Vitamin B12 cannot be produced by the human body, and must be obtained from the diet. When foods containing B12 are eaten, the vitamin is usually bound to protein and is released by proteases released by the<unk> ncreas into the small bowel. Following its release, most B12 is absorbed by the body in the small bowel (ileum) after binding to a protein known as intrinsic factor. Intrinsic factor is produced by<unk> rietal cells of the gastric mucosa (stomach lining) and the intrinsic factor-B12-complex is absorbed by enterocytes in the ileum's cubam receptors.<unk>  is characterised by B12 deficiency caused by the absence of intrinsic factor. Other disorders that can disrupt the absorption of vitamin B12 in the small intestine include celiac disease, Crohn's disease, and HIV. Atrophic gastritis showing<unk> tchy atrophy of oxyntic mucosa<unk>  may be considered as an end stage of autoimmune atrophic gastritis, a disease characterised by stomach atrophy and the presence of antibodies to<unk> rietal cells and intrinsic factor. Autoimmune atrophic gastritis, is localised to the body of the stomach, where<unk> rietal cells are located. Antibodies to intrinsic factor and<unk> rietal cells cause the destruction of the oxyntic gastric mucosa, in which the<unk> rietal cells are located, leading to the subsequent loss of intrinsic factor synthesis. Without intrinsic factor, the ileum can no longer absorb the B12. Atrophic gastritis is often a precursor to gastric cancer. Although the exact role of Helicobacter pylori infection in<unk>  remains controversial, evidence indicates H. pylori is involved in the<unk> thogenesis of the disease. A long-standing H. pylori infection may cause gastric autoimmunity by a mechanism known as molecular mimicry. Antibodies produced by the immune system can be cross-reactive and may bind to both H. pylori antigens and those found in the gastric mucosa. The antibodies are produced by activated B cells that recognise both<unk> thogen and self-derived peptides. The autoantigens believed to cause the autoreactivity are the alpha and beta subunits of the sodium-potassium pump. In a study, B12 deficiency caused by Helicobacter pylori was positively correlated with CagA positivity and gastric inflammatory activity, rather than gastric atrophy. Less commonly, H. pylori and Zollinger-Ellison syndrome may cause a form of nonautoimmune gastritis that can lead to<unk> . Impaired B12 absorption can also occur following gastric removal (gastrectomy) or gastric bypass surgery. In these surgeries, either the<unk> rts of the stomach that produce gastric secretions are removed or they are bypassed. This means intrinsic factor, as well as other factors required for B12 absorption, are not available. However, B12 deficiency after gastric surgery does not usually become a clinical issue. This is probably because the body stores many years' worth of B12 in the liver and gastric surgery<unk> tients are adequately supplemented with the vitamin. Although no specific<unk>  susceptibility genes have been identified, a genetic factor likely is involved in the disease.<unk>  is often found in conjunction with other autoimmune disorders, suggesting common autoimmune susceptibility genes may be a causative factor. In spite of that, previous family studies and case reports focusing on<unk>  have suggested that there is a tendency of genetic heritance of<unk>  in<unk> rticular, and close relatives of the<unk> <unk> tients seem to have higher incidence of<unk>  and associated<unk>  conditions. Moreover, it was further indicated that the formation of antibodies to gastric cells was autosomal dominant gene determined, and the presence of antibodies to the gastric cells might not be necessarily related to the occurrence of atrophic gastritis related to<unk> .
Pernicious anemia
Zinc deficiency
Iron poisoning
Zinc toxicity
Hookworm infection
Fruit allergy
Pinworm infection
African iron overload