A 68-year-old patient developed atrophic gastritis and, 2 years later, developed a macrocytic, hyperchromic anemia. His anemia has most likely occurred due to which one of the following reasons?
This patient has trouble absorbing vitamin B12 for two reasons. The first is that the stomach no longer produces adequate levels of intrinsic factor. Atrophic gastritis leads to the loss of the glandular cells of the stomach and replacement of those cells with intestinal and fibrous tissues. This will lead to a loss of function of the stomach cells, and less intrinsic factor will be produced and secreted. Additionally, B12 bound to proteins in the diet will have difficulty in being removed from their carrier proteins because of the lack of stomach acid. After the body's stores of B12 are exhausted (about 2 years), the anemia will develop because of the inability of reticulocytes to grow and divide. The loss of acid would fail to stimulate pancreatic bicarbonate, so the pH would stay the same in the duodenum and would not increase, such that folate absorption continues normally. The terminal ileum is not involved in atrophic gastritis but can be involved in Crohn disease. Iron deficiency would give a microcytic, hypochromic anemia, not the observed anemia. Heme synthesis is not impaired under these conditions.
The atrophic gastritis leads to vitamin B12 malabsorption.
The atrophic gastritis raises the pH in the duodenum, leading to folate malabsorption.
The terminal ileum is also involved, so iron is malabsorbed.
The atrophic gastritis leads to increased red blood cell absorption by the spleen.
Endocrinology