A search of the literature of iron related disease .. reveals low
vitamin D .
What significance is the fact iron destroys vitamin D or more precisely
in those with iron overload .. vitamin D is decreased .. in those with
supplemental iron induced iron overload .. vitamin D is decreased.
Bleeding / venesection / bloodletting / phlebotomy .. RESTORES ..
vitamin D .
<<snip>>
The results reveal that the low serum 25-OHD concentration in patients
with hemochromatosis is directly related to the extent of iron loading
and it is improved by venesection therapy.
<<snip>>
Iron induced decreased vitamin D.
<<snip>>
when transferrin is saturated with iron, may impair bone formation and
aggravate osteomalacia.
<<snip>>
Saccharated ferric oxide (SFO)-induced osteomalacia: in vitro
inhibition by SFO of bone formation and 1,25-dihydroxy-vitamin D
production in renal tubules.
Sato K, Nohtomi K, Demura H, Takeuchi A, Kobayashi T, Kazama J, Ozawa H
Bone. 1997 Jul ; 21(1): 57-64
A 60-year-old man with portal hypertensive gastropathy due to type C
liver cirrhosis developed severe bone pains, marked hypophosphatemia
with inappropriately increased urinary excretion of phosphate (%TRP;
9.6%), and hyperalkaline phosphatasia, after intravenous administration
of saccharated ferric oxide (SFO) at a dose of 80-240 mg/week over a
period of more than 5 years. The total iron infused was estimated to be
more than 25 g. On a diagnosis of SFO-induced osteomalacia, the
infusion of iron was immediately discontinued, and phosphate and
vitamin D2 (1000 IU/day) were administered. Serum levels of 25-OHD2
increased after 1 week, whereas levels of 1,25-(OH)2D2 did not increase
until 3 months later, accompanied by improvement of renal tubular
reabsorption of phosphate and gradual improvement of the bone pains.
The patient has been doing well for the last 2 years, with normal serum
levels of phosphate, calcium, and alkaline phosphatase, without any
supplementation of phosphate, vitamin D, or iron-containing agents. In
primary culture of neonatal mouse renal tubules, in which 1,25-(OH)2D3
was produced from 25-OHD3 in response to PTH, SFO significantly
inhibited PTH-induced production of 1,25-(OH)2D3 at 30 mumol/L, which
is attainable in the urine of patients receiving a therapeutic
intravenous dose of SFO. Furthermore, SFO decreased the calcium content
and inhibited 45Ca incorporation in cultured fetal mouse parietal bones
at 3 mumol/L. Such SFO concentration may be transiently observed in the
plasma of patients receiving excessive intravenous doses of SFO for a
prolonged period. These in vitro findings together with the clinical
observations suggest that SFO, after filtration through the glomerulus
and reabsorption in the proximal renal tubules, impaired proximal renal
tubular function, such as tubular reabsorption of phosphate and 1
alpha-hydroxylase activity, leading to hypophosphatemic osteomalacia.
Furthermore, it is highly likely that SFO in the peripheral blood, when
transferrin is saturated with iron, may impair bone formation and
aggravate osteomalacia. Although SFO-induced osteomalacia is reversible
simply by discontinuation of the agent, excessive and prolonged
administration of SFO should be avoided.
-------------------------------------------------------------------------------------------
1: Gastroenterology. 1985 Apr;88(4):865-9. Related Articles, Links
Low serum 25-hydroxyvitamin D in hereditary hemochromatosis: relation
to iron status.
Chow LH, Frei JV, Hodsman AB, Valberg LS.
Under normal conditions, vitamin D absorbed from the diet or
synthesized in the skin is transported to the liver where it undergoes
hydroxylation. The purpose of this study was to determine whether
excess hepatic iron affects this process and the subsequent production
of 1,25-dihydroxyvitamin D (1,25-[OH]2D) in the kidney. Mean serum
25-hydroxyvitamin D (25-OHD) concentrations in untreated hereditary
hemochromatosis were 13 +/- 6 (SD) in 9 patients with cirrhosis, 13 +/-
6 in 5 patients with hepatic fibrosis, and 22 +/- 6 in 10 patients with
normal hepatic architecture aside from siderosis and were significantly
lower than the levels found in 24 controls matched for age, sex, and
season, p less than 0.05. The mean serum 25-OHD levels in the two
groups with hemochromatosis and hepatic damage were significantly lower
than the value in the group with normal hepatic architecture, p less
than 0.05. Serum 25-OHD levels in individual patients were inversely
related to the size of body iron stores as measured by exchangeable
body iron, r = -0.64, or serum ferritin, r = -0.47, p less than 0.05.
In 15 patients removal of excess body iron by venesection therapy
produced a significant increase in the mean serum 25-OHD from 20 ng/ml
to 30 ng/ml, p less than 0.05. In contrast, mean serum 1,25-[OH]2D
levels were similar in iron-loaded and control subjects, indicating
that the regulation of this metabolite was intact in patients with
hemochromatosis. The results reveal that the low serum 25-OHD
concentration in patients with hemochromatosis is directly related to
the extent of iron loading and it is improved by venesection therapy.
PMID: 3838288 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
http://health.enotes.com/genetic-disorders-encyclopedia/major-histoco...
Major histocompatibility complex
HLA disease associations
Disease MHC allele Approximate relative risk
Ankylosing spondylitis B27 77?90
Patients with ankylosing spondylitis may have extremely low levels of
25(OH)D.
http://tinyurl.com/8tonv
Celiac disease DR3 + DR7 5?10
A low 25-(OH)D vitamin concentration was a typical biochemical
abnormality in our patients (64% of men and 71% of women).
http://tinyurl.com/b7b9d
Diabetes, Type 1 DR3 5
decreased zinc and 25OHD serum levels in poorly controlled
insulin-dependent (Type I) diabetic patients
http://tinyurl.com/73fsu
Diabetes, Type 1 DR4 5?7
Diabetes, Type 1 DR3 + DR4 20?40
Graves disease DR3 5
[High prevalence of secondary hyperparathyroidism due to vitamin D
insufficiency in Graves' disease]
http://www.hubmed.org/search.cgi?q=25-hydroxyvitamin+D+and+graves
Hemochromatosis A3 6?20
Lupus DR3 1?3
There was a high prevalence of hypovitaminosis D (65.2%),
http://tinyurl.com/8wfws
Multiple sclerosis DR2 2?4
Vitamin D Defends Against MS
http://www.hon.ch/News/HSN/516850.html
Myasthenia gravis B8 2.5?4
Psoriasis vulgaris Cw6 8
These data suggest that exogenous active forms of vitamin D3 are
effective for treatment of psoriasis and that the endogenous
1,25-dihydroxyvitamin D level also may be involved in the development
of this skin disease.
http://tinyurl.com/9c88e
Rheumatoid arthritis DR4 3?6
We suggest that there is a disturbance in vitamin D metabolism in RA.
http://tinyurl.com/df6zv
---------------------------------------------------------------------------------------------
Prabhala, A., R. Garg, and P. Dandona,
Severe myopathy associated with vitamin D deficiency in western New
York.
Arch Intern Med, 2000. 160(8): p. 1199-203.
Five cases of severe myopathy associated with vitamin D deficiency are
described. Each patient was confined to a wheelchair because of
weakness and immobility. Two were elderly, 1 was a 37-year-old African
American with type 1 diabetes mellitus, 1 was being treated for
carcinoid syndrome, and 1 was severely malnourished due to poor oral
intake. In each, weakness had previously been attributed to other
causes, including old age, concomitant diabetic neuropathy, or general
debility. Correct diagnosis was made initially by a high index of
suspicion, following the demonstration of clinical proximal myopathy;
confirmation was made by the demonstration of low 25-hydroxyvitamin D
and elevated parathyroid hormone concentrations. Treatment with vitamin
D caused a resolution of body aches and pains and a restoration of
normal muscle strength in 4 to 6 weeks. Four patients became fully
mobile and had normal 25-hydroxyvitamin D concentrations, and the fifth
also became mobile. In the 4 fully recovered cases, parathyroid hormone
levels on follow-up were lower but still elevated. This finding
suggests a degree of autonomy of parathyroid secretion known to occur
in cases of long-standing vitamin D deficiency. Myopathy, due to
chronic vitamin D deficiency, probably contributes to immobility and
ill health in a significant number of patients in the northern United
States. An awareness of this condition may significantly improve
mobility and quality of life in patient populations vulnerable to
vitamin D deficiency.
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://jesuswasavegetarian.7h.com
Man Is A Herbivore!
http://pages.ivillage.com/ironjustice/manisaherbivore
DEAD PEOPLE WALKING
http://pages.ivillage.com/ironjustice/deadpeoplewalking
jva02@yahoo.com - 19 Jan 2006 17:40 GMT
Here's what I know:
I'm 40. For 15 years, my ankle pain got progressively worse.
Instead of investigating the cause, doctors gave me pain killers, vioxx
and told me I had flat feet. Then I ran into a great doctor who found
my feritin level was over 1000.
After one and a half years of weekly hlebotomies, my iron, saturation
level and feritin levels were brought to normal levels. I now just
need to give blood about four times a year.
My ankle-pain is gone. It's amazing. ;-)
ironjustice@aol.com - 19 Jan 2006 18:19 GMT
>>After one and a half years of weekly hlebotomies, my iron, saturation
level and feritin levels were brought to normal levels. I now just
need to give blood about four times a year.
My ankle-pain is gone. It's amazing. ;-)<<
How are the .. headaches ..
Some guy over on the iron list is giving blood three times a week ..
Must be freaked out ..
<<snip>>
Depending on the level of iron overload, people living with HH may
donate blood more than once a week.
<<snip>>
http://www.duckandcats.com/may99.htm
Sylv - 19 Jan 2006 18:20 GMT
> Then I ran into a great doctor who found
>my feritin level was over 1000.
Do you have hemochromatosis, the genetic disease that causes a build-up
of iron in the body? If not, did they tell you what was causing the
iron excess?
I like it when doctors look for the cause of pain rather than just
passing out the prescriptions.
Sylvia
jva02@yahoo.com - 05 Feb 2006 15:51 GMT
> > Then I ran into a great doctor who found
> >my feritin level was over 1000.
[quoted text clipped - 7 lines]
>
> Sylvia
Sorry for the long response.
I was wrong about the feritin level. I pulled out the lab work.
It was actually 5,100. Yep, it's hemochromatosis.
As for the headaches, it's a strange story, but indirectly, that's how
the hemochromatosis was found. I started getting migraines about
4 years ago. I went to a doctor that sent me to a neurologist, who did
an MRI... which showed a brain tumor in my temporal lobe. I had
surgery
a week later. The first pathology was one of those "you have a year to
live"
things. It turned out to be benign (Thank you Lord).
Long road to becoming a productive citizen again.
Anyway, the also showed my brain was discolored - iron penetrates the
blood barrier. For the kicker, the migraines are caused by alergies to
MSG and other stuff. But I don't get them as much as I did with high
iron.
John