Iron dysregulation and inflammatory stress erythropoiesis associates with long-term outcome of COVID-19, 2024, Hanson et al

Sean said:
30mg is correct.

IIRC, in Europe they use the comma instead of the period for the decimal point, to avoid confusion because the period can also represent multiplication.
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I'm not sure that's why. I think the comma and the period are simply used in the opposite way (at least here in Hungary but I guess elsewhere too).

For example:

In English you would write 3.5 g, meaning 3 and a half grams. In some other countries this is 3,5 g because they use the comma in this context.

In English, you you would write 3,500 meaning 3500. In some other countries this would be 3.500, also meaning 3500. The period is optional though.

So they simply use the comma and the period differently but they use both.
 
Stumbled on a study by Broadbent and Coutts 2015, where they found:
A previous or current medical diagnosis of iron deficiency/anaemia occurred in 45.8% of the CFS group, significantly greater (p = 0.001) than non-CFS.
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The sample was small, though - 24 patients and 18 controls - and
The female-to-male ratios for CFS and non-CFS were17:7 and 13:5 respectively
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so I'd want to see if it was replicated in a larger study with equal female:male ratios.
 
Just a note on interpretation of the results for this study, since I explored this data in-depth as part of a validation for another LC study I was a part of.

Ferritin is a carrying molecule that is primarily present within cells in the body. Transferrin is the primary molecule that carries iron in the bloodstream (hemoglobin notwithstanding).

Some amount of ferritin leaks out of cells and is present in the blood plasma--because of this, free blood ferritin levels may often be used as a proxy for available iron stores in the body. The logic being that more ferritin in the blood = there's enough iron stored in ferritin in the cells to go around.

However, if there are differences in how greedily cells are holding onto that iron, levels of ferritin in the blood may not correlate that well to the actual presence of iron in the body.

The theoretical explanation based on these results is that there is an increased sequestration of iron in certain innate immune cells starting during infection and it continues beyond infection in individuals who experience LC. In simple terms, the rest of the body experiences "anemia" because certain innate immune cells are really active thieves.

This "iron theft" is often seen during acute infection and is induced as a response to certain cytokines. The main question in LC is why these cells don't return to normal behavior after infection is cleared. That question is somewhat beyond the scope of this paper.

Because they are still "thieving" iron, further iron supplementation may or may not help. It is hard to tell how much of that supplemented iron will actually end up where it is supposed to go vs. getting rounded up by those same greedy immune cells.

It's also hard to determine which LC symptoms are coming from the direct behavior of those immune cells vs. less iron availability for other cells. So even if you are able to get more iron to the rest of the body, that may only fix a portion of the problem.
 
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jnmaciuch said:
Just a note on interpretation of the results for this study, since I explored this data in-depth as part of a validation for another LC study I was a part of.

Ferritin is a carrying molecule that is primarily present within cells in the body. Transferrin is the primary molecule that carries iron in the bloodstream (hemoglobin notwithstanding).

Some amount of ferritin leaks out of cells and is present in the blood plasma--because of this, free blood ferritin levels may often be used as a proxy for available iron stores in the body. The logic being that more ferritin in the blood = there's enough iron stored in ferritin in the cells to go around.

However, if there are differences in how greedily cells are holding onto that iron, levels of ferritin in the blood may not correlate that well to the actual presence of iron in the body.

The theoretical explanation based on these results is that there is an increased sequestration of iron in certain innate immune cells starting during infection and it continues beyond infection in individuals who experience LC. In simple terms, the rest of the body experiences "anemia" because certain innate immune cells are really active thieves.

This "iron theft" is often seen during acute infection and is induced as a response to certain cytokines. The main question in LC is why these cells don't return to normal behavior after infection is cleared. That question is somewhat beyond the scope of this paper.

Because they are still "thieving" iron, further iron supplementation may or may not help. It is hard to tell how much of that supplemented iron will actually end up where it is supposed to go vs. getting rounded up by those same greedy immune cells.

It's also hard to determine which LC symptoms are coming from the direct behavior of those immune cells vs. less iron availability for other cells. So even if you are able to get more iron to the rest of the body, that may only fix a portion of the problem.
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Bookmarking this answer for the next time I try and talk to my GP about why my ferritin is low but other rbc results are OK!
 
Eleanor said:
Bookmarking this answer for the next time I try and talk to my GP about why my ferritin is low but other rbc results are OK!
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For what it's worth, in this study they did find other typical markers of anemia (particularly hemoglobin) and elevated ferritin.

Low ferritin in the absence of other markers has also been observed in other cases (Hashimoto's comes to mind, as I also have hashimoto's and unexplained low ferritin). As far as I know, that's never been explained--it's possible there's some other ferritin-specific phenomenon that's going on, but we can really only make wild speculations about that at this point.

It is probably a different phenomenon than whatever explains the iron results in this paper, though it might be related for all we know!
 
Utsikt said:
Do you have a link to the study?
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I don't, because for me the link goes to a Chinese language something or other:
Link to Published Version: https://doi.org/10.15640/ijhs.v3n4a7
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But you can download the pdf by searching for it in Suzanne Broadbent's publications https://research.usc.edu.au/esploro...=any,contains,3483878740002621&page=1&lang=en

The citation is:
Broadbent, S., & Coutts, R. (2015). Irregularities in red cell distribution width and lymphocyte
concentration in individuals with Chronic Fatigue Syndrome. International Journal of Health Sciences, 3(4),
71–78.
 
Karen Kirke said:
I don't, because for me the link goes to a Chinese language something or other:

But you can download the pdf by searching for it in Suzanne Broadbent's publications https://research.usc.edu.au/esploro...=any,contains,3483878740002621&page=1&lang=en

The citation is:
Broadbent, S., & Coutts, R. (2015). Irregularities in red cell distribution width and lymphocyte
concentration in individuals with Chronic Fatigue Syndrome. International Journal of Health Sciences, 3(4),
71–78.
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Thank you! I found it here:
https://www.researchgate.net/public..._in_individuals_with_Chronic_Fatigue_Syndrome
 
Utsikt said:
Thank you! I found it here:
https://www.researchgate.net/public..._in_individuals_with_Chronic_Fatigue_Syndrome
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The CFS group CD3+CD4+ cell count (Table 3) was lower than the non-CFS (p = 0.049) but the concentrations of other lymphocyte sub-populations, absolute cell counts and percentages of positive cells, measured by TBNK flow cytometric analysis were not significantly different between groups.
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jnmaciuch said:
The theoretical explanation based on these results is that there is an increased sequestration of iron in certain innate immune cells starting during infection and it continues beyond infection in individuals who experience LC. In simple terms, the rest of the body experiences "anemia" because certain innate immune cells are really active thieves.

This "iron theft" is often seen during acute infection and is induced as a response to certain cytokines. The main question in LC is why these cells don't return to normal behavior after infection is cleared. That question is somewhat beyond the scope of this paper.

Because they are still "thieving" iron, further iron supplementation may or may not help. It is hard to tell how much of that supplemented iron will actually end up where it is supposed to go vs. getting rounded up by those same greedy immune cells.

It's also hard to determine which LC symptoms are coming from the direct behavior of those immune cells vs. less iron availability for other cells. So even if you are able to get more iron to the rest of the body, that may only fix a portion of the problem.
Click to expand...
I also am dealing with long-term problems with low ferritin levels, and trying to get them back up and keep them there, with no other abnormal iron related measures and no sign of anaemia.

Standard oral iron supplements are a disaster (ferrous sulphate, and Maltofer – the pill form is just awful, no better than the ferrous sulphate pill, and while the liquid form is far better for gut pain it still wreaks the same havoc with the gut function that the pill forms do).

Currently trying a new-ish one called SiderAL Forte which seems to completely sidestep the awful side effects of the standard ones – as I understand it, it works by bypassing the gut immune response to excess dietary iron by hiding the iron in micro-capsules that get into the blood before releasing the iron.

No obvious side effects so far, and the side effects from the other forms seem to have gone, and I am generally feeling considerably better for it. Though early days with it and yet to have tests to see how well it is working on the ferritin levels (coming up soon).

SiderAL Forte is available in Europe and some other countries, but for some reason not yet here in Australia. So I have to order it from overseas. Not particularly cheap, but if it proves to do the job, especially with no side effects, than I am happy to keep paying for it.

If that does not work than the only option left is regular IV infusions at the hospital.
 
Evergreen said:
Ferritin, transferrin saturation and serum iron are the only ones that are low for me at this point. All other measures, including haemoglobin, are in the normal ranges. What I have is iron deficiency, and if I don’t get an iron infusion, that will keep going until haemoglobin also drops below the normal range, and it’s offically iron deficiency anaemia rather than just iron deficiency.
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Just to note that I had the iron infusion, and they took bloods just before. In the 5-6 weeks since the last blood tests, haemoglobin had dropped out of the normal range (from the middle of the range). I had side effects - they started 2-3 days after the infusion and lasted 2 days (this is typical and it did not resemble PEM). Mainly nausea, painful, weak muscles and exhaustion - much more reminiscent of an infection than PEM. Started with a near-faint. The nausea lasted longest. Resolved nicely. Really glad I had it when I did. The infusion, that is, not the nausea!

Edited to add last line.
 
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I thought this might be of interest and/or use to someone with suspected anemia caused by low iron :

https://irondisorders.org/wp-content/uploads/2019/12/Handout-HowdoIknow_Anemia2020.pdf

It is just one page. The table at the bottom is of particular interest, I think, but isn't a complete list of patterns of results indicating anemia.

The link is entitled "How do I know if I'm anemic?"

At one time I had very low iron and ferritin as a result of a long-term, chronic GI bleed. As well as serum iron and ferritin being very low, my TIBC was below range. Under normal circumstances when someone has low iron and ferritin it would result in TIBC being high in range or over the range.
 
Arnie Pye said:
I thought this might be of interest and/or use to someone with suspected anemia caused by low iron :

https://irondisorders.org/wp-content/uploads/2019/12/Handout-HowdoIknow_Anemia2020.pdf

It is just one page. The table at the bottom is of particular interest, I think, but isn't a complete list of patterns of results indicating anemia.

The link is entitled "How do I know if I'm anemic?"

At one time I had very low iron and ferritin as a result of a long-term, chronic GI bleed. As well as serum iron and ferritin being very low, my TIBC was below range. Under normal circumstances when someone has low iron and ferritin it would result in TIBC being high in range or over the range.
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That must have been horrible. Hope you got it sorted.

The table would certainly be helpful if all you know is that your haemoglobin is low, and your doctor isn't following up.

TIBC doesn't often appear on my blood tests, but when it does, I'm in the normal range, pretty much in the middle. That includes when I was in hospital with severe iron-deficiency anaemia and now, when it's milder.

Cleveland Clinic says:
If you have a low TIBC level and a high blood iron level, it could mean you have hemochromatosis (iron overload). Low TIBC and low iron can be a sign of certain conditions, like:
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The NHS only highlights liver disease as a possible cause of low TIBC:
https://www.nhs.uk/conditions/tibc-test/
 
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