Causes
Most commonly (in temperate climates), the cause for impaired binding of vitamin B12 by intrinsic factor is autoimmune atrophic gastritis, in which autoantibodies are directed against parietal cells (resulting in their loss), as well as against the intrinsic factor itself (rendering it unable to bind B12).
Less frequently, loss of parietal cells may simply be part of a widespread atrophic gastritis of nonautoimmune origin, such as that frequently occurring in elderly people affected with long-standing chronic gastritis of any cause (including Helicobacter pylori infection).
Forms of B12 deficiency other than pernicious anemia must be considered in the differential diagnosis of megaloblastic anemia. For example, a B12-deficient state which causes megaloblastic anemia and which may be mistaken for classical PA may be caused by infection with the tapeworm Diphyllobothrium latum, possibly due to the parasite's competition for B12.
A similar disorder involving impaired B12 absorption can also occur following gastric removal (gastrectomy) or gastric bypass surgery, especially the Roux-en-Y bypass. In this procedure, the stomach is separated into two sections, one a very small pouch for holding small amounts of food, and the other (the remainder of the stomach), which becomes nonfunctional. Therefore, the mucosal cells are no longer available; nor is the required intrinsic factor. This results in inadequate GI absorption of B12, and may result in a syndrome indistinguishable from PA. Gastric bypass or gastrectomy patients must take B12 as in treatment of PA: either oral megadoses, or by injection.
Read more about this topic: Pernicious Anemia