Low iron storage and mild anemia in postural tachycardia syndrome in adolescents, 2013, Jarjour and Jarjour

Copied post, from NIH: Decoding the Mysteries of Postural Orthostatic Tachycardia Syndrome


From PubMed: Clin Auton Res.
. 2013 Aug;23(4):175-9. doi: 10.1007/s10286-013-0198-6. Epub 2013 May 30.
Low iron storage and mild anemia in postural tachycardia syndrome in adolescents
Imad T Jarjour 1, Laila K Jarjour
Affiliations

• PMID: 23720007
  
• DOI: 10.1007/s10286-013-0198-6

Abstract


Objective: We reported low iron storage in neurally mediated syncope (NMS). While reduced red cell mass indicative of anemia has been reported in POTS, iron indices and hemoglobin (Hb) data were not reported. We investigated whether POTS, like NMS, is associated with low iron storage and anemia.

Methods: Thirty two children evaluated in 2007 and 2008 for probable POTS by a standing or tilt test or both at Texas Children's Hospital were included in a retrospective study. We measured serum ferritin (SF) and Hb values. We defined iron deficiency as SF < 12 μg/L, low iron storage as SF ≤ 25 μg/L, anemia as low Hb values for age and sex, and POTS as ≥2 symptoms of orthostatic intolerance >3 months and increased HR of >30 BPM or HR of >120 BPM within 10 min of standing or 70° tilt.

Results: Twenty four children had POTS, ages 12-18 years, 17 (71 %) were females. Value range (median) of SF 2-289 μg/L (25), Hb 11.5-14.6 (12.5) in females and 12-15.9 g/L (13.6) in males. Patients with POTS, when compared with normal US pediatric population had higher prevalence of low iron storage (50 vs. 14 %), iron deficiency (25 % of teenage girls vs. 9 %, and 16 % of teenage boys vs. 1 %), and anemia (18 % of teenage girls vs. 1.5 %, and 43 % of teenage boys vs. 0.1 %).

Interpretation: Low iron storage and mild anemia are associated with POTS suggesting that low iron storage is a potentially pathophysiologic factor in both POTS and NMS.

Link here:

https://pubmed.ncbi.nlm.nih.gov/23720007/

 

When I was younger and already ill, I was treated for low iron levels. It had nothing to do with a low iron diet or not eating enough.

 

There've been a couple of hints of iron playing a role in ME, too. By memory it may have been Birch and McGregor who independently of each other found issues of iron getting into cells. I can't remember but I doubt they distinguished between ME with and without POT so hard to tell if their iron findings related to one or the other or both.

There seem to be many different causes for iron not getting into cells, both genetic and epigenetic, and not everyone has the same issue - which makes it hard to pinpoint the problem - only the end result is the same: too little intracellular iron and/or poor utilisation of what little there is. It's unclear to me how well the standard iron panel test reflects intracellular iron, especially in people with dysregulated iron transport in and out of cells.

I find this whole area interesting because I have hereditary haemochromatosis (HHC), in other words too much iron, the opposite of anaemia. But I have a rare form of HHC where there's a disconnect between the amount of iron floating around in the serum and the amount of iron estimated to be stored in body tissues. Normally these move roughly in tandem, either both are up or both are down. In my case, without extremely aggressive treatment, it's one up and the other down. My serum is saturated with iron even while tissue storage tests come out normal. It's only when tissue storage tests get close to anemia levels that the serum levels drop into the normal range.

So my non-expert thinking is that there must be a problem with getting the iron from the serum into cells - loop back to the first paragraph about potentially too little intracellular iron in pwME.

Which looks very much like a lose-lose situation: simultaneous iron deficiency (in cells) and overload (in serum). Excessive serum iron is toxic but aggressive treatment to reduce it may exacerbate a possible intracellular iron deficiency which may worsen ME and/or POT. Argh!

I wonder if other people with HHC plus ME and/or POTS have the same problem? If so, that would support the hypothesis that iron (transport into cells) plays a role, if not a causative one then maybe as an aggravating factor.