Good morning
I work in the NHS predominantly with elderly patients . Since the pandemic all my patients have been prescribed oral b12. Many of these patient still have b12D symptoms but the GPS are adamant that because their blood results improve on oral that they are no longer deficient. My question is if blood serum improves on b12 oral are they being absorbed and are these patients are no longer deficient?
I am not an expert, and I am sure there will be other replies from other members of the forum who know much more than I do.
But - I have a diagnosed functional B12 deficiency, which means that although I can get b12 into my blood stream, I can’t seem to be able to either transport it / access it or store it… so even if my serum total B12 levels appear normal, at a cellular level I am deficient (shown by high levels of metabolites (Methylmalonic acid (in my case), and homocysteine). So a proportion of your patients may be functionally deficient - ie not able to transport, access or store B12 - but can appear to have ‘normal’ total serum B12. MMA (methylmalonic acid) and homocysteine tests only seem to be authorised by hospitals, not by GPs, so I imagine that probably 95 per cent of people with a functional B12 deficiency probably don’t know about it. For me, only injections of hydroxocobalamin work… I was on the maximum dose of cyanocobalamin tablets for 2 months but still had high MMA.
Other reasons probably include the difference between total B12 and active B12. In my experience, only total B12 serum levels are ever tested, which includes B12 that is not ‘bioavailable’ or ‘active’, plus the ‘active’ B12. It may be that some of your patients have very low ‘active’ B12 levels, which are being masked by the high total B12 serum level.
I am sure that there could be other reasons, and I am sure someone else more knowledgeable will be along soon!
Thing is, B12 deficiency is such a complex matter yet we're working up against a system with limited time or knowledge to address it correctly.
Each patient will have a different story, reason, timeline for deficiency. Some of them may even have been quite anaemic. Everyone needs to get injections to get the levels up quickly and thoroughly - something tablets or sublinguals aren't capable of doing.
After they've been loaded up, they need maintenance to keep the levels high and let the B12 get back into cells over time.
Then, on top of that, if they have absorption issues, then swallowing tablets is unlikely to really do much of anything at all when it comes to B12. It could do for some, but if they do have PA then they may aswell eat a boiled sweet instead. At least that would give them a suger boost and taste of something - but the pills would be doing exactly the same thing (i.e. nothing to address their deficiencies).
GP's only work off numbers - they don't know enough about B12 to delve any deeper. They haven't received nearly enough training and are only looking out for anaemia.
So if the pills are 'increasing their numbers' then your patients could well be absorbing the B12. But if they didn't get loading doses and have ongoing symptoms then the oral isn't going to be enough to keep the healing going.
In essence, oral does not work as well as injection. Injection bypasses any risk of absorption issue and floods the blood with B12. Oral has a much lower absorption process but oral is also divided into sublingul and tablet. And if it's tablet it's usually a low dose. In which case you'd be better off giving them a boiled sweet for all the good it's doing.
Hi Kapat1,
Thank you for taking an interest and showing concern about the patients you care for.
Firstly, doctors should not be testing serum B12 blood once treatment has started according to the British Haematological Society. So, Dr C, GP in Essex would not that save you time and money ? (This is in reference to a previous post).
Like Pickle500 and Dilly_blue have said we are no experts but serum testing is just that. No idea what’s happening at cellular level. Doctors are not trained in pharmacokinetics or pharmacodynamics that’s your chemists, mathematicians, biochemists and pharmacists.
But when I worked for the NHS whenever I gave a medication, twenty minutes or so later I would follow up and either ask the question, Are you still in pain or the like. Or with informed consent, test the effectiveness of the medication. I’d write in the notes the action the drug had had and the comfort of the person I cared for. If it hadn’t worked then I’d offer something else.
Best wishes
relatively small scale study in Switzerland about 8 years ago, concluding that oral is inferior to IM when looking at secondary markers.Truth is, oral works for some but not for everyone and as there is no way of knowing who falls into which class I would think it would be inadvisable to use oral as the primary treatment on a routine basis
When B12 enters the mouth it is joined to a substance called haptocarrin. Haptocarrin s job is to protect B12 from stomach acid until it gets to the ilium. There intrinsic factor separates it from the haptocarrin and joins it to trans cobalamin 2. This substance enables the cobalamin to be used by the cells. Joined to haptocarrin it is totally useless to the cells. If you have a problem with producing intrinsic factor then all that happens is that the B12 circulates round the body joined to haptocarrin uselessly. So no amount of testing B12 serum levels will tell you if there is a deficiency or if there’s an absorption problem.
Similarly, if you have a problem producing haptocorrin - from saliva glands - when eating, your B12 source ( extrinsic factor, from food ) would not have the protection it requires.
The advice given to GPs is not to retest B12 once a deficiency has been found and injections started. BCSH, NICE, BNF - they all say the same thing. Should be enough, shouldn't it ?
The only time when I can see the necessity for retesting (along with other tests) is if the injected B12 is seen NOT to be effective - if MMA is building up in the bloodstream alongside the introduced B12, it would imply a connection is not taking place that will transport to cell and tissue level. Functional B12 deficiency - if renal problems and small intestine bacterial overgrowth (SIBO) ruled out as causes.
The BMJ research document - summary below - demonstrates that it’s symptoms not numbers that are important and, hopefully, GPs will be able to access the full document (behind a paywall).
At the bottom of page 4 ' under 'Parental Treatment' :
…………..
"Parenteral treatment
"Data from randomised controlled trials and observational studies for parenteral treatment are lacking; however, the expert consensus for standard treatment in the United Kingdom is to begin parenteral treatment with intramuscular hydroxocobalamin. This bypasses the possibility of the debate about whether the treatment will be adequately taken, absorbed, and metabolised.
Standard initial treatment for patients without neurological involvement is 1000 μg intramuscularly three times a week for two weeks.
If there are neurological symptoms then 1000 μg intramuscularly on alternate days should be continued for up to three weeks or until there is no further improvement. In irreversible cases, for example, pernicious anaemia, the treatment should be continued for life. "
…………..
Also at the bottom of page 4 ' under, 'How is Response to treatment assessed'), it outlines that, once treatment is given, blood levels will inevitably increase but it is the clinical condition of the patient that is important:
"Cobalamin and holotranscobalamin levels are not helpful because they increase with vitamin B12 influx regardless of the effectiveness of treatment, and retesting is not usually required."
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