B12 deficiency and autoimmune disorders

It seems strange that B12 deficiency is involved in both under-activation and over-activation of the immune system. However, it's true, because one cause of vitamin B12 deficiency is pernicious anemia, an autoimmune disorder in which the body attacks its own cells.

Most physicians incorrectly use the term pernicious anemia. This diagnosis is properly reserved for the autoimmune phenomenon that results in disease and dysfunction of the stomach (gastric atrophy, poor stomach acid production, intrinsic factor deficiency, and gastric autoantibodies directed against intrinsic factor and/or parietal cells). Therefore, a person who has a B12 deficiency stemming from Crohn's disease, gastric bypass surgery, celiac disease, or dietary causes does not have "pernicious anemia." (However, patients as well as physicians need to understand that no matter what the cause of B12 deficiency, it can be just as deadly or "pernicious" if not diagnosed and treated. Cobalamin deficiency is cobalamin deficiency, and all forms must be treated and their underlying causes identified.)

Autoimmune pernicious anemia is a condition in which the stomach lining that contains the parietal cells is destroyed through an autoimmune mechanism. The parietal cells secrete intrinsic factor, which is necessary for B12 absorption. Without intrinsic factor, B12 deficiency ensues. It is thought that this failure of intrinsic factor secretion is a result of gastric mucosal atrophy (wasting of the stomach lining). The gastric atrophy is caused by immune destruction of the acid- and pepsin-secreting portions of the stomach lining.

Pernicious anemia patients have poor gastric acid production and often complain of a bloated and prolonged full feeling after eating. Progressive destruction of the parietal cells causes decreased secretion of hydrochloric acid and enzymes required to release food-bound vitamin B12. Over time, this leads to wasting and inflammation of the stomach lining and achlorhydria (no stomach acid). The destruction of the stomach lining is thought to be the end stage of the autoimmune process. Typically, antibodies to parietal cells and/or intrinsic factor are seen in pernicious anemia patients.

New research is questioning whether pernicious anemia is an autoimmune disorder or possibly caused by an infectious disease, Helicobacter pylori (H. pylori). Researchers are investigating the possibility that long-standing H. pylori leads to atrophic gastritis and is the catalyst for the induction of gastric autoimmunity. This new theory is still under debate.24 Regardless of the cause, patients with autoimmune pernicious anemia need monitoring by esophagogastroduodenoscopy (EGD) because of their increased risk for gastric cancer and carcinoids (a type of neuroendocrine tumor). Chronic elevation of the hormone gastrin (which occurs in PA patients) may cause tumors called gastrinomas.

Approximately one in 25 patients with PA develops gastric carcinoids.25 Researchers who followed PA patients for 6.7 years found that those with

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