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Old 09-08-2012
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Default Hemochromatosis and Wilsons disease doubt

Could someone tell me
a) why is there low transferrin in Hereditary hemochromatosis?

b) why is there low ceruloplasmin in Wilsons disease?

Any help would be appreciated
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Old 09-08-2012
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1) wilson's disease---in normal individuals dietary copper enter intestinal epithelial cells and reach liver by transporter(DMT1)..in liver,it binds to ceruloplasmin and release into bile...
in wilson's there is mutation in transportation and binding with ceruloplasmin..so, though ceruloplasmin is released it is ineffective in binding to copper ..so ceruloplasmin becomes inactivated and it's level decreases

2) hemochromatosis-----in normal individuals dietary iron is transported in blood by transferrin and extra iron is stored in ferritin...when iron levels in blood decreases,transferrin levels increase normally (vice versa---decreased transferrin levels in blood lead to iron overload)--because when iron level decrease more transferrin is produced by liver for needed transports and viceversa.....
in hemochromatosis------there is mutation leading to excessive absorption of iron ,so as increased iron levels...ferritin takes it and storage in body tissues(as hemosiderin etc)......as there is iron overload liver won't synthesize transferrin


hope it understands
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Old 09-08-2012
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Quote:
Originally Posted by tarsuc View Post
Could someone tell me
a) why is there low transferrin in Hereditary hemochromatosis?

b) why is there low ceruloplasmin in Wilsons disease?

Any help would be appreciated
Hemochromatosis is an Fe overload state.whenever feritin(which is soluble storage form of iron)is high,the liver stops making transferrin hence it's low.the reverse is the case in iron def state.

Wilsons dx is an AR disorder.the disease itself is simply the inability of ceruloplasmin to enter circulation.this leads to copper accumulation within tissues and oxidative damage
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