I would like to hear other members thoughts on questions I have about the current understanding of parietal cell loss, either due to autoimmune antibodies, or atrophic gastritis.
I gather that it is currently believed that Pernicious Anemia patients can still access their liver store of B12, despite having either Parietal Cell or Intrinsic Factor autoimmune antibodies, and that the maintenance injection supplies adequate B12 to last the patient until their next injection. However, this biliary B12 is not instantly accessible but has to be picked up from bile by IF to be reabsorbed following enterohepatic circulation.
Now, it would seem reasonable to question how a patient is able to access biliary B12 if:
1) They have IF antibodies
2) They have Parietal Cell antibodies preventing them from producing IF
3) They have no IF due to the loss of the parietal cells.
It is also increasingly being seen that patients are developing gastric atrophy, leading to achlorhydria, following longterm use of acid-suppressant medicines. Surely, if the parietal cells have atrophied, they are not producing either hydrochloric acid or IF so there is no way for these patients to access their biliary B12?
It is also thought that patients whose sole problem is achlorhydria can access 'free' B12 in supplements since hydrochloric acid is not necessary to do so, but it is claimed that they can also access their liver store. However, no explanation is given of how this can be done since they will need IF to access the biliary B12 and, of course, if their parietal cells have atrophied then they are not producing IF.
I had asked a prominent UK gastroenterologist to comment on this subject and, although he agreed to do so, he has not given his comments so I can only assume he had no answer. I would really appreciate to hear what others think about this issue.
I gather that it is currently believed that Pernicious Anemia patients can still access their liver store of B12, despite having either Parietal Cell or Intrinsic Factor autoimmune antibodies, and that the maintenance injection supplies adequate B12 to last the patient until their next injection. However, this biliary B12 is not instantly accessible but has to be picked up from bile by IF to be reabsorbed following enterohepatic circulation.
Now, it would seem reasonable to question how a patient is able to access biliary B12 if:
1) They have IF antibodies
2) They have Parietal Cell antibodies preventing them from producing IF
3) They have no IF due to the loss of the parietal cells.
It is also increasingly being seen that patients are developing gastric atrophy, leading to achlorhydria, following longterm use of acid-suppressant medicines. Surely, if the parietal cells have atrophied, they are not producing either hydrochloric acid or IF so there is no way for these patients to access their biliary B12?
It is also thought that patients whose sole problem is achlorhydria can access 'free' B12 in supplements since hydrochloric acid is not necessary to do so, but it is claimed that they can also access their liver store. However, no explanation is given of how this can be done since they will need IF to access the biliary B12 and, of course, if their parietal cells have atrophied then they are not producing IF.
I had asked a prominent UK gastroenterologist to comment on this subject and, although he agreed to do so, he has not given his comments so I can only assume he had no answer. I would really appreciate to hear what others think about this issue.
