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Blood work help.

bonacris

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Jan 15, 2015
Messages
584
I got a my results back and everything is within range except my iron.

Iron 48 umol/L range 12-31
Transferrin 2.8 g/L range 2.0-3.6
calculated TIBC 70 umol/L range 50-85
Transferrin Saturation 68% range 21-45

I dont take an iron supplement or a multi vitamin. Anything I can do to get this back in range or is it something too be concerned about
 
You could phlebotomize, or see your primary to further evaluate why your Transferrin Saturation% is a bit high.

I probably stick it to the latter.
 
We both know you are smarter than that Stewie. tsk tsk
 
We both know you are smarter than that Stewie. tsk tsk

I could have suggested he should speak to his primary to rule out homozygous for C282Y or H63D mutation, in which we both know is indicative of hereditary hemochromatosis.

Tho he may of ate a 16oz filet mignon the night before his lab's :)
 
I could have suggested he should speak to his primary to rule out homozygous for C282Y or H63D mutation, in which we both know is indicative of hereditary hemochromatosis.

Tho he may of ate a 16oz filet mignon the night before his lab's :)


Hahahaha....hemochromatosis...Hahahaha. Thanx for the laugh aloud, Stewie. :D
 
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I could have suggested he should speak to his primary to rule out homozygous for C282Y or H63D mutation, in which we both know is indicative of hereditary hemochromatosis.

Tho he may of ate a 16oz filet mignon the night before his lab's :)

I'll give you a hint. The other lab test needed starts with the letter "F".
 
I'll give you a hint. The other lab test needed starts with the letter "F".


Ferritin is helpful, tho isn't diagnostic in his particular situation, correct?

He could have some sort of bacterial or viral infection (recently past or present) that would transiently increase his ferritin, therefore wouldn't give a true indication of his Fe status.
 
Last edited:
Ferritin is helpful, tho isn't diagnostic in his particular situation, correct?

He could have some sort of bacterial or viral infection (recently past or present) that would transiently increase his ferritin, therefore wouldn't give a true indication of his Fe status.

Remember this when you decide to go back into the world of clinical medicine, serum ferritin should be obtained whenever ordering iron studies for a patient. :)
 
Remember this when you decide to go back into the world of clinical medicine, serum ferritin should be obtained whenever ordering iron studies for a patient. :)

I wholeheartedly agree. If you was to look back through several of my posts over the years regarding one's Fe status, you'll see I've continually mentioned ferritin as base requirement when assessing one's Fe status.

With that out of the way. I've been under the impression if one's Transferrin Saturation % is 55>% , ferritin takes a backseat in a differential diagnosis as iron overloaded is certain. Either be accidentally or hereditary.

I've also come to the concussion that especially on these 'over-consumption of antioxidant forums'--- such as here, these anti-kryptonite connoisseurs may skew their ferritin status in a positive way. Understandably ferritin is considered the 'longterm' storage of Fe, a lot of these antioxidants can act as potential iron chelators, therefore lower bound Fe. Although, I don't believe these antioxidants affect TFs%.

To conclude. I didn't want to invoke fear mongering with my opening post by suggesting he chooses the 'latter' with discussing this with his primary.

What else will right shift> Transferrin Saturation % outside of HFE?
 
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Also, if by chance he has sickle cell (if his ethnicity fits in) he'd been screened for sideroblasts long ago, correct?
 
I wholeheartedly agree. If you was to look back through several of my posts over the years regarding one's Fe status, you'll see I've continually mentioned ferritin as base requirement when assessing one's Fe status.

I believe you but know that I am entirely too lazy to look anything up. Now a 24 hour ICU shift? No problem. An internet search or to "google" something you know that you already know? Not gonna happen.

With that out of the way. I've been under the impression if one's Transferrin Saturation % is 55>% , ferritin takes a backseat in a differential diagnosis as iron overloaded is certain. Either be accidentally or hereditary.

Part of what makes a great diagnostician is the ability to look at labs and see when "normal" isn't normal. You know docs commonly say or write "WNL"? To me that means "We Never Look". :rolleyes:

I've also come to the concussion that especially on these 'over-consumption of antioxidant forums'--- such as here, these anti-kryptonite connoisseurs may skew their ferritin status in a positive way. Understandably ferritin is considered the 'longterm' storage of Fe, a lot of these antioxidants can act as potential iron chelators, therefore lower bound Fe. Although, I don't believe these antioxidants affect TFs%.

To conclude. I didn't want to invoke fear mongering with my opening post by suggesting he chooses the 'latter' with discussing this with his primary.

What else will >shift Transferrin Saturation % outside of HFE?

Hemosiderosis, frequent/multiple blood transfusions, sickle cell anemia, thalassemia major, chronic alcoholism, drinking well water via iron pipes, pica, and my favorite - sideroblastic anemia.
 
Also, if by chance he has sickle cell (if his ethnicity fits in) he'd been screened for sideroblasts long ago, correct?

There is a prenatal DNA test which looks for the point mutation but I stay the hell away from OB-GYN b/c it sucks.

We would screen patients using Hb electrophoresis which sounds crazy complicated but is really simple and easy to do and interpret.

The other way to dx SCD is via peripheral blood smear on a plain light microscope when a patient presents with his/her first sicked cell crisis. Pretty sure Stevie Wonder could dx that one.
 
I've also come to the concussion that especially on these 'over-consumption of antioxidant forums'--- such as here, these anti-kryptonite connoisseurs may skew their ferritin status in a positive way. Understandably ferritin is considered the 'longterm' storage of Fe, a lot of these antioxidants can act as potential iron chelators, therefore lower bound Fe. Although, I don't believe these antioxidants affect TFs%.

Might want to get that checked out before you develop CTE. :p
 

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