Study group discussion: Mechanism of anemia in anemia of chronic disease

Why in chronic diseases you get anemia?

Due to poor absorptiomu of iron

Because of the inflammatory factor.. It locks up iron in the bone marrow.

I don't think it's due to inadequate absorption.

It's due to reduced absorption. But there is a reason to it. You guys heard of the protein hepcidin?
In anaemia of chronic disease, liver synthesizes hepcidin.
Hepcidin is a key that locks up iron in the bone marrow and prevents it’s release to transferrin.
That’s why, ferritin is increased. (Stores are there, but unavailable!)

Hepcidin block transporters in the intestine.

Good explanation!

Study link! http://medicowesome.blogspot.in/2013/08/difference-between-iron-deficiency.html

So reduced absorption is true?

Maybe the bone marrow too..The stores are adequate in chronic disease of anemia.

But main cause is the hepcidin locking the stores.

I'll look it up.

It's true..But there are other reasons too.

The ferroportin is present in both intestinal cells and macrophages.
Hepcidin performs its different functions via a single biochemical mechanism: hepcidin-ferroportin interaction. Intestinal epithelial cells and reticuloendothelial macrophages use the same transporter, ferroportin, to transport iron in the plasma. Moreover, macrophages and enterocytes exhibit strong upregulated ferroportin expression in the erythropoietic response in an iron-restricted state.
So I guess both the mechanisms are absolutely correct!

Nice.

What is the regulatory factor in the absorption of iron from duodenum?

Is it the transferrin levels? Their level of binding?

It's the Ferroportin.

Oh yes..The channel that transfers iron from epithelial cells into the blood, right?

Ferroportin is present in the entrocytes (cells lining the duodenum)

The level of ferritin that indicates adequate stores?
It's 15mg/dl
Below that level, it is diagnostic of falling iron stores.

I just read a research paper on it.. The hepcidin stuff can be used therapeutically, theoretically.
Interesting stuff.
Hepcidin agonists could be used to prevent or improve the accumulation of iron in both transfused and non-transfused β-thalassemic patients and even in anemia with iron storage. Hepcidin antagonists could be used in patients with diseases that cause hepcidin excess and occur with a framework of IDA or systemic IDA.