The Mechanism for Omeprazole Induced Vitamin B12 Deficiency and Risk of Developing Macrocytic Anemia, Hyperhomocysteinemia, and/or Neuropathy
The Mechanism for Omeprazole Induced Vitamin B12 Deficiency and Risk of Developing Macrocytic Anemia, Hyperhomocysteinemia, and/or Neuropathy
Summary:
The chronic use of proton pump inhibitors such as omeprazole (Prilosec) is fairly common in medical practice especially for gastroesophageal reflux disease (GERD) or in patients at increased risk of peptic ulcer disease (PUD), but has been associated with causing vitamin B12 deficiency.If vitamin B12 is ingested in its free (or nonprotein bound) form, it will bind to a carrier protein known as R-binders or transcobalamin I that is secreted by both the salivary glands in the oropharynx and the gastric mucosal cells within the stomach.If the vitamin B12 is ingested in its protein bound form, it must first undergo a proteolytic cleavage in the stomach or duodenum where it will bind to an R-binder and enter into the duodenum for further cleavage.Upon entry into the second segment of the duodenum, the pancreas will secrete additional protease which will then degrade the R-binders holding onto the vitamin B12. It is at this point that vitamin B12 will bind to or complex with intrinsic factor for the remainder of its journey to the ileum of the small intestine for absorption.Omeprazole's ability to suppress gastric acid production can impair the conversion of pepsinogen to pepsin, which can affect the ability of protein bound vitamin B12 to be freed for additional preparations for absorption will be compromised.
Editor-in-Chief: Anthony J. Busti, MD, PharmD, FNLA, FAHA
Reviewers: Donald S. Nuzum, PharmD, BCACP, CDE
Last Reviewed: October 2015
MESH Terms & Keywords
Vitamin B12 Deficiency, Proton Pump Inhibitor, Omeprazole, Prilosec, Macrocytic Anemia, Hyperhomocysteinemia, Neuropathy
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