This first article describes one cause of B12 deficiency (other than PA) as gastritis that is 'where the patient produces antibodies that destroy either the Parietal Cells or Intrinsic Factor or both.' So is this very much different in reality to actual PA which is described in the article below as more accurately 'Autoimmune Metaplastic Atrophic Gastritis'. i.e. they are both B12 deficiencies, one caused by autoimmune antibodies affecting the Parietal cells, and the other (true PA) caused by autoimmune antibodies affecting the intrinsic factor?
AMAG is one type of atrophic gastritis - an autoimmune type.as it particularly attacks the mechanisms that allow B12 to be absorbed in the terminal ileum it will lead to B12 deficiency.
Other types of atrophic gastritis may not affect B12 absorption so dramatically and some are curable and the damage can be reversed (though I think there is quite a lot of evidence that they can also lead to AMAG/there is a cross-over).
As AMAG is auto-immune it can be treated but it can't be cured.
The first articleis about the causes of B12 deficiency, including dietary deficiency.
The second article is specifically about AMAG
B12 deficiency has the same symptoms whatever the cause but it can have different causes. Different causes have different consequences and treatments. Some have other consequences.
Thanks. I'm kind of with you. Up until the point that there is a type of autoimmune gastritis, where there are parietal cell antibodies, so this presumably also can't be cured? It seems the only difference is in PA, autoimmune antibodies attack the IF, and in the other autoimmune antibodies attack the Parietal Cells that produce the IF. (notwithstanding that gastritis has other causes other than autoimmune).
the auto-immune gastritis that produces PC antibodies is PA. PCA isn't recommended as a test by the WHO as there are problems with both sensitivity and specificity - ie it gives a high rate of false positivesl
OK, so PA can be caused by either IF antibodies attacking the IF, or PC antibodies attacking the Parietal cells? But PC antibodies can also be caused by other things. So to confirm the pc antibodies type of PA, what else would need to be tested to be sure?
Don't think PCA are caused by other things just that its difficult to distinguish PCA from other metabolites which is what leads to false positives.If you have a positive for IF then it is extremely unlikely you don't have PA.
They are looking into a test using gastrin levels though I don't think its a widespread test yet.
I'm positive PCA, negative IF, borderline low B12 (most recent 292). Have started injections under care of a private doctor. But trying to work out what exactly is the root issue. Hoping to get an NHS referral to a gastroenterologist.
PCA is not recommended as a diagnostic test for PA in UK.
It is still possible to have PA with a negative result in IFA or PCA test.
I came across some local B12 deficiency guidelines recently that suggested a small percentage of people with PA are negative for both IFA and PCA antibodies.
Mine too I think. I do have some questions to ask when I go back for my follow up - a discussion like on this thread is something I want to have with him ideally.
I think it is all very confusing, and I strongly feel that a major step towards getting B12 issues recognised and understood more would be if the naming / classification of types of issue was overhauled.
I really suspect that if you say ‘B12 deficiency’ to an average person (or to an average medical practitioner), the first assumption is that you just have a bad diet, and the second is that you have pernicious anaemia (with full-blown anaemia / blood cell issues).
I have been thinking about what a new system of naming it should be like. I think the term ‘pernicious anaemia’ should be got rid of, and ‘B12 deficiency’ should be limited to a proven nutritional deficit / dietary cause, without absorption /transport / storage components..
I think all B12 issues are just not taken seriously because of the commonly held view of the term ‘deficiency’.
Some initial thoughts included:
B12 Pathway Disorder Type 1 (B12 PD Type 1) (maybe Type 1 could be ‘absorption’, as seems to be most common reason??)
B12 Pathway Disorder Type 2 (B12PD Type 2) (maybe Type 2 could be transport and/or storage??)
... and the ‘Type’ could be subdivided into Type 1a or 1b or 1c etc to signify what are the primary manifestations... eg haematological (macrocyclic anaemia), neurological, neuromuscular, or a combination.. eg Type 1bc???
I think whatever system would need to be expanded to accommodate cross-over situations (eg I have strong suspicions that long term functional deficiency results in a degradation of the body’s ability.to absorb, (and possibly to store???) so there should be a category (or two) that relate to absorption and transport (and storage)?? Or absorption and transport??
Or prefixes could be used... perhaps ‘autoimmune’ ‘acquired’ inherited’ or ‘multiple’ (for those cross-over situations).
So:
Eg... Autoimmune B12 Pathway Disorder type 1 bc
Now - I am not a medical professional, and have not given this much thought at all, but I think it is definitely worthy of discussion / debate. Any other suggestions / ideas welcomed!
I have just realised I have hijacked the thread / gone off tangent (I sincerely apologise for this), I suspect I lack a bit of confidence! I might try and paste it into a new thread later today when I am back in front of my laptop Sorry!!
From my point of view, a B12 deficiency caused by autoimmune antibodies to Parietal Cells causing gastritis seems very similar indeed to a B12 deficiency caused by autoimmune antibodies to IF i.e. true Pernicious Anaemia, which the PAS suggest should be renamed AMAG. I wasn't sure if I was missing something obvious but I don't think I am.
There's a few diseases like this and I seem to get them all 😆 (PCOS, it's an endocrine disorder that sometimes affects the ovaries causing cysts, but not always, it really needs a rebrand as well).
Personally doubt it would help. It doesn't help with the clasification of diabetes where GPs tend to be aware of just type 1 and type 2 and miss out on a whole range of fringe types - and even if they recognise them tend to have an amazingly poor grasp of them. I remember being told by a hospital consultant that MODY was a type 2 diabetes - it isn't it is much closer to type 1 and even there there are at least 14 different sub-types of MODY. Admittedly the consultant was not an endocrinologist but given the range of disorders covered by endocrinologists I wouldn't be surprised to come across a specialist who came out with the same nonsense about MODY (Mature onset diabetes of the Young).
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Sorry!!
PA with no antibodies?
Gut Instinct
Confusing biopsy results
