Phlebotomy anyone?

[Merlyn]

My ferritin level in December was 66, it was not tested this time:

Iron Level 20 (10-30) umol/L

Iron Binding Capacity 45 (45-75) umol/L

Iron Saturation 0.44 (0.14-0.50)


I have no idea how to interpret the iron saturation because everything I've ever seen has been in percentage...


I assume this means that I am up near the top for iron saturation, and that the reference ranges are probably too broad. I would like some input? I have an appointment Thursday with the Dr. yet again, and it will be to ask for phlebotomy... if I have been iron loading for five decades, they would have no way of knowing just how much I have secreted away. But being within reference range is going to create problems I can see it coming. I ran into this with thyroid, you can be half dead, but the lab result tells you you are just fine...

[Bethr]

Hi beth just got my period feeling more energetic, and less tight. I guess tightness is spasticity but i never get jumpy just super tight, Example I can walk across the room today. A couple dats ago barely wall walk. I was looking at blood work from a couple months ago that showed h63d GENE mutatation but my iron levels do not appear particularly elevated. What am I looking for exactly. It is funny on the weekend of nov 14 i went to a party after I had just had a ton of blood drawn for all those tests and I was significantly more mobiile . I never really conected the dots but wow I wonder if it was all the blood being removed. Hmmm

Hi jak7ham9,
I've posted this elsewhere, but wanted to let you know that if you have a combination of the H63D gene and something called PCT you can load iron without showing very high levels of iron on blood tests.

A doctor could easily miss it. They don't generally check transferrin saturation on a routine iron blood test. You need that test.
You need to read up on PCT (porphyria Cutanea Tarda) and the other porphyrias. You can carry the genetics for PCT and not have obvious symptoms like me. I get the rash, not so much now, but for 30 years+ from age 16 it never went away. They told me it was eczema at the time.
PCT attacks have many symptoms similar to MS, but they can be differentiated, that includes lesions and spasticity and combined with a HH gene you also get fatigue and stiff joints.

Porphyria cutanea tarda

Porphyria cutanea tarda (PCT) is characterized by the defective uroporphyrinogen III decarboxylase enzyme. There are 3 types of porphyria cutanea tarda with typical skin manifestations; patients present with skin fragility, erosions, vesicles, bullae, and milia in sun-exposed areas of the skin. Sometimes, there is the presence of periorbital mottled hyperpigmentation and hypertrichosis, sclerodermoid changes, and ulceration.

Hemochromatosis gene (HFE) mutations and the hepatitis C virus (HCV) are both risk factors for PCT. In a French cohort of PCT patients with both C282Y and H63D were more frequent in PCT+ patients than in controls, but there was no difference in HFE genotype according to HCV seropositivity.19 Up to two thirds of Saxon patients with PCT carry the classic HFE mutations (C282Y and/or H63D). PCT is associated with antibodies to HCV. PCT is an important extrahepatic manifestation of HCV-infection.20 In a Swedish cohort, 38% of male patients with PCT had a history of alcohol abuse.21

Magnetic resonance imaging (MRI)

MRI of acute intermittent porphyria demonstrates multiple large, contrast-enhancing, subcortical white matter lesions, which regress with glucose and hematin infusions. Diffusion-weighted MRI is normal, and MR spectroscopy excludes acute demyelination or tissue necrosis. MRI findings of acute intermittent porphyria can differ from those in posterior reversible encephalopathy syndrome by virtue of intense contrast enhancement. Because diffusion-weighted MRI and MR spectroscopy are normal, the lesions are likely caused by reversible vasogenic edema and transient breakdown of the blood-brain barrier.52

T2-weighted MRI sequences demonstrated multiple white-matter, high-signal lesions in 4 of 16 acute intermittent porphyria gene carriers (25%).53 Kupferschmidt and colleagues54 described 2 patients with acute intermittent porphyria who presented with cortical blindness. MRI showed bilateral occipital lesions, and the investigators speculated that these lesions were caused by vasospasm-induced ischemia due to unopposed cerebral vasoconstriction that resulted from a deficiency of nitrous oxide synthase, a major vascular dilator.

The striking feature of the MRI findings in these cases and in those of acute intermittent porphyria described in the literature is that the lesions are bioccipital and partially or totally reversible. These characteristics are typical of MRI findings seen in patients with hypertensive encephalopathy, and many patients presenting with acute intermittent porphyria attacks have high blood pressure on presentation.55

In cases of porphyria cutanea tarda, MRI of the liver shows poorly defined areas, which, on T2-weighted sequences, exhibit a hypersignal with fat saturation. Treatment of porphyria cutanea tarda may lead to clinical remission and resolution of radiologic abnormalities

Add a bit of extra iron overload because of a hemochromatosis gene and you can see why it is a bad combination, but it's not MS.
I have this combination and it's reversible with phlebotomy.
I've had phlebotomy and I'm feeling like I'm back in my 20's again.
Maybe my lesion has now disappeared, hope so.

The other interesting thing is, in menstruating women you feel better when menstruating, worse in the luteal phase prior to menstruating! This is significant, that was my main clue. I've cracked it!

Cheers....hope that's helpful

[jimmylegs]

fyi

http://www.ncbi.nlm.nih.gov/pubmed/568576
Hypovitaminemia A in idiopathic hemochromatosis and hepatic cirrhosis. Role of retinol-binding protein and zinc.
Brissot P, Le Treut A, Dien G, Cottencin M, Simon M, Bourel M.

Serum levels of vitamin A, its specific carrier protein retinol-binding protein (RBP), and zinc were determined in 34 cases of idiopathic hemochromatosis, 33 cases of alcoholic cirrhosis, 10 cases of non-alcoholic cirrhosis, and in 35 normal controls. In both alcoholic and non-alcoholic cirrhosis, vitamin A and RBP levels were very significantly reduced, whereas a significantly low zinc was observed only in the alcoholic cirrhosis group. In idiopathic hemochromatosis, vitamin A values were significantly lower compared to normals, whereas serum RBP levels were normal and serum zinc was very close to that of the controls. A significant correlation was found between vitamin A and RBP levels in the entire group of 112 patients. These results, (1) in alcoholic and non-alcoholic cirrhosis, confirm a dramatic vitamin A deficiency and the major role played by decreased RBP, but tend to deemphasize the possible role of zinc deficiency; (2) in idiopathic hemochromatosis, affirm a significant serum vitamin A deficiency supposedly by a different mechanism from that of alcoholic cirrhosis since in idiopathic hemochromatosis plasma RBP levels are normal. The role of this vitamin A disorder should be considered in the interpretation of clinical signs of idiopathic hemochromatosis such as ichthyosis and visual disorders.

without seeing the full text i can't see what 'very close' means in terms of zinc levels in patients and controls. however, if i do get a chance to go for the full text i am willing to bet it's not higher than controls, and also that the patient average is not 18.2 umol/L! it is known that the human body needs adequate zinc in order to handle vitamin A properly. AND, zinc repairs cirrhosis, which occurs both in alcoholism and iron overload.

[jak7ham9]

hi bethe I always feel much worse before my period much better when I get it. also though my left jugular is stenosed and reduced flow too. I will get saturation checked. I would get someone to draw blood if I could. I ordered deferiprone (iron chelator) a month ago and it still is not here

[Bethr]

hi bethe I always feel much worse before my period much better when I get it. also though my left jugular is stenosed and reduced flow too. I will get saturation checked. I would get someone to draw blood if I could. I ordered deferiprone (iron chelator) a month ago and it still is not here

Chelation won't help with PCT (it will help with the iron overload due to PCT). You need to get it checked out (gene test, urine test???), PCT makes you overload iron (because of the HH gene) without the usual high ferritin etc. and the PCT puts porphyrins into your system. This gives you the neurological symptoms and lesions. Iron chelation will not get rid of the porphyrins. The treatment for PCT is phlebotomy, same as HH.

It could be a red herring, but then again you never know. Why would MS have a monthly cycle? That was the clue that put me on my search.
I suppose i could have put it down to Pre-menstrual syndrome, (most doctors would), but the fatigue and sleeping had a monthly cycle too, which was more than weird. The sleeping/tiredness was extreme.

I self medicated by giving a blood donation. Instant stop to sleeping/fatigue, and it proved something was up and i was on the right path.

If you have lesions caused by PCT they apparently reverse when you are treated.
Lesions from PCT can have similar symptoms to MS, lost vision, spasticity etc. i lost the use of my right hand for a while.

Hope that helps.

[Merlyn]

Okay, my iron test I think proves my theory that heterozygote people like me can load iron, just at a slightly slower rate. We also have more elevated transferrin than ferritin... bear with me here...

I was anemic in my teens and 20s, and if it were iron loading anemia, the transferrin would've picked up iron and deposited it in places where it should not go rather than in the liver... with hemochromatosis type iron abnormality, usually this anemia eventually corrects. People outgrow it. As I did. Transferrin is the protein that deposits iron into the brain. It is also elevated in Alzheimer's... I don't know about Parkinson's at this time, but my guess is is yes I will have to look it up. So what is happening with me, is that my ferritin would never alarm anyone because it is in such a normal state. But the transferrin is so close to showing hemochromatosis that I know that I am depositing iron in the brain and central nervous system rather than the liver. This is how you get the neurological impairment of MS over many years, as the iron accumulates in the CNS. It takes decades, but it happens. What is amazing me is that they could be preventing MS with preventative phlebotomies done at an early age for anybody that shows up with this skewered ferritin/transferrin ratios. These are very nonstandard tests, they must be ordered and even then they are not going to alarm the doctors if you are still was in this bizarre reference range. But what we are looking at in MS (and Parkinson's and Alzheimer's) is long time accumulation that eventually results in disability. If we iron loaded at a faster rate and the ferritin became abnormally elevated, it would alert people to the abnormal iron metabolism. But because we are just under the wire, and we load iron at a slightly slower rate, no one sees it in the blood tests for ferritin... this is probably one category of iron abnormality. There are also the porphyria iron abnormalities that are genetic, and I don't know enough about it to comment on that, but people without condition have abnormalities in iron metabolism also... I can study everything at one time, so can't do much commenting there. But if you are anemic I would check out the porphyria link also.

Phlebotomy brings down the transferrin levels! They could be preventing both Alzheimer's and Parkinson's through phlebotomy also if the transferrin levels were elevated! I thoroughly believe that my disability could have been prevented through preemptive phlebotomy. I have an appointment on Thursday with my Dr. and I think I will be able to convince him to go ahead and try this. People on hemochromatosis forum say they feel remarkably better when the transferrin level comes down. For the first time in a long time I feel there may be something I can do for PP MS. As soon as I can get these phlebotomies I will and I will keep you updated of course because this is just remarkable! At last, an explanation for what occurs in some cases of primary progressive MS! And not only that, I method of treatment! Am I happy? You bet, and I fully expect to feel better with very little treatment, very few phlebotomies.

[ForeverSpring]

You have motivated me to take action on this.

Due to surgery, I have not had a period for over 30 years, so cannot use that as an indicator.

Yesterday I made an appointment for March 1 to donate blood when the blood drive comes to town. I am curious to see how it will affect me. It has been years since my last blood donation, and I never paid any attention to that.

Before going to the local clinic to request the tests for iron overload, it would be helpful to have some “reason” in their eyes for doing so. March 1 is only four weeks away.

Meanwhile, I have stopped taking my daily multi-vitamin/multi-mineral tablet, which contains 50% RDA for iron. I had known the iron was in there, but never before realized the harm it could do.

Since it is so common and so easily overlooked, the iron-overload question is one that everybody should investigate. Otherwise, there is no way of knowing you have the overload, until after serious damage has been done.

Thanks for presenting your experiences and information! Plenty to think about!

ForeverSpring

[Merlyn]

Oh thank you, for volunteering to give blood and see how you feel. I guess this is going to make you feel much better. People on hemochromatosis forum say they feel much much better when the transferrin levels come down... this is done through phlebotomy. It seems so simple right now for me, all of the devastating health problems that could be simply prevented.

Being on those those birth control pills that prevents bleeding has got to be just horrible for people with MS.

I am now positive mentally that I had iron loading anemia in my teens and 20s, and I switched to cast-iron cookware to absorb iron from my food... big mistake. I used to tell other people to buy cast-iron, that advice!

http://www.ironoverload.org/anemia.htm

[jak7ham9]

ok don't think i am crazy but what about leeches. You buy abunch keep them in water then stick on 10-20 when you nned them . Stick them back in water when they fall off. www.leeches.biz I know it sounds wacky but read about it.

[ForeverSpring]

ok don't think i am crazy but what about leeches. You buy abunch keep them in water then stick on 10-20 when you nned them . Stick them back in water when they fall off. www.leeches.biz I know it sounds wacky but read about it.

You are not crazy, and I know that they do the job, but . . . ew-w-w-w-w-w-w!

When I lived in hot, humid, southern Tennessee, there were huge slugs everywhere. They caused that same, creepy reaction!

Thanks, but no thanks!

However, if you have no aversion to them, and can live with them in your home, and do not mind handling them, then go for it!

ForeverSpring

[shye]

Bethr,
Why did you ask about sensitivity to metal in cheap jewelry?
I have had this, esp in the past (don't wear any jewelry now, so not sure).
Daon't recall seeing this mentioned in any porphyric stuff I've read.

And the small blisters, I get them sometimes, esp when getting all the other symptoms of porphyria.

BUT again, MS could be iron dysregulation, ie, too high OR too low.
As I say, my recent TIBC was too low, have a script to do all irons again, but fasting this time. Hope to do it 2/1/10; and I have a history consistent with porphyria, and tests for porphyria were inconclusive (one part yes, one part no show), but is an extraordinarily difficult test to get done, you should be experiencing an attack when testing!
Am exploring just getting the gene test done.

[Merlyn]

Also, look at my TIBC (Total Iron Binding Capacity)... right down at the very bottom...

http://www.digitalnaturopath.com/cond/C517593.html

While low TIBC is commonly explained by the presence of hemochromatosis, it can also be caused by hypoproteinemia from malnutrition, anemia with infection and chronic disease, and nephrosis

I was at 45... reference range was 45-75

more and more, I do not think we can separate some forms of MS from hemochromatosis, we are just milder iron loaders, but we get nuked just the same

[shye]

Bethr'
just read the stuff I missed above that you posted--
where are your MS lesions? If they are head only, that might be an indication also.
I have noticed that there is a group of MSers posting that seems to have similar problems--optic neuritis, brain fog and a few other things (brain fog- can't recall this moment ), and are still fairly okay with walking--and this group ONLY has brain lesions, no spinal lesions.
I am in that group--and when diagnosed, (only found this out when recently obtained record), the speculation by neurologist was that my problems could be vascular, not MS (but was also NOT inconsistent with MS). Yes, the typical mish-mosh we get so often!
But now, from the abstraact you posted, possibly those brain lesions could be caused by Porphyria!! Eureka--now to take my MRI to get it evaluated by a porphyria specialist!
This all gets curiouser and curiouser. Working on the vascular idea, I recently got two Magnesium venous infusions, and am now taking high dose Mg (Albion chelation process)(for years was just taking Mg citrate), and am already a million times better--this of course could indicate either vascular or "just MS", since magnesium is needed for nerve transmission, as well as needed for muscle, cardiovascular, brain, circulatory, etc etc--needed in over 300 processes.
There are just so many variables here--

[Merlyn]

My letter to Ironic Health:

I have contacted you recently, but I did not have my iron panel results yet.


My ferritin level in December was 66, it was not tested this time:

Iron Level 20 (10-30) umol/L

Iron Binding Capacity 45 (45-75) umol/L

Iron Saturation 0.44 (0.14-0.50)


my transferrin saturation level is 44%
ie: Iron 20 as a percentage of IBC 45 = 44%

They look at hemochromatosis for menstruating women at 45%+ so close, and so damaging.


Okay, my iron test I think proves my theory that heterozygote people like me can load iron, just at a slightly slower rate. I find the Iron Binding Capacity interesting in that it is very often low in hemochromatosis...

I was anemic in my teens and 20s, and if it were iron loading anemia, the transferrin would've picked up iron and deposited it in places where it should not go rather than in the liver... with hemochromatosis type iron abnormality, usually this anemia eventually corrects. People outgrow it, I understand. I did. Transferrin is the protein that deposits iron into the brain. It is also elevated in Alzheimer's... and Parkinson's to I gather? So what is happening with me, I gather, is that my ferritin would never alarm anyone because it is in such a normal state. But the transferrin is so close to showing hemochromatosis . I know that I am depositing iron in the brain and central nervous system rather than the liver. This is how you get the neurological impairment of MS over many years, as the iron accumulates in the CNS. It takes decades, but it happens. What is amazing me is that they could be preventing MS with preventative phlebotomies done at an early age for anybody that shows up with this skewered ferritin/transferrin ratios. These are very nonstandard tests, but think of the money they would save! But what we are looking at in MS (and Parkinson's and Alzheimer's) is long time accumulation that eventually results in disability. If we iron loaded at a faster rate and the ferritin became abnormally elevated, it would alert people to the abnormal iron metabolism. But because we are just under the wire, and we load iron at a slightly slower rate, so no one sees it in the blood tests for ferritin...

Phlebotomy brings down the transferrin levels! They could be preventing both Alzheimer's and Parkinson's through phlebotomy also if the transferrin levels were elevated! I thoroughly believe that my disability could have been prevented through preemptive phlebotomy. I have an appointment on Thursday with my Dr. and I think I will be able to convince him to go ahead and try this. People on hemochromatosis forum say they feel remarkably better when the transferrin level comes down. For the first time in a long time I feel there may be something I can do for PP MS. As soon as I can get these phlebotomies I will and I will keep you updated of course because this is just remarkable! At last, an explanation for what occurs in some cases of primary progressive MS! And not only that, I method of treatment! Am I happy? You bet, and I fully expect to feel better with very little treatment, very few phlebotomies.

Mr. Ignatieff announced in the Globe and Mail today that he wants to investigate dementias/brain diseases. I do believe we could prevent Alzheimer's through phlebotomy also. Stop the iron from accumulating in the first place, rather than trying to deal with the end state of disease!

Some people are even starting to question whether the 45% is too high.


http://wwwironoverload.org/anemia.htm

[shye]

Merlyn,
Some of us could be TOO low in iron--appears to work both ends of the iron problem..