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Old 09-25-2010, 06:46 AM
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mrsD mrsD is offline
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Join Date: Aug 2006
Location: Great Lakes
Posts: 33,508
15 yr Member
mrsD mrsD is offline
Wisest Elder Ever
mrsD's Avatar
 
Join Date: Aug 2006
Location: Great Lakes
Posts: 33,508
15 yr Member
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Back in 1999 we were all on the "older format" at BT, some of us that is...

rose appeared there with her experience with low B12, and she used to provide the AMA Journal paper by Dr. Chris Snow MD which appeared that year and was a turning point for medicine in this country, for interpreting serum B12 levels. For a while this paper was only available to members of the AMA and it was not online. Rose sent me that article thru the mail, back then as she did for many other posters.

Well, that article is now available online and here is the link to it:
http://archinte.ama-assn.org/cgi/con...ll/159/12/1289
Quote:
As discussed above, patients with Cbl deficiency may have overt neurologic disease in the absence of hematologic findings. Patients with neurologic symptoms and signs and a normal complete blood cell count require a modified diagnostic approach because of several considerations. First, folate deficiency is an unlikely cause of neurologic disease. Second, the neurologic disease of Cbl deficiency may be irreversible if treatment is withheld or delayed; because Cbl therapy is nontoxic, the risk-benefit ratio favors treatment in questionable cases. Finally, an apparent response to therapy (or lack of response to therapy) is less definitive in ruling in or ruling out Cbl deficiency than is the serial measurement of abnormal initial hematologic parameters. Even in patients with a normal complete blood cell count, it may be worthwhile to monitor the MCV after treatment because a significant decline within the normal range provides additional evidence of Cbl deficiency.

An approach to the diagnosis of Cbl deficiency in patients with isolated neurologic findings is outlined in Figure 4. Relevant to the development of this algorithm is a study23 of 419 patients with Cbl deficiency, 12 of whom had serum Cbl levels greater than 148 pmol/L (200 pg/mL). All 12 had elevated levels of serum Hcy and serum MMA. Five patients with normal serum Cbl levels had neurologic disease, and 1 of the 5 had a level greater than 221 pmol/L (300 pg/mL). All 5 patients had a clinical neurologic response to Cbl therapy and normalization of metabolite levels.
(note: picomoles is a European and other country lab report, and we use pg/ml in US-- this link explains how to convert them:
http://neurotalk.psychcentral.com/post627358-43.html )

This article is often quoted in the bibliographies of other papers now, so it is nice to have it to refer to. Some of the information and graphs in it were picked up by AAFP, in their online reference for doctors, in 2003. I gave that link in the first post on this thread, so I won't repeat it here.

Over the years the formulas for oral B12 have changed. I have yet to see the new enhanced absorption one yet, but I understand it is coming. Methyl B12 (bioactive form) oral is available now and it supercedes the cyano (which is not active and is synthetic) by far. Methyl B12 is also available by injection from compounding pharmacies and is mostly used by the autism community, but any doctor can order it.

Also parallel discoveries in pharmaceutical dosage forms and bioavailability about microgram absorption of drugs failing when food is present in the GI tract (esp. fiber) have not yet trickled over to oral B12 recommendations, we often see in papers.
Thyroid and digoxin have been found to not be absorbed when food is present, so now carry the recommendation to take on an empty stomach. Since the oral forms of B12 are in micrograms also, and since they are passively absorbed orally, this recommendation I think should apply to them. Testing for intrinsic factor (the Schilling's test) has been dropped by many labs today. So many doctors and patients have no idea if they have working intrinsic factor or not. The antibody test to parietal cells is sometimes used but it is expensive and often not done either. When intrinsic factor is working, oral B12 will be absorbed better. But when people present with significant neurological symptoms one has to wonder if intrinsic factor is NOT working as it should. So expecting only passive absorption of B12 in the intestine is what we have to go on.
The AAFP link has some nice color illustrations to show how B12 is absorbed ideally, so please check that out.
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