Hi
I wonder if anyone could kindly explain about the reticulate test please? I’m on a loading dose of b12 & had this test after 2 injections. Ive had a loading dose before, but quite sure this test didn’t take place last time around?I’ve tried to find information out, but can’t seem to find an answer? Some info seems to be suggest about expecting a reticulate crisis & the count going over range to show the b12 is working?
any ideas gratefully received please…
Many thanks.
Hi,
"I wonder if anyone could kindly explain about the reticulate test please?"
Just wondered if you meant "reticulocyte" test?
A reticulocyte is an immature red blood cell.
The reticulocyte test checks the bone marrow's ability to produce red blood cells.
Link about Reticulocyte test
labtestsonline.org.uk/tests...
NICE published a new B12 deficiency guideline on March 6th 2024.
Worth a look if you haven't already read it.
I left detailed replies in this recent forum thread which might be of interest.
Help Needed! Have I got Pernicious Anaemia?
Thank you sleepy bunny for understanding my very poor spelling! I've read that through thank you,but am still a bit befuddled. Does everyone have this test at this stage? My MCH was above range on 1st test,32.7, lymphocytes below range.
I can't quite work out how test relates to b12 deficiency,in terms of diagnosis or as to whether its checking about response of injections?
Many thanks...
Hi Jo5454. I spent many years performing reticulocyte counts, amongst many others, and it's an easy answer. Reticulocytes [retics] are 'juvenile' red blood cells. They remain retics for about two days, when they mature. Red cells last around 115 days in circulation, before they're removed, mainly by the spleen. So at any one time, the retic count is around 1%-2% of the total. If you're anaemic, a retic count might throw some light on the subject. If you're destroying cells early [a haemolytic anaemia] then your retic count will be raised, so long as your body has enough of everything to keep up with the rate of destruction. There is a lot of spare capacity to do this. If however you run out of folate, for example, then the bone marrow shuts down production and the Hb level falls, sometimes quite rapidly.
If you're B12 or folate deficient, then replacement therapy will cause a spectacular rise in your retic count. Within a few days, we see a sharp rise in the retic count. Waiting to see the Hb rise takes considerably longer, so requesting a retic count a week after starting B12 and/or folate is sensible. It's not performed on every case, every time however. The more anaemic you are, the greater the response. Simply sitting back and waiting for the Hb to rise is the more usual approach, and that's quite normal. However, a retic count will generally tell if you've hit the target with the first shot. In iron deficiency, the same rule applies, but it takes a bit longer for the retic count to rise.
Your MCH was raised at the first test almost certainly due to megaloblastic change in your marrow, and that's related to deficiency of B12 or folate. Treatment of the deficiency will cause the MCH to fall in a few weeks. Another interesting test, part of the FBC [Retic count is an 'extra' test] is the RDW. The Red Cell Distribution Width is a measure of the size distribution of the red cells. Normally, it's around 13.5-16.5. When treatment starts, the new cells are a different size so the RDW increases, and reaches a maximum in a few weeks, as the new cells replace the old ones, then it comes back to normal at around 4 months.
If you donate blood, then your body responds with a brief retic spike to replace the missing cells.
Wow, thank you very much, I hit the jackpot there in getting an explanation. Thank you for taking time to explain and type that all, it’s really interesting.
I had 2 inj before Easter, then had to have 7 days gap before the retic test & 3rd inj, Can I ask why you think my relic count hasn’t risen high like you describe please? It’s 75, bang in middle of normal?I had a bad headache/nausea after 5 days?
My ferritin is 48, though in past an iron profile has shown that at 48 my TIBC on my than one occasion has been way over range at 117, which I’ve been advised means I need to take more iron?
My folate is 7, fairly low in range, I eat healthily, but have ordered some methyl folate as I have the gene which means I don’t absorb folate quite as well.
My lymphocytes were .77, under range on 1st test but had raised to 1 in 2nd test.
I’m concerned due to the retic not rising it may be felt b12 may not be my issue & not a good argument for b12 inj, but the amount of electric shocks & buzzing I’m experiencing down left hand side tells me somethings happening😀(I was diagnosed with functional defic 1st time round, high MMA, homocysteine raised, been trying subs thro covid, but health very poor again.)
Sorry to fire so many more questions, but I’ve really appreciate your response.Thank you…
This isn't as simple as it seems, as there are numerous other factors in play.
Were you anaemic before you started the treatment, and if so, how anaemic? If your Hb wasn't sub-normal then your retic response would be considerably lower. Plus it's possible to miss a peak in response. As we know, many folks diagnosed with 'Pernicious Anaemia' are not anaemic.
If you have a viral infection that can shut down your red cell production to a degree, and there are enough viruses around, aren't there?! [They don't all do it, but there are some common ones that do. Most of the time we're not aware of this, as we recover.]
Recovery from deficiency is complex. Your bone marrow responds in a few days, and sorts out your red cells, although it will take four months to completely replace the old ones. However, the rest of your body, nerves etc can take much longer.
Stick with it. It certainly sounds like you're being listened to, and you have a good doctor.
Thank you once again! My Hb was in the range, not sure if ferritin reading is accurate due to general very poor health after an infection & antibiotics 8 wks ago.
I see, yes, guess could have missed the response, the blood test was 9 days after the 1st inj.
First time around I had to sort it all out with the help of so many good people on here,pay for tests, etc. Guess that’s why I’m keen to feel fully armed this time around, in case I needed to be battle ready, but yes, seem to have been very lucky & found an understanding Dr who’s willing to listen now.
It’s all really fascinating thank you. So I’m thinking now I had a bad spell cple yrs aft starting those inj,mch was raised again, TSH up & ferritin bottom range, so the mch could’ve been due to lack of iron then & not necessarily b12 maybe? That helps a lot in knowing what to watch for in future, I shall take whole jolly lot now & give myself a boost!
So does the raised MCH cause the red cell width to grow? Last Dr never commented on MCH, I’ve just seen it on results.
I must’ve used up my quota of questions now, but it’s really interesting & yve put it in such an understandable way, thank you.Kind regards…
Right-oh, here we go once more, step by step. It's a bit long, but stick with it.
If you're short of iron, you make smaller red cells [microcytes]. These have a lower MCH. If you replace the iron, then you start making bigger cells, and the MCH rises. When you are in a stable state, your RDW will tend towards normal, even if not in the reference range. When your bone marrow starts making new cells that are replete with iron, they'll be normal sized. As you've now got two populations; one iron-deficient and one iron-replete, the RDW increases, and reaches a maximum about half-way through treatment. The same rule applies if you're deficient in B12 or folate, whereas the cells are bigger, MCH higher, and on treatment they get smaller, and the MCH decreases. So, any change in the MCH will be reflected in the MCV and thus the RDW. The MCH and the MCV tell us much the same thing.
If you're not actually anaemic, then you won't get a big spike in your retic count on treatment, but it will possibly increase a bit, for a while. But you are simply replacing old, dodgy cells with new, healthy ones. The macrocytes do actually work just as well as normocytes in terms of oxygen and carbon dioxide transport. Microcytes in iron deficiency work pretty well too.
Whilst all this is going on, your kidneys are monitoring the degree of oxygenation of your blood. If they detect that your oxygen carrying capacity is reduced then they secrete a hormone, Erythropoietin [Epo], and that helps you to make more red cells to recover from the anaemia. Then the Epo secretion shuts down again to normal levels.
So, here we go: if you're anaemic, and deficient, then correcting the deficiency allows you to make more cells and these are retics in the first couple of days, then they mature, but more follow on. If your iron stores are OK but not vast, then treating the B12 or folate deficiency can result in your iron stores being depleted, and you end up iron deficient, so it's important that we are looked after by folks who understand and react to the changes.
Thank you! Firstly, silly me, I did know (in a very basic way I must add) thatlack of iron makes red cells smaller & b12 larger, so think I had a senior moment there, tho was just off for no.5 loading dose so maybe that’ll help!😁
But I certainly didn’t know the reasons why which is what is so very interesting to read, thank you again for taking the time. I’m not sure it’s really ever dawned on me that we have to wait for new cells to be made healthily & in better condition, I was more of the thinking that if I take iron it would plump out & help the ones I’d got floating around,etc!
So when settling back to regulate injections, e.g. are we saying that just after the injection & for however long we’ve got enough for, the new blood cells will be healthy, correct size, etc, but as the time goes on towards next injection and symptoms very often return before this, it’s signalling the blood cells are not looking/being produced as they should again please?
Yes, last time around my ferritin lowered furthered after loading dose,so I’m taking iron & will try methyl folate as soon as arrives!
Can I also ask, if MCH is over range why is MCV not? It was 93, then raised to 97 after 2 injections.
Heaps of thanks & I hope you slept well after a busy day in the office helping us out yesterday😀
Ooh, this is getting technical [as if it wasn't already!] but here we go. In simplified terms. Sorry, but it's a bit wordy and 'done on the fly'.
Red cells are made in the bone marrow. If we have deficiency of B12 or folate, then we have difficulty in making DNA. As cells mature, they divide, so one cell makes two, and so on. They divide when they've made enough DNA to make two sets of chromosomes. If however, they don't quite make enough, they miss out a division and mature, so they're bigger than they would have been. If we have a deficiency of Iron, but everything else is OK, then the precursors can manage another division before maturation, so they're smaller than otherwise. Once a red cell has matured, it's what's known as an 'end cell' so it's no longer capable of further division, as it's lost its nucleus and chromosomes. It still has some DNA in the mitochondria [present in retics] but as the cell matures, the mitochondria go too. so, despite being surrounded by all sorts of goodies, the old red cell is stuck, living on glucose to generate energy, until it gets to around 115 days, give or take. Then, the spleen dismantles the effete red cell and recycles much of the contents. The haem bit of haemoglobin is where the iron resides. The iron is recycled, but the rest of haem is largely discarded, and the breakdown products are coloured. I'll be polite here, but the contents of the toilet bowl rely heavily on red cell breakdown for their colouring...
MCV and MCH: It depends a little on methodology, but if you get a healthy retic response and you're anaemic, then when retics are released, they're actually a bit bigger than mature red cells, but as they mature, they get a bit smaller. The haemoglobin inside them was made before the red cell left the bone marrow. So, the MCH is how much haemoglobin was made in the assembly process. The MCV is how big the cell is, by volume. There's another magic number, the MCHC, which is the mass concentration of Hb within the red cell, as a percentage. If, say, your MCV was 100, and your MCH was 33, your MCHC would be 33. The MCHC tends to around 33 regardless of MCV, unless you're iron deficient, or you have another issue making haemoglobin. In which case the MCHC will be reduced, because the MCH is lower than you'd expect for the MCV. If you're deficient in something and it's replaced then the results will come back to 'normal' but it will take a while, as you're only replacing around 1% of your red cells each day. If you're anaemic, then you make more to address the degree of anaemia.
Hope this helps!
Amaaaazing! So the cells are larger in b12 defic, because they haven’t been able to divide due to lack of making inadequate dna? I feel like trying to draw a picture of it all !
I’m still a little confused, uh oh!😀and maybe I just need to read it a few more times & it’s my error…if we are deficient in iron too, but the red cells lacking in b12 can’t go on any further what happens then regarding iron? The only way we could see smaller cells due to iron deficiency would be if we are topped up with adequate b12? If that question makes any sense please?
Thank you for the mch explanation too, that’s really helpful. All truly fascinating.
Right-oh; here's another term for you: Nuclear/cytoplasmic asynchrony. So, the cell matures when it's got mature cytoplasm. The nucleus is busy making more DNA to get to '2N' chromosomes, but if it fails, and gets to more than 1N but less than 2N, it can't divide, the cytoplasm matures, and the cell leaves the marrow, minus nucleus, and bigger.
If on the other hand, there's not enough iron to go round, then there's less Hb being made, and the cell might manage another division. However, if you've got multiple deficiencies, then the Iron deficiency and the B12 deficiency result in somewhere in-between. So, your red cell precursors are busily trying to make Hb. They can make globin chains, they can make various bits of haem, but if there's not enough iron, they can't actually make 'complete' haemoglobin. But they're trying their best!
Got you,I hope, thank you! So with multiple deficiencies of b12 & iron,you are reliant onHb result being lower to give an idea of iron deficiency,rather than size of cell necessarily? Also read back & you mention folate def can cause the increase in size also, would you consider a bottom of range folate blood result to possibly mean deficiency, or are we talking of it needing to be well under? Or maybe again,it's like the b12 serum level,what is considered normal range, doesn't fit all?
My word its a fascinating,but incredibly complex world going on inside us isn't it!
Thank you so much for explaining all of this, this site is very lucky to have you, you have incredible knowledge & the patience of a Saint. I shall gradually read back thro your other replies too. I do have a question about TIBC & ferritin,but will post that separately another day! Kind regards...
Thank you for your kind words. It keeps my brain active as well, so I don't mind.
B12 and folate are both important in DNA synthesis. The shortage of either will result in megaloblastic change in the bone marrow. From a lab point of view, it's impossible to discriminate between the two substances when we encounter a macrocytic anaemia, which is why we have the assays available. We would normally do both B12 and folate, but we might actually measure red cell folate too, because the result isn't as reliant on recent folate intake. When you have megaloblastic change in the marrow, that results in macrocytosis in the peripheral blood. When you have iron deficiency, your bone marrow will have micronormoblastic changes and that results in a microcytic hypochromic anaemia.
Let me have a guess at ferritin, TIBC, serum iron etc.
Ferritin is a storage protein for iron. The 'end stage' for iron storage is deposition in bone and tissues, and the ferritin is converted to haemosiderin. Transferrin is a transport protein for iron. The TIBC [total iron binding capacity] is a measure of the total capacity that your transferrin has. Serum iron is a reflection of the amount of iron being carried by transferrin, and TIBC is in effect the spare iron carrying capacity. In iron deficiency, the actual total amount of transferrin is usually increased. The saturation is reduced. So, serum Iron and TIBC is a classical way of detecting Iron Deficiency. Ferritin measurement has fewer technical problems than Iron and TIBC. To complicate matters, Ferritin is an acute phase reactant, to levels increase in inflammatory conditions, so it's not infallible. It goes up and down without your iron status changing. Some laboratories stopped measuring Iron and TIBC when assays for serum Ferritin became available. We learned to accept the changes, but there is still a role for both. There are yet other tests for measuring Iron status, but I'll leave those until someone brings one up!
Thanks heaps, that's a marvellous explanation once again! I'll put a question about iron results on main post as I have a few more asks about it!
So you may wish to go on holiday for a few days for a break
Not sure I phrased that quite rightbFlipperTD! I meant seeing as I’d gone onto another theme had better start another post, so that it helps folk looking for iron answers as know your interesting information tends to generate further questions & interest. Reading that back, could sound like I was telling you to pack your suitcase! Oh dear, I know what I mean these days, but that doesn’t mean others do🤪Maybe jab 6 will help today🙂
“When I use a word,” Humpty Dumpty said, in rather a scornful tone, “it means just what I choose it to mean – neither more nor less.” [Thank you, Lewis Carroll]
Oh, if only I could pack my suitcase. I've got other appointments filling the time up, but soon, I hope to get a chance!
Enjoy jab 6. It'll do you a power of good.
🙂Thats made me smile thank you! Yes,we have a lot to thank Lewis Carroll for. Think I may be more in line with old Bagpuss,yawning at the moment, than the wise Cheshire cat,but as those busy little mice sang,'We will fix it!'...hope that holiday arrives sooner than later!
Unless youve packed yr bags & left the building already,its me again! I've been looking at red cell folate tests you mentioned,do you think a pinprick test is sufficient for testing this please? I'm concerned now that low folate could be an issue after mine was bottom of range,non-fasting test & wonder if I should investigate further before trying methylfolate? I was on monthly injections previously & seems I struggled then to keep well,better for fortnight each time & hard to keep MCH down,so am wondering if folate is also an issue, I do have the gene that has part difficulty in absorbing. I'm awaiting to hear the regularity of injections this time & just trying to get as much info before I do! Many thanks once again.
Red Cell Folate isn't done in all labs that measure serum folate for a few reasons too tedious to cover here. It is typically done from an EDTA [FBC] sample, and they're better from venous samples. If it was my lab, I wouldn't encourage folks to do fingerprick red cell folate samples, as life's difficult enough already.
Thank you! I'll keep looking for somewhere venous then! One hole in arm is prob preferable to 4 fingers on a not so good attempt😀
That's about the level of it. One hole but a good one, rather than every fingertip. More nerve endings in your fingers than in your antecubital fossa [inside your elbow] so you tend to feel fingerpricks much more than the work of a skilled needle-pusher.
Thank you...know youve said aside from the red cell folate theres little way of differentiarungg between MCH causing b12 or folate deficiency. On further reading found articles saying thyroid dysfunction may cause MCH to be raised too.
Is there a way you are to tell this within the blood, or is it simply (who am I kidding,none of this is simple:)!) the fact that b12 & folate are all tied in with thyroid problems & it's an indicator in this sense please?
I've tend to steer clear of the macrocytosis that can be found in thyroid disorders, as I'm not really up to speed with it. I know it happens, but I don't know the answer. If you consult a 'Metabolic Map' [the Nicholson Metabolic Map is quite enough to blow your mind] then the interlinking of all the processes does make you realise how complex these things are, and they're probably more complicated than that. And more complicated still.
Yep, my mind has been blown! Resembles something of a complex London underground map and some & a very confusing some at that! Thank you,but if you find it complex there's little hope of me deciphering it,but on a better day when eyes haven't desserted me as well as brain, I will be interested to have another look. Have contacted some places abt red cell folate test,awaiting replies,but it's def not as common as the serum folate. Failing that it will be throwing methylfolate,b12 at it,along with other homocysteine requirements & see what happens.
Thank you again for the tremendous amount of time you've shared this week helping. If we could dvide you up,like all this cell division & have 1 of you at all the medical centres in the country,it would be a far better & unstood place. ⭐
Thank you! Donald Nicholson's map is bewilderingly complicated. My only connections to it are 1. having a copy, and 2. knowing the department where he worked. It is a case of finding the bit you're interested in and following it round, and being amazed.
For the biochemistry nerds who would like hardcopy, there is a nice A3 format book with large readable graphics , "Metabolism At A Glance", fourth edition from J.G. Salway on Wiley Blackwell. It is best accompanied with Lehninger's "Principles Of Biochemistry" 8th Edition , a standard text.
The Map: sigmaaldrich.com/deepweb/as...
That is amazing - just off to buy a huge monitor and large format printer...
For the 'Janet and John' end of the market, there's the Biochemists Songbook by Harold Baum, and ideally learning the songs too. Michaelis Menten kinetics is still hard-wired in my head, thanks to Professor Baum.
Thanks FlipperTD, I will check those out, sounds like a fun way to learn!
To Professor Sir Hans Krebs, F.R.S. in honour of his 80th birthday and to my wife Glenda who only nags me for my own good
Page 8
Some of these songs found their way to Sir Hans Krebs in Oxford, who very kindly encouraged me to continue producing them, and subsequently suggested (perhaps not too seriously) that I write an entire Introduction to Biochemistry in this format. My wife had been making a similar suggestion for some time, and the combined encouragement of two such remarkable patrons led to an increase in my scribbling activity —I began to compose on buses Nos. 85, 85A, 14 and 30 as well—and hence to the completion of the present collection. Consequently, only around half of these songs have so far been subject to the test of public performance.
Cheers.
To the tune of 'The Red Flag'...
"The substrate changed by an enzyme, initially, in unit time,
Varies if not in excess,
With substrate concentration, [s]."
Before you know it, you've absorbed the fact that [[V x S] / Km + S] gives you the answer, whether you like it or not. Michaelis Menten kinetics in a song. The songs rhyme and scan.
Can I ask out of interest please, whether you found many who were in range with serum folate test, but folate deficient when checking with the red cell folate test? I'm wondering if its common. I've been advised now to repeat the serum folate & iron test in 8 wks, so not sure what do for the best. Do I forge ahead with private tests,supplements or is it important to see what happens with just the b12 first in terms of how my system is working? Many thanks...
Several questions here, but here goes.
I don't have data for the serum vs red cell folate results, but serum folate responds very quickly to changes in dietary intake of folate. Red cell folate would be much slower than that. I tend to think of it a bit like Blood Sugar versus HbA1c testing. Blood sugar reflects recent intake, whereas HbA1c reflects long-term control because it's bound in the red cell, and as we know, they last 4 months. The usual assumption is that once the B12 injections have started then it's not worth retesting that, and if you were B12 deficient to start with, you don't start folate until your B12 treatment was started. 8 weeks sounds like a reasonable interval, but I'm a humble scientist, not a doctor, so it's guesswork! I still reckon that monitoring the FBC values over time gives a good indication of what's going on.
Good luck!
Many thanks once again. Yes that's a good comparison to blood sugar in terms of short/longer term picture.I guess the only way I will know if it's just a b12 deficiency & not folate too is to hold off supplementation until the 8 wk test & maybe my money will be better spent at that stage doing a FBC to check mch & red cell test then too if needed. Think we 're only offered a folate & iron test by nhs at that stage,but I can always ask! Guess I'd be better too waiting until that stage to do an iron profile. I have raised homocysteine so had intended to get on & take folate with zinc,b6, but perhaps better do it one stage at a time.
Thanks once more.
If you've been started on B12 then folate is a good idea, especially with a raised homocysteine.
Good luck.
Yes,I guess actually,maybe best to just get on with it, then when they test in 8 wks at least I'll know if its helped raise levels. Gosh, what a ditherer I've become,bring back my head! Thank you.
Dithering's good. You're thinking about what's going on. Keep Calm and Carry On. With the way things are going, we might be needing those signs... But I don't think so!
Thanks,next time I'm told I'm dithering I'll remember that! Go through the tunnel & aim for the light,but don't keep bashing head into the sides also springs to mind.!
Listen, just in case the light at the end is on the front of an approaching train. Or it might just be someone bringing more work, and carrying a torch. If it's a canal tunnel and you're 'legging' the boat through the tunnel, just keep on.
I'd never actually considered the light being an oncoming train it was enough to be in the dark,damp tunnel😂 but once again,you've made us think & yes absolutely,just keep on!
I've wondered why in the old days of horse-drawn barges, the bargees didn't encourage the horses to lay on their backs and 'walk' the barge through the tunnel? Or, given that horses can swim, maybe tow the barge that way. Although I suspect that many of the canals aren't really deep enough for horse swimming, This is getting very, very silly! I suspect that the thought police will now be after me.
😆They missed a trick there! Never mind the thought police, I'd watch out for the herds of horses marching your way wielding placards!Oh well, after we all worked hard with our science lessons last wk,we deserve a smile!
All good reading here, so even though I wasn't diagnosed with PA I knew something was wrong with me, a blood test showed I had B12 issues, even though I've had no type of infections, but I've always had stomach issues over the years, and numerous general anesthetics, even taking omeprazole for long periods, I can't do without my 3 monthly injection and once had to take a course of folic acid tablets to help with worsening symptoms, so surly I'm classed as someone who's pernicious anemia but never given this title??? Or is it general layman's terms used to describe B12 deficiency???
Pernicious Anaemia is a specific condition which results in a low B12, so PA is a cause of B12 deficiency. A deficiency of B12 can however occur due to other reasons. Dietary B12 deficiency can occur, and should respond to a change in diet. A dietary B12 deficiency will respond to B12 injections, but a revision of diet would fix it too, although B12 in the syringe will fix it quicker! There are other causes too, for example the Fish Tapeworm, diphyllobothrium latum, is a competitor for B12, and pinches the B12 from your gut before you get chance to absorb it. We were all taught about it in our lectures, but never actually [or knowingly] came across a case in the UK, but that's not to say it doesn't happen.
So, B12 deficiency MIGHT be due to PA, but then again, it might not be. It requires further investigations to be certain, and that's beyond the scope of this site.
Helicobacteur Pylori can be another cause, can’t it that can be ruled out,
Functional b12 deficiency,bas I was diagnosed with, was down to low Active b12/high MMA, but I’ve only had 1 intrinsic factor test, negative and seems it can take several tries before P.A shows up…
Thanks for that.
Some folks never actually develop Intrinsic Factor antibodies that we can measure but it doesn't stop them having PA. IFAb-negative PA probably accounts for around 50% of the total. Our old friend the Schilling Tests were helpful, complicated, expensive and still fault-prone if they weren't done properly, but they've gone the way of the Dodo and the Dinosaurs, I'm afraid.
Helicobacter Pylori is horrible, and common, but at least it's detectable and treatable.
I was actually treated for that many years ago with a course of antibiotics after a stomach bleed , maybe this was the initial start of my issues , thanks for your helpful advice 🙂
Sounds like it could well be. Have you been tested recently for HPylori? You mention general anaesthetics,flipperTD or someone else may be able to clarify it, but I’m sure I’ve read that b12s ability to be absorbed can be switched off by anaesthetic, linking to use of nitric oxide? Don’t quote me, until I try to find out more! Sorry you’re having such problems…
No more tests for that complaint , I believed that you couldn't get this condition again if treated, but I'm unsure about this, yes I've mentioned about the general anesthetics myself and I've had numerous operations under a general anesthetic and maybe this has caused my deficiency issues, your posts have been highly informative, thanks again for getting back, and hopefully more people can understand this condition 😀 👍
That's a nice thought only being able to get HP once. I've had a Google & seems that it is unlikely for more than once,but does mention it could bevposs to get a different strain? I'm sure I've read on here before of folk getting it more than once, but how likely that is,I've no idea.Maybe that's partly one reasonwhy b12 def seems to be more common with more use of gen anaesthetics? I'm thinking if I need a planned op I'd make sure I'm well stocked up.of b12 before & after,some way or other, if poss to be on safe side!
Unless the cause can be found with this def & reversed, then otherwise guess we have to focus on getting the right treatment, but often easier said than done,isnt it!
Thanks for yr kind words & hope you soon get answers.
Oh I didn't know there's different strains, I was told after my stomach bleed I'd have to stay on omeprazole for the rest of my life, however I only take it when I have a bout of acid reflux, or indigestion as some folk call it, I think they're using different gasses in the general anesthetics these days, I'm not 100% sure though, obviously there's a link between omeprazole or antacid medication that causes problems with absorption, obviously I've fallen into a certain group of people who were suspected to have B12 issues due to the links on many of the reasons ,I've required the injections for several years now, I think I'd be struggling without them, once again thank you for your input on this subject 🤗
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