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Old 11-04-2006, 01:59 AM
Moyvore Moyvore is offline
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Join Date: Nov 2006
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There have been an number of recent articles in the medical literature in effect endorsing your years of posts about B12 misdiagnosis:

Cobalamin-responsive disorders in the ambulatory care setting: unreliability of cobalamin, methylmalonic acid, and homocysteine testing.

Solomon LR. Department of Medicine, Yale University Health Services

(Full text, with link to free pdf file)

Editorial comment on Solomon, same journal:

Unreliability of current assays to detect cobalamin deficiency: "nothing gold can stay"

Responses and rejoinder:

To the editor:
Cobalamin-responsive disorders and unreliability of cobalamin, methylmalonic acid, and homocysteine testing

To the editor:
Is testing for clinical cobalamin deficiency truly unreliable?

A subsequent UK confirmation:

Haematologica. 2006 Feb;91(2):231-4.

The limited value of methylmalonic acid, homocysteine and holotranscobalamin in the diagnosis of early B12 deficiency.

"The symptomatic effects of high dose B12 therapy
warrant further investigation in larger studies. Our findings
are in keeping with the recent report by Solomon
that the metabolite markers MMA and tHCY cannot be
regarded as the gold standards for assessing B12 deficiency."

There have been reports describing B12 deficiency with high serum B12 levels in immunological or kidney issues.

Eur Neurol. 2006;56(1):62-5.

Chronic renal failure promotes severe variant of vitamin B12 deficiency
(Letter, no abstract provided)

"The vitamin B 12 deficiency in patients with chronic renal insufficiency is however much more difficult to assess and poorly understood. There is evidence that patients with renal dysfunction might develop a vitamin B 12 resistance [10] . Here we report a foudroyant case of SCD [subacute combined degeneration] with severe affection of the white matter of the brain and spinal cord in a patient with chronic renal failure."

"The patient had been on vitamin B 12 supplementation for 2 years (1,000  g/month).

"In conclusion, severe SCD courses combined with epilepsy, cognitive decline and reduced vigilance, and normal levels of vitamin B 12 , homocysteine and MMA
should be considered in the spectrum of cobalamin-deficiency-associated neurological disorders, especially in patients with chronic renal failure. Such fulminant
courses of the disease might be related to a generalized resistance to vitamin B 12 in such patients and may require earlier and much larger therapeutic cobalamin doses than previously considered."

[10] was:

Nephron Clin Pract. 2005;99(2):c42-8. .

Cellular uptake of vitamin B12 in patients with chronic renal failure.

"...CONCLUSIONS: Our results show that vitamin B12 uptake is impaired in [mononuclear cells] from renal patients, with no evidence that the surface receptor is down-regulated. High serum concentrations of holoTC [holo-transcobalamin] are common in renal patients and might be related to a generalized resistance to this vitamin. Serum concentrations of vitamin B12 within the reference range are not likely to ensure vitamin delivery into the cells. Supraphysiological doses of vitamin B12 may be necessary to deliver a sufficient amount of the vitamins to the cells via mechanisms largely independent of holoTC receptor."

I wonder if you have noted any poster on this List with B12 issues (masked or not) has reported either a diminished sense of thirst (noted camel effect) and or sporatically (or constantly) elevated blood urea nitrogen levels (BUN). It turns out that diminished kidney function (which may be associated with reduced fluid intake) apparently can have a material influence on B12 serum to tissue transfer.

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