulates the cholesterol, I was thinking this might be a place to start. Certainly a little extra lecithin wont hurt, it is a major component of cell membrane function as well.

My thing is, if you've corrected bad dietary habits, and done other things to reduce risk factors and still seem to be forming stones, then something is still deficient.

Anyway, read below.
Pathogenesis of gallstones
Robert Coben, MD

Excerpt:

Stages in Cholesterol Gallstone Formation:


1. Formation of saturated bile: The most critical factor is the ratio of cholesterol/bile acids.
In general the likelihood of stone formation is increased by anything that raises cholesterol level or lowers bile acid levels, such as: .. CUT..

2. Nucleation: The next step in cholesterol gallstone formation is nucleation of cholesterol into crystals, followed by agglomeration of crystals and growth of the microlith into
macroscopic gallstones.


Nucleation

Nucleation promoters:
Even when supersaturated with cholesterol, fresh bile from
subjects without Gallstones rarely contains cholesterol crystals. The same bile, when incubated, forms crystals very slowly (up to 15 days). Bile of patients with cholesterol gallstones, on the other hand, usually does contain cholesterol crystals, and its nucleation time, when incubated, is much more rapid (mean of 2.9 days). Nucleation of cholesterol occurs far more rapidly from gallbladder bile of patients with cholesterol Gallstones than from hepatic bile in the same patients, even when hepatic bile samples are supersaturated with cholesterol. The addition of even small amounts of gallbladder bile to the hepatic bile samples causes rapid nucleation. These observations have led to the isolation of proteins in the gallbladder that promote or retard the nucleation of cholesterol crystals. At least five proteins have been identified as putative nucleation promoters, in addition to gallbladder mucoprotein. High doses of aspirin reduce the incidence of Gallstones in a prairie-dog model, perhaps by inhibiting the synthesis of a nucleation promoter. Success in other species has been variable.

. Growth: The crystal acquires additional cholesterol to form a visible stone. Cholesterol
stones often contain alternating layers of cholesterol crystals and mucoprotein. Pure
cholesterol crystals are quite soft. Protein adds strength to the stone. This stage of
stone formation is largely influenced by gallbladder stasis. In theory, microscopic
cholesterol crystals would be regularly ejected from the gallbladder if its contractions were
effective enough. Gallstones forming in patients with high spinal cord injury or treated
with the somatostatin analog Octreotide have been largely associated with impaired
gallbladder motility.



4. Gallbladder sludge, or thickened gallbladder mucoprotein with tiny entrapped cholesterol
crystals, is thought to be the usual precursor of gallstones. Sludge may also occur in
asymptomatic patients with prolonged fasting and can be seen on standard
ultrasonography of the gallbladder. Sludge can sometimes cause biliary pain,
cholecystitis, or acute pancreatitis, but may also resolve without treatment. The antibiotic
ceftriaxone can precipitate in the gallbladder and bile ducts as sludge.




Bile Duct Stones

Primary bile duct stones are stones formed in the biliary tree as the result of bile stasis, e.g.
above a stricture, around foreign material such as a suture, or in association with infection.
They are often earthy, muddy stones that can reach large dimensions, and are composed
predominantly of calcium bilirubinate and minor amounts of cholesterol or fatty acids. These
stones do not dissolve well in lipid solvents and may be found in the intrahepatic or
extrahepatic bile ducts.



Secondary bile duct stones are found in the bile ducts in association with gallbladder stones,
either having migrated out of the gallbladder or having formed concomitantly in the bile ducts.
Their matrix reflects the composition of gallbladder stones, i.e. predominantly cholesterol in
~80%, and black pigment in ~20% of cases. Black pigment stones are usually idiopathic, but
may be associated with chronic hemolysis or cirrhosis. Bacterial infection is not thought to be
important in the pathogenesis of either type of secondary stones.
 

 
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