mani
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whats the cause of hypercholesterolemia in obstructive jaundice?
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| Sakaki-
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Bile contains cholesterol, and in obstructive jaundice, the secretion of bile is blocked, resulting in cholestasis.
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| mani
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but one factor is that bile is needed for fat absorption from GIT. In Obstr jaundice this is impaired and this should decrease serum cholesterol. Another thing is that cholestrol contained in the bile is endogenous and is not meant for excretion. so even if it is retained or returned to blood this shouldnt elevate serum cholestrol
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| Sakaki-
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Hey--finally found something in a book about it.
Do you have a reference that refers to the endogenous nature of the cholesterol contained in the bile (such that it is not meant for excretion)? I would love to see one, as I always thought that there was fecal elimination of cholesterol. You are right about the decreased serum cholesterol absorption.
Anyways, the book (Lipoproteins in Helath and Disease ed. by Betteridge, Illingworth, and Shepherd) states four putative mechanisms:
-regurgitation of biliary cholesterol
-redistribution of itssue cholesterol into plasma
-increased hepatic synthesis of cholesterol
-impaired removel of cholesterol from the circulation
Rupture of the bile canaliculi may release bile into the blood but does not account sufficiently.
Redistribution of tissue cholesterol into plasma is more likely. In biliary obstruction, the reflux of biliary phospholipid (mainly lecithin) may result in a rise in plasma cholesterol from liver, skin and possibly brain. This excess cholesterol is from both preformed and newly synthesized cholesterol; ultimately, there is a small increase in the cholesterol/protein ratio in LDL (due to abstraction from tissues into the particle).
Increased hepatic cholesterol synthesis does not seem to be essential for hypercholesterolemia, though it is sometimes associated with biliary obstruction. In fact, in patients with chronic cholestasis, fecal neutral sterol and bile acid outputs are reduced (implying decreased synthesis).
Impaired removal of cholesterol from the circulation is also possible; chylomicron remnant uptake is impaired in rats with biliary obstruction. Therefore, these remnants accumulate. It is believed that this may be due to bile-salts, the precursor of LP-X as well as LP-X itself (lipoprotein X, which accumulates). Phospholipid emulsions from the bile may also decrease the fractional catabolic rate of LDL. There may be abnormalities of hepatocyte membrane composition (due to alterations in the lipid profile), as well as defective LDL clearance from bile-salt retention. ApoE-enriched HDL may compete for the LDL receptor.
So mainly, it's likely impaired removal of cholesterol from the circulation (from bile components and possibly LP-X), and the redistribution of tissue cholesterol (induced by phospholipids in the bile - mainly lecithin).
I hope this post wasn't too long...it is not completely understood why hypercholesteremia results.
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